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14,600 | Survivors of ventricular fibrillation have persistent cardiovascular risk factors late in follow-up. | Implantable cardioverter-defibrillators (ICDs) prevent arrhythmic death, but do not modify disease progression. The prevalence of persistent cardiovascular risk factors in patients receiving an ICD and their adherence to optimal pharmacological therapy at late follow-up is unknown. The aim of this study was to assess the prevalence of cardiovascular and specific sudden cardiac arrest (SCA) risk factors, and the pharmacological treatment in ICD recipients who survived SCA caused by ventricular fibrillation (VF).</AbstractText>Cross-sectional study. A total of 100 consecutive ICD patients who survived SCA due to documented VF, not due to a transient or reversible cause or an arrhythmogenic disease, were interviewed and examined at the routine outpatient clinic.</AbstractText>The mean age of the patients was 60 ± 11 years, and they were analysed at a median interval of 1092 days after SCA. The majority of patients had coronary artery disease. The New York Heart Association class at the time of implantation was ≥ II in 62%. A single chamber device was used in 49% and a resynchronization device in 12%. At the routine control, the most prevalent risk factors were overweight or obesity (63%), hypertension (41%), and smoking (16%). Pharmacological therapy was suboptimal in 18-32% of the patients. Eight per cent of the patients had known diabetes and 29% had elevated HbA1c levels. While only 7% had pre-existing overt heart failure, 43% had N-terminal pro-brain natriuretic peptide levels ≥ 100 pmol/l. High sensitivity C-reactive protein was ≥ 3 mg/l in 52% of the patients. Family history was positive for sudden cardiac death (SCD) in 46% of the patients.</AbstractText>Despite regular medical consultation, a large proportion of the patients had persistent cardiovascular risk factors and were often suboptimally treated. Unexpectedly, latent heart failure and unrecognized diabetes are observed in a large proportion of the patients, as well as elevated inflammatory markers. Genetic analysis may be rewarding, as 46% of the patients had a family history of SCD. Full medical attention, optimizing drug therapy, and counselling of these patients is necessary.</AbstractText> |
14,601 | Incidence, prognosis, and factors associated with cardiac arrest in patients hospitalized with acute coronary syndromes (the Global Registry of Acute Coronary Events Registry). | Contemporary data are lacking with respect to the incidence rates of, factors associated with, and impact of cardiac arrest from ventricular fibrillation or tachycardia (VF-CA) on hospital survival in patients admitted with an acute coronary syndrome (ACS). The objectives of this multinational study were to characterize trends in the magnitude of in-hospital VF-CA complicating an ACS and to describe its impact over time on hospital prognosis.</AbstractText>In 59 161 patients enrolled in the Global Registry of Acute Coronary Events Study between 2000 and 2007, we determined the incidence, prognosis, and factors associated with VF-CA.</AbstractText>Overall, 3618 patients (6.2%) developed VF-CA during their hospitalization for an ACS. Incidence rates of VF-CA declined over time. Patients who experienced VF-CA were on average older and had a greater burden of cardiovascular disease, yet were less likely to receive evidence-based cardiac therapies than patients in whom VF-CA did not occur. Hospital death rates were 55.3% and 1.5% in patients with and without VF-CA, respectively. There was a greater than 50% decline in the hospital death rates associated with VF-CA during the years under study. Patients with a VF-CA occurring after 48 h were at especially high risk for dying during hospitalization (82.8%).</AbstractText>Despite reductions in the magnitude of, and short-term mortality from, VF-CA, VF-CA continues to exert an adverse effect on survival among patients hospitalized with an ACS. Opportunities exist to improve the identification and treatment of ACS patients at risk for VF-CA to reduce the incidence of, and mortality from, this serious arrhythmic disturbance.</AbstractText> |
14,602 | A novel gain-of-function KCNJ2 mutation associated with short-QT syndrome impairs inward rectification of Kir2.1 currents. | Short-QT syndrome (SQTS) is a recently recognized disorder associated with atrial fibrillation (AF) and sudden death due to ventricular arrhythmias. Mutations in several ion channel genes have been linked to SQTS; however, the mechanism remains unclear. This study describes a novel heterozygous gain-of-function mutation in the inward rectifier potassium channel gene, KCNJ2, identified in SQTS.</AbstractText>We studied an 8-year-old girl with a markedly short-QT interval (QT = 172 ms, QTc = 194 ms) who suffered from paroxysmal AF. Mutational analysis identified a novel heterozygous KCNJ2 mutation, M301K. Functional assays displayed no Kir2.1 currents when M301K channels were expressed alone. However, co-expression of wild-type (WT) with M301K resulted in larger outward currents than the WT at more than -30 mV. These results suggest a gain-of-function type modulation due to decreased inward rectification. Furthermore, we analysed the functional significance of the amino acid charge at M301 (neutral) by changing the residue. As with M301K, in M301R (positive), the homozygous channels were non-functional, whereas the heterozygous channels demonstrated decreased inward rectification. Meanwhile, the currents recorded in M301A (neutral) showed normal inward rectification under both homo- and heterozygous conditions. Heterozygous overexpression of WT and M301K in neonatal rat ventricular myocytes exhibited markedly shorter action potential durations than the WT alone.</AbstractText>In this study, we identified a novel KCNJ2 gain-of-function mutation, M301K, associated with SQTS. Functional assays revealed no functional currents in the homozygous channels, whereas impaired inward rectification demonstrated under the heterozygous condition resulted in larger outward currents, which is a novel mechanism predisposing SQTS.</AbstractText> |
14,603 | [The effects of mild hypothermia on cardiac function and myocardial structure in a rabbits model of ventricular fibrillation after restoration of spontaneous circulation]. | To examine the impact of mild hypothermia on cardiac function, myocardial tissue integrity, and 48 hours mortality in a rabbits model of ventricular fibrillation after restoration of spontaneous circulation (ROSC).</AbstractText>The rabbits were randomly divided into four groups: normothermic post ROSC (NTPR, n = 10), mild hypothermia post ROSC (HTPR, n = 10), normothermic control (NTC, n = 8) and mild hypothermia control (HTC, n = 8). Ventricular fibrillation was induced by trans-epicardium electric-shook with alternating current in all the animals and ROSC was achieved through administration of adrenaline (i.v.) and artificial ventilation in group NTPR and HTPR. The body temperature of the animals was kept either at (39.0 ± 0.5) centigrade (NTPR and NTC) or (33.5 ± 0.5) centigrade (HTPR and HTC) for 4 hours after surgery for hemodynamic index data collection 0.5, 1, 2, 3 and 4 hours after surgery, 48 hours later, the mortality in the animals was recorded, and myocardial tissue samples were collected from survived animals for morphological examination by light and electric microscopy and analysis of apoptosis by terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL) staining. The content of ATP, ADP and AMP in the tissue samples was measured by high performance liquid chromatography (HPLC) for the calculation of energy charges (EC).</AbstractText>(1)Hemodynamic indexes: as compared to the NTC group, HTC group exhibited significantly lower levels of heart rate (HR) and -dp/dt max in all the time points. No significant difference between the two groups in the levels of +dp/dt max and mean artery pressure (MAP) was found in all the time points but 0.5 hour. There was no significant difference in the levels of left ventricular end-diastolic pressure (LVEDP), left ventricular end-systolic pressure (LVESP), and femoral artery blood pressure between the two groups.(2) In comparison with NTPR group, HTPR group exhibited significantly (all P < 0.05) lower levels of HR (bpm) and -dp/dt max in all time points (ROSC 0.5, 1, 2, 3, 4 hours: HR 216.5 ± 33.3 vs. 292.9 ± 38.4, 218.2 ± 28.0 vs. 294.3 ± 37.0, 227.5 ± 25.4 vs. 291.4 ± 25.3, 232.4 ± 27.4 vs. 278.1 ± 30.8, 230.6 ± 22.0 vs. 285.1 ± 38.2; -dp/dt max 1847.1 ± 241.2 vs. 2383.3 ± 470.9, 1860.7 ± 167.8 vs. 2154.6 ± 319.5, 1822.3 ± 389.7 vs. 2239.7 ± 379.0, 1950.6 ± 412.9 vs. 2229.6 ± 392.4, 1875.7 ± 555.6 vs. 2396.7 ± 420.1). There was no significant difference between the two groups in the levels of LVEDP, +dp/dt max, LVESP, and femoral artery blood pressure. (3)Optical and electron microscopy revealed myocardium injury in samples from animals underwent ROSC. However, in comparison with the NTPR group, samples from HTPR group exhibited less damage to the myocardium structure. (4) Apoptosis index (AI) of myocardium was significantly (P < 0.05) higher in NTPR group (42.02%) than in HTPR group (26.39%). (5) Tests of myocardial energy: ATP level (μmol/g) in HTPR was significantly (P < 0.05) higher than NTPR (0.97 ± 0.26 vs. 0.65 ± 0.16). EC in NTPR was significant lower than it in two control groups [(0.33 ± 0.13)% vs. (0.52 ± 0.12)%, (0.55 ± 0.06)%, both P < 0.05], whereas no such difference was found between HTPR [(0.41 ± 0.12)%] and two control groups. (6) 48 hours survival rate in HTPR group was significantly higher (P = 0.043) as compared to NTPR group (100% vs. 60%).</AbstractText>Myocardial dysfunction and myocardium tissue injury both develop in post-resuscitation rabbits with ventricular fibrillation. In these animals, reducing body temperature to the level of mild hypothermia after ROSC may improve the 48 hours survival rate, probably via mechanisms that suppress myocardial cell apoptosis. In our study, such intervention produced no obvious negative impact neither on the cardiac function nor hemodynamics.</AbstractText> |
14,604 | A specific sign for differential diagnosis of atypical atrioventricular nodal reentrant tachycardia from atrial tachycardia. | Narrow QRS tachycardia with atrial activation occurring before ventricular activation was induced in a 34-year-old woman with dilated cardiomyopathy. During tachycardia late ventricular extrastimulus delivered when His bundle was refractory failed to reset the tachycardia while early ventricular extrastimulus caused paradoxical delay of the subsequent atrial response and terminated the tachycardia with a QRS not being followed by an atrial response. This is a rare but specific sign for excluding atrial reentry as the mechanism of tachycardia when P wave or atrial activation is registered before QRS response. |
14,605 | Role of the alternans of action potential duration and aconitine-induced arrhythmias in isolated rabbit hearts. | Under conditions of Na(+) channel hyperactivation with aconitine, the changes in action potential duration (APD) and the restitution characteristics have not been well defined in the context of aconitine-induced arrhythmogenesis. Optical mapping of voltage using RH237 was performed with eight extracted rabbit hearts that were perfused using the Langendorff system. The characteristics of APD restitution were assessed using the steady-state pacing protocol at baseline and 0.1 µM aconitine concentration. In addition, pseudo-ECG was analyzed at baseline, and with 0.1 and 1.0 µM of aconitine infusion respectively. Triggered activity was not shown in dose of 0.1 µM aconitine but overtly presented in 1.0 µM of aconitine. The slopes of the dynamic APD restitution curves were significantly steeper with 0.1 µM of aconitine than at baseline. With aconitine administration, the cycle length of initiation of APD alternans was significantly longer than at baseline (287.5 ± 9.6 vs 247.5 ± 15.0 msec, P = 0.016). The functional reentry following regional conduction block appears with the progression of APD alternans. Ventricular fibrillation is induced reproducibly at pacing cycle length showing a 2:1 conduction block. Low-dose aconitine produces arrhythmogenesis at an increasing restitution slope with APD alternans as well as regional conduction block that proceeds to functional reentry. |
14,606 | Transmyocardial drilling revascularization combined with heparinized bFGF-incorporating stent activates resident cardiac stem cells via SDF-1/CXCR4 axis. | To investigate whether transmyocardial drilling revascularization combined with heparinized basic fibroblast growth factor (bFGF)-incorporating degradable stent implantation (TMDRSI) can promote myocardial regeneration after acute myocardial infarction (AMI).</AbstractText>A model of AMI was generated by ligating the mid-third of left anterior descending artery (LAD) of miniswine. After 6 h, the animals were divided into none-treatment (control) group (n=6) and TMDRSI group (n=6). For TMDRSI group, two channels with 3.5 mm in diameter were established by a self-made drill in the AMI region, into which a stent was implanted. Expression of stromal cell-derived factor-1(α) (SDF-1(α)) and CXC chemokine receptor 4 (CXCR4), cardiac stem cell (CSC)-mediated myocardial regeneration, myocardial apoptosis, myocardial viability, and cardiac function were assessed at various time-points.</AbstractText>Six weeks after the operation, CSCs were found to have differentiated into cardiomyocytes to repair the infarcted myocardium, and all above indices showed much improvement in the TMDRSI group compared with the control group (P<0.001).</AbstractText>The new method has shown to be capable of promoting CSCs proliferation and differentiation into cardiomyocytes through activating the SDF-1/CXCR4 axis, while inhibiting myocardial apoptosis, thereby enhancing myocardial regeneration following AMI and improving cardiac function. This may provide a new strategy for myocardial regeneration following AMI.</AbstractText>Copyright © 2011 Elsevier Inc. All rights reserved.</CopyrightInformation> |
14,607 | Psychic trauma as cause of death. | of study Psychic trauma is described as the action of 'an emotionally overwhelming factor' capable of causing neurovegetative alterations leading to transitory or persisting bodily changes. The medico-legal concept of psychic trauma and its definition as a cause in penal cases is debated. The authors present three cases of death after psychic trauma, and discuss the definition of cause within the penal ambit of identified 'emotionally overwhelming factors'.</AbstractText>The methodological approach to ascertainment and criterion-based assessment in each case involved the following phases: (1) examination of circumstantial evidence, clinical records and documentation; (2) autopsy; (3) ascertainment of cause of death; and (4) ascertainment of psychic trauma, and its coexisting relationship with the cause of death.</AbstractText>The results and assessment of each of the three cases are discussed from the viewpoint of the causal connotation of psychic trauma. In the cases presented, psychic trauma caused death, as deduced from assessment of the type of externally caused emotional insult, the subjects' personal characteristics and the circumstances of the event causing death.</AbstractText>In cases of death due to psychic trauma, careful methodological ascertainment is essential, with the double aim of defining 'emotionally overwhelming factors' as a significant cause of death from the penal point of view, and of identifying the responsibility of third parties involved in the death event and associated dynamics of homicide.</AbstractText> |
14,608 | New methods for the analysis of heartbeat behavior in risk stratification. | Developing better methods for risk stratification for tachyarrhythmic sudden cardiac remains a major challenge for physicians and scientists. Since the transition from sinus rhythm to ventricular tachycardia/fibrillation happens by different mechanisms in different people, it is unrealistic to think that a single measure will be adequate to provide a good index for risk stratification. We analyze the dynamical properties of ventricular premature complexes over 24 h in an effort to understand the underlying mechanisms of ventricular arrhythmias and to better understand the arrhythmias that occur in individual patients. Two dimensional density plots, called heartprints, correlate characteristic features of the dynamics of premature ventricular complexes and the sinus rate. Heartprints show distinctive characteristics in individual patients. Based on a better understanding of the natures of transitions from sinus rhythm to sudden cardiac and the mechanisms of arrhythmia prior to cardiac arrest, it should be possible to develop better methods for risk stratification. |
14,609 | Augmented single-unit muscle sympathetic nerve activity in heart failure with chronic atrial fibrillation. | Atrial fibrillation (AF) is a common complication in heart failure (HF) patients. However, it remains unclear whether irregular ventricular response patterns induced by AF increase sympathetic nerve activity. We measured resting multi- and single-unit muscle sympathetic nerve activity (MSNA) in 21 age-matched HF patients with chronic AF (n = 11) rhythm or sinus rhythm (SR, n = 10). The multi-unit MSNA, which was expressed as total activity, was similar between HF + AF patients and HF + SR patients. However, the single-unit MSNA in HF + AF patients was significantly greater than that in HF + SR patients (62 ± 9 spikes min(-1) vs. 42 ± 4 spikes min(-1), P < 0.05). Moreover, the incidence of multiple firing of single-unit MSNA within a given burst was augmented in HF + AF patients as compared with HF + SR patients (48 ± 8% vs. 26 ± 3%, P < 0.01). A significant negative relationship was observed between the reduced diastolic pressure induced by a prolonged cardiac interval in AF subjects and single-unit MSNA frequency within one cardiac interval in each HF + AF subject. The firing characteristics of single-unit MSNA were different between HF patients with AF and HF patients with SR; particularly, those with a prolonged long RR interval showed multiple firings of single-unit MSNA. These findings suggest that AF per se leads to the instantaneous augmentation of single-unit MSNA induced by decreased diastolic pressure, which might partially contribute to disease progression in HF patients. |
14,610 | Long-term outcomes in hypertrophic cardiomyopathy caused by mutations in the cardiac troponin T gene. | Hypertrophic cardiomyopathy caused by mutations in the cardiac troponin T gene (TNNT2) has been associated with a high risk of sudden cardiac death (SCD) and mild left ventricular hypertrophy. However, previous studies are limited by sample size, cross-sectional design, and few data in relatives.</AbstractText>Five hundred fifty-two unrelated hypertrophic cardiomyopathy probands were screened for TNNT2 mutations. First-degree relatives were invited for clinical and genetic evaluation. Ninety-two individuals (20 probands and 72 relatives) carried TNNT2 mutations (51 [55%] male; 30±17 years). ECGs and echo were available in 87 (95%) and 88 (96%) individuals, respectively. ECG was normal in 13 (68%) children (<16 years) and 13 (19%) adults. Echo was normal in 18 (90%) children and 16 (24%) adults; 7 (10%) adults had a normal ECG and echo. Thirteen (65%) of 20 families had a history of SCD. Follow-up was available for 75 patients (mean, 9.9±5.2 years); 2 of 16 adults and 2 of 18 children with normal echoes developed left ventricular hypertrophy. Twenty-three (22%) received an implantable cardioverter-defibrillator (20 for primary prophylaxis). One child and 3 adults died of SCD and 2 adults were resuscitated from ventricular fibrillation. One patient had an appropriate implantable cardioverter-defibrillator discharge. The rate of cardiovascular death, transplant, and implantable cardioverter-defibrillator discharge was 1.6% (0.016 person/y; 95% confidence interval, 0.83-2.79%), and SCD 0.93% (0.0093 person/y; 95% confidence interval, 0.37-1.92%).</AbstractText>Left ventricular hypertrophy is rare in children with TNNT2 mutations. Left ventricular hypertrophy is absent in the minority of adults, but most have an abnormal ECG. Despite adverse family histories, the rate of cardiovascular death during follow-up was similar to that reported in large referral populations.</AbstractText> |
14,611 | Panoramic optical mapping shows wavebreak at a consistent anatomical site at the onset of ventricular fibrillation. | The first seconds of ventricular fibrillation (VF) are well organized and can consist of just one to two rotating waves (rotors). New rotors are spawned when local propagation block causes wave fragmentation. We hypothesized that this process, which leads to fully developed VF, begins at a consistent anatomic site.</AbstractText>We initiated VF with a stimulus timed to the local T-wave in 10 isolated pig hearts. Hearts were stained with a voltage-sensitive dye and four video cameras recorded electrical propagation panoramically across the epicardium. In each VF episode, we identified the position of the first wavebreak event that produced new rotor(s) that persisted for at least one cycle. The first such wavebreak occurred along the anterior right ventricular insertion (ARVI) in 26 of 32 VF episodes. In these episodes, wavebreak sites were 6 ± 4 mm from the midline of the ARVI. In the remaining 6 episodes, wavebreak sites were 24 ± 5 mm from the midline on either the LV or RV. During rapid pacing, conduction speed was locally depressed at the ARVI when waves crossed parallel to the midline. Action potential duration (APD) was slightly longer (2.2 ± 2.1 ms) at the ARVI compared with other sites (P< 0.01). Temporal APD alternans were small and not unique to the break site, suggesting that dynamic APD properties were not the cause of wavebreak.</AbstractText>The ARVI is the dominant site for wavebreak at the onset of VF in normal myocardium. This may be due to the anatomic complexity of the region.</AbstractText> |
14,612 | Anaesthesia for cardioversion: a prospective randomised comparison of propofol and etomidate combined with fentanyl. | External electrical cardioversion is mostly performed solely under sedatives or hypnotics, although the procedure is painful. The aim of this prospective randomised study was to compare two anaesthetic protocols that included analgesia.</AbstractText>Patients with persistent atrial fibrillation were randomised to receive intravenously either fentanyl 50 μg and propofol 0.5 mg/kg (group P) or fentanyl 50 μg and etomidate 0.1 mg/kg (group E), while breathing spontaneously 100% oxygen. In the case of inadequate anaesthesia, repeated doses of 20 mg propofol (group P) or 4 mg etomidate (group E) were given as often as necessary until loss of eyelid reflex. Cardioversion was achieved with an extracardiac biphasic electrical shock ranging from 200 to 300 J, performed three times at most.</AbstractText>Forty-six patients (25 in group P, 21 in group E), aged 64 ± 9 years, were enrolled in the study. There were no differences between the study groups concerning left ventricular ejection fraction, the dimension of the left atrium, the number of shocks needed or the number of unsuccessful cardioversions. Patients in group E had a shorter time from injection of the induction agents until loss of consciousness (49 vs. 118 s, p=0.003) and until the first shock was given (61 vs. 135 s, p=0.004). Systolic blood pressure decreased significantly (repeated measurements ANOVA with Bonferroni adjustment) in group P when the baseline value was compared to that after anaesthesia induction (mean decrease 15.2 mmHg, 95% CI 5.6-24.8 mmHg, p=0.001) and to the value after recovery (mean decrease 15.2 mmHg, 95% CI 4.8-25.7 mmHg, p=0.002). Manual ventilation was required in 7 and 9 patients in groups P and E, respectively (p=0.360).</AbstractText>Both anaesthetic regimens provided excellent conditions for external electric cardioversion. In addition, etomidate in combination with fentanyl had a shorter induction time and ensured haemodynamic stability.</AbstractText> |
14,613 | Sudden cardiac arrest and sudden cardiac death on dialysis: Epidemiology, evaluation, treatment, and prevention. | Sudden cardiac death is the most common cause of death in dialysis patients and is usually preceded by sudden cardiac arrest due to ventricular tachycardia or ventricular fibrillation. A variety of risk factors have been identified that predispose the sudden cardiac arrest and sudden cardiac death in dialysis patients. Primary prevention of sudden cardiac arrest in dialysis patients may be accomplished by avoiding the use of low potassium dialysate. Pharmacotherapy with beta-blockers angiotensin converting enzyme inhibitors and angiotensin receptor blockers and use of implantable cardioverter defibrillators (ICDs) may also prevent sudden cardiac arrest and sudden cardiac death in high-risk dialysis patients. Secondary prevention of sudden cardiac death may be accomplished by similar pharmacotherapy and by the use of ICDs. Indications for ICD use in dialysis patients are similar to those for nondialysis patients; however, survival rates following ICD implantation in dialysis patients are substantially lower than in non-dialysis patients. |
14,614 | The relationship between D-dimer level and the development of atrial fibrillation in patients with systolic heart failure. | Heart failure (HF) is one of the most common and leading cause of death worldwide. Clinical trials provide evidence that the development of atrial fibrillation (AF) is a marker of poor prognosis in patients with HF. Furthermore, elevated D-dimer level is associated with increased cardiovascular mortality independent of AF in HF patients. We investigated whether plasma D-dimer levels in patients with hospitalized systolic HF could predict development of AF. A total of 150 consecutive patients with sinus rhythm who admitted to the emergency department with hospitalized systolic HF were evaluated. All hospitalized patients were obtained D-dimer levels within the first 24 h following admission. Atrial fibrillation developed in 31 (20.7%) patients during follow-up period of 6.3 ± 5 months. Patients who developed atrial fibrillation had significantly increased levels of D-dimer [608 (339-1,022) ng/ml versus 1,100 (608-2,599) ng/ml, P = 0.001]. Optimal cut-off level of D-dimer to predict development of AF was found to be >792 ng/ml. D-dimer >792 ng/ml, right ventricular dilatation, age, systolic pulmonary pressure, left atrium size, moderate to severe tricuspid regurgitation, and beta blocker usage were found to have prognostic significance in univariate analysis. In multivariate Cox proportional-hazards model, D-dimer levels >792 ng/ml (HR = 3.019, P = 0.006), and right ventricular dilatation (HR = 8.676, P = 0.003) were associated with an increased risk of new-onset AF. In conclusion, D-dimer could predict development of AF in patients with hospitalized systolic HF. |
14,615 | [Practical questions around individual with a pacemaker or an implantable cardioverter defibrillator]. | An individual with a pacemaker can ask his GP for information about potential problems associated with the device. Should a pacemaker continue to be used by end-of-life patients? Should a pacemaker be stopped in a limited care situation? What precautions should be taken when treating a patient with a pacemaker? Pacemakers and implantable defibrillators are sensitive to electromagnetic interference (EMI). Medically, MRIs are theoretically contraindicated, even though examinations could be performed without a major problem, and special precautions should be taken when using an electrosurgical cutter or radiotherapy. In case of death, a doctor or embalmer must remove the patient's pacemaker due to its risk of explosion during cremation. Doctors who sign cremation forms have a legal obligation to provide such information. It may affect an employee's ability to work. Are there some professions that are not well suited for individuals with a pacemaker? |
14,616 | Prognostic value of exercise echocardiography in patients with hypertrophic cardiomyopathy. | Although exercise echocardiography may assess left ventricular (LV) function and LV outflow tract (LVOT) gradients during exercise in patients with hypertrophic cardiomyopathy (HCM), its value for predicting outcomes has not been studied. The aim of this study was to determine whether exercise echocardiography predicts outcomes in patients with HCM.</AbstractText>LV function and LVOT gradients were evaluated during exercise echocardiography in 239 patients with HCM.</AbstractText>Sixty patients (25.1%) had LVOT obstruction at rest, and 43 (18%) developed exercise-induced LVOT obstruction. The mean resting LV ejection fraction was 69 ± 9%, and the mean resting wall motion score index was 1.00 ± 0.06. Wall motion abnormalities during exercise were seen in 19 patients (7.9%). During follow-up of 4.1 ± 2.6 years, 19 patients had hard events (cardiac death, cardiac transplantation, appropriate discharge of a defibrillator, stroke, myocardial infarction, or hospitalization for heart failure), and 41 patients had composite end points of hard or soft events (including atrial fibrillation and syncope). Exercise wall motion abnormalities occurred in 31.5% of patients with hard events compared with 5.9% of patients without hard events (P < .001). After adjustment, LV wall thickness (hazard ratio [HR], 1.13; 95% confidence interval [CI], 1.05-1.21; P = .002), resting wall motion score index (HR, 21.59; 95% CI, 2.38-196.1, P = .006), and metabolic equivalents (HR, 0.74; 95% CI, 0.63-0.88; P = .001) remained independent predictors of hard events. Change in wall motion score index was also independently associated with hard events (HR, 52.30; 95% CI, 3.81-718.5; P = .003) and with the composite end point (HR, 39.51; 95% CI, 3.79-412.4; P = .002). LVOT obstruction was not associated with either end point.</AbstractText>Assessment of exercise capacity and LV systolic function during exercise echocardiography may have a role in risk stratification of patients with HCM.</AbstractText>Copyright © 2012 American Society of Echocardiography. Published by Mosby, Inc. All rights reserved.</CopyrightInformation> |
14,617 | Rationale and design of the treatment of preserved cardiac function heart failure with an aldosterone antagonist trial: a randomized, controlled study of spironolactone in patients with symptomatic heart failure and preserved ejection fraction. | Despite increasing prevalence of heart failure (HF) in patients with preserved ejection fraction (PEF), there are no available therapies proven to reduce morbidity and mortality. Aldosterone, a potent stimulator of myocardial and vascular fibrosis, may be a key mediator of HF progression in this population and is therefore an important therapeutic target.</AbstractText>The TOPCAT trial is designed to evaluate the effect of spironolactone, an aldosterone antagonist, on morbidity, mortality, and quality of life in patients with HF-PEF.</AbstractText>Up to 3,515 patients with HF-PEF will be randomized in double-blind fashion to treatment with spironolactone (target dose 30 mg daily) or matching placebo. Eligible patients include those with age ≥50 years, left ventricular ejection fraction ≥45%, symptomatic HF, and either a hospitalization for HF within the prior year or an elevated natriuretic peptide level (B-type natriuretic peptide ≥100 pg/mL or N-terminal pro-B-type natriuretic peptide ≥360 pg/mL) within the 60 days before randomization. Patients with uncontrolled hypertension and those with known infiltrative or hypertrophic cardiomyopathy are excluded. The primary end point is the composite of cardiovascular death, hospitalization for HF, or aborted cardiac arrest. Key secondary end points include quality of life, nonfatal cardiovascular events, and new-onset atrial fibrillation. Ancillary studies of echocardiography, tonometry, and cardiac biomarkers will provide more insight regarding this understudied population and the effects of spironolactone therapy.</AbstractText>TOPCAT is designed to assess definitively the role of spironolactone in the management of HF-PEF.</AbstractText>Copyright © 2011 Mosby, Inc. All rights reserved.</CopyrightInformation> |
14,618 | Electrocardiographic determinants of the polymorphic QRS morphology in idiopathic right ventricular outflow tract tachycardia. | Premature ventricular contractions (PVCs) arising from the right ventricular outflow tract (RVOT) can trigger polymorphic ventricular tachycardia (PVT) or ventricular fibrillation (VF) in patients with no structural heart disease. We aimed to clarify the ECG determinants of the polymorphic QRS morphology in idiopathic RVOT PVT/VF.</AbstractText>The ECG parameters were compared between 18 patients with idiopathic PVT/VF (PVT-group) and 21 with monomorphic VT arising from the RVOT (MVT-group). The coupling interval (CI) of the first VT beat was comparable between the 2 groups. However, the prematurity index (PI) of the first VT beat was smaller in the PVT-group than in the MVT-group (P < 0.001). Furthermore, the QT index, defined as the ratio of the CI to the QT interval of the preceding sinus complex, was also smaller for the PVT/VF in the PVT-group than that for the VT in the MVT-group (P < 0.01). In the PVT-group, the CI of the first VT beat was comparable between that of VT and isolated PVCs, but the PI of the first VT beat was shorter for VT than isolated PVCs (P < 0.05). The PI was the only independent determinant of the polymorphic QRS morphology (odd ratio = 2.198; 95% confidence interval = 1.321-3.659; P = 0.002).</AbstractText>The smaller PIs of the first VT beat may result in a polymorphic QRS morphology.</AbstractText>© 2011 Wiley Periodicals, Inc.</CopyrightInformation> |
14,619 | The effect of atrial preference pacing on paroxysmal atrial fibrillation incidence in myotonic dystrophy type 1 patients: a prospective, randomized, single-bind cross-over study. | Atrial Preference Pacing (APP) is a pacemaker (PM) algorithm that supports a continuous atrial stimulation instead of a spontaneous atrial rhythm to prevent supraventricular tachyarrhythmias. The role of the APP in the prevention of atrial fibrillation (AF) is still controversial. The aim of our study was to evaluate the effect of preventive atrial pacing on AF incidence in myotonic dystrophy type I patients during a 12-month follow-up period.</AbstractText>We studied 40 patients with myotonic dystrophy type 1 (MD1) who underwent dual-chamber PM implantation for first- and second-degree atrioventricular block. After a 1-month stabilization period, they were randomized to APP algorithm programmed OFF or ON for 6 months each, using a cross-over design. The number of AF episodes during active treatment (APP ON phases) was lower than those registered during no treatment (APP OFF phases). No statistically significant difference was found in AF episodes duration between the two phases. During the APP OFF phases and APP ON phases, the atrial pacing percentage was 0 and 98%, respectively, while the ventricular pacing percentage did not show statistically significant difference (10 vs. 8%, P =0.2). Atrial premature beats count was significantly greater during APP OFF phases than during APP ON phases. Lead parameters remained stable over time and there were no lead-related complications.</AbstractText>Based on these 12-month follow-up data, it is concluded that APP is an efficacy algorithm for preventing paroxysmal AF in MD1 patients who underwent dual-chamber PM implantation for atrioventricular conduction disorders.</AbstractText> |
14,620 | [Problems with placement and using of automated external defibrillators in Czech Republic]. | The use of automated external defibrillators improves the survival of adults who suffer from cardiopulmonary arrest. Automated external defibrillators detect ventricular fibrillation with almost perfect sensitivity and specificity. Authors describe the use of automated external defibrillator during cardiopulmonary resuscitation in a patient with sudden cardiac arrest during ice-hockey match. The article reports also the use of automated external defibrillators in children. |
14,621 | Alterations of the intercellular coupling protein, connexin-43, during ventricular fibrillation and sinus rhythm restoration demonstrated in male and female rat hearts: A pilot study. | Ventricular fibrillation (VF) is a life-threatening arrhythmia, whose occurrence precedes the development of myocardial arrhythmogenic substrate resulting from either chronic or acute pathophysiological conditions. The authors' previous and current studies suggest that downregulated and/or heterogeneously distributed cell-to-cell coupling protein - connexin-43 (Cx43) - facilitates the development of malignant arrhythmias. It was hypothesized that VF itself deteriorates Cx43, and may hamper cardioversion into sinus rhythm. The purpose of the present study was to examine whether myocardial expression and the phosphorylated status of Cx43 is altered due to VF and during sinus rhythm restoration. Experiments were performed using 10-month-old male and female Wistar rats. Isolated Langendorff-mode-perfused rat hearts were subjected to the following events: basal condition, electrically induced VF lasting 2 min, electrically induced VF lasting 10 min, and sustained VF followed by spontaneous sinus rhythm restoration due to transient stop perfusion. The hearts were snap frozen at each event; ventricular tissue was sent for Cx43 immunoblotting using rabbit antiCx43 polyclonal antibody to detect phosphorylated (P-Cx43) as well as unphosphorylated (noP-Cx43) forms of Cx43, and mouse antiCx43 monoclonal antibody to detect noP-Cx43 only. Compared with basal conditions, total Cx43 expression did not change during experiments in either male or female rat hearts. However, P-Cx43 and the ratio of P-Cx43 to total Cx43 decreased significantly due to VF lasting 2 min and 10 min in male rat hearts only. In parallel, there was a significant increase in noP-Cx43 due to VF lasting 2 min and 10 min in male rat hearts only. Surprisingly, an enhancement of noP-Cx43 linked with suppression of P-Cx43 was detected during stop perfusion-induced termination of VF lasting 2 min, followed by sinus rhythm restoration in both male and female rat hearts. Sinus rhythm was not restored after 10 min of VF, which caused pronounced Cx43 dephosphorylation. In conclusion, there is a downregulation of Cx43 due to sustaining of VF, and it occurs earlier in male rat hearts compared with female rat hearts. It appears that transient no-flow-related inhibition of cell-to-cell coupling, as indicated by an increase in nonP-Cx43, can terminate VF followed by sinus rhythm restoration depending on the degree of previous Cx43 downregulation. |
14,622 | Effects of theophylline on anesthetized malignant hyperthermia-susceptible pigs. | Theophylline was shown to induce contracture development in porcine malignant hyperthermia (MH) susceptible (MHS) skeletal muscles in vitro. The purpose of the current study was to investigate the in vivo effects of theophylline in MHS and MH normal (MHN) swine.</AbstractText>MH-trigger-free general anesthesia was performed in MHS and MHN swine. Theophylline was administered intravenously in cumulative doses up to 93.5 mg·kg⁻¹. The clinical occurrence of MH was defined by changes of central-venous pCO₂, central-venous pH, and body core temperature.</AbstractText>Theophylline induced comparable clinical alterations in the anesthetized MHS and MHN swine, especially in regard to hemodynamic data. No pig developed hypermetabolism and/or MH according to defined criteria. All animals died with tachycardia followed by ventricular fibrillation.</AbstractText>The cumulative theophylline doses used in this study were much higher than doses used therapeutically in humans, as demonstrated by measured blood concentrations. Theophylline is thus not a trigger of MH in genetically determined swine.</AbstractText> |
14,623 | Left atrial speckle tracking analysis in patients with mitral insufficiency and history of paroxysmal atrial fibrillation. | The occurrence of atrial fibrillation (AF), especially in patients with mitral regurgitation (MR), is related to the degree of left atrial (LA) myopathy, remodeling and fibrosis, that are responsible of LA electrical inhomogeneity and abnormal conduction velocities. Speckle tracking echocardiography (STE) has recently enabled the quantification of longitudinal myocardial LA deformation dynamics. Our aim was to investigate by STE the effects of the occurrence of paroxysmal AF on LA myocardial deformation, in a population of patients with asymptomatic chronic MR. We compared two groups of a total of 197 patients with MR: 54 with history of paroxysmal AF and 143 with MR alone. Subgroups were created according to MR degree. Peak atrial longitudinal strain (PALS) was measured in all subjects. Values were obtained by averaging all segments (global PALS), measured in the 4-chamber and 2-chamber views. Compared to the mild MR group (46.1 ± 4.9%), global PALS was lower in moderate MR group (22.1 ± 5.8%) and further reduced in the severe MR group (13.9 ± 4.2%; overall P < 0.0001 by ANOVA, P < 0.05 for all pair-wise comparisons). Besides, in each MR group, patients with history of paroxysmal AF presented a global PALS significantly reduced (overall P < 0.0001 by ANOVA). After multivariate analysis, global PALS was significantly and independently associated with paroxysmal AF. STE enables noninvasive quantification of LA dysfunction due to MR and paroxysmal AF. MR have a major negative impact on LA function. In patients with MR, the history of paroxysmal AF is associated to a further impair of LA myocardial reservoir function. |
14,624 | Predicting heart failure outcome from cardiac and comorbid conditions: the 3C-HF score. | Prognostic stratification in heart failure (HF) is crucial to guide clinical management and treatment decision-making. Currently available models to predict HF outcome have multiple limitations. We developed a simple risk stratification model, based on routinely available clinical information including comorbidities, the Cardiac and Comorbid Conditions HF (3C-HF) Score, to predict all-cause 1-year mortality in HF patients.</AbstractText>We recruited in a cohort study 6274 consecutive HF patients at 24 Cardiology and Internal Medicine Units in Europe. 2016 subjects formed the derivation cohort and 4258 the validation cohort. We entered information on cardiac and comorbid candidate prognostic predictors in a multivariable model to predict 1-year outcome.</AbstractText>Median age was 69 years, 35.8% were female, 20.6% had a normal ejection fraction, and 65% had at least one comorbidity. During 5861 person-years follow-up, 12.1% of the patients met the study end-point of all-cause death (n=750) or urgent transplantation (n=9). The variables that contributed to outcome prediction, listed in decreasing discriminating ability, were: New York Heart Association class III-IV, left ventricular ejection fraction <20%, no beta-blocker, no renin-angiotensin system inhibitor, severe valve heart disease, atrial fibrillation, diabetes with micro or macroangiopathy, renal dysfunction, anemia, hypertension and older age. The C statistic for 1-year all-cause mortality was 0.87 for the derivation and 0.82 for the validation cohort.</AbstractText>The 3C-HF score, based on easy-to-obtain cardiac and comorbid conditions and applicable to the 1-year time span, represents a simple and valuable tool to improve the prognostic stratification of HF patients in daily practice.</AbstractText>Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.</CopyrightInformation> |
14,625 | How to establish an arrhythmia unit in the 21st century. | Arrhythmia and cardiac electrophysiology services are an innovative and fast-growing branch of clinical cardiology. Initiating an arrhythmia unit involves proper selection of personnel, as well as technical, structural, and organizational requirements. Proper selection of personnel includes specialized and well-trained physicians, nurses, and medical technicians in the electrophysiology laboratories and on the hospital wards. Standard electrophysiology laboratories must support the full spectrum of catheter-based diagnosis and therapies of cardiac arrhythmias. This includes state-of-the-art fluoroscopy and 3-dimensional mapping systems used during complex procedures such as catheter ablation of atrial fibrillation or ventricular tachycardia. Furthermore, technical requirements need to support pacemaker and defibrillator implantation as one of the core tasks of a specialized arrhythmia unit. Outpatient clinics should fulfill technical capabilities to perform a diverse spectrum of pre-and postinterventional diagnostics, guaranteeing proper patient follow-up. Structural requirements should focus on close physical integration of individual functional units allowing for an effective and safe workflow. Finally, organizational requirements such as networking between arrhythmia specialists and referring physicians and hospitals are essential for patient recruitment and high-quality postdischarge patient care. Regular educational programs for physicians, nurses, and technicians are essential in such an innovative and fast-growing field of cardiology. |
14,626 | Effects of valsartan on ventricular arrhythmia induced by programmed electrical stimulation in rats with myocardial infarction. | The impact of angiotensin II receptor blockers (ARBs) on electrical remodelling after myocardial infarction (MI) remains unclear. The purpose of the present study was to evaluate the effect of valsartan on incidence of ventricular arrhythmia induced by programmed electrical stimulation (PES) and potential link to changes of myocardial connexins (Cx) 43 expression and distribution in MI rats. Fifty-nine rats were randomly divided into three groups: Sham (n = 20), MI (n = 20) and MI + Val (20 mg/kg/day per gavage, n = 19). After eight weeks, the incidence of PES-induced ventricular tachycardia (VT) and fibrillation (VF) was compared among groups. mRNA and protein expressions of Cx43, angiotensin II type 1 receptor (AT1R) in the LV border zone (BZ) and non-infarct zone (NIZ) were determined by real-time PCR and Western blot, respectively. Connexins 43 protein and collagen distribution were examined by immunohistochemistry in BZ and NIZ sections from MI hearts. Valsartan effectively improved the cardiac function, reduced the prolonged QTc (163.7 ± 3.7 msec. versus 177.8 ± 4.5 msec., P < 0.05) after MI and the incidence of VT or VF evoked by PES (21.1% versus 55%, P < 0.05). Angiotensin II type 1 receptor expression was significantly increased in BZ and NIZ sections after MI, which was down-regulated by valsartan. The mRNA and protein expressions of Cx43 in BZ were significantly reduced after MI and up-regulated by valsartan. Increased collagen deposition and reduced Cx43 expression in BZ after MI could be partly attenuated by Valsartan. Valsartan reduced the incidence of PES-induced ventricular arrhythmia, this effect was possibly through modulating the myocardial AT1R and Cx43 expression. |
14,627 | Bilirubin attenuates bufadienolide-induced ventricular arrhythmias and cardiac dysfunction in guinea-pigs by reducing elevated intracellular Na(+) levels. | Bufadienolides, known ligands of the sodium pump, have been shown to inhibit the proliferation of several cancer cell types. However, their development to date as anticancer agents has been impaired by a narrow therapeutic margin resulting from their potential to induce cardiotoxicity. In the present study, we examined the effects of bilirubin, an endogenous antioxidant, on the cardiotoxicity of bufadienolides (derived from toad venom) in guinea-pigs. The results showed that bufadienolides (8 mg/kg) caused ventricular arrhythmias, conduction block, cardiac dysfunction and death in guinea-pigs. Pretreatment with bilirubin (75 and 150 mg/kg) significantly prevented bufadienolide-induced premature ventricular complexes, ventricular tachycardia, ventricular fibrillation and death. Bilirubin also markedly improved the inhibition of cardiac contraction in bufadienolide-treated guinea-pigs as evidenced by increases in left ventricular systolic pressure and decreases in left ventricular diastolic pressure in vivo. Furthermore, bilirubin significantly reduced the intracellular sodium content ([Na(+)]( i )) in ex vivo bufadienolide-stimulated guinea-pig ventricular myocytes loaded with the sodium indicator Sodium Green. An antitumor study showed that bilirubin did not compromise the ability of bufadienolides to inhibit gastric cancer cell MGC-803 proliferation. These results suggested that bilirubin can attenuate bufadienolide-induced arrhythmias and cardiac dysfunction in guinea-pigs by reducing elevated [Na(+)]( i ) and may improve bufadienolide therapeutic index in cancer treatment. |
14,628 | Ablation and pacing: improving brain perfusion and cognitive function in patients with atrial fibrillation and uncontrolled ventricular rates. | The aim of our study was to determine if ablation and pacing improved brain perfusion (BP) and cognitive function (CF) in patients with medically refractory rapidly conducted atrial fibrillation (Med Refr RCAF).</AbstractText>The study included 17 patients with Med Refr RCAF (average age 55.3 ± 4.5 years). All patients underwent brain single photon emission computed tomography scanning with (99m) Tc-hexamethylpropylene amine oxime and comprehensive neuropsychological testing before and after 3 months following pacemaker implantation. The BP was significantly lower in all regions in patients with Med Refr RCAF compared with the control group. The greatest BP decrease was revealed in the inferior frontal (P = 0.002) and posterior parietal (P = 0.024) brain regions. These patients showed cognitive deficit in 94%. There was a direct correlation between BP and CF parameters. Ablation followed by pacemaker implantation had a positive effect on BP and CF in all patients with Med Refr RCAF. Thus, BP increased in the right inferior frontal (P = 0.01), in the left superior frontal (P = 0.007), and in the left temporal (P = 0.005) cortex. These patients demonstrated improvements in immediate and delayed verbal memory, immediate and delayed visual memory, abstract mentation, attention, psychomotor speed, as well as in learning.</AbstractText>Patients with atrial fibrillation and rapid ventricular rates refractory to medical treatment have marked signs of brain hypoperfusion and impaired CF. Ablation and pacing improve left ventricular systolic function, thereby increasing BP and improving CF.</AbstractText>©2011, The Authors. Journal compilation ©2011 Wiley Periodicals, Inc.</CopyrightInformation> |
14,629 | Brain natriuretic peptide and biomarkers of myocardial ischemia increase after defibrillation threshold testing. | During implantable cardioverter defibrillator insertion, induced ventricular fibrillation followed by test shocks (defibrillation threshold testing [DFT]) is utilized to confirm effective device function. The effect of DFT on ventricular function is uncertain. Brain natriuretic peptide (BNP) is a marker of ventricular dysfunction and hemodynamic stress. We hypothesized that DFT causes increased BNP levels.</AbstractText>BNP, creatine kinase, creatine kinase-MB (CK-MB), and troponin I (cTnI) were measured in 31 patients (mean age 71.4 years; 12 women) at preinsertion (T1), at 2-4 hours (T2), and at 8-12 hours (T3) after DFT. Biomarker levels were compared in patients receiving one shock (Group A) or two shocks (Group B).</AbstractText>After DFT all biomarkers increased above baseline levels but did not reach levels diagnostic for myocardial infarction. From T1 to T2, elevations in CK-MB and cTnI occurred in the highest proportion of patients (CK-MB 90% and cTnI 84%). From T1 to T3, elevation in BNP and cTnI were most prevalent (BNP 83% and cTnI 90%). Significant increases were measured in BNP levels from T1 to T3 (P = 0.0003), CK-MB levels from T1 to T2 (P < 0.0001), and cTnI levels from T1 to T2 (P < 0.0001) and from T1 to T3 (P < 0.0001). CK-MB levels did not increase significantly from T1 to T3 (P = 0.51).</AbstractText>BNP levels rise progressively after DFT accompanied by early CK-MB increases and sustained increases in cTnI. These data suggest that DFT is associated with hemodynamic stress and left ventricular dysfunction, as evidenced by increases in BNP.</AbstractText>©2011, The Authors. Journal compilation ©2011 Wiley Periodicals, Inc.</CopyrightInformation> |
14,630 | How healthy were the arteries of Phidippides? | Subacute and chronic cardiac adaptations to marathon running may increase risk for sudden death. Herein, it is proposed that cardiac arrhythmogenic remodeling resulting from prolonged strenuous exertion may also have a systemic vascular component. Marathon running reduces coronary perfusion pressure and causes acute endothelial damage, possibly via altering concentrations of circulating angiogenic growth factors with novel vasoregulatory properties. Marathon runners have increased arterial stiffness and augmented pressure from wave reflections contributing to a widening of pulse pressure. Pulsatile hemodynamics may contribute to target organ damage. Moreover, each of these vascular maladaptations (increased arterial stiffness, augmented pressure from wave reflections, and widened pulse pressure) has been associated with atrial fibrillation and may provide a substrate for lethal arrhythmogenesis in the marathon runner. |
14,631 | Ventricular tachycardia and sudden death after primary PCI-reperfusion therapy: impact on primary prevention of sudden cardiac death. | Current approaches to coronary artery disease (CAD) and acute myocardial infarction (MI) may not be well represented in most primary prevention trials of sudden cardiac death (SCD).</AbstractText>The contemporary and ongoing registry of the Rostock infarction network (Drip & Ship) represents a well-defined cohort of patients subjected to percutaneous coronary intervention (PCI) for ST-elevation infarction (STEMI) and served as the database for both candidates for an ICD for primary prevention of SCD and for sudden death (SCD) or ventricular tachycardia (VT) during follow-up.</AbstractText>A total of 855 consecutive patients were treated with PCI for STEMI or NSTEMI in the region of Rostock (Germany) between 2001 and 2004. While all cause mortality was still 17.2%, the SCD rate was low at 1.3% during 728 ± 366 days of follow-up. Within that time 85 patients (9.9%) developed an indication for ICD therapy due to an impaired LV function (LVEF ≤ 35%) and heart failure. Univariate predictors of an ICD indication were delayed reperfusion (p = 0.001), a high creatine kinase (CK) max (p = 0.009), a persistent wide QRS complex (p = 0.001), previous cerebrovascular events (p = 0.033), and chronic renal failure (p = 0. 001). However, only 16.5% of these patients qualifying for an ICD actually received an ICD; nevertheless, the actual SCD rate was only 3.5%, while 5.4% (46 patients) suffered VTs or ventricular fibrillation (VF). The SCD/VT rate in the entire infarct population was associated with time to reperfusion (0.032), left bundle-branch block (0.002), a longer history of CAD (0.032), and VT during follow-up.</AbstractText>While mortality in patients with STEMI is still alarming even with PCI, the risk of SCD may be considerably decreased even in patients with an LVEF below 35%. With the current approach to primary prevention of sudden cardiac death, approximately 10% of postinfarction patients qualify for ICD therapy; however this may only reach a quarter of patients prone to SCD.</AbstractText> |
14,632 | Predictors of sustained ventricular arrhythmia episodes in patients with primary ICD indication: male gender and AF in primary ICD prophylaxis. | Implantable cardioverter-defibrillators (ICD) reduce mortality in patients with severely impaired left ventricular function. In randomized studies, female patients are underrepresented and data on ICD therapy is limited. Atrial fibrillation (AF) is a determinant of poor prognosis but has not been consistently evaluated. We evaluated the risk factors for the occurrence of ventricular arrhythmia episodes in patients with primary ICD prophylaxis.</AbstractText>Consecutive patients after ICD implantation for primary prophylaxis were followed. During follow-up, detected sustained episodes of ventricular arrhythmia were documented. Multivariate analysis controlled for propensity score was used to evaluate the correlation between gender, history of AF, and the occurrence of ventricular arrhythmia episodes.</AbstractText>A total of 400 patients (19.8% female; n = 79) were included. During follow-up, 64 patients (16%) had appropriate ICD therapy episodes. Men (18%) had significantly more often episodes than women (8%; p = 0.025). Patients with a history of AF (102, 25.5%) had significantly more often episodes (30%) compared to patients without a history of AF (11%; p < 0.001). In a multivariate model, only gender (p = 0.02) and history of AF (p < 0.001) were significantly associated predictors of the occurrence of appropriate ICD therapies during follow-up. Based on the propensity score model, the adjusted hazard ratio for male gender was 2.7 (p = 0.02) and 2.6 (p = 0.0004) for history of AF.</AbstractText>Male gender and history of AF are independent predictors for the occurrence of sustained ventricular arrhythmia in primary ICD prophylaxis. Further studies need to evaluate whether history of AF in female patients might be an indicator for higher risk of sudden cardiac arrhythmic death.</AbstractText> |
14,633 | Mice with cardiac overexpression of peroxisome proliferator-activated receptor γ have impaired repolarization and spontaneous fatal ventricular arrhythmias. | Diabetes mellitus and obesity, which confer an increased risk of sudden cardiac death, are associated with cardiomyocyte lipid accumulation and altered cardiac electric properties, manifested by prolongation of the QRS duration and QT interval. It is difficult to distinguish the contribution of cardiomyocyte lipid accumulation from the contribution of global metabolic defects to the increased incidence of sudden death and electric abnormalities.</AbstractText>In order to study the effects of metabolic abnormalities on arrhythmias without the complex systemic effects of diabetes mellitus and obesity, we studied transgenic mice with cardiac-specific overexpression of peroxisome proliferator-activated receptor γ 1 (PPARγ1) via the cardiac α-myosin heavy-chain promoter. The PPARγ transgenic mice develop abnormal accumulation of intracellular lipids and die as young adults before any significant reduction in systolic function. Using implantable ECG telemeters, we found that these mice have prolongation of the QRS and QT intervals and spontaneous ventricular arrhythmias, including polymorphic ventricular tachycardia and ventricular fibrillation. Isolated cardiomyocytes demonstrated prolonged action potential duration caused by reduced expression and function of the potassium channels responsible for repolarization. Short-term exposure to pioglitazone, a PPARγ agonist, had no effect on mortality or rhythm in WT mice but further exacerbated the arrhythmic phenotype and increased the mortality in the PPARγ transgenic mice.</AbstractText>Our findings support an important link between PPARγ activation, cardiomyocyte lipid accumulation, ion channel remodeling, and increased cardiac mortality.</AbstractText> |
14,634 | Identification of high-risk syncope related to ventricular fibrillation in patients with Brugada syndrome. | Syncope in patients with Brugada syndrome is usually associated with ventricular tachyarrhythmia, but some episodes of syncope can be related to autonomic disorders.</AbstractText>The purpose of this study was to investigate the characteristics of syncope to differentiate high-risk syncope episodes from low-risk events in patients with Brugada syndrome.</AbstractText>We studied 84 patients with type 1 electrocardiogram and syncope. Patients were divided into 2 groups: patients with prodrome (prodromal group; n = 41) and patients without prodrome (nonprodromal group; n = 43).</AbstractText>Ventricular fibrillation (VF) was documented at index event in 19 patients: 4 patients (21%) with documented VF experienced a prodrome prior to the onset of VF, whereas 15 patients (79%) did not have symptoms prior to documented VF (P <.01). Twenty-seven patients in the prodromal group and 7 patients in the nonprodromal group were considered to have syncope related to autonomic dysfunction. Syncope in other patients was defined as unexplained syncope. During the follow-up period (48 ± 48 months), recurrent syncope due to VF occurred in 13 patients among patients with only unexplained syncope and was more frequent in the nonprodromal group (n = 10) than in the prodromal group (n = 3; P = .044). In multivariate analysis, blurred vision (hazard ratio [HR] 0.20) and abnormal respiration (HR 2.18) and fragmented QRS (HR 2.39) were independently associated with the occurrence of VF.</AbstractText>Syncope with prodrome, especially blurred vision, suggests a benign etiology of syncope in patients with Brugada syndrome.</AbstractText>Copyright © 2012 Heart Rhythm Society. Published by Elsevier Inc. All rights reserved.</CopyrightInformation> |
14,635 | Electrocardiographic changes during therapeutic hypothermia. | Induced mild therapeutic hypothermia (MTH) is an effective treatment to improve outcome after out-of-hospital resuscitation. Adverse events are rare, but arrhythmias and bleeding complications have been reported. So far, only few data about electrocardiographic changes and associated events have been reported.</AbstractText>Between 6/2005 and 3/2011, 109 comatose survivors of out-of-hospital cardiac arrest admitted to our institution underwent MTH. In an observational single-center study, we analyzed preclinical course, electrocardiographic changes, arrhythmias, laboratory parameters and complication rates before, during and after MTH.</AbstractText>MTH led to a significant decrease of heart rate (85.0±23.3 min(-1) at admission; 59.1±20.5 min(-1) during, p<0.01 and 63.1±19.2 after hypothermia p<0.05) a significant prolongation of PR (0.17±0.04 s before, 0.18±0.05 s during, p<0.05; and 0.17±0.04 s after hypothermia, p<0.01) and QTc intervals (0.47±0.05 s before, 0.49±0.05 s during, p<0.01; and 0.46±0.05 s after hypothermia, p<0.01). Two patients developed ventricular fibrillation during hypothermia, both had an acute myocardial infarction. No significant MTH related changes in electrolytes or coagulation parameters were observed. Major bleeding complications occurred in four cases (3.7%) with a trend towards more bleedings after use of preclinical thrombolysis (21.4% with to 6.4% without thrombolysis, p=0.057). We did not find increased risk for bleeding complications in patients with double platelet inhibition after PCI (14.3% compared to 9.5% without PCI, p=0.63) compared to those without PCI.</AbstractText>Under strict clinical and laboratory parameter control, induced mild therapeutic hypothermia can be applied to most patients after out-of-hospital cardiac arrest with no increased risk for arrhythmias despite significant electrocardiographic changes.</AbstractText>Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.</CopyrightInformation> |
14,636 | Acute myocarditis and ventricular fibrillation as initial presentation of pediatric systemic lupus erythematosus. | Acute myocarditis and ventricular arrhythmia are rarely seen as the initial presentation of systemic lupus erythematosus (SLE) in children. We reported the case of a 12-year-old girl with congestive heart failure, acute myocarditis and pericardial effusion as a primary manifestation of SLE. Sudden cardiovascular collapse due to ventricular fibrillation (VF), ventricular tachycardia (VT) and cardiac tamponade occurred. After resuscitation and pericardiocentesis, frequent VF/VT refractory to anti-arrhythmic therapy was supported by venoarterial extracorporeal membrane oxygenation. Early diagnosis and a combination treatment for heart failure, arrhythmias and immunosuppression may result in a favorable outcome. |
14,637 | [Description of a new mutation in a female patient with Fabry disease]. | Fabry disease is caused by intracellular accumulation of glycosphingolipids in various tissues, secondary to mutations in the GLA gene (Xq22). Classically described as affecting hemizygous males with no residual alpha-galactosidase A activity, it is now known to affect both sexes, with later and less severe manifestations in females. The manifestations of this disease are systemic: neurological, cutaneous (angiokeratomas), renal, cardiovascular (left ventricular hypertrophy, valve thickening or rhythm disturbances), cochlear-vestibular, and cerebrovascular. In the absence of treatment there is progressive damage to vital organs with renal failure, stroke, heart failure or rhythm perturbations, leading to severe impairment of quality of life as well as reduced life expectancy. We describe the case of a female patient with a history of cryptogenic ischemic stroke at the age of 38 years and chronic renal failure with proteinuria, who presented to the emergency room with atrial fibrillation. The echocardiogram revealed concentric left ventricular hypertrophy, diastolic dysfunction and decreased longitudinal strain in the basal septum. In the context of a screening protocol, she was diagnosed with Fabry disease and a previously undescribed mutation was identified. |
14,638 | [Prognostic implications of left ventricular end-diastolic pressure in acute coronary syndromes with left ventricular ejection fraction of 40% or over]. | There is still debate concerning the impact of left ventricular end-diastolic pressure (LVEDP) on long-term prognosis after an acute coronary syndrome (ACS).</AbstractText>To assess LVEDP and its prognostic implications in ACS patients with left ventricular ejection fraction (LVEF) ≥40%.</AbstractText>We performed a prospective, longitudinal study of 1329 ACS patients from a single center between 2004 and 2006. LVEDP was assessed at the beginning of the coronary angiogram. Patients with LVEF >40% were excluded (n=489). The population was divided into three groups: A - LVEDP ≤19 mmHg (n=186); B - LVEDP >19 and ≤27 mmHg (n=172); and C - LVEDP >27 mmHg (n=131). The primary endpoint of the analysis was readmission for congestive heart failure in the year following the index admission.</AbstractText>Mean LVEDP was 22.8±7.8 mmHg. The groups were similar age, gender, cardiovascular risk factors, cardiovascular history, and medication prior to admission. There was an association between higher LVEDP and: admission for ST-elevation acute myocardial infarction (35.4 vs. 45.9 vs. 56.7%, p<0.01), higher peak levels of cardiac biomarkers, and lower LVEF (56.5±7.0 vs. 55.3±7.6 vs. 53.0±7.5%, p<0.01). There were no significant differences between the groups in terms of coronary anatomy, medical therapy during hospital stay and at discharge, or in-hospital mortality. With regard to the primary endpoint, cumulative freedom from congestive heart failure was higher in group A patients (99.4 vs. 97.6 vs. 94.4%, log rank p=0.02). In a multivariate Cox regression model, a 5-mmHg increase in LVEDP (HR 1.97, 95% CI 1.10-3.54, p=0.02) remained an independent predictor of the primary endpoint when adjusted for age, systolic function, atrial fibrillation, peak troponin I, renal function, and prescription of diuretics and beta-blockers.</AbstractText>In selected population LVEDP was a significant prognostic marker of future admission for congestive heart failure.</AbstractText>Copyright © 2011 Sociedade Portuguesa de Cardiologia. Published by Elsevier España. All rights reserved.</CopyrightInformation> |
14,639 | [Toxicological and medico-legal analyses of sudden deaths resulting from butane inhalation]. | Butane is known to be a suffocating gas with narcotic activity, especially at high concentrations. Within the past five years, a few cases of sudden deaths in teenage boys who had inhaled butane, a component of gas for lighters, were investigated in the Forensic Medicine Department, Medical University of Silesia, Katowice. Analyses of biological materials secured at autopsies and evidence from places of deaths was carried out using GC/FID. Butane was found in blood, lung and brain samples of the deceased. Moreover, histopathological examinations were performed. Results of autopsies and additional analyses were appraised from the point of view of their significance and usefulness in giving medico-legal opinions on the cause of death. |
14,640 | Primary carnitine deficiency and sudden death: in vivo evidence of myocardial lipid peroxidation and sulfonylation of sarcoendoplasmic reticulum calcium ATPase 2. | Primary carnitine deficiency is an autosomal recessive disorder caused by mutations in the SLC22A5 gene which results in impaired carnitine transport, cytosolic fatty acid accumulation and impaired beta oxidation. The disease is associated with cardiomyopathy and arrhythmias, but the mechanism is unknown. We hypothesized that carnitine deficiency results in increased myocardial oxidative stress.</AbstractText>We evaluated a 22-year-old woman with primary carnitine deficiency and ventricular fibrillation, as well as her first-degree relatives.</AbstractText>Sequencing of SLC22A5 identified two deleterious mutations (A142S and R488H) and a novel mutation predicted to be a splice variant. Histology demonstrated increased myocardial lipid deposition and swollen mitochondria. Immunohistochemistry demonstrated accumulation of the reactive aldehyde 4-hydroxy-2-nonenal, indicative of increased lipid peroxidation, and sulfonylation of sarcoendoplasmic reticulum calcium ATPase 2 at cysteine 674.</AbstractText>These findings suggest that increased oxidant stress may contribute to myocardial dysfunction and arrhythmogenesis in this disorder.</AbstractText>Copyright © 2011 S. Karger AG, Basel.</CopyrightInformation> |
14,641 | Impaired β-adrenergic receptor signalling in post-resuscitation myocardial dysfunction. | Post-resuscitation myocardial dysfunction is a major cause of fatality in patients receiving successful cardiopulmonary resuscitation. The mechanism of post-resuscitation myocardial dysfunction is largely unknown, although is generally considered related to ischaemia occurring during cardiac arrest and resuscitation and/or reperfusion injury after restoration of circulation. A key mechanism responsible for reduced contractile reserves in chronic heart failure is impaired β-adrenergic receptor signalling. Thus, we hypothesised that β-adrenergic receptor signalling is markedly abnormal in the post-resuscitation period following cardiopulmonary resuscitation.</AbstractText>Male landrace domestic pigs were randomised into a sham group (anaesthetised and instrumented, no ventricular fibrillation) or cardiopulmonary resuscitation (CPR) group (ventricular fibrillation) (n=8 per group). Haemodynamic and echocardiographic data were recorded. β-Adrenergic receptor signalling was assessed at 6h after the operation by measuring myocardial adenylate cyclase activity, β-adrenergic receptor density and β-adrenergic receptor kinase expression.</AbstractText>Left ventricular function in the CPR group was significantly decreased at 6 h after restoration of spontaneous circulation. Basal and isoproterenol-stimulated adenylate cyclase activity was blunted in the CPR group compared with the sham group. Total β-AR density was significantly decreased in CPR group compared with the sham group. Myocardial β-adrenergic receptor kinase expression was 2.03-fold greater in the CPR group than in the sham group.</AbstractText>β-Adrenergic receptor signalling is markedly impaired in the post-resuscitation period, which may be a mechanism of post-resuscitation myocardial dysfunction.</AbstractText>Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.</CopyrightInformation> |
14,642 | Outcome when adrenaline (epinephrine) was actually given vs. not given - post hoc analysis of a randomized clinical trial. | IV line insertion and drugs did not affect long-term survival in an out-of-hospital cardiac arrest (OHCA) randomized clinical trial (RCT). In a previous large registry study adrenaline was negatively associated with survival from OHCA. The present post hoc analysis on the RCT data compares outcomes for patients actually receiving adrenaline to those not receiving adrenaline.</AbstractText>Patients from a RCT performed May 2003 to April 2008 were included. Three patients from the original intention-to-treat analysis were excluded due to insufficient documentation of adrenaline administration. Quality of cardiopulmonary resuscitation (CPR) and clinical outcomes were compared.</AbstractText>Clinical characteristics were similar and CPR quality comparable and within guideline recommendations for 367 patients receiving adrenaline and 481 patients not receiving adrenaline. Odds ratio (OR) for being admitted to hospital, being discharged from hospital and surviving with favourable neurological outcome for the adrenaline vs. no-adrenaline group was 2.5 (CI 1.9, 3.4), 0.5 (CI 0.3, 0.8) and 0.4 (CI 0.2, 0.7), respectively. Ventricular fibrillation, response interval, witnessed arrest, gender, age and endotracheal intubation were confounders in multivariate logistic regression analysis. OR for survival for adrenaline vs. no-adrenaline adjusted for confounders was 0.52 (95% CI: 0.29, 0.92).</AbstractText>Receiving adrenaline was associated with improved short-term survival, but decreased survival to hospital discharge and survival with favourable neurological outcome after OHCA. This post hoc survival analysis is in contrast to the previous intention-to-treat analysis of the same data, but agrees with previous non-randomized registry data. This shows limitations of non-randomized or non-intention-to-treat analyses.</AbstractText>Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.</CopyrightInformation> |
14,643 | Risk factors for recurrent stroke after coronary artery bypass grafting. | Preventing stroke after coronary artery bypass grafting (CABG) remains a therapeutic goal, due in part to the lack of identifiable risk factors. The aim of this study, accordingly, was to identify risk factors in CABG patients with a previous history of stroke.</AbstractText>Patients with a history of stroke who underwent CABG at Beijing An Zhen hospital from January 2007 to July 2010 were selected (n = 430), and divided into two groups according to the occurrence of postoperative stroke. Pre-operative and post-operative data were retrospectively collected and analyzed by univariate and multivariate logistic regression analyses.</AbstractText>Thirty-two patients (7.4%) suffered post-operative stroke. Univariate analysis identified several statistically significant risk factors in the post-operative stroke group, including pre-surgical left ventricular ejection fractions (LVEF) ≤50%, on-pump surgery, post-operative atrial fibrillation (AF), and hypotension. Multivariable analysis identified 4 independent risk factors for recurrent stroke: unstable angina (odds ratio (OR) = 2.95, 95% CI: 1.05-8.28), LVEF ≤50% (OR = 2.77, 95% CI: 1.23-6.27), AF (OR = 4.69, 95% CI: 1.89-11.63), and hypotension (OR = 2.55, 95% CI: 1.07-6.04).</AbstractText>Unstable angina, LVEF ≤50%, post-operative AF, and post-operative hypotension are independent risk factors of recurrent stroke in CABG patients with a previous history of stroke.</AbstractText> |
14,644 | [Coronary artery spasm during neurosurgical anesthesia]. | We experienced a case of coronary artery spasm during neurosurgical anesthesia. A 69-year-old man was scheduled for craniotomy for cerebello-pontine angle meningioma. He had a history of cigarette smoking, but no history or evidence of ischemic heart disease. After the dura mater was opened, marked ST elevation on the ECG monitor followed by ventricular fibrillation was noticed. After successful resuscitation, the surgery was cancelled. Because the coronary angiography, immediately after surgery, demonstrated normal coronary arteries, coronary artery spasm was considered to be the cause of the ECG change. Possible triggering factor in this case was vagal stimulation due to surgical manipulation. Careful anesthetic management is required to prevent intraoperative coronary artery spasm even in patients without a history of ischemic heart disease during neurosurgery. |
14,645 | [Hypertension complicated with heart disease]. | Hypertension facilitates development and progression of cardiac diseases such as left ventricular hypertrophy (LVH), coronary artery disease (CAD), arrhythmia and heart failure. Strict blood pressure control over 24 hours is essential for the primary and secondary prevention of these cardiac diseases. Inhibitors of renin-angiotensin system(RASI) such as ACE inhibitors and angiotensin II receptor blockers(ARB) and long-acting calcium channel blockers(CCB) are effective in improving LVH. CCB and beta-blockers are preferentially chosen for CAD. RASI is expected to reduce the incidence of atrial fibrillation. RASI, beta-blockers and aldosterone blockers have been shown to improve the prognosis of heart failure patients. In addition, diuretics and long-acting CCB are used for the adequate control of body fluid volume and blood pressure. |
14,646 | Prevalence of heart failure and atrial fibrillation in minority ethnic subjects: the Ethnic-Echocardiographic Heart of England Screening Study (E-ECHOES). | Limited data exists on the prevalence of heart failure amongst minority groups in the UK. To document the community prevalence and severity of left ventricular systolic dysfunction, heart failure, and atrial fibrillation, amongst the South Asian and Black African-Caribbean groups in the UK.</AbstractText>We conducted a cross-sectional study recruiting from September 2006 to July 2009 from 20 primary care centres in Birmingham, UK. 10,902 eligible subjects invited, 5,408 participated (49.6%) and 5,354 had complete data (49.1%). Subjects had median age 58.2 years (interquartile range 51.0 to 70.0), and 2544 (47.5%) were male. Of these, 1933 (36.3%) had BMI>30 kg/m(2), 1,563 (29.2%) had diabetes, 2676 (50.0%) had hypertension, 307 (5.7%) had a history of myocardial infarction, and 104 (1.9%) had history of arrhythmia. Overall, 59 (1.1%) had an Ejection Fraction<40%, and of these 40 (0.75%) were NYHA class ≥2; 51 subjects (0.95%) had atrial fibrillation. Of the remaining 19 patients with an EF<40%, only 4 patients were treated with furosemide. A further 54 subjects had heart failure with preserved ejection fraction.</AbstractText>This is the largest study of the prevalence of left ventricular systolic dysfunction, heart failure and atrial fibrillation in under-researched minority communities in the UK. The prevalence of heart failure in these minority communities appears comparable to that of the general population but less than anticipated given the high rates of cardiovascular disease in these groups. Heart failure continues to be a major cause of morbidity in all ethnic groups and preventive strategies need to be identified and implemented.</AbstractText> |
14,647 | Cardiopulmonary resuscitation before defibrillation in the out-of-hospital setting: a literature review. | Many studies over the past decade have investigated delaying initial defibrillation to perform cardiopulmonary resuscitation (CPR), as it has been associated with increased rates of restoration of spontaneous circulation and/or survival. Since 2006, a number of studies have investigated these procedures. The objective of this study was to undertake a literature review examining the commencement of CPR before defibrillation in the out-of-hospital setting.</AbstractText>A literature review was undertaken using the electronic medical databases Ovid Medline, EMBASE, CINHAL Plus, Cochrane Systematic Review and Meditext, from their commencement to the end of June 2011. Keywords used in the search included: CPR, defibrillation, ventricular fibrillation, VF, EMS, EMT, paramedic, emergency medical service, emergency medical technician, prehospital, out-of-hospital and ambulance. References of relevant articles were also reviewed.</AbstractText>Of the 3079 articles located, 10 met the inclusion criteria. The results of these studies showed conflicting results. All retrospective studies (n=6) indicated a benefit in performing pre-shock CPR on patients with ventricular fibrillation for durations between 90 and 180 s. Conversely, all randomised controlled trials demonstrated no benefit from providing CPR before defibrillation compared with immediate defibrillation for return of spontaneous circulation, neurological outcome and/or survival to hospital discharge. However, none of the studies reported evidence that CPR before defibrillation is harmful.</AbstractText>Conflicting evidence remains regarding the benefit of CPR before defibrillation. The establishment of a consistent timeframe of chest compressions before defibrillation in the out-of-hospital setting will provide uniformity in standards in clinical practice and education and training.</AbstractText> |
14,648 | Vernakalant: conversion of atrial fibrillation in patients with ischemic heart disease. | Vernakalant is a novel, relatively atrial-selective antiarrhythmic drug. This analysis assessed the efficacy and safety of intravenous vernakalant for the rapid conversion of atrial fibrillation (AF) to sinus rhythm in patients with a history of ischemic heart disease (IHD).</AbstractText>The presence of IHD was extracted from the medical history of patients from four randomized placebo-controlled studies and one open label study. The efficacy analysis included patients with recent onset AF (consistent with the European labeled indication), while the safety analysis included all patients with AF or atrial flutter (AFL) (3h to 45 days duration) who were exposed to study drug.</AbstractText>A total of 1052 adult patients were enrolled and treated; 274 patients (91 placebo, 183 vernakalant) with a history of IHD and 778 patients (224 placebo, 554 vernakalant) without IHD. Conversion of AF to sinus rhythm was not influenced by IHD. In patients with recent onset AF, the placebo-subtracted conversion rate with vernakalant was 45.7% in the IHD group and 47.3% in the non-IHD group. In the 24h following treatment, the rate of treatment-emergent serious adverse events and discontinuations due to adverse events was similar in both the IHD and non-IHD groups, and there was no case of torsades de pointes, ventricular fibrillation, or death in patients with IHD.</AbstractText>Vernakalant was safe and well tolerated in AF/AFL patients with a history of IHD, and was significantly more effective than placebo for the acute conversion of AF regardless of IHD status.</AbstractText>Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.</CopyrightInformation> |
14,649 | Electrical therapies in cardiac arrest. | Recognition and appropriate treatment of ventricular fibrillation or pulseless ventricular tachycardia is an essential skill for healthcare providers. Appropriate defibrillation can improve survival and benefit patient outcome. Similarly, increased public access to automatic electronic defibrillators has been shown to improve out-of-hospital survival for cardiac arrest. When combined with high-quality cardiopulmonary resuscitation, electrical therapies are an important aspect of resuscitation in the patient with cardiac arrest. This article focuses on the use of electrical therapies, including defibrillation, cardiac pacing, and automated external defibrillators, in cardiac arrest. |
14,650 | End-tidal CO2 as a predictor of survival in out-of-hospital cardiac arrest. | The objective of this study was to evaluate initial end-tidal CO2 (EtCO2) as a predictor of survival in out-of-hospital cardiac arrest.</AbstractText>This was a retrospective study of all adult, non-traumatic, out-of-hospital, cardiac arrests during 2006 and 2007 in Los Angeles, California. The primary outcome variable was attaining return of spontaneous circulation (ROSC) in the field. All demographic information was reviewed and logistic regression analysis was performed to determine which variables of the cardiac arrest were significantly associated with ROSC.</AbstractText>There were 3,121 cardiac arrests included in the study, of which 1,689 (54.4%) were witnessed, and 516 (16.9%) were primary ventricular fibrillation (VF). The mean initial EtCO2 was 18.7 (95%CI = 18.2-19.3) for all patients. Return of spontaneous circulation was achieved in 695 patients (22.4%) for which the mean initial EtCO2 was 27.6 (95%CI = 26.3-29.0). For patients who failed to achieve ROSC, the mean EtCO2 was 16.0 (95%CI = 15.5-16.5). The following variables were significantly associated with achieving ROSC: witnessed arrest (OR = 1.51; 95%CI = 1.07-2.12); initial EtCO2 >10 (OR = 4.79; 95%CI = 3.10-4.42); and EtCO2 dropping <25% during the resuscitation (OR = 2.82; 95%CI = 2.01-3.97).The combination of male gender, lack of bystander cardiopulmonary resuscitation, unwitnessed collapse, non-vfib arrest, initial EtCO2 ≤10 and EtCO2 falling > 25% was 97% predictive of failure to achieve ROSC.</AbstractText>An initial EtCO2 >10 and the absence of a falling EtCO2 >25% from baseline were significantly associated with achieving ROSC in out-of-hospital cardiac arrest. These additional variables should be incorporated in termination of resuscitation algorithms in the prehospital setting.</AbstractText> |
14,651 | Distinct effects of acute pretreatment with lipophilic and hydrophilic statins on myocardial stunning, arrhythmias and lethal injury in the rat heart subjected to ischemia/reperfusion. | Although both lipophilic and more hydrophilic statins share the same pathway of the inhibition of HMG-CoA reductase, their pleiotropic cardioprotective effects associated with the ability to cross cellular membranes, including membranes of heart cells, may differ. To test this hypothesis, isolated rat hearts were Langendorff-perfused either with simvastatin (S, 10 micromol/l) or pravastatin (P, 30 micromol/l), 15 min prior to ischemia. Control untreated hearts (C) were perfused with perfusion medium only. Postischemic contractile dysfunction, reperfusion-induced ventricular arrhythmias and infarct size were investigated after exposure of the hearts to 30-min global ischemia and 2-h reperfusion. Both lipophilic S and hydrophilic P reduced the severity of ventricular arrhythmias (arrhythmia score) from 4.3 +/- 0.2 in C to 3.0 +/- 0 and 2.7 +/- 0.2 in S and P, respectively, (both P < 0.05), decreased the duration of ventricular tachycardia and suppressed ventricular fibrillation. Likewise, the extent of lethal injury (infarct size) determined by tetrazolium staining and expressed in percentage of risk area, was significantly lower in both treated groups, moreover, the effect of P was more pronounced (27 +/- 2 % and 10 +/- 2 % in S and P groups, respectively, vs. 42 +/- 1 % in C; P < 0.05). In contrast, only S, but not P, was able to improve postischemic recovery of left ventricular developed pressure (LVDP; 48 +/- 12 % of preischemic values vs. 25 +/- 4 % in C and 21 +/ -7 % in P groups; P < 0.05). Our results suggest that differences in water solubility of statins indicating a different ability to cross cardiac membranes may underlie their distinct cardioprotective effects on myocardial stunning and lethal injury induced by ischemia/reperfusion. |
14,652 | Atrial fibrillation in patients with sick sinus syndrome: the association with PQ-interval and percentage of ventricular pacing. | In the recently published DANPACE trial, incidence of atrial fibrillation (AF) was significantly higher with single-lead atrial (AAIR) pacing than with dual-chamber (DDDR) pacing. The present analysis aimed to evaluate the importance of baseline PQ-interval and percentage of ventricular pacing (VP) on AF.</AbstractText>We analysed data on AF during follow-up in 1415 patients included in the DANPACE trial. In a subgroup of 650 patients with DDDR pacemaker, we studied whether %VP, baseline PQ-interval, and programmed atrio-ventricular interval (AVI) was associated with AF burden measured as time in mode-switch (MS) detected by the pacemaker. In the entire DANPACE study population, the incidence of AF was significantly higher in patients with baseline PQ-interval >180 ms (P< 0.001). Among 650 patients with DDDR pacemaker, telemetry data were available for 1.337 ± 786 days, %VP was 66 ± 33%, AF was detected at planned follow-up in 160 patients (24.6%), MS occurred in 422 patients (64.9%), and AF burden was marginally higher with baseline PQ-interval >180 ms (P= 0.028). No significant association was detected between %VP and %MS (Spearman's ρ 0.056, P= 0.154). %MS was not different between minimal-paced programmed AVI ≤ 100 and >100 ms (median value), respectively (P= 0.60).</AbstractText>The present study indicates that a longer baseline PQ-interval is associated with an increased risk of AF in patients with sick sinus syndrome. Atrial fibrillation burden is not associated with the percentage of VP or the length of the programmed AVI.</AbstractText> |
14,653 | Targeting cardiac mast cells: pharmacological modulation of the local renin-angiotensin system. | Enhanced production of angiotensin II and excessive release of norepinephrine in the ischemic heart are major causes of arrhythmias and sudden cardiac death. Mast cell-dependent mechanisms are pivotal in the local formation of angiotensin II and modulation of norepinephrine release in cardiac pathophysiology. Cardiac mast cells increase in number in myocardial ischemia and are located in close proximity to sympathetic neurons expressing angiotensin AT1- and histamine H3-receptors. Once activated, cardiac mast cells release a host of potent pro-inflammatory and pro-fibrotic cytokines, chemokines, preformed mediators (e.g., histamine) and proteases (e.g., renin). In myocardial ischemia, angiotensin II (formed locally from mast cell-derived renin) and histamine (also released from local mast cells) respectively activate AT1- and H3-receptors on sympathetic nerve endings. Stimulation of angiotensin AT1-receptors is arrhythmogenic whereas H3-receptor activation is cardioprotective. It is likely that in ischemia/reperfusion the balance may be tipped toward the deleterious effects of mast cell renin, as demonstrated in mast cell-deficient mice, lacking mast cell renin and histamine in the heart. In these mice, no ventricular fibrillation occurs at reperfusion following ischemia, as opposed to wild-type hearts which all fibrillate. Preventing mast cell degranulation in the heart and inhibiting the activation of a local renin-angiotensin system, hence abolishing its detrimental effects on cardiac rhythmicity, appears to be more significant than the loss of histamine-induced cardioprotection. This suggests that therapeutic targets in the treatment of myocardial ischemia, and potentially congestive heart failure and hypertension, should include prevention of mast cell degranulation, mast cell renin inhibition, local ACE inhibition, ANG II antagonism and H3-receptor activation. |
14,654 | Dronedarone prevents microcirculatory abnormalities in the left ventricle during atrial tachypacing in pigs. | Atrial fibrillation induces ischaemic microcirculatory flow abnormalities in the ventricle, contributing to the risk for acute coronary syndromes. We evaluated the effect of dronedarone on ventricular perfusion during rapid atrial pacing (RAP).</AbstractText>Coronary and fractional flow reserve (CFR/FFR) were measured in the left anterior descending artery in 29 pigs. Six received RAP, six received RAP with dronedarone (RAP/D), seven received dronedarone alone, four received RAP with amiodarone (RAP/A), and six received neither (sham). In ventricular tissue, oxidative stress/ischaemia-related gene and protein expression was evaluated by RT-PCR and Western blotting; Isoprostanes were measured by GC-MS procedures.</AbstractText>CFR was decreased in the RAP group, compared with other groups. FFR was not different between groups. Effective refractory period was reduced in RAP compared with RAP/D. RAP-activated PKC phosphorylation tended to be decreased by dronedarone (P= 0.055) RAP induced NOX-1 and NOX-2 protein and the mRNA for hypoxia-inducible factor-1α (HIF-1α). Dronedarone reduced the pacing-dependent increase in the expression of NOX-2 protein and of HIF-1α mRNA. The oxidative stress marker, F(2)-isoprostane, was increased by RAP and this increase was attenuated by dronedarone. Other oxidative stress/ischaemia-related genes were induced by RAP compared with sham and were decreased by dronedarone treatment. In HL1 cells, dronedarone significantly inhibited the increased phosphorylation of PKCα after oxidative stress, with an almost significant effect (P= 0.059) on that after RAP.</AbstractText>Dronedarone abolished RAP-induced ventricular microcirculatory abnormalities by decreasing oxidative stress/ischaemia-related gene and protein expression in the ventricle.</AbstractText>© 2011 The Authors. British Journal of Pharmacology © 2011 The British Pharmacological Society.</CopyrightInformation> |
14,655 | Clinical trials update from the European Society of Cardiology Meeting 2011: ARISTOTLE, SMART-AV: QLV substudy, SHIFT: echocardiography and quality of life substudies, European CRT Survey, and Basic Science Update. | This article provides information and a commentary on key trials relevant to the pathophysiology, prevention, and treatment of heart failure presented at the European Society of Cardiology meeting held in Paris, France in August 2011. Unpublished reports should be considered as preliminary, since analyses may change in the final publication. Results from ARISTOTLE suggest that apixaban is more effective than warfarin for the prevention of stroke in patients with atrial fibrillation. Electrical dyssynchrony, measured by the time from onset of electrical activity on the surface ECG to activation of myocardium by intrinsic conduction at the pacing site (QLV), was a strong and independent predictor of improvement in ventricular function after cardiac resynchronization therapy (CRT) in an observational analysis of a subgroup of patients from the SMART-AV study. Subgroup analyses from SHIFT suggest that heart rate reduction with ivabradine causes favourable left ventricular remodelling and improves quality of life in patients with symptomatic systolic heart failure and an increased heart rate. The European CRT Survey reported outcome data. |
14,656 | Protective effects of therapeutic hypothermia in post-resuscitation myocardium. | Post-resuscitation therapeutic hypothermia has been recommended because of its neuroprotective effects. However, a few studies have reported the effects of therapeutic hypothermia on the heart, especially in ventricular fibrillation cardiac arrest. The aim of this study was to determine whether therapeutic hypothermia attenuates post-resuscitation myocardial injury in a swine cardiac arrest model.</AbstractText>A prospective animal study was performed in the university hospital animal research laboratory. Ventricular fibrillation cardiac arrest was induced in domestic pigs weighing 35-40 kg. After 6 min of no flow time, cardiopulmonary resuscitation was provided to pigs, and the restoration of spontaneous circulation (ROSC) was achieved. The subjects were randomly allocated to a normothermic (NT group, n=5) or hypothermic (HT group, n=5) group. In the HT group, therapeutic hypothermia (core temperature 32-34 °C) was maintained for 24h, and rewarming was performed over a period of 8 h. In the NT group, core temperature was maintained at 37 °C throughout the experiments. Sixty hours after ROSC, blood and myocardial tissues were harvested.</AbstractText>Serum troponin I was not significantly different between the groups. However, myocardial histological damage was attenuated in the HT group. Myocardial ATP contents were higher in the HT group than in the NT group. Immunohistochemistry for apoptosis-related protein showed that survivin expression was higher in the HT group, and XAF1 and cleaved caspase-3 expressions were lower in the HT group than in the NT group.</AbstractText>Therapeutic hypothermia attenuated histological myocardial injury in ventricular fibrillation cardiac arrest model of pigs while preserving more ATP and decreased apoptosis.</AbstractText>Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.</CopyrightInformation> |
14,657 | Comparison of role of early (less than six hours) to later (more than six hours) or no cardiac catheterization after resuscitation from out-of-hospital cardiac arrest. | Despite reports of patients with resuscitated sudden cardiac arrest (rSCA) receiving acute cardiac catheterization, the efficacy of this strategy is largely unknown. We hypothesized that acute cardiac catheterization of patients with rSCA would improve survival to hospital discharge. A retrospective cohort of 240 patients with out-of-hospital rSCA caused by ventricular tachycardia or fibrillation was identified from 11 institutions in Seattle, Washington from 1999 through 2002. Patients were grouped into those receiving acute catheterization within 6 hours (≤6-hour group, n = 61) and those with deferred catheterization at >6 hours or no catheterization during the index hospitalization (>6-hour group, n = 179). Attention was directed to survival to hospital discharge, neurologic status, extent of coronary artery disease, presenting electrocardiographic findings, and symptoms before arrest. Propensity-score methods were used to adjust for the likelihood of receiving acute catheterization. Survival was greater in patients who underwent acute catheterization (72% in the ≤6-hour group vs 49% in the >6-hour group, p = 0.001). Percutaneous coronary intervention was performed in 38 of 61 patients (62%) in the ≤6-hour group and 13 of 170 patients (7%) in the >6-hour group (p <0.0001). Neurologic status was similar in the 2 groups. A significantly larger percentage of patients in the acute catheterization group had symptoms before cardiac arrest and had ST-segment elevation on electrocardiogram after resuscitation. Age, bystander cardiopulmonary resuscitation, daytime presentation, history of percutaneous coronary intervention or stroke, and acute ST-segment elevation were positively associated with receiving cardiac catheterization. In conclusion, in this series of patients who sustained out-of-hospital cardiac arrest, acute catheterization (<6 hours of presentation) was associated with improved survival. |
14,658 | Predictors of clinical efficacy of 'Ablate and Pace' therapy in patients with permanent atrial fibrillation. | To evaluate the 2-year clinical improvement after 'Ablate and Pace' therapy and to identify the variables able to influence the efficacy of this therapy in patients with permanent atrial fibrillation (AF). Design Prospective multicentre observational study. Setting Cardiology departments of 19 general hospitals in Italy, Spain and Greece.</AbstractText>171 patients with drug-refractory severely symptomatic permanent AF considered for AV junction ablation. Interventions Patients underwent AV junction ablation, received a right ventricular (RV) pacing or echo-guided cardiac resynchronisation (CRT) pacing and were followed-up to 24 months. Main outcome measures Non-responders to Ablate and Pace therapy were defined those patients who, during the follow-up period had clinical failure (defined as death or hospitalisation due to heart failure, or worsening heart failure) or showed no improvement in their clinical condition.</AbstractText>Responders were 63% of RV-paced patients and 83% of CRT-paced patients. Another 27% showed no clinical improvement (7%) or worsened (20%) (non-responders group). On multivariable Cox regression analysis, CRT mode and echo-optimised CRT were the only independent protective factors against non-response (HR=0.24, 95% CI 0.10-0.58, p=0.001 and HR=0.22, 95% CI 0.07-0.77, p=0.018 respectively). On comparing freedom from non-response, a trend in favour of echo-optimised CRT versus simultaneous biventricular pacing (p=0.077) was seen.</AbstractText>In patients affected by severely symptomatic permanent AF, Ablate and Pace therapy yielded a clinical benefit in 63% of RV-paced patients and 83% of CRT-paced patients. CRT pacing and echo-optimised CRT were the only independent predictor of clinical benefit.</AbstractText> |
14,659 | Predicting long-term mortality after first coronary revascularization: – the Kyoto model –. | We explored the determinants of mortality in order to develop and validate the Kyoto model, which predicts outcomes after percutaneous coronary intervention (PCI) and coronary artery bypass grafting (CABG).</AbstractText>A total of 9,393 patients who underwent their first coronary revascularization without concomitant valvular, left ventricular, or major vascular surgery were followed over a median follow-up of 3.5 years in the CREDO-Kyoto Registry. We fitted separate Cox regression to mortality after PCI and CABG. The best-fitting model was internally validated by 10-fold cross-validation. The Cox regression identified the following predictors: age, sex, body mass index, ejection fraction, atrial fibrillation, diabetes mellitus, hyperlipidemia, current smoker, stroke, peripheral vascular disease, chronic obstructive pulmonary disease, malignancy, kidney disease, anemia, liver cirrhosis, diseased vessel, left main disease, proximal left anterior descending artery disease, and total occlusion. This model simulated that the 3-year mortality for a hypothetical 70-year-old man with 2-vessel disease is 2.0% after PCI and 2.6% after CABG, or 4.2% and 5.1% if he has diabetes and chronic kidney disease. The Hosmer-Lemeshow test showed no significant deviations between the observed and predicted events. The C statistics were greater than 0.78.</AbstractText>The Kyoto model can assist clinicians and patients in adherence to medication and lifestyle changes after revascularization and in individualized decision making. A web application is available at http://www.biostatistics.jp/prediction/kyoto-model.</AbstractText> |
14,660 | The relation of ventricular arrhythmia electrophysiological characteristics to cardiac phenotype and circadian patterns in hypertrophic cardiomyopathy. | The triggers of ventricular arrhythmias (VAs) leading to sudden cardiac death in hypertrophic cardiomyopathy (HCM) are ill defined. We sought to examine the electrophysiological characteristics of VAs in HCM and study their relation to cardiac phenotype and circadian patterns using stored intracardiac electrocardiograms from implantable cardioverter defibrillators (ICDs).</AbstractText>A single centre, observational cohort study of 230 consecutively evaluated ICD recipients with HCM [median age 42 years, 97% primary prevention, 51% with anti-tachycardia pacing (ATP)]. Fifty-six non-clustered VAs (39 initially treated with ATP and 17 with shocks) from 29 patients were analysed. Monomorphic ventricular tachycardia was the culprit arrhythmia in 86% of cases, ventricular fibrillation/flutter in 9%, and polymorphic ventricular tachycardia in 5%. Prior to the onset of VA the rhythm was sinus in 67%, atrial fibrillation/flutter in 19%, and 15% were paced ventricularly; tachycardia (cycle length <600 ms) was present in 25%. Ventricular arrhythmias were triggered by premature ventricular complexes (PVCs) in 72%, which were late-coupled (84%). Short-long-short initiation was seen in 2% and 26% of VAs were sudden-onset without preceding PVCs. Ventricular arrhythmia peaked at midday (with 20% occurring between 2300 and 0700), on Sundays and in May. The cardiac phenotype and time of the day did not predict the mode of initiation. Age at ICD implantation was the only independent predictor of VA cycle length (linear regression coefficient 0.67, 95% CI 0.02-1.32, P= 0.04). Anti-tachycardia pacing terminated 67% of VAs, but patients with ATP therapy had a similar incidence of appropriate shocks (log-rank test P= 0.25) and syncope (log rank P= 0.23) to patients with shock as initial therapy.</AbstractText>Most VAs are monomorphic ventricular tachycardias triggered by late-coupled PVCs. They are frequently terminated by ATP, but ATP does not reduce the frequency of ICD shocks. Younger HCM patients have more rapid VAs, which may explain the peak of sudden cardiac death in early adulthood. The circadian periodicity is different from that observed in ischaemic heart disease, and is likely to relate to the distinct character of the arrhythmogenic substrate in HCM and its modulators.</AbstractText> |
14,661 | A fully automatic, implantable cardioverter-defibrillator algorithm to prevent inappropriate detection of ventricular tachycardia or fibrillation due to T-wave oversensing in spontaneous rhythm. | T-wave oversensing (TWOS) may cause inappropriate shocks in patients with implantable cardioverter-defibrillator (ICD). Programming options to prevent TWOS are usually implemented only after TWOS has occurred, and they may compromise sensing of ventricular fibrillation (VF).</AbstractText>To evaluate an ICD algorithm that differentiates TWOS from ventricular tachycardia (VT) or VF to prevent inappropriate detection of VT/VF when TWOS occurs.</AbstractText>We developed a TWOS algorithm based on both the differential frequency content of R vs T waves and their alternating pattern. Algorithm parameters were developed from a database of stored electrograms. The algorithm was validated on a hardware system consisting of actual ICD circuitry by using an independent database of stored electrograms including inappropriate detections of both VT/VF caused by spontaneous TWOS and induced true VF to assess delays in detection.</AbstractText>We tested 83 inappropriate detections of VF due to TWOS from 22 patients. All 22 patients had at least 1 successful rejection of TWOS, and rejection was effective in 80 of the 83 episodes. After adjustment for multiple episodes per patient, specificity was 96.6% (95% confidence interval 90.3%-98.8%). In 166 episodes of true VF in 92 patients, the sensitivity for VF detection was 100% (95% confidence interval 98.2%-100%) at a nominal sensitivity of 0.3 mV; the new TWOS algorithm did not delay the detection of VF.</AbstractText>A novel TWOS rejection algorithm is designed to operate in real time. The algorithm reduced inappropriate detections of VF in spontaneous TWOS episodes by 96.6% while maintaining 100% sensitivity for detecting true VF.</AbstractText>Copyright © 2012 Heart Rhythm Society. Published by Elsevier Inc. All rights reserved.</CopyrightInformation> |
14,662 | [Effects of ventricular demand and dual-chamber pacing models on the long-term clinical outcome and cardiac remodeling in patients with symptomatic bradycardia]. | To assess the effects of VVI (ventricular demand) and DDD (dual-chamber) pacing models on cardiac remodeling and the long-term clinical outcome of patients with symptomatic bradycardia.</AbstractText>All patients with DDD and VVI pacing models at our hospital from January 1991 to January 2003 were retrospectively analyzed.</AbstractText>After a follow-up period of over 8 years in DDD and VVI groups (97 ± 27, 107 ± 44 months), left atrial diameter [(45 ± 12) mm vs (39 ± 12) mm, P < 0.01] and left ventricular end-diastolic diameter [(53 ± 11) mm vs (50 ± 9) mm, P = 0.01] in 57 patients with VVI pacing model were markedly enlarged than those at pre-implantation. And tricuspid regurgitation increased (42.4% vs 16.9%, P < 0.05). But in 59 patients with DDD pacing model, except for increased tricuspid regurgitation (42.1% vs 10.5%, P < 0.01), left atrial diameter [(37 ± 5) mm vs. (35 ± 5) mm, P = 0.07] and left ventricular end-diastolic diameter [(47 ± 7) mm vs (47 ± 5) mm, P = 0.32] were not significantly different. Mitral regurgitation significantly increased only in the VVI group (P < 0.01). The increases of left ventricular end-diastolic diameter (P = 0.04), mitral valve (P = 0.02) and tricuspid regurgitation (P < 0.01) were much more pronounced in the VVI group than those in the DDD group. Left ventricular ejection fraction (LVEF) showed no difference with that at pre-implantation (P = 0.11 in DDD group, P = 0.05 in VVI group). But the LVEF value was lower (P = 0.04) while the incidence of thrombosis was higher (P = 0.03) in the VVI group than those in the DDD group at post-implantation. However, the incidence of atrial fibrillation (P = 0.14), hospitalization (P = 0.08) and survival (P = 0.77) showed no significant difference between two groups.</AbstractText>DDD pacing offers more benefits over VVI pacing through improving cardiac functions and arresting left ventricular remodeling. However, neither groups showed any difference in decreasing mortality rate and hospitalization. Moreover, both pacing modes fail to reverse cardiac electrical and anatomical remodeling. It is imperative to explore more physiological pacing site and rational atrioventricular (AV) interval to improve the prognosis of patients.</AbstractText> |
14,663 | [Focus on beta-blockers for vascular specialists in 2012]. | Since they were launched on the market in 1964, cardiovascular indications for beta-blockers have been validated and accepted worldwide. Numerous studies and meta-analysis have confirmed their benefits. They reduce mortality in post infarction and acute coronary syndrome populations and also in people with stable coronary heart disease. Moreover, heart failure with systolic left ventricular dysfunction is a major indication for this therapeutic class, providing a 30% decrease in mortality. In patients with permanent atrial fibrillation, beta-blockers are recommended for rate control. In hypertension patients, first-line drug treatment with beta-blockers is currently discussed. Indeed, several studies have shown that patients randomized in the beta-blocker arms experienced more coronary heart and cerebrovascular diseases than comparators. Their lesser effect on central blood pressure decrease could partially explain those results. Nevertheless, beta-blockers are still considered as first-line drugs for hypertension in the French and European guidelines. Long-term comparative studies focusing on central blood pressure are needed. Concerning the other indications for beta-blockers in vascular diseases, their use perioperatively to reduce surgical cardiovascular risk raised much hope, but the most recent results are disappointed and even suggest possible higher mortality. Finally, except for patients with critical ischemia of the lower limbs, presence of peripheral artery disease should probably be considered as a condition favoring their prescription. |
14,664 | Inhibition of c-Src tyrosine kinase prevents angiotensin II-mediated connexin-43 remodeling and sudden cardiac death. | The aim of this study was to test whether c-Src tyrosine kinase mediates connexin-43 (Cx43) reduction and sudden cardiac death in a transgenic mouse model of cardiac-restricted overexpression of angiotensin-converting enzyme (ACE8/8 mice).</AbstractText>Renin-angiotensin system activation is associated with an increased risk for arrhythmia and sudden cardiac death, but the mechanism is not well understood. The up-regulation of c-Src by angiotensin II may result in the reduction of Cx43, which impairs gap junction function and provides a substrate for arrhythmia.</AbstractText>Wild-type and ACE8/8 mice with and without treatment with the c-Src inhibitor 1-(1,1-dimethylethyl)-1-(4-methylphenyl)-1H-pyrazolo[3,4-d]pyrimidin-4-amine (PP1) were studied. Telemetry monitoring, in vivo electrophysiologic studies, Western blot analyses for total and phosphorylated c-Src and Cx43, immunohistochemistry staining for Cx43, and functional assessment of Cx43 with fluorescent dye diffusion were performed.</AbstractText>The majority of the arrhythmic deaths resulted from ventricular tachycardia degenerating to ventricular fibrillation (83%). Levels of total and phosphorylated c-Src were increased and Cx43 reduced in ACE8/8 mice. PP1 reduced total and phosphorylated c-Src levels, increased Cx43 level by 2.1-fold (p < 0.005), increased Cx43 at the gap junctions (immunostaining), improved gap junctional communication (dye spread), and reduced ventricular tachycardia inducibility and sudden cardiac death. The survival rate increased from 11% to 86% with 4 weeks of PP1 treatment (p < 0.005). Treatment with an inactive analog did not change survival or Cx43 levels.</AbstractText>Renin-angiotensin system activation is associated with c-Src up-regulation, Cx43 loss, reduced myocyte coupling, and arrhythmic sudden death, which can be prevented by c-Src inhibition. This suggests that an increase in c-Src activity may help mediate renin-angiotensin system-induced arrhythmias and that c-Src inhibitors might exert antiarrhythmic activity.</AbstractText>Copyright © 2011 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.</CopyrightInformation> |
14,665 | Implantable cardioverter-defibrillator patients who are upgraded and respond to cardiac resynchronization therapy have less ventricular arrhythmias compared with nonresponders. | The purpose of this study was to evaluate the impact of upgrading implantable cardioverter-defibrillator (ICD) therapy to cardiac resynchronization therapy (CRT) combined with defibrillator (CRT-D) on the occurrence of ventricular arrhythmia (VA) and appropriate ICD therapies.</AbstractText>CRT has been shown to improve left ventricular (LV) systolic function and induce reverse LV remodeling. In addition, it has been hypothesized that CRT may reduce the incidence of VA.</AbstractText>Heart failure patients receiving an upgrade from ICD to CRT-D were evaluated. Patients were considered responders to CRT if LV end-systolic volume reduced ≥15% at 6 months of follow-up. Episodes of VA, triggering device therapy (anti-tachycardia pacing and shocks) were recorded before and after upgrade for the overall population. In addition, these outcomes were compared between CRT responders and nonresponders during the follow-up period after CRT response was assessed.</AbstractText>One hundred fifteen patients (93 males [81%], age 65 ± 12 years) were evaluated during a mean follow-up of 54 ± 34 months before CRT-D upgrade and 37 ± 27 months after upgrade. In CRT responders (n = 70), the frequency of VA requiring appropriate device therapy demonstrated a trend toward a decrease from 0.51 ± 0.79 to 0.30 ± 0.59 per patient per year after CRT-D upgrade (p = 0.052). In CRT nonresponders (n = 45), the frequency of VA requiring appropriate device therapy significantly increased from 0.40 ± 0.69 to 1.21 ± 2.53 per patient per year after CRT-D upgrade (p = 0.014).</AbstractText>After upgrade from ICD to CRT-D, nonresponders to CRT showed a significant increase in VA burden requiring appropriate device therapy.</AbstractText>Copyright © 2011 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.</CopyrightInformation> |
14,666 | Brugada-like syndrome in infancy presenting with rapid ventricular tachycardia and intraventricular conduction delay. | Brugada syndrome is a potentially serious channelopathy that usually presents in adulthood and has only rarely been described in infancy. In the absence of metabolic or structural cardiac disease, rapid ventricular tachycardia (>200 bpm) and primary cardiac conduction disease are uncommon in infancy. We hypothesized that infants having rapid ventricular tachycardia and conduction abnormalities and not having structural or metabolic pathogeneses were likely to have mutations in depolarizing current channels.</AbstractText>A retrospective review of all clinical materials from a single institution over a 9-year period from all infants <2 years old and having a discharge diagnosis of ventricular tachycardia or ventricular fibrillation was performed. Among 32 infants fulfilling inclusion criteria, 12 had a structurally normal heart, and 9 of them had either prolonged QRS duration or Brugada pattern while in sinus rhythm. Of those 5 infants not having a definitive pathogenesis, electrophysiological testing had been performed in 4, and genetic testing had been performed in all 5 of those infants. During electrophysiological testing, a prolonged HV interval was present in 2 of 4, inducible ventricular tachycardia was present in 1 of 4, and a type 1 Brugada pattern was induced by intravenous procainamide in 3 of 4. Genetic testing revealed disease-causing mutations in depolarizing sodium (SCN5A) or calcium (CaCNB2b) channels in all 5 infants.</AbstractText>Infants having rapid ventricular tachycardia and conduction abnormalities in the absence of structural or metabolic abnormalities are likely to have disease-causing mutations in cardiac depolarizing channels.</AbstractText> |
14,667 | Early and long-term results of combined cardiac surgery and neoplastic resection in patients with concomitant severe heart disease and neoplasms. | It is a surgical dilemma when patients present with both severe heart disease and neoplasms. The best surgical treatment remains controversial. This study aimed to analyze the early and long-term results of simultaneous surgical treatment of severe heart disease and neoplasms.</AbstractText>We reviewed the clinical records of 15 patients who underwent simultaneous neoplastic resection and cardiac surgery between September 2006 and January 2011. There were 5 male and 10 female patients. The mean age was (59.2 ± 12.5) years and the mean left ventricular ejection fraction was (57.4 ± 11.0)%. All patients were followed up completely for a period of 12 to 51 months (mean, (33.1 ± 11.2) months).</AbstractText>Fifteen patients underwent simultaneous cardiac surgery and neoplastic resection. Cardiac procedures consisted of off pump coronary artery bypass grafting (n = 7), aortic valve replacement (n = 3), mitral valve replacement (n = 3), mitral valve replacement with coronary artery bypass grafting (n = 1) and left atrial myxoma resection (n = 1). Neoplastic resection consisted of lung cancer resection (n = 5), colonic cancer resection (n = 3), gallbladder resection (n = 1), colonic cancer resection with gallbladder resection (n = 1), hysterectomy (n = 2), hysterectomy with bilateral salpingo-oophorectomy (n = 2) and left ovariectomy (n = 1). Pathological examination confirmed malignant disease in 10 patients and benign disease in 5 patients. There were no perioperative myocardial infarctions, stroke, pericardial tamponade, renal failure or hospital deaths. The most frequent complications were atrial fibrillation (33.3%), pneumonia (26.7%), low cardiac output syndrome (6.7%) and delayed healing of surgical wounds (6.7%). There was 1 late death 42 months after surgery for recurrent malignant disease. At 1 and 3 years, survival rates were 100% (Kaplan-Meier method).</AbstractText>Simultaneous cardiac surgery and neoplastic resection was not associated with increased early or late morbidity or mortality. Cardiopulmonary bypass does not appear to adversely affect survival in patients with malignant disease. The long-term survival was determined by tumor stage.</AbstractText> |
14,668 | Disturbed left atrial mechanical function in paroxysmal atrial fibrillation: a speckle tracking study. | We aimed to assess left atrial (LA) intrinsic myocardial function and its relationship to left ventricular (LV) filling pattern in a group of paroxysmal atrial fibrillation (PAF) patients.</AbstractText>Twenty-three PAF patients (age 68 ± 7 year, 10 males) were studied using speckle tracking echocardiography and compared with 18 age and sex matched controls. LA segmental longitudinal strain (S), strain rate (SR) and myocardial velocities during atrial systole were measured as were LA diameters. E/A and E/Em were also measured.</AbstractText>LA longitudinal diameter was larger in patients (5.5 ± 0.6 vs. 4.8 ± 0.6 cm, p<0.01) and global LA S (-9.2 ± 4.3 vs. -12.9 ± 4.6%, p=0.01) and SR (-1.1 ± 0.5 vs. -1.6 ± 0.7 1/s, p<0.01) were reduced and correlated with E/A (r=0.52, p=0.01 and r=0.43, p<0.05, respectively). LA lateral S and SR were uniformly reduced compared with controls (p<0.05 for all). Both septal and lateral wall SR correlated with E/A (p<0.05 for all), only septal S correlated with E/A (p<0.05). LA myocardial velocities were highest at the annular level and lowest at the rear in both patients and controls (p<0.01 for all).</AbstractText>In PAF patients, LA systolic function is suppressed and is directly related to the pattern of LV filling which itself may suggest raised pressures. While intrinsic global and segmental function can reproducibly be studied by S and SR, myocardial velocities reflect only regional motion, thus less sensitive in demonstrating localize dysfunction.</AbstractText>Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.</CopyrightInformation> |
14,669 | Comparison of the durations of mild therapeutic hypothermia on outcome after cardiopulmonary resuscitation in the rat. | Current studies have demonstrated that applying therapeutic hypothermia for 12 to 24 hours after resuscitation from cardiac arrest improves the outcomes of cardiopulmonary resuscitation. The present study investigated whether a shorter duration of therapeutic hypothermia induced quickly and early after resuscitation would provide an equal improvement in the outcomes of cardiopulmonary resuscitation.</AbstractText>Ventricular fibrillation was induced and untreated for 8 minutes in 24 male Sprague-Dawley rats. Defibrillation was attempted after 8 minutes of cardiopulmonary resuscitation. Seven minutes after resuscitation, animals were randomized into 4 groups (n=6 each): normothermic, hypothermic-2 hours, hypothermic-5 hours, and hypothermic-8 hours. Animals in the hypothermic groups received rapid cooling, which was started 7 minutes after restoration of spontaneous circulation and maintained at 33±0.5°C for 2, 5, or 8 hours. Normothermic animals were maintained at 37±0.2°C. All animals were anesthetized and ventilated for 8 hours after resuscitation. Blood temperature was significantly decreased in the hypothermic groups. Postresuscitation myocardial function, neurological deficit scores, and 72-hour survival were significantly better in animals treated with hypothermia regardless of the duration of cooling. However, significantly better postresuscitation tissue microcirculation, myocardial ejection fraction, and neurological deficit scores were observed in the hypothermic-2 hours animals.</AbstractText>In a rat model of cardiopulmonary resuscitation, a shorter duration of mild hypothermia induced rapidly and early after restoration of spontaneous circulation improved postresuscitation microcirculation, myocardial and cerebral functions, and survival as well as, or better than, prolonged duration of hypothermia after resuscitation.</AbstractText> |
14,670 | Safety and efficacy of dronedarone in the treatment of atrial fibrillation/flutter. | Dronedarone is an amiodarone analog but differs structurally from amiodarone in that the iodine moiety was removed and a methane-sulfonyl group was added. These modifications reduced thyroid and other end-organ adverse effects and makes dronedarone less lipophilic, shortening its half-life. Dronedarone has been shown to prevent atrial fibrillation/flutter (AF/AFl) recurrences in several multi-center trials. In addition to its rhythm control properties, dronedarone has rate control properties and slows the ventricular response during AF. Dronedarone is approved in Europe for rhythm and rate control indications. In patients with decompensated heart failure, dronedarone treatment increased mortality and cardiovascular hospitalizations. However, when dronedarone was used in elderly high risk AF/AFl patients excluding such high risk heart failure, cardiovascular hospitalizations were significantly reduced and the drug was approved in the USA for this indication in 2009 by the Food and Drug Administration. Updated guidelines suggest dronedarone as a front-line antiarrhythmic in many patients with AF/Fl but caution that the drug should not be used in patients with advanced heart failure. In addition, the recent results of the PALLAS trial suggest that dronedarone should not be used in the long-term treatment of patients with permanent AF. |
14,671 | Arrhythmia-induced cardiomyopathies: the riddle of the chicken and the egg still unanswered? | The hypothesis testing of inappropriate fast, irregular, or asynchronous myocardial contraction provoking cardiomyopathy has been the primary focus of numerous research efforts, especially during the last few decades. Rapid ventricular rates resulting from supraventricular arrhythmias and atrial fibrillation (AF), irregularity of heart rhythm-basic element of AF-and asynchrony, as a consequence of right ventricular pacing, bundle branch block, or frequent premature ventricular complexes, have been established as primary causes of arrhythmia-induced cardiomyopathy. The main pathophysiological pathways involved have been clarified, including neurohumoral activation, energy stores depletion, and abnormalities in stress and strain. Unfortunately, from a clinical point of view, patients usually seek medical advice only when symptoms develop, while the causative arrhythmia may be present for months or years, resulting in myocardial remodelling, diastolic, and systolic dysfunction. In some cases, making a definite diagnosis may become a strenuous exercise for the treating physician, as the arrhythmia may not be present and, additionally, therapy must be applied for the diagnosis to be confirmed retrospectively. The diagnostic process is also hardened due to the fact that strict diagnosing criteria are still a matter of discrepancy. Therapy options include pharmaceutical agents trials, catheter-based therapies and, in the context of chronic ventricular pacing, resynchronization. For the majority of patients, partial or complete recovery is expected, although they have to be followed up thoroughly due to the risk of recurrence. Large, randomized controlled trials are more than necessary to optimize patients' stratification and therapeutic strategy choices. |
14,672 | Temporary ventricular overdrive pacing for electrical storm after coronary artery bypass grafting. | A 57-year-old man who had been receiving chemotherapy for multiple myeloma complained of chest pain and was diagnosed with coronary artery disease. Coronary artery bypass grafting without cardiopulmonary bypass was performed smoothly, and extubation was done in the operating room. The next evening, cluster of ventricular tachycardia and fibrillation triggered by ventricular premature contractions occurred and required multiple electrical defibrillations. Despite intravenous administration of lidocaine, amiodarone, magnesium, and β-blocker, the storm sustained and was suppressed only by temporary ventricular overdrive pacing. He was discharged on foot. |
14,673 | Atrial fibrillation pathophysiology: implications for management. | Atrial fibrillation (AF), the most common sustained cardiac arrhythmia, is an important contributor to population morbidity and mortality. An arrhythmia that is particularly common in the elderly, AF is growing in prevalence with the aging of the population. Our understanding of the basic mechanisms that govern AF occurrence and persistence has been increasing rapidly. This article reviews the basic pathophysiology of AF over a broad range of levels, touching on the tissue mechanisms that maintain the arrhythmia, the relationship between clinical presentation and basic mechanisms, ion channel and transporter abnormalities that lead to ectopic impulse formation, basic models and tissue determinants of reentry, ion channel determinants of reentry, the nature and roles of electric and structural remodeling, autonomic neural components, anatomic factors, interactions between atrial and ventricular functional consequences of AF, and the basic determinants of atrial thromboembolism. We then review the potential implications of the basic pathophysiology of the arrhythmia for its management. We first discuss consequences for improved rhythm control pharmacotherapy: targeting underlying conditions, new atrium-selective drug targets, new targets for focal ectopic source suppression, and upstream therapy aiming to prevent remodeling. We then review the implications of basic mechanistic considerations for rate control therapy, AF ablation, and the prevention of thromboembolic events. We conclude with some thoughts about the future of translational research related to AF mechanisms. |
14,674 | An appropriate defibrillation threshold obtained by the combined connection between two shock leads and ICD generator. | A 60-year-old man with arrhythmogenic right ventricular cardiomyopathy was readmitted for the battery exchange of his implantable cardioverter-defibrillator (ICD). Since (i) he had been treated with a dual-coil shock lead (Sprint Fidelis, Medtronic) and (ii) pre-operative venography showed mild collateral flow to the left subclavian vein, a single-coil lead was additionally implanted. However, the single-coil defibrillation system was unable to terminate the induced ventricular fibrillation (VF), thus dual defibrillation shock pathways were created using the connection to the superior vena cava coil of the Fidelis lead. The combined connections of the two shock leads provided an appropriate margin of the defibrillation threshold. |
14,675 | Efficacy and safety of celivarone, with amiodarone as calibrator, in patients with an implantable cardioverter-defibrillator for prevention of implantable cardioverter-defibrillator interventions or death: the ALPHEE study. | Celivarone is a new antiarrhythmic agent developed for the treatment of ventricular arrhythmias. This study investigated the efficacy and safety of celivarone in preventing implantable cardioverter-defibrillator (ICD) interventions or death.</AbstractText>Celivarone (50, 100, or 300 mg/d) was assessed compared with placebo in this randomized, double-blind, placebo-controlled, parallel-group study. Amiodarone (200 mg/d after loading dose of 600 mg/d for 10 days) was used as a calibrator. A total of 486 patients with a left ventricular ejection fraction ≤40% and at least 1 ICD intervention for ventricular tachycardia or ventricular fibrillation in the previous month or ICD implantation in the previous month for documented ventricular tachycardia/ventricular fibrillation were randomized. Median treatment duration was 9 months. The primary efficacy end point was occurrence of ventricular tachycardia/ventricular fibrillation-triggered ICD interventions (shocks or antitachycardia pacing) or sudden death. The proportion of patients experiencing an appropriate ICD intervention or sudden death was 61.5% in the placebo group; 67.0%, 58.8%, and 54.9% in the celivarone 50-, 100-, and 300-mg groups, respectively; and 45.3% in the amiodarone group. Hazard ratios versus placebo for the primary end point ranged from 0.860 for celivarone 300 mg to 1.199 for celivarone 50 mg. None of the comparisons versus placebo were statistically significant. Celivarone had an acceptable safety profile.</AbstractText>Celivarone was not effective for the prevention of ICD interventions or sudden death.</AbstractText>http://www.clinicaltrials.gov. Unique identifier: NCT00993382.</AbstractText> |
14,676 | Dronedarone in high-risk permanent atrial fibrillation. | Dronedarone restores sinus rhythm and reduces hospitalization or death in intermittent atrial fibrillation. It also lowers heart rate and blood pressure and has antiadrenergic and potential ventricular antiarrhythmic effects. We hypothesized that dronedarone would reduce major vascular events in high-risk permanent atrial fibrillation.</AbstractText>We assigned patients who were at least 65 years of age with at least a 6-month history of permanent atrial fibrillation and risk factors for major vascular events to receive dronedarone or placebo. The first coprimary outcome was stroke, myocardial infarction, systemic embolism, or death from cardiovascular causes. The second coprimary outcome was unplanned hospitalization for a cardiovascular cause or death.</AbstractText>After the enrollment of 3236 patients, the study was stopped for safety reasons. The first coprimary outcome occurred in 43 patients receiving dronedarone and 19 receiving placebo (hazard ratio, 2.29; 95% confidence interval [CI], 1.34 to 3.94; P=0.002). There were 21 deaths from cardiovascular causes in the dronedarone group and 10 in the placebo group (hazard ratio, 2.11; 95% CI, 1.00 to 4.49; P=0.046), including death from arrhythmia in 13 patients and 4 patients, respectively (hazard ratio, 3.26; 95% CI, 1.06 to 10.00; P=0.03). Stroke occurred in 23 patients in the dronedarone group and 10 in the placebo group (hazard ratio, 2.32; 95% CI, 1.11 to 4.88; P=0.02). Hospitalization for heart failure occurred in 43 patients in the dronedarone group and 24 in the placebo group (hazard ratio, 1.81; 95% CI, 1.10 to 2.99; P=0.02).</AbstractText>Dronedarone increased rates of heart failure, stroke, and death from cardiovascular causes in patients with permanent atrial fibrillation who were at risk for major vascular events. Our data show that this drug should not be used in such patients. (Funded by Sanofi-Aventis; PALLAS ClinicalTrials.gov number, NCT01151137.).</AbstractText> |
14,677 | Risk of mortality for ventricular arrhythmia in ambulatory LVAD patients. | There are limited data regarding the incidence and prognostic significance of ventricular arrhythmias (VA) in ambulatory continuous flow left ventricular assist device (LVAD) patients.</AbstractText>Sixty-one consecutive patients from November 1, 2006 through December 31, 2010 with an LVAD and implantable cardioverter defibrillator that survived to discharge from the LVAD implantation admission were studied. Follow-up began from date of discharge with both devices in situ and ended with death, transplant, on June 1, 2011. Pre-LVAD VA history was related to the primary endpoints of post-LVAD VA, mortality, and the combined endpoint of post-LVAD VA/mortality.</AbstractText>During a mean follow-up of 622 days 19 patients (31%) experienced VA (14 episodes of VT, 5 episodes of VF). Pre-LVAD VA was predictive of post-LVAD VA (hazard ratio [HR] 2.91, P = 0.026) and the combined post-LVAD VA/mortality endpoint (HR 2.70, P = 0.021) but only displayed a nonsignificant association with mortality (HR 2.30, P = 0.11). In multivariate analysis, pre-LVAD VA remained a significant predictor of post-LVAD VA (HR 2.84, P = 0.03) and the combined post-LVAD VA/mortality endpoint (HR 2.65, P = 0.025). Post-LVAD VA was the strongest univariate predictor of mortality (HR 13.92, P < 0.001) and remained so after multivariate adjustment (HR 9.69, P = 0.001). Post-LVAD VA occurred at a mean of 1 year from mortality events with 45% within 1 month.</AbstractText>Pre-LVAD VA is a significant predictor of post-LVAD VA but not of mortality. VA in the continuous flow LVAD population carries a significant risk of mortality often within the first month.</AbstractText>© 2011 Wiley Periodicals, Inc.</CopyrightInformation> |
14,678 | The determinants of clinical outcome and clinical response to CRT are not the same. | The purpose of treatment is to alter outcomes favourably. From a clinical perspective, these outcomes may include symptoms, quality of life, disability, morbidity and mortality. However, a good outcome does not mean that the intervention was effective and a seemingly poor outcome could have been worse without intervention. Patients may have a good outcome either because their disease was due to run a benign course, or because they responded to the intended treatment or because they responded to some other ancillary treatment. Clearly, there is a link between response and outcome but it is loose and uncertain. The clinical substrate being treated is often a stronger determinant of outcome than the response to the intervention. The concepts of outcome and response can both be useful when deciding whether or not to implant a device but they are not the same and their determinants will differ. Patients with dilated cardiomyopathy and those with inter-ventricular mechanical dyssynchrony have a better prognosis than those who do not have these features, but this is true whether or not they receive cardiac resynchronisation therapy (CRT). Many characteristics predict outcome in patients considered for CRT but none consistently predict response. On the other hand, guidelines recommend CRT in populations that have not yet been adequately studied, such as those with atrial fibrillation. Clinicians should follow the criteria for patient selection in the landmark trials when selecting patients for CRT, should extrapolate with caution from these and should be extremely cautious in the interpretation of observational data. |
14,679 | The electrophysiological properties of ranolazine: a metabolic anti-ischemic drug or an energy-efficient antiarrhythmic agent? | Ranolazine, a newer anti-ischemic agent that appears to induce a more efficient utilization of adenosine triphosphate at the cellular level, has been shown to be clinically beneficial in patients with chronic stable angina. More recently, the antiarrhythmic effects of the drug have been described in patients with acute coronary syndromes, as well as in those with atrial fibrillation, when combined with other agents. Experimentally, the predominant inhibitory effects on late I(Na), I(Ca), I(Na-Ca), and I(Ks), with little or no effect on I(to) or I(K1), have been demonstrated. Different experimental models have shown the potential beneficial effect of the drug in both supraventricular and ventricular arrhythmias. Interestingly, despite its potential prolongation of the QT interval, ranolazine does not appear to induce ventricular arrhythmias in animal models. Whether the antiarrhythmic effect is secondary to a more efficient energy production by the cardiac cell or by its direct effect on ion channels is still unclear. The effect of ranolazine on other ionic currents, as well as its potential as a clinically relevant antiarrhythmic agent, still needs to be studied. |
14,680 | Efficacy and safety of ventricular tachycardia ablation with mechanical circulatory support compared with substrate-based ablation techniques. | Catheter ablation of ventricular tachycardia (VT) can be limited by haemodynamic instability. In these cases, substrate-based ablation is typically performed. An alternative is to perform activation and entrainment mapping during VT supported by a percutaneous left ventricular assist device (pVAD). We sought to compare the complication and success rates of pVAD-assisted VT ablation with scar-based techniques.</AbstractText>Thirteen consecutive patients with haemodynamically unstable VT underwent pVAD-assisted ablation (pVAD group) and were retrospectively compared with 18-matched patients undergoing a substrate-based VT ablation (non-pVAD group). There was no significant difference in age or ejection fraction between the groups although pVAD patients tended to have more shocks in the preceding months. Procedure times were longer for the pVAD group. The number of monomorphic VTs induced was greater in the pVAD group (3.2 vs. 1.6, P= 0.04); however, after ablation, there was no difference in inducibility between the pVAD and non-pVAD group (10 of 13 vs. 12 of 18; 77 vs. 67%, P = 0.69). There was no difference in acute complications including stroke or death. At 9 ± 3 months, 1-year freedom from implantable cardioverter-defibrillator (ICD) shocks/therapies for sustained VT were similar (P= 0.96). In multivariable analysis, the absence of atrial fibrillation (hazard ratio=0.15, P= 0.04) was associated with a lower incidence of ICD shocks.</AbstractText>In high-risk patients, pVAD-assisted VT ablation guided by activation and entrainment mapping is a feasible alternative to substrate mapping and allows outcomes comparable to substrate mapping.</AbstractText> |
14,681 | Reduced ventricular proarrhythmic potential of the novel combined ion-channel blocker AZD1305 versus dofetilide in dogs with remodeled hearts. | AZD1305 is an investigational antiarrhythmic agent for management of atrial fibrillation. It blocks various cardiac ion currents at different potencies and has atrial-predominant electrophysiological effects. We investigated the electrophysiological and proarrhythmic effects of AZD1305 versus dofetilide in dogs with chronic complete atrioventricular block and myocardial hypertrophic remodeling.</AbstractText>AZD1305 was administered to anesthetized mongrel dogs before and >2 weeks after the induction of atrioventricular block and ventricular and atrial electrophysiological parameters were assessed. In all dogs, the selective I(Kr) blocker dofetilide was used to examine susceptibility to acquired torsades de pointes in chronic atrioventricular block and for comparison. At normal sinus rhythm, AZD1305 increased QT and RR intervals from 290±7 to 397±15 ms (+37%, P<0.0001) and from 603±22 to 778±32 ms (+29%, P=0.002), respectively. In the same animals at chronic atrioventricular block, AZD1305 increased the QT interval from 535±28 to 747±36 ms (+40%, P<0.0001), similar to the QT prolongation by dofetilide (511±22 to 703±45 ms [+38%, P<0.0001]). AZD1305 slightly slowed the idioventricular rhythm. Whereas all (n=14) chronic atrioventricular block animals exhibited torsades de pointes on dofetilide, the arrhythmia was induced in only 4 of 11 dogs after AZD1305. Beat-to-beat variability of left-ventricular monophasic-action-potential duration increased after dofetilide (2.3±0.2 to 6.3±0.7 ms; P<0.0001) but not after AZD1305 (2.8±0.3 to 3.7±0.3 ms; P=0.20) despite similar left-ventricular monophasic-action-potential duration prolongations.</AbstractText>Despite causing similar degrees of repolarization delay as the selective I(Kr) blocker dofetilide, the combined ion-channel blocker AZD1305 induces less repolarization instability and has a lower ventricular proarrhythmic potential in the remodeled dog heart.</AbstractText> |
14,682 | Radiofrequency ablation of cardiac arrhythmias: past, present and future. | The treatment of cardiac arrhythmias has been revolutionized by the ability to definitively treat many patients with radiofrequency catheter ablation, rather than requiring lifelong medication. This review covers the history of how this has developed and the methods used currently and explores what the future holds for this rapidly evolving branch of Cardiology. |
14,683 | Total epinephrine dose during asystole and pulseless electrical activity cardiac arrests is associated with unfavourable functional outcome and increased in-hospital mortality. | Epinephrine is the drug of choice during advanced cardiac life support. The cumulative dose of epinephrine applied during resuscitation was shown to be independently associated with unfavourable outcome after ventricular fibrillation cardiac arrest in humans. Our objective was to investigate the association between the cumulative dose of epinephrine applied during resuscitation and unfavourable functional outcome and in-hospital mortality, in patients with asystole and pulseless electric activity.</AbstractText>Data on 946 patients admitted to the emergency department after resuscitation of witnessed in-hospital and out-of hospital cardiac arrest with asystole or pulseless electric activity were retrieved from the cardiac arrest registry of the emergency department at the Vienna General Hospital/Medical University of Vienna. Data were documented according to Utstein Style. The risk factor was cumulative epinephrine categorized into quartiles. The endpoints were unfavourable functional outcome and in-hospital mortality.</AbstractText>The median cumulative amount of epinephrine administered was 2mg (IQR 0-5), ranging from 1 to 50mg. Of all patients 643/946 (68%) had an unfavourable functional outcome, 649/946 (69%) died during hospital stay. The multivariable analysis showed a statistically significant increasing risk for unfavourable functional outcome and in-hospital mortality outcome with increasing cumulative doses of epinephrine (unfavourable functional outcome: OR 1-1.45-2.25-2.95 over quartiles of epinephrine; in hospital mortality: OR 1-1.35-2.15-2.82 over quartiles of epinephrine).</AbstractText>Our results show that an increasing cumulative dose of epinephrine during resuscitation of patients with asystole and pulseless electric activity is an independent risk factor for unfavourable functional outcome and in-hospital mortality.</AbstractText>Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.</CopyrightInformation> |
14,684 | Mild-to-moderate kidney dysfunction and the risk of sudden cardiac death in the setting of acute myocardial infarction. | Although end-stage renal disease is known to elevate the risk of sudden cardiac death (SCD), the role of less severe renal impairment in SCD is unclear.</AbstractText>The purpose of this study was to examine the association between mild-to-moderate renal impairment and first ischemic ventricular fibrillation (VF).</AbstractText>Renal function in patients included in the Arrhythmia Genetics in the NEtherlands Study (AGNES) were compared. Cases (n = 337, age 56 ± 1 year, 80% men) were defined as patients who had survived VF at the time of their first acute ST elevation myocardial infarction (STEMI), and controls (n = 339, age 58 ± 1 years, 80% men) were defined as those without VF during their first acute STEMI. Estimated glomerular filtration rate (eGFR) at the time of acute STEMI was computed using the 4-variable Modification of Diet in Renal Disease equation.</AbstractText>At eGFR less than 105 mL/min, a decrease in eGFR was associated with elevated odds of developing VF during STEMI. The association was essentially flat at eGFR levels >105 mL/min. The lowest eGFR quintile was associated with a >6-fold increase in odds of developing VF compared to the fourth quintile. This association between eGFR and VF at the time of STEMI remained significant after adjusting for potential confounders including electrolyte levels.</AbstractText>Mild-to-moderate kidney dysfunction is associated with a significantly elevated risk of VF in the setting of acute STEMI. Further studies are needed to investigate the precise mechanisms by which mild kidney function results in VF.</AbstractText>Copyright © 2012 Heart Rhythm Society. Published by Elsevier Inc. All rights reserved.</CopyrightInformation> |
14,685 | Long-term effects of catheter ablation for lone atrial fibrillation: progressive atrial electroanatomic substrate remodeling despite successful ablation. | Whether curative ablation can prevent progression of the atrial electroanatomic remodeling associated with atrial fibrillation (AF) is not known.</AbstractText>The purpose of this study was to determine whether successful radiofrequency ablation (RFA) of AF can prevent progression of the atrial substrate associated with AF.</AbstractText>Detailed right atrial electroanatomic maps from 11 patients without apparent structural heart disease undergoing RFA of AF at baseline and ≥6 months following successful RFA were compared to 11 control patients undergoing electrophysiologic evaluation of supraventricular tachycardia. Bipolar voltage, conduction, effective refractory periods (ERPs), and signal complexity were assessed.</AbstractText>At baseline compared with the control group, the AF group demonstrated (1) lower voltage (P <.001); (2) slowed conduction (P = .005); (3) more prevalent complex signals (P <.001); (4) prolonged regional refractoriness (P <.05), and (5) left atrial dilation (P = .01). At 10 ± 13 month follow-up, the AF group demonstrated the following compared to baseline: (1) lower voltage (P <.05); (2) either no improvement or further slowing of conduction; (3) further prolongation of regional refractoriness (P <.05); and (4) reversal of left atrial dilation (P <.05).</AbstractText>Patients with lone AF demonstrate evidence of an abnormal atrial substrate at baseline compared to control patients without AF. This substrate does not appear to reverse even after successful catheter ablation. These findings may have implications for long-term outcomes of ablation and for timing of ablative intervention.</AbstractText>Copyright © 2012 Heart Rhythm Society. Published by Elsevier Inc. All rights reserved.</CopyrightInformation> |
14,686 | Racial differences in sudden cardiac death among hypertensive patients during antihypertensive therapy: the LIFE study. | In the general population, blacks appear to have a higher risk of sudden cardiac death (SCD).</AbstractText>To determine whether black hypertensive patients have a higher SCD incidence.</AbstractText>The incidence of SCD was examined in 533 black and 8660 nonblack hypertensive patients with electrocardiographic left ventricular hypertrophy randomly assigned to losartan- or atenolol-based treatment.</AbstractText>During a mean follow-up of 4.8 ± 0.9 years, SCD occurred in 178 patients (1.9%); 5-year SCD incidence was significantly higher in black than in nonblack patients (3.9% vs 1.9%; P = .007). In univariate Cox analyses, black patients had a 97% higher risk of SCD (hazard ratio 1.97; 95% confidence interval 1.19-3.25; P = .015). In multivariate Cox analyses adjusting for randomized treatment, age, sex, body mass index, diabetes, history of heart failure, atrial fibrillation, myocardial infarction, ischemic heart disease, stroke, peripheral vascular disease, smoking, serum total and high-density lipoprotein cholesterol level, creatinine level, glucose level, and urine albumin/creatinine ratio and for incident myocardial infarction, in-treatment heart rate, QRS duration, diastolic and systolic pressure, Cornell voltage-duration product, and Sokolow-Lyon voltage left ventricular hypertrophy treated as time-varying covariates, black race remained associated with a 98% increased risk of SCD (hazard ratio 1.98; 95% confidence interval 1.12-3.59; P = .020).</AbstractText>Black hypertensive patients are at increased risk of SCD. The higher risk of SCD in black patients persists after adjusting for the higher prevalence of risk factors in black patients, in-treatment blood pressure, and the established predictive value of in-treatment electrocardiographic left ventricular hypertrophy and heart rate for SCD in this population.</AbstractText>Copyright © 2012 Heart Rhythm Society. Published by Elsevier Inc. All rights reserved.</CopyrightInformation> |
14,687 | [Therapeutic hypothermia after pediatric cardiac arrest]. | Therapeutic hypothermia (TH) improves neurological outcome in adults after ventricular fibrillation cardiac arrest and in neonates with hypoxic ischemic encephalopathy. The effect of TH in children is under investigation.</AbstractText>To assess the feasibility, efficacy and safety of a pilot program of TH in pediatric cardiac arrest.</AbstractText>Prospective study in a pediatric intensive care unit. An external cooling method with a servo system was used on all patients according to an established protocol. Values expressed as median (IQ range).</AbstractText>Six patients were included, of whom 5 had an out of hospital cardiac arrest. The mean age was 33 months (16-120) and Glasgow coma scale 6 (4-7). The T° prior to the induction of TH was 39.2° C (39.1-39.4). The median T° used was 34.0° C (33.5-34.8° C), which was reached in 4h. (3-7) after the start and maintained for 48h. (45-54). The rewarming was carried out over a period of 14h. (12-16). Hypokalemia was the most common adverse event found. Five patients survived to hospital discharge with a Glasgow Coma Scale of 13 (11-14). At 6 months follow up the Pediatric Cerebral Performance Category score was ≤ 2 in three patients.</AbstractText>In this pilot study, the use of mild therapeutic hypothermia with a protocol that included rapid sequence induction with an external surface cooling technique was feasible, effective and safe in children with cardiac arrest.</AbstractText>Copyright © 2011 Asociación Española de Pediatría. Published by Elsevier Espana. All rights reserved.</CopyrightInformation> |
14,688 | Percutaneous implantation of the Edwards SAPIEN transcatheter heart valve for conduit failure in the pulmonary position: early phase 1 results from an international multicenter clinical trial. | The purpose of this study was to evaluate the safety and effectiveness of the Edwards SAPIEN transcatheter heart valve (Edwards Lifesciences LLC, Irvine, California) in the pulmonary position in patients with moderate to severe pulmonary regurgitation with or without stenosis.</AbstractText>Transcatheter pulmonary valve replacement is evolving, but to date, experience has been limited to the Melody valve (Medtronic Inc., Minneapolis, Minnesota).</AbstractText>Eligible patients with dysfunctional right ventricle-to-pulmonary artery conduits were screened if body weight was ≥35 kg and the in situ conduit diameter was ≥16 mm and ≤24 mm. Standardized implantation and follow-up protocols were used.</AbstractText>Thirty-six patients from 4 centers were recruited between April 2008 and May 2010. Mean body weight was 73.4 ± 22.9 kg. Successful valve deployment was achieved in 33 of 34 attempts (97.1%). Valve migration occurred in 3 patients, with 2 requiring surgical retrieval; however, 1 patient underwent successful perventricular valve implantation. Further intraprocedure complications included pulmonary hemorrhage (n = 2), ventricular fibrillation (n = 1), and stent migration (n = 1). Pullback gradient across the conduit decreased from 26.8 ± 18.4 mm Hg to 11.7 ± 8.0 mm Hg (p < 0.001). The right ventricular/aortic pressure ratio decreased from 0.6 ± 0.2 to 0.4 ± 0.1 (p < 0.001). Peak Doppler gradient across the right ventricular outflow tract decreased from 41.9 ± 27.9 mm Hg to 19.1 ± 13.3 mm Hg (p < 0.001). At 6-month follow-up, all patients were alive. The number of patients with New York Heart Association functional class I increased from 5 at baseline to 27 at follow-up. Pulmonary regurgitation was ≤2+ in 97% of patients. Freedom from reintervention was 97% with 1 patient undergoing elective placement of a second valve due to conduit-induced distortion of the initial implant.</AbstractText>Transcatheter pulmonary valve replacement using the Edwards SAPIEN transcatheter heart valve is safe and effective in patients with dysfunctional right ventricle-to-pulmonary artery conduits.</AbstractText>Copyright © 2011 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.</CopyrightInformation> |
14,689 | Myocardial performance index derived from preejection period: a novel and feasible parameter in evaluation of cardiac performance in patients with permanent atrial fibrillation. | Using tissue Doppler echocardiography, we can measure preejection period (PEPa), defined as the interval measured from the onset of QRS to the onset of the systolic mitral annular velocity pattern, isovolumic relaxation time (IVRTa), defined as the interval measured from the end of systolic mitral annular velocity pattern to the onset of diastolic mitral annular velocity pattern, and ejection time (ETa), defined as the interval measured from the onset to the end of systolic mitral annular velocity pattern on the same cardiac cycle. The aim of this study is to test the applicability of PEPa-derived myocardial performance index (MPI), defined as the ratio of PEPa + IVRTa to ETa, as an indicator of combined left ventricular systolic and diastolic function in patients with permanent atrial fibrillation.</AbstractText>Echocardiographic examination was performed in 54 consecutive patients with permanent atrial fibrillation. Clinical and echocardiographic parameters were compared and analyzed.</AbstractText>After a multivariate analysis, the average RR interval on the tissue Doppler image (β=-0.328, P = 0.002), left ventricular ejection fraction (β=-0.260, P = 0.024), and early diastolic mitral annular velocity (β=-0.408, P < 0.001) were the major determinants of PEPa-derived MPI.</AbstractText>PEPa-derived MPI had a significant correlation with echocardiographic left ventricular diastolic and systolic function. It may be a novel and feasible indicator in assessment of global left ventricular function in patients with permanent atrial fibrillation.</AbstractText>© 2011, Wiley Periodicals, Inc.</CopyrightInformation> |
14,690 | Telmisartan: just an antihypertensive agent? A literature review. | The modulation of the renin angiotensin aldosterone system (RAAS) is an important pathway in managing high blood pressure, and its overexpression plays a key role in target end-organ damage. Telmisartan is an angiotensin II receptor blocker (ARB) with unique pharmacologic properties, including the longest half-life among all ARBs; this leads to a significant and 24-h sustained reduction of blood pressure. Telmisartan has well-known antihypertensive properties, but there is also strong clinical evidence that it reduces left ventricular hypertrophy, arterial stiffness and the recurrence of atrial fibrillation, and confers renoprotection.</AbstractText>This paper reviews telmisartan's pharmacological properties in terms of efficacy for hypertension control and, importantly, focuses on its new therapeutic indications and their clinical implications.</AbstractText>ONTARGET (ongoing telmisartan alone and in combination with ramipril global endpoint trial) demonstrated, that telmisartan confers cardiovascular protective effects similar to those of ramipril, but with a better tolerability. Moreover, recent investigations focused on the capability of telmisartan to modulate the peroxisome proliferator-activated receptor-gamma (PPAR-γ), an established target in the treatment of insulin resistance, diabetes and metabolic syndrome, whose activation is also correlated to anti-inflammatory and, finally, anti-atherosclerotic properties. Telmisartan shows peculiar features that go beyond blood pressure control. It presents promising and unique protective properties against target end-organ damage, potentially able to open a scenario of new therapeutic approaches to cardiovascular disease.</AbstractText> |
14,691 | Influence of ramiprilat and losartan on ischemia reperfusion injury in rat hearts. | HYPOTHESIS/INTRODUCTION: Our aim was to investigate whether a non-hypotensive dose of ramiprilat and losartan has myocardial protective effects during myocardial ischemia/reperfusion in vivo.</AbstractText>Three groups of rats were given 10 mg/kg per day of losartan for one (L-1W), four (L-4W) or 10 (L-10W) weeks. Another three groups were given 50 µg/kg per day of ramiprilat for one (R-1W), four (R-4W) or 10 (R-10W) weeks. The animals underwent 30 min of left anterior descending artery occlusion and subsequent reperfusion for 120 min.</AbstractText>Myocardial infarct size (IS) was reduced in R-1W (28.4 ± 6.3%, p < 0.001), R-4W (27.8 ± 7.4, p < 0.001), L-4W (31.8 ± 6%, p < 0.05) and L-10W (25.3 ± 5.7, p < 0.001) groups compared with a saline group (48.3 ± 7.8%). A significant reduction in the number of ventricular ectopic beats (VEBs) was noted in groups R-1W (209 ± 41, p < 0.01), R-4W (176 ± 39, p < 0.01), L-4W (215 ± 52, p < 0.05) and L-10W (191 ± 61, p < 0.01 vs. saline 329 ± 48). The incidence of irreversible ventricular fibrillation (VF) and mortality were decreased significantly only in L-10W group. There were no significant decreases in episodes of VT, the incidence of irreversible VF and mortality in all of the groups treated with ramiprilat.</AbstractText>These data indicate that losartan and ramiprilat protect the heart against ischemia/reperfusion injury independently of their hemodynamic effects but in a time-dependent manner.</AbstractText> |
14,692 | Outcome after implantable cardioverter-defibrillator in patients with Brugada syndrome: the Gulf Brugada syndrome registry. | Among patients with Brugada syndrome (BS) and aborted cardiac arrest, syncope, or inducible ventricular fibrillation at electrophysiologic study (EPS), the only currently recommended therapy is an implantable cardioverter-defibrillator (ICD), but these are not without complications. We assessed the total number of shocks (appropriate and inappropriate) and complications related to ICD in patients with BS.</AbstractText>Twenty-five patients implanted with ICD for BS in 6 Gulf centers between January 1, 2002, and December 31, 2010, were reviewed. Implantable cardioverter-defibrillator indication was based on aborted cardiac arrest (24%), syncope (56%), or in asymptomatic patients with positive EPS (20%). During a follow-up of 41.2 ± 17.6 months, 3 patients (all with prior cardiac arrest) had appropriate device therapy. Four patients developed complications; 3 of them had inappropriate shocks.</AbstractText>In our cohort, appropriate device therapy was limited to cardiac arrest survivors, whereas none of those with syncope and/or positive EPS had arrhythmias. Overall complication rate was relatively high, including inappropriate ICD shocks.</AbstractText>Copyright © 2012 Elsevier Inc. All rights reserved.</CopyrightInformation> |
14,693 | Pre-implantation psychological functioning preserved in majority of implantable cardioverter defibrillator patients 12 months post implantation. | The impact of ICD therapy on patient well being has typically focused on mean differences between groups, thereby neglecting changes within individuals. Using an intra-individual approach, we examined (i) the prevalence of implantable cardioverter defibrillator (ICD) patients maintaining their pre implantation level of psychological functioning at 12 months, and (ii) factors associated with deterioration in functioning.</AbstractText>Consecutively implanted ICD patients (n=332) completed a set of standardized and validated patient reported measures at baseline and at 12 months post implantation.</AbstractText>The majority of patients (72.8% to 81.7%) preserved their pre implantation level of psychological functioning 12 months post implantation. In adjusted analysis, ICD shock (all ps<.001) and Type D personality (all ps<.05) were independent predictors of deterioration in psychological functioning at 12 months across all domains, while baseline psychological status was associated with an improvement (all ps<.05). Patients with a primary prevention indication experienced a decrease in ICD concerns (p=.03) and anxiety (p=.006), and older patients (p=.04) a decrease in anxiety symptoms during the follow-up period. By contrast, patients with left ventricular dysfunction (p=.007) and atrial fibrillation (p=.02) were more likely to experience an increase in anxiety.</AbstractText>The majority of ICD patients maintained their pre implantation level of psychological functioning at 12 months. A subset of patients was at risk of poor psychological adaptation, attributable to ICD shocks, Type D personality, atrial fibrillation, and left ventricular dysfunction, while primary prevention indication and older age had a protective effect against deterioration in functioning.</AbstractText>Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.</CopyrightInformation> |
14,694 | Impact of alcohol habits and smoking on the risk of new-onset atrial fibrillation in hypertensive patients with ECG left ventricular hypertrophy: the LIFE study. | The incidence of new-onset atrial fibrillation (AF) is increased by uncontrolled hypertension, and antihypertensive treatment reduces new-onset AF. However, it is unclear whether alcohol intake and smoking influence the risk of new-onset AF during antihypertensive treatment.</AbstractText>In the Losartan Intervention For Endpoint reduction in Hypertension (LIFE) study, a double-blinded, randomized, parallel-group study, 9193 hypertensive patients with electrocardiogram (ECG)-documented left ventricular hypertrophy (LVH), randomized to once-daily losartan- or atenolol-based antihypertensive therapy were followed for a mean of 4.8 years. At baseline, 8831 patients (54% women, mean age 67 years, mean blood pressure 174/98 mmHg after placebo run-in) had neither a history of AF nor AF on ECG, and they were thus at risk of developing this condition during the study.</AbstractText>New-onset AF occurred in 353 (4%) patients. Univariate Cox analyses showed that intake of alcohol > 10 units/week compared with less or no alcohol intake predicted new-onset AF (Hazard ratio, HR = 1.60 [95% CI 1.02-2.51], p = 0.043). Multivariate Cox regression analysis showed that intake of alcohol > 10 units/week predicted new-onset AF (p = 0.010) independently of most other univariate predictors, except when also baseline serum cholesterol, serum potassium and urinary albumin/creatinine ratio were included in the model (HR = 1.60 [95% CI 0.94-2.72], p = 0.081). Impact of smoking was not significant in Cox univariate or multivariate analyses, and there were no significant interactions between high alcohol intake and either smoking or gender on the risk of getting AF.</AbstractText>Up to 10 drinks of alcohol per week appears to be safe with respect to the risk for AF in hypertensive patients with LVH. Our data suggest that alcohol intake above this level may be marginally deleterious, while no effect of smoking on risk of AF was detected in hypertensive patients with LVH.</AbstractText> |
14,695 | [Long-term follow-up after catheter-ablation of atrioventricular junction and pacemaker implantation in patients with uncontrolled atrial fibrillation and heart failure]. | Atrioventricular (AV) junction ablation coupled with pacemaker implantation is an effective therapeutic option for rate control in atrial fibrillation (AF) and heart failure (HF). However, there is controversy regarding the long-term outcome of the procedure, since right ventricular stimulation can lead to left ventricular remodelling and HF.</AbstractText>The aim of the study was to determine a 5-year outcome of the procedure on survival, HF control and myocardial function in patients with HF and uncontrolled AF.</AbstractText>All patients with AF and HF who underwent AV-junction ablation with pacemaker implantation in our institution were followed after the procedure. HF diagnosis was established if > or = 2 of the following criteria were present: 1) ejection fraction (EF) < or = 45%; 2) previous episode of congestive HF (CHF); 3) NYHA-class > or = 2; and 4) use of drug-therapy for HF.</AbstractText>Study included 32 patients (25 males; 53.4 +/- 9.6 years). The mean heart rate was 121 +/- 25 bpm before and 75 +/- 10 bpm after ablation (p=0.001). Over the follow-up of 5.0 +/- 4.0 years nine patients (28.1%) died (five died suddenly, three of terminal CHF and one of stroke). After the procedure, CHF occurrence was reduced (p=0.001), as well as the annual number of hospitalizations (p=0.001) and the number of drugs for CHF (p=0.028). In addition, NYHA-class and EF were improved, from 3.3 +/- 0.7 to 1.6 +/- 0.8 (p<0.001) and from 39 +/- 11% to 51 +/- 10% (p<0.001), respectively.</AbstractText>In HF patients with uncontrolled AF, 5-year mortality after AV-junction ablation and pacemaker implantation was 28%. In the majority of these patients good rate of AF and HF control were achieved, as well as the improvement of functional status and myocardial contractility.</AbstractText> |
14,696 | Predictors for the development of severe tricuspid regurgitation with anatomically normal valve in patients with atrial fibrillation. | Atrial fibrillation (AF) may be a risk factor for severe functional tricuspid valve regurgitation (FTR). We aimed to determine the predictors of severe FTR in patients with AF.</AbstractText>From our echocardiographic laboratory database, we searched for and reviewed the medical records of consecutive patients with severe FTR and AF seen at Mayo Clinic in Arizona from 2002 through 2009. Our search identified 42 patients who met all inclusion criteria. These patients (cases) with severe FTR and AF were compared with 38 patients (controls) with AF who had no greater than mild tricuspid regurgitation. Case patients with severe FTR were older than controls (mean, 81 years vs. 76 years; P < 0.001) and more frequently had chronic AF (69% vs 26%; P < 0.001). Mean right atrial volume (86 mL/m(2) vs 46 mL/m(2) ; P < 0.001), right ventricular volume (42 mL ± 33 mL vs 22 mL ±8 mL; P < 0.001) and tricuspid annular diameter (3.6 cm vs 3.0 cm; P < 0.001) were larger in cases than in controls. Patients with severe FTR also had a higher prevalence of right-sided heart failure (69% vs 16%; P < 0.001). After adjusting for age and gender, right atrial and right ventricular volumes were independent predictors for the development of severe FTR in patients with AF (odds ratio, 1.7 [95% CI, 1.3-2.8] for every 10 mL/m(2) increase in right atrial volume; P = 0.0002 and odds ratio, 3.1 [95% CI, 1.5-8.9] for every 10 mL increase in right ventricular volume; P = 0.0002).</AbstractText>Severe FTR occurs in older patients with chronic AF as a result of marked right atrial and right ventricular dilatation; and enlargement of the tricuspid annulus in the absence of pulmonary hypertension. More importantly, severe FTR leads to increased prevalence of right-sided heart failure underscoring the nonbenign nature of chronic AF.</AbstractText>© 2011, Wiley Periodicals, Inc.</CopyrightInformation> |
14,697 | A new way to analyze resuscitation quality by reviewing automatic external defibrillator data. | High quality cardiopulmonary resuscitation (CPR) plays an important role in survival of out-of-hospital cardiac arrests (OHCAs). We have developed an algorithm to automatically identify the quality of chest compressions from data retrieved from automatic external defibrillators (AEDs).</AbstractText>Electrocardiographic (ECG) signals retrieved from AEDs were analyzed by a newly developed algorithm to identify fluctuations in CPR. The algorithm contained three steps. First, it decomposed the AED signals into several intrinsic mode fluctuations (IMFs) by empirical mode decomposition (EMD). Second, it identified the dominant IMFs that carried the chest compression signals and weighted the IMFs to both enhance the chest compression oscillations and filter the noise. Third, it calculated the autocorrelation function (ACF) of the reconstructed signals and tested their periodicity. Using this algorithm, several CPR quality indicators were automatically calculated minute-by-minute and compared with those derived by audio and visual review of AED data by experienced physicians.</AbstractText>A total of 77 (29 women, 48 men) OHCA patients were enrolled, and 351 one-min segments were analyzed. The results showed that the CPR quality parameters calculated from the algorithm were highly correlated with those from the manual review (all P<0.001). The limits of agreement by Bland-Altman analysis were acceptable for chest compression number, total flow time, and no flow time, but not for CPR rate. We also demonstrated that only 41.8±29.8% of time was spent in chest compressions and only 7.5±16.8% was spent in adequate chest compressions.</AbstractText>Our results demonstrated that several indicators of CPR quality can be precisely and automatically determined by analyzing the ECG signals from AEDs using EMD and autocorrelograms.</AbstractText>Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.</CopyrightInformation> |
14,698 | The efficacy of terlipressin versus adrenaline in swine cardiopulmonary resuscitation. | The objective of the present study was to evaluate the efficacy of terlipressin (TP) vs. adrenaline (ADR) in increasing coronary perfusion pressure (CPP) and return of spontaneous circulation (ROSC) in swine CPR.</AbstractText>Under anesthesia with ketamine/thiopental, ventricular fibrillation was induced in 44 female immature pigs, remaining unassisted for 10 minutes, followed by 2 minutes of manual CPR (100 compression/10 ventilations/min with air). Animals were, then, divided into four groups: 1) ADR (45μg.kg(-1)); 2) saline-placebo (10mL); 3) TP 20μg.kg(-1)); and TP (20μg.kg(-1)) + ADR (45μg.kg(-1)). Defibrillation was performed after 2 minutes, observing surviving animals for a 30-minute period. Electrocardiogram, systemic BP, DBP, and PetCO(2) were monitored continuously.</AbstractText>Terlipressin did not differ from placebo regarding the effects on CPP, with low rates of ROSC in both groups (1/11 vs. 2/11; p=NS). Adrenaline increased CPP from 13±12 to 54±15mmHg (p<0.0001), similar effect to TP + ADR (from 21±10 to 45±13mmHg; p<0.0001), with high rates of ROSC/survivors in both groups (10/11 vs. 9/11, respectively). Among survivors, greater MAP was observed in the TP + ADR group vs. ADR (105±19mmHg vs. 76±21mmHg; p=0.0157) groups.</AbstractText>Adrenaline and TP + ADR were effective on maintaining CPP/ROSC in this experimental model, but isolated TP did not differ from placebo. However, in surviving animals in the TP + ADR group, greater hemodynamic stability was observed after ROSC, suggesting that TP can be a useful medication in the management of post-CPR hypotension.</AbstractText>Copyright © 2011 Elsevier Editora Ltda. All rights reserved.</CopyrightInformation> |
14,699 | Predictive value of preoperative electrocardiography for perioperative cardiovascular outcomes in patients undergoing noncardiac, nonvascular surgery. | The utility of routine preoperative electrocardiography (ECG) for assessing perioperative cardiovascular risk in patients undergoing noncardiac, nonvascular surgery (NCNVS) is unclear.</AbstractText>There would be an association between preoperative ECG and perioperative cardiovascular outcomes in patients undergoing NCNVS.</AbstractText>A total of 660 patients undergoing NCNVS were prospectively evaluated. Patients age >18 years who underwent an elective, nonday case, open surgical procedure were enrolled. Troponin I concentrations and 12-lead ECG were evaluated the day before surgery, immediately after surgery, and on the first 5 postoperative days. Preoperative ECG showing atrial fibrillation, left or right bundle branch block, left ventricular hypertrophy, frequent premature ventricular complexes, pacemaker rhythm, Q-wave, ST-segment changes, or sinus tachycardia or bradycardia were classified as abnormal. The patients were followed up during hospitalization and were evaluated for the presence of perioperative cardiovascular events (PCE).</AbstractText>Eighty patients (12.1%) experienced PCE. Patients with abnormal ECG findings had a greater incidence of PCE than those with normal ECG results (16% vs 6.4%; P < 0.001). Mean QTc interval was significantly longer in the patients who had PCE (436.6 ± 31.4 vs 413.3 ± 16.7 ms; P < 0.001). Univariate analysis showed a significant association between preoperative atrial fibrillation, pacemaker rhythm, ST-segment changes, QTc prolongation, and in-hospital PCE. However, only QTc prolongation (odds ratio: 1.15, 95% confidence interval: 1.06-1.2, P < 0.001) was an independent predictor of PCE according to the multivariate analysis. Every 10-ms increase in QTc interval was related to a 13% increase for PCE.</AbstractText>Prolongation of the QTc interval on the preoperative ECG was related with PCE in patients undergoing NCNVS.</AbstractText>© 2011 Wiley Periodicals, Inc.</CopyrightInformation> |
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