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15,100 | Systemic hypothermia to prevent radiocontrast nephropathy (from the COOL-RCN Randomized Trial). | Radiocontrast nephropathy (RCN) develops in a substantial proportion of patients with chronic kidney disease (CKD) after invasive cardiology procedures and is strongly associated with subsequent mortality and adverse outcomes. We sought to determine whether systemic hypothermia is effective in preventing RCN in patients with CKD. Patients at risk for RCN (baseline estimated creatinine clearance 20 to 50 ml/min) undergoing cardiac catheterization with iodinated contrast ≥50 ml were randomized 1:1 to hydration (control arm) versus hydration plus establishment of systemic hypothermia (33°C to 34°C) before first contrast injection and for 3 hours after the procedure. Serum creatinine levels at baseline, 24 hours, 48 hours, and 72 to 96 hours were measured at a central core laboratory. The primary efficacy end point was development of RCN, defined as an increase in serum creatinine by ≥25% from baseline. The primary safety end point was 30-day composite rate of adverse events consisting of death, myocardial infarction, dialysis, ventricular fibrillation, venous complication requiring surgery, major bleeding requiring transfusion ≥2 U, or rehospitalization. In total 128 evaluable patients (mean creatinine clearance 36.6 ml/min) were prospectively randomized at 25 medical centers. RCN developed in 18.6% of normothermic patients and in 22.4% of hypothermic patients (odds ratio 1.27, 95% confidence interval 0.53 to 3.00, p = 0.59). The primary 30-day safety end point occurred in 37.1% versus 37.9% of normothermic and hypothermic patients, respectively (odds ratio 0.97, 95% confidence interval 0.47 to 1.98, p = 0.93). In conclusion, in patients with CKD undergoing invasive cardiology procedures, systemic hypothermia is safe but is unlikely to prevent RCN. |
15,101 | Rabbit-specific ventricular model of cardiac electrophysiological function including specialized conduction system. | The function of the ventricular specialized conduction system in the heart is to ensure the coordinated electrical activation of the ventricles. It is therefore critical to the overall function of the heart, and has also been implicated as an important player in various diseases, including lethal ventricular arrhythmias such as ventricular fibrillation and drug-induced torsades de pointes. However, current ventricular models of electrophysiology usually ignore, or include highly simplified representations of the specialized conduction system. Here, we describe the development of an image-based, species-consistent, anatomically-detailed model of rabbit ventricular electrophysiology that incorporates a detailed description of the free-running part of the specialized conduction system. Techniques used for the construction of the geometrical model of the specialized conduction system from a magnetic resonance dataset and integration of the system model into a ventricular anatomical model, developed from the same dataset, are described. Computer simulations of rabbit ventricular electrophysiology are conducted using the novel anatomical model and rabbit-specific membrane kinetics to investigate the importance of the components and properties of the conduction system in determining ventricular function under physiological conditions. Simulation results are compared to panoramic optical mapping experiments for model validation and results interpretation. Full access is provided to the anatomical models developed in this study. |
15,102 | Reliability of the Cerebral Performance Category to classify neurological status among survivors of ventricular fibrillation arrest: a cohort study. | The Cerebral Performance Category (CPC) score is widely used in research and quality assurance to assess neurologic outcome following cardiac arrest. However, little is known about the inter- and intra-reviewer reliability of the CPC.</AbstractText>We undertook an investigation to assess the inter-reviewer and source document reliability of the CPC among a cohort of survivors from out-of-hospital ventricular fibrillation cardiac arrest (n = 131) in a large metropolitan area between November 1, 2003 and December 31, 2005. Subjects with a CPC of 1 or 2 were classified as favorable outcome and those with CPC 3 or greater were classified as unfavorable outcome. One abstractor first used the discharge summary alone to determine the CPC. All 3 abstractors independently reviewed the entire hospital record. Reliability was assessed by determining the proportion of determinations that agreed between abstractors and the respective kappa statistics. We also evaluated the implications for determining survival with favorable neurological outcome when survival to hospital discharge was 20% and 30%.</AbstractText>When the entire hospital record was used to determine CPC, favorable neurologic outcome (CPC 1 or 2) was recorded in 92% by abstractor 1, 89% by abstractor 2, and 74% by abstractor 3. Agreement was 96% (kappa = 0.78) between abstractors 1 and 2, 84% (kappa = 0.49) between abstractors 2 and 3, 82% (kappa = 0.38) between abstractors 1 and 3. The 3-way kappa was 0.50. Agreement was 90% (kappa = 0.71) between the discharge summary alone and the entire hospital record. If the results from review of the entire record are applied to a circumstance where survival to discharge is 20%, favorable neurologic status would occur in 18.4% for abstractor 1, 17.8% for abstractor 2, and 14.8% for abstractor 3. For survival to hospital discharge of 30%, favorable neurologic status would occur in 27.6% for abstractor 1, 26.7% for abstractor 2, and 22.2% for abstractor 3.</AbstractText>In this cohort study of survivors of out-of-hospital ventricular fibrillation cardiac arrest, the use of the CPC to classify favorable versus unfavorable neurological status at hospital discharge produced variable inter- and intra-reviewer agreement. The findings provide useful context to interpret outcome evaluations that report CPC.</AbstractText> |
15,103 | Heart failure enhances arrhythmogenesis in pulmonary veins. | 1. Heart failure (HF) predisposes to atrial fibrillation (AF) as a result of substrate remodelling. The present study aimed to investigate the impact of HF on the electrical remodelling of the pulmonary veins (PV) and left atrium (LA). 2. The electrical activity was recorded in LA and PV from control rabbits and rabbits with rapid ventricular pacing-induced HF, using a multi-electrode array system and conventional microelectrodes. 3. Compared with the control-PV (n = 21), the HF-PV (n = 13) had a higher incidence and frequency of rapid pacing-induced spontaneous activity (85 vs 29%, P = 0.005; 3.5 ± 0.2 vs 1.7 ± 0.1 Hz, P < 0.001) and high-frequency irregular electrical activity (92 vs 38%, P = 0.01; 23 ± 1 vs 19 ± 1 Hz, P = 0.003), greater depolarized resting membrane potential (-59 ± 1 vs -70 ± 2 mV, P < 0.001), higher incidence of early afterdepolarizations (EAD; 69 vs 6%, P = 0.001) and delayed afterdepolarizations (DAD; 92 vs 25%, P = 0.001), and slower conduction velocity (38 ± 2 vs 63 ± 2 cm/s, P < 0.05). In comparison to the HF-LA, the HF-PV had a higher incidence of spontaneous activity and high-frequency irregular electrical activity (85 vs 39%, P = 0.04; 92 vs 46%, P = 0.03), and higher incidence of EAD and DAD, and those differences were not found between the control-LA and control-PV. The control-PV with high-frequency irregular electrical activity had a higher incidence of DAD and spontaneous activity as compared with those without it. 4. HF contributed to an increased automaticity, triggered activity and conduction disturbance in the PV. The PV possessed more arrhythmogenic properties, which might play an important role in the genesis of AF in HF. |
15,104 | Purkinje-related arrhythmias part ii: polymorphic ventricular tachycardia and ventricular fibrillation. | There has been growing evidence that the Purkinje network plays a pivotal role in both the initiation and perpetuation of ventricular fibrillation (VF). A triggering ventricular premature beat (VPB) with a short-coupling interval could arise from either the right or left Purkinje system in patients with polymorphic ventricular tachycardia (VT) or VF, and that can be suppressed by the catheter ablation of the trigger. A focal breakdown in the "gating mechanism" at the Purkinje system resulting in a short-circuiting of the transmission across the gate at the distal Purkinje network might predispose to reentrant circuits of polymorphic VT/VF. Many investigators also reported the successful ablation of Purkinje-related VF with an acute or remote myocardial infarction. The same approach with good short-term results has been reported in a small number of patients with other heart diseases (i.e., amyloidosis, chronic myocarditis, nonischemic cardiomyopathy). Catheter ablation of the triggering VPBs from the Purkinje system can be used as an electrical bailout therapy in patients with VF storm. |
15,105 | High-energy defibrillation increases the dispersion of regional ventricular repolarization. | This study evaluated the effects of shock energy on the dispersion of regional ventricular repolarization (DRVR), post-shock rhythm and sinus recovery time (SRT), and the relationship between DRVR and post-shock ventricular arrhythmias.</AbstractText>Ten open-chest dogs were anesthetized. Ventricular fibrillation (VF) was electrically induced and recorded from a 6 × 6 unipolar electrode plaque (4 mm spacing) sutured on the left ventricular epicardium. Defibrillation threshold (DFT) was determined after 20 s of VF. DRVR was measured before VF, during the earliest post-shock sinus rhythm, and during sinus rhythm 30 s following shocks. Post-shock rhythm and SRT were evaluated after energies of 100% DFT, 125% DFT, 175% DFT, and 250% DFT.</AbstractText>In the100% DFT group, the DRVR of the earliest sinus rhythm and 30 s after successful defibrillation was not significantly different than that before VF. But the DRVRs were significantly increased in 125% DFT, 175% DFT, and 250% DFT group. DRVR after defibrillation in the 250% DFT group was higher than those in the 100% DFT and 125% DFT groups. SRT in the 250% DFT group was significantly longer than that in the other groups .The incidence of post-shock ventricular tachycardia was increased when a high-shock energy was applied (P = 0.041).</AbstractText>DRVR was increased by application of high-energy defibrillation associated with SRT prolongation. The increased DRVR may play an important role in the onset of post-shock ventricular tachycardia.</AbstractText> |
15,106 | Safety, efficacy, and performance of new discrimination algorithms to reduce inappropriate and unnecessary shocks: the PainFree SST clinical study design. | Implantable cardioverter defibrillator (ICD) shock therapy improves survival of patients at risk for sudden cardiac death. The high sensitivity of ICDs to detect tachycardia events is accompanied by reduced specificity resulting in inappropriate and unnecessary shocks. Up to 30% of ICD patients may experience inappropriate shocks, which are most commonly caused by lead noise, oversensing of T-waves, and supraventricular tachycardias. The new Protecta ICD and cardiac resynchronization therapy devices have been designed to minimize inappropriate and unnecessary shocks through novel SmartShock(TM) technology algorithms targeting these causes.</AbstractText>The PainFree SST study is a prospective, multicentre clinical trial, which will be conducted in two consecutive phases. Phase I will assess safety and any delay that may arise in ventricular fibrillation (VF) arrhythmia detection time using new algorithms. Phase II will evaluate reduction of inappropriate and unnecessary shocks at 1 year of follow-up. Additional objectives will include Quality of Life, healthcare utilization, safety of extending the ventricular tachyarrhythmia/VF interval detection duration (18 out of 24 vs. 30 out of 40 intervals), and reasons for inappropriate shock. Up to 2000 subjects in 150 centres worldwide will be enrolled with a follow-up of at least 1 year. Subjects enrolled in Phase I will continue in Phase II of the study and data from all enrolled subjects will contribute to the analysis of Phase II objectives.</AbstractText>Inappropriate and unnecessary shock delivery remains a significant clinical issue for patients receiving device therapies, which has considerable consequences for patients and the healthcare system. The PainFree SST study will investigate the ability of new algorithms to reduce inappropriate shocks. Results from this study are expected in mid-2013.</AbstractText> |
15,107 | Irregular ventricular activation results in QT prolongation and increased QT dispersion: a new insight into the mechanism of AF-induced ventricular arrhythmogenesis. | Atrial fibrillation (AF) has been shown to be associated with increased risk of ventricular arrhythmias. We have previously shown reverse electrical remodeling of the ventricles following successful restoration of sinus rhythm in patients with persistent AF. The purpose of this study was to assess the relative role of irregular ventricular activation in mediating the previously observed changes.</AbstractText>Twenty-two patients referred for an invasive electrophysiologic study were randomized to 30 minutes of regular or irregular atrioventricular (AV) sequential pacing at 100 beats per minute (bpm) with a programmed AV interval of 100 ms. Irregular pacing was triggered from prerecorded digital signal with a mean rate of 100 bpm, and a standard deviation of 150 ms (25% of the mean rate). In the regular pacing group, QT and QTc decreased from 448 ± 102 ms and 453 ± 105 ms to 428 ± 109 ms and 442 ± 104 ms, respectively (P < 0.001 for QT interval and P < 0.001 for QTc interval). There was no significant change in QT dispersion. In the irregular pacing group, QT and QTc increased from 477 ± 104 ms and 486 ± 78 ms to 489 ± 106 ms and 500 ± 106 ms (P < 0.01 for QT interval and P = 0.03 for QTc interval). In addition, there was a significant increase in QT dispersion from 50 ± 22 ms to 66 ± 22 ms (P = 0.001). Since the rate and pacing sites were similar between the groups, we attribute the repolarization changes in the irregular pacing group to the irregular activation of the ventricles.</AbstractText>The detrimental effects of irregular pacing go beyond the hemodynamic changes and include electrical remodeling that favors an arrhythmogenic substrate.</AbstractText>© 2011 Wiley Periodicals, Inc.</CopyrightInformation> |
15,108 | Effect of rosiglitazone on cardiac electrophysiology, infarct size and mitochondrial function in ischaemia and reperfusion of swine and rat heart. | Rosiglitazone, a peroxisome proliferator-activated receptor γ agonist, has been used to treat type 2 diabetes. Despite debates regarding its cardioprotection, the effects of rosiglitazone on cardiac electrophysiology are still unclear. This study determined the effect of rosiglitazone on ventricular fibrillation (VF) incidence, VF threshold (VFT), defibrillation threshold (DFT) and mitochondrial function during ischaemia and reperfusion. Twenty-six pigs were used. In each pig, either rosiglitazone (1 mg kg(-1)) or normal saline solution was administered intravenously for 60 min. Then, the left anterior descending coronary artery was ligated for 60 min and released to promote reperfusion for 120 min. The cardiac electrophysiological parameters were determined at the beginning of the study and during the ischaemia and reperfusion periods. The heart was removed, and the area at risk and infarct size in each heart were determined. Cardiac mitochondria were isolated for determination of mitochondrial function. Rosiglitazone did not improve the DFT and VFT during the ischaemia-reperfusion period. In the rosiglitazone group, the VF incidence was increased (58 versus 10%) and the time to the first occurrence of VF was decreased (3 ± 2 versus 19 ± 1 min) in comparison to the vehicle group (P < 0.05). However, the infarct size related to the area at risk in the rosiglitazone group was significantly decreased (P < 0.05). In the cardiac mitochondria, rosiglitazone did not alter the level of production of reactive oxygen species and could not prevent mitochondrial membrane potential changes. Rosiglitazone increased the propensity for VF, and could neither increase defibrillation efficacy nor improve cardiac mitochondrial function. |
15,109 | Antioxidant and cardioprotective effects of Danshensu (3-(3, 4-dihydroxyphenyl)-2-hydroxy-propanoic acid from Salvia miltiorrhiza) on isoproterenol-induced myocardial hypertrophy in rats. | Myocardial hypertrophy has been linked to the development of a variety of cardiovascular diseases, and is a risk factor for myocardial ischemia, arrhythmias, and sudden cardiac death. The objective of the present study was to evaluate the cardioprotective effects of Danshensu (DSS), a water-soluble active component of Danshen, on cardiac hypertrophy in rats. We are the first to report that DSS reversed Cx43 down-regulation in ventricular tissue. Cardiomyopathy in rats was produced using isoproterenol (Iso) treatment (2.5 mg/kg/d, s.c.) for seven days. DSS (3 and 10 mg/kg/d, i.p.) and Valsartan (Val) (10 mg/kg, i.g.) were administered on days 4-7 of Iso-treatment. Heart weight index, hemodynamic parameters, and ECG II parameters were monitored and recorded; protein expression of left ventricular connexin 43 (Cx43) and the activity of the redox system were assayed, and arrhythmias were produced using a coronary ligation/reperfusion procedure. The results demonstrated that DSS treatment significantly decreased heart weight/body weight (HW/BW) and left ventricular weight/body weight (LVW/BW) ratios. The protective role of DSS against Iso-induced myocardial hypertrophy was further confirmed using ECG. The incidences of ventricular tachycardia and ventricular fibrillation (VT, VF) and arrhythmic scores were higher in the model group and were suppressed by DSS. DSS decreased the serum and myocardium levels of creatine kinase, lactate dehydrogenase, and malondialdehyde (CK, LDH, and MDA) and increased serum activity of superoxide dismutase (SOD) in a dose-dependent manner. Cx43 expression in the left ventricle was down-regulated, and there was significant oxidative stress in this model of cardiomyopathy. DSS reversed the down-regulated Cx43 protein levels and showed potent anti-oxidative activities and cellular protection. These data demonstrate that DSS can prevent cardiac I/R injury and improve cardiac function in a rat model of hypertrophy, the effects partially resulting from antioxidants and the protection from Cx43 expression. |
15,110 | [Malignant fascicular ventricular tachycardia degenerating into ventricular fibrillation in a patient with early repolarization syndrome]. | A 45-year-old man was hospitalized for syncope due to fascicular ventricular tachycardia degenerating into ventricular fibrillation (VF). The electrocardiogram showed an early repolarization syndrome. The arrhythmia was repetitive and disappeared after oral hydroquinidine. An implantable cardioverter-defibrillator (ICD) was implanted; subsequently, the patient was arrhythmia free at 9 months follow-up. |
15,111 | [About an implantable cardioverter-fibrillator]. | A 61-year-old man has been implanted with a Ventritex Profile MD V-186 HV3 ICD for ischemic cardiomyopathy with sustained inducible VT. Three years later, this patient received several inappropriate shocks during the device's interrogation. These shocks provoked ventricular fibrillation. They were caused by a failing soldering between the system random accessory memory (SRAM) module and the hybrid circuit of the device. The device was explanted in emergency. |
15,112 | Ventricular and supraventricular arrhythmias and heart failure in a patient with left ventricular noncompaction and Brugada syndrome. | We report a 47 year-old male patient with coexistence of left ventricular noncompaction and Brugada syndrome. He presented malignant ventricular arrhythmias followed by cardioverter- -defibrillator implantation, atrial fibrillation and flutter and progressive heart failure. This case could be an example of the coexistence of two rare diseases of various genetic patterns that only partially showed overlapping symptomatology and complications, particularly ventricular arrhythmias. |
15,113 | Assessment of ventricular and left atrial mechanical functions, atrial electromechanical delay and P wave dispersion in patients with scleroderma. | The aim of this study was to investigate ventricular functions and left atrial (LA) mechanical functions, atrial electromechanical coupling, and P wave dispersion in scleroderma patients.</AbstractText>Twenty-six patients with scleroderma and twenty-four controls were included. Left and right ventricular (LV and RV) functions were evaluated using conventional echocardiography and tissue Doppler imaging (TDI). LA volumes were measured using the biplane area- -length method and LA mechanical function parameters were calculated. Inter-intraatrial electromechanical delays were measured by TDI. P wave dispersion was calculated by 12-lead electrocardiograms.</AbstractText>LV myocardial performance indices (MPI) and RV MPI were higher in patients with scleroderma (p = 0.000, p = 0.000, respectively) while LA passive emptying fraction was decreased and LA active emptying fraction was increased (p = 0.051, p = 0.000, respectively). P wave dispersion and inter-intraatrial electromechanical delay were significantly higher in patients with scleroderma (25 [10-60] vs 20 [0-30], p = 0.000, 16.50 [7.28-26.38] vs 9.44 [3.79-15.78] and 11.33 [4.88-16.06] vs 4.00 [0-12.90], p < 0.05, respectively). Interatrial electromechanical delay was negatively correlated with LV E wave, (p = 0.018). LV E wave was demonstrated to be a factor independent of the interatrial electromechanical delay (R² = = 0.270, b = -0.52, p = 0.013).</AbstractText>This study showed that in scleroderma patients, global functions of LV, RV and mechanical functions of LA were impaired, intra-interatrial electromechanical delays were prolonged and P wave dispersion was higher. LV E wave was demonstrated to be a factor that is independent of the interatrial electromechanical delay. Reduced LV E wave may also give additional information on the process of risk stratification of atrial fibrillation.</AbstractText> |
15,114 | Electrolyte disorders and arrhythmogenesis. | Electrolyte disorders can alter cardiac ionic currents kinetics and depending on the changes can promote proarrhythmic or antiarrhythmic effects. The present report reviews the mechanisms, electrophysiolgical (EP), electrocardiographic (ECG), and clinical consequences of electrolyte disorders. Potassium (K⁺) is the most abundent intracellular cation and hypokalemia is the most commont electrolyte abnormality encountered in clinical practice. The most significant ECG manifestation of hypokalemia is a prominent U wave. Several cardiac and non cardiac drugs are known to suppress the HERG K⁺ channel and hence the I(K), and especially in the presence of hypokalemia, can result in prolonged action potential duration and QT interval, QTU alternans, early afterdepolarizations, and torsade de pointes ventricular tachyarrythmia (TdP VT). Hyperkalemia affects up to 8% of hospitalized patients mainly in the setting of compromised renal function. The ECG manifestation of hyperkalemia depends on serum K⁺ level. At 5.5-7.0 mmol/L K⁺, tall peaked, narrow-based T waves are seen. At > 10.0 mmol/L K⁺, sinus arrest, marked intraventricular conduction delay, ventricular techycardia, and ventricular fibrillation can develop. Isolated abnormalities of extracellular calcium (Ca⁺⁺) produce clinically significant EP effects only when they are extreme in either direction. Hypocalcemia, frequently seen in the setting of chronic renal insufficiency, results in prolonged ST segment and QT interval while hypercalcemia, usually seen with hyperparathyroidism, results in shortening of both intervals. Although magnesium is the second most abudent intracellular cation, the significance of magnesium disorders are controversial partly because of the frequent association of other electrolyte abnormalities. However, IV magnesium by blocking the L-type Ca(⁺⁺) current can successfully terminate TdP VT without affecting the prolonged QT interval. Finally, despite the frequency of sodium abnormalities, particularly hyponatremia, its EP effects are rarely clinically significant. |
15,115 | Diastolic heart failure: predictors of mortality. | Diastolic heart failure (HF) as defined by the symptoms and signs of HF, preserved ejection fraction and abnormal diastolic function is estimated to occur in half of all patients presenting with HF. Patients with preserved ejection fraction are older and more often female. The underlying etiology of HF differs, with hypertension being more common in patients with preserved ejection fraction and ischemic heart disease predominant among those with reduced ejection fraction. Diastolic HF is associated with high mortality comparable with that of HF with depressed ejection fraction with a five year survival rate after a first episode of 43% and a higher excess mortality compared with the general population. Despite significant disease burden, clinical and biological prognostic factors in diastolic HF remain poorly understood. There is limited data from well designed studies regarding the effective treatment strategies for this group of patients. The purpose of this review is to summarize the mortality data and predictors of mortality in patients with diastolic HF for better understanding of the prognosis. In patients with diastolic HF older age, male gender, non-Caucasian ethnicity, history of coronary artery disease and atrial fibrillation are associated with poor prognosis. Anemia and B-type natriuretic peptide are significant laboratory variable that predict mortality. Two dimensional echocardiography and tissue Doppler imaging measurements including left ventricular ejection fraction, E/Ea ratio ≥ 15, restrictive transmiral filling (deceleration time £ 140 ms) and Em < 3.5 cm/s are predictors of adverse outcomes in diastolic HF patients. |
15,116 | Cardiac arrest caused by torsades de pointes tachycardia after successful atrial flutter radiofrequency catheter ablation. | A 66-year-old woman underwent successful radiofrequency catheter ablation for long-lasting, drug refractory fast atrial flutter. Two days later she had a cardiac arrest due to torsades de pointes (TdP) tachycardia attributed to relative sinus bradycardia and QT interval prolongation. After successful resuscitation further episodes of TdP occurred, which were treated with temporary pacing. Because of concomitant systolic dysfunction due to ischemic and valvular heart disease she was finally treated with an implantable defibrillator. In conclusion we strongly advise prolonged monitoring for 2 or more days for patients with structural heart disease following successful catheter ablation for long lasting tachyarrhythmias. |
15,117 | Atrial remodeling, autonomic tone, and lifetime training hours in nonelite athletes. | Endurance athletes have an increased risk of developing atrial fibrillation (AF) at 40 to 50 years of age. Signal-averaged P-wave analysis has been used for identifying patients at risk for AF. We evaluated the impact of lifetime training hours on signal-averaged P-wave duration and modifying factors. Nonelite men athletes scheduled to participate in the 2010 Grand Prix of Bern, a 10-mile race, were invited. Four hundred ninety-two marathon and nonmarathon runners applied for participation, 70 were randomly selected, and 60 entered the final analysis. Subjects were stratified according to their lifetime training hours (average endurance and strength training hours per week × 52 × training years) in low (<1,500 hours), medium (1,500 to 4,500 hours), and high (>4,500 hours) training groups. Mean age was 42 ± 7 years. From low to high training groups signal-averaged P-wave duration increased from 131 ± 6 to 142 ± 13 ms (p = 0.026), and left atrial volume increased from 24.8 ± 4.6 to 33.1 ± 6.2 ml/m(2) (p = 0.001). Parasympathetic tone expressed as root of the mean squared differences of successive normal-to-normal intervals increased from 34 ± 13 to 47 ± 16 ms (p = 0.002), and premature atrial contractions increased from 6.1 ± 7.4 to 10.8 ± 7.7 per 24 hours (p = 0.026). Left ventricular mass increased from 100.7 ± 9.0 to 117.1 ± 18.2 g/m(2) (p = 0.002). Left ventricular systolic and diastolic function and blood pressure at rest were normal in all athletes and showed no differences among training groups. Four athletes (6.7%) had a history of paroxysmal AF, as did 1 athlete in the medium training group and 3 athletes in the high training group (p = 0.252). In conclusion, in nonelite men athletes lifetime training hours are associated with prolongation of signal-averaged P-wave duration and an increase in left atrial volume. The altered left atrial substrate may facilitate occurrence of AF. Increased vagal tone and atrial ectopy may serve as modifying and triggering factors. |
15,118 | Reverse remodeling and the risk of ventricular tachyarrhythmias in the MADIT-CRT (Multicenter Automatic Defibrillator Implantation Trial-Cardiac Resynchronization Therapy). | We aimed to evaluate the relationship between echocardiographic response to cardiac resynchronization therapy (CRT) and the risk of subsequent ventricular tachyarrhythmias (VTAs).</AbstractText>Current data regarding the effect of CRT on the risk of VTA are limited and conflicting.</AbstractText>The risk of a first appropriate implantable cardioverter-defibrillator (ICD) therapy for VTA (including ventricular tachycardia, ventricular fibrillation, and ventricular flutter) was compared between high- and low-echocardiographic responders to CRT defibrillator (CRT-D) therapy (defined as ≥ 25% and <25% reductions, respectively, in left ventricular end-systolic volume [LVESV] at 1 year compared with baseline) and ICD-only patients enrolled in the MADIT-CRT (Multicenter Automatic Defibrillator Implantation Trial-Cardiac Resynchronization Therapy).</AbstractText>The cumulative probability of a first VTA at 2 years after assessment of echocardiographic response was highest among low responders to CRT-D (28%), intermediate among ICD-only patients (21%), and lowest among high responders to CRT-D (12%), with p < 0.001 for the overall difference during follow-up. Multivariate analysis showed that high responders to CRT-D experienced a significant 55% reduction in the risk of VTA compared with ICD-only patients (p < 0.001), whereas the risk of VTA was not significantly different between low responders and ICD-only patients (hazard ratio [HR]: 1.26; p = 0.21). Consistently, assessment of response to CRT-D as a continuous measure showed that incremental 10% reductions in left ventricular end-systolic volume were associated with corresponding reductions in the risk of subsequent VTA (HR: 0.80; p < 0.001), VTA/death (HR: 0.79; p < 0.001), ventricular tachycardia (HR: 0.80; p < 0.001), and ventricular fibrillation/ventricular flutter (HR: 0.75; p = 0.044).</AbstractText>In patients with left ventricular dysfunction enrolled in the MADIT-CRT trial, reverse remodeling was associated with a significant reduction in the risk of subsequent life-threatening VTAs. (Multicenter Automatic Defibrillator Implantation Trial-Cardiac Resynchronization Therapy [MADIT-CRT]; NCT00180271).</AbstractText>Copyright © 2011 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.</CopyrightInformation> |
15,119 | GWAS for discovery and replication of genetic loci associated with sudden cardiac arrest in patients with coronary artery disease. | Epidemiologic evidence suggests a heritable component to risk for sudden cardiac arrest independent of risk for myocardial infarction. Recent candidate gene association studies for community sudden cardiac arrests have focused on a limited number of biological pathways and yielded conflicting results. We sought to identify novel gene associations for sudden cardiac arrest in patients with coronary artery disease by performing a genome-wide association study.</AbstractText>Tagging SNPs (n = 338,328) spanning the genome were typed in a case-control study comparing 89 patients with coronary artery disease and sudden cardiac arrest due to ventricular tachycardia or ventricular fibrillation to 520 healthy controls.</AbstractText>Fourteen SNPs including 7 SNPs among 7 genes (ACYP2, AP1G2, ESR1, DGES2, GRIA1, KCTD1, ZNF385B) were associated with sudden cardiac arrest (all p < 1.30 × 10(-7)), following Bonferroni correction and adjustment for population substructure, age, and sex; genetic variation in ESR1 (p = 2.62 × 10(-8); Odds Ratio [OR] = 1.43, 95% confidence interval [CI]:1.277, 1.596) has previously been established as a risk factor for cardiovascular disease. In tandem, the role of 9 genes for monogenic long QT syndrome (LQT1-9) was assessed, yielding evidence of association with CACNA1C (LQT8; p = 3.09 × 10(-4); OR = 1.18, 95% CI:1.079, 1.290). We also assessed 4 recently published gene associations for sudden cardiac arrest, validating NOS1AP (p = 4.50 × 10(-2), OR = 1.15, 95% CI:1.003, 1.326), CSMD2 (p = 6.6 × 10(-3), OR = 2.27, 95% CI:1.681, 2.859), and AGTR1 (p = 3.00 × 10(-3), OR = 1.13, 95% CI:1.042, 1.215).</AbstractText>We demonstrate 11 gene associations for sudden cardiac arrest due to ventricular tachycardia/ventricular fibrillation in patients with coronary artery disease. Validation studies in independent cohorts and functional studies are required to confirm these associations.</AbstractText> |
15,120 | The induction of mild hypothermia improves systolic function of the resuscitated porcine heart at no further sympathetic activation. | Mild hypothermia (MH) after cardiac arrest attenuates hypoxic brain injury and improves survival. As MH increases contractility in normal hearts, we hypothesized that MH improves cardiovascular function after cardiac arrest.</AbstractText>In 16 anaesthetized pigs (64 ± 2 kg), ventricular fibrillation was induced electrically for 5 min. At 10 min after resuscitation and return of spontaneous circulation (ROSC), pigs were assigned to normothermia (NT, 38°C, n = 8) or MH (33°C, n = 8, intravascular cooling).</AbstractText>At ROSC 6 h vs. baseline, heart rate (HR) was unchanged in NT, but decreased in MH. Cardiac output (CO, l min(-1)) decreased in MH (3.5 ± 0.2 vs. 5.5 ± 0.4, P < 0.05) more than in NT (4.8 ± 0.4 vs. 5.7 ± 0.4, P = ns). Mixed venous oxygen saturation decreased in NT (56 ± 2 vs. 66 ± 3%, P < 0.05), but remained constant in MH (64 ± 2 vs. 65 ± 2%) due to a 35% decrease of whole body oxygen consumption. Left ventricular (LV) dP/dt(max) (mmHg s(-1)) decreased in NT (1163 ± 97 vs. 1665 ± 134, P < 0.05), but was preserved in MH (1602 ± 102 vs. 1603 ± 96), whereas LV relaxation was profoundly slowed during MH. Pressure-volume analysis confirmed improved LV systolic function during MH, but also demonstrated decreased LV end-diastolic distensibility, which was further potentiated by right atrial pacing at baseline HR. MH did not increase plasma catecholamine levels. Spectral analysis of heart rate variability revealed reduced sympathetic activation during MH.</AbstractText>The induction of MH after cardiac resuscitation improves systolic myocardial function without further sympathetic activation. A reduced metabolism during MH outweighs a decreased CO and thereby acts favourably on systemic oxygen supply/demand balance.</AbstractText>© 2011 The Authors. Acta Physiologica © 2011 Scandinavian Physiological Society.</CopyrightInformation> |
15,121 | [Alcohol, acid, vitamins and heart]. | We report on a 67-year-old male patient with chronic alcoholism, who presented with acute dyspnea, a strongly reduced left ventricular cardiac function and a severe lactic acidosis. In face of a low thiamine serum level and a rapid improvement after parenteral thiamine administration we were able to diagnose a Shoshin-Beriberi syndrome with cardiogenic shock and reversible dilated cardiomyopathy. The epidemiology, pathophysiology, clinics and treatment of the rare cardiac manifestation of this vitamine deficiency are discussed. |
15,122 | A novel mutation in the RYR2 gene leading to catecholaminergic polymorphic ventricular tachycardia and paroxysmal atrial fibrillation: dose-dependent arrhythmia-event suppression by β-blocker therapy. | Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a genetic condition that presents with exercise-induced polymorphic arrhythmias. We describe a case report of a 25-year-old woman who had a cardiac arrest due to ventricular fibrillation. Genetic analysis revealed a novel missense mutation in exon 90 of the ryanodine receptor (RyR2) gene resulting in substitution of arginine for serine at residue 4153 (S4153R). The patient received an implantable cardioverter-defibrillator and low-dose β-blocker therapy. She had recurrent polymorphic ventricular arrhythmias treated with appropriate cardioverter-defibrillator shocks and paroxysmal atrial fibrillation. Titration of β-blocker to a much higher dose suppressed further episodes of ventricular arrhythmia and paroxysmal atrial fibrillation, resulting in reduction in device therapies. |
15,123 | Eicosapentaenoic acid reduces ischemic ventricular fibrillation via altering monophasic action potential in pigs. | Although high intake of n-3 fatty acids is associated with reduced mortality of patients with ischemic heart disease, especially reduction in sudden cardiac death (SCD), the detailed mechanisms remain to be elucidated. Thus, the present study was designed to examine whether long-term treatment with eicosapentaenoic acid (EPA), a major component of n-3 fatty acids, reduces ischemia-induced ventricular fibrillation (VF) in pigs in vivo, and if so, what molecular mechanisms are involved. Male pigs were treated with either a control chow (control group) or a control chow plus EPA (600 mg/kg/day, PO, EPA group) for 3 weeks and were subjected to myocardial ischemia for 90 min (n=8 each) with measurement of the monophasic action potential (MAP), as a marker of ventricular electrophysiological activities. The EPA treatment significantly attenuated the occurrence of VF (control 5.1±1.7 vs. EPA 1.5±0.8 times/animal, P<0.05) and markedly reduced the mortality (control 50% vs. EPA 0%, P<0.05), with the attenuation of MAP duration shortening during ischemia (control -28.1±3.0% vs. EPA -18.2±1.4%, P<0.05). These beneficial effects of EPA were abolished by pre-treatment with cromakalim, a K(ATP) channel opener (0.3 μg/kg/min, IC). Furthermore, EPA significantly inhibited the mRNA and protein expression of Kir6.2, a major component of sarcolemmal K(ATP) channels, in both the ischemic region and non-ischemic regions. These results indicate that long-term treatment with EPA reduces ischemia-induced VF and SCD in pigs in vivo, for which attenuation of MAP duration shortening may be involved. |
15,124 | Activated human platelet products induce proarrhythmic effects in ventricular myocytes. | Sudden cardiac death remains one of the most prevalent modes of death and is mainly caused by ventricular fibrillation (VF) in the setting of acute ischemia resulting from coronary thrombi. Animal experiments have shown that platelet activation may increase susceptibility of ischemic myocardium to VF, but the mechanism is unknown. In the present study, we evaluated the effects of activated blood platelet products (ABPPs) on electrophysiological properties and intracellular Ca(2+) (Ca(2+)(i)) homeostasis. Platelets were collected from healthy volunteers. After activation, their secreted ABPPs were added to superfusion solutions. Rabbit ventricular myocytes were freshly isolated, and membrane potentials and Ca(2+)(i) were recorded using patch-clamp methodology and indo-1 fluorescence measurements, respectively. ABPPs prolonged action potential duration and induced early and delayed afterdepolarizations. ABPPs increased L-type Ca(2+) current (I(Ca,L)) density, but left densities of sodium current, inward rectifier K(+) current, transient outward K(+) current, and rapid component of the delayed rectifier K(+) current unchanged. ABPPs did not affect kinetics or (in)activation properties of membrane currents. ABPPs increased systolic Ca(2+)(i), Ca(2+)(i) transient amplitude, and sarcoplasmic reticulum Ca(2+) content. ABPPs did not affect the Na(+)-Ca(2+) exchange current (I(NCX)) in Ca(2+)-buffered conditions. Products secreted from activated human platelets induce changes in I(Ca,L) and Ca(2+)(i), which result in action potential prolongation and the occurrence of early and delayed afterdepolarizations in rabbit myocytes. These changes may trigger and support reentrant arrhythmias in ischemia models of coronary thrombosis. |
15,125 | Epicardial scar in a patient with no apparent heart disease. | A 35-year-old man, who had an episode of aborted sudden cardiac death due to ventricular fibrillation, suffered from multiple storms of ventricular tachycardia (VT). Conventional cardiac examinations did not reveal any structural heart diseases, and he had been treated by an implantable cardioverter defibrillator since 2007. At the latest admission, epicardial but not endocardial voltage mapping revealed a small area of low voltage at the left ventricular (LV) postero-lateral wall where a delayed potential was recorded during sinus rhythm. Excellent pacemapping with a prolonged stimulus to QRS interval was obtained from the area, and a mid-diastolic potential was recorded during the VT. Radiofrequency application terminated the VT and any VT became noninducible after the ablation. In some patients diagnosed as LV-VT with no apparent heart disease, arrhythmogenic substrate may exist on the epicardial surface of the ventricle. |
15,126 | Endothelin-1 attenuates the hemodynamic response to exogenous epinephrine in a porcine ischemic ventricular fibrillation cardiac arrest model. | Endothelin-1 (ET-1) increases in the ischemically induced ventricular fibrillation (VF) swine model of cardiac arrest and affects outcome by potentially attenuating the hemodynamic response to epinephrine. Fifty-one swine underwent percutaneous left anterior descending occlusion. Seven minutes postonset of ischemic VF, cardiopulmonary resuscitation (CPR) was initiated. If VF persisted after 3 shocks, 1 mg of epinephrine was given. ET-1 (collected at baseline and every 5 min until VF onset) was assayed with ELISA. Bayesian multivariate logistic regression analysis compared peak ET-1 levels with the binary outcome of a positive coronary perfusion pressure response of >20 mmHg following epinephrine. Sixteen animals (31%) failed to achieve a positive response. Restoration of spontaneous circulation (ROSC) was observed in 1/16 (6.3%) of epinephrine nonresponders and 20/35 (57.1%) of epinephrine responders (P = 0.0006). The median peak ET-1 level was 2.71 pg/mL [interquartile range (IQR) 1.06-4.40] in nonresponders and 1.69 pg/mL (IQR 0.99-2.35) in responders. ET-1 levels were inversely associated with epinephrine response with a median posterior odds ratio (OR) of a coronary perfusion pressure response of 0.72 (95% confidence interval [CI] 0.48-1.06) for each one-unit increase in ET-1 and a probability that the associated OR is <1 of 0.95. Peak ET-1 levels predict a lack of a hemodynamic response to epinephrine during treatment of cardiac arrest during ischemic VF. |
15,127 | AV nodal ablation-induced Gerbode defect (LV-RA Shunt). | A Gerbode defect that comprises a left ventricular to right atrial shunt is usually a congenital cardiac condition. Rarely, acquired Gerbode defects secondary to aortic or tricuspid valve endocarditis have been reported. We present a case of a Gerbode defect caused by catheter ablation of the AV node in a patient with a severely dilated cardiomyopathy and refractory atrial fibrillation. |
15,128 | Automated defibrillation. | There is much evidence that defibrillation is the most effective treatment for cardiac arrest caused by ventricular fibrillation or pulseless ventricular tachycardia, but only where automated external defibrillators (AEDs) are installed and staff are trained to use them. |
15,129 | Primary angioplasty in a high-volume tertiary center in Turkey: in-hospital clinical outcomes of 1625 patients. | We evaluated in-hospital results of primary percutaneous coronary intervention (PCI) in a high-volume tertiary center.</AbstractText>We retrospectively evaluated 1625 patients (1323 males, 302 females; mean age 56.0 ± 11.6 years) who underwent primary PCI for acute ST-elevation myocardial infarction between January 2006 and April 2008. All coronary angiography procedures were performed using the femoral artery route. In-hospital clinical and angiographic results were recorded.</AbstractText>On admission, 23% of the patients had diabetes mellitus, 49.6% had anterior myocardial infarction, and 4.9% had cardiogenic shock. The mean duration of pain was 171.2 ± 121.2 minutes, and the mean door-to-balloon time was 31.6 ± 7.2 minutes. Infarct-related artery was the left anterior descending artery in 49.7%, multivessel disease was present in 40.9%, TIMI 2/3 flow was present in 23.6%, and high-grade thrombus was observed in 66.8%. Primary PCI involved balloon dilatation (5.7%) and stent implantation (94.3%). The incidence of angiographic no-reflow was 11.9%. The mean hospital stay was 5.2 ± 3.3 days. All-cause mortality occurred in 71 patients (4.4%). Other in-hospital events were reinfarction (1.4%), target vessel revascularization (1.9%), hemorrhagic/ischemic stroke (0.6%), stent thrombosis (1.2%), major bleeding (3.8%), blood transfusion (4.8%), heart failure (10.5%), atrial fibrillation (4%), and ventricular tachycardia (3.9%).</AbstractText>Primary PCI is an effective method in achieving complete revascularization of the infarct-related artery. Successful in-hospital results not only depend on the experience and equipment of the center, but also on how rapidly reperfusion is achieved.</AbstractText> |
15,130 | [The impact of chronic kidney disease on in-hospital clinical outcomes in patients undergoing primary percutaneous angioplasty for ST-segment elevation myocardial infarction]. | We investigated the effect of chronic kidney disease (CKD) on in-hospital results in patients undergoing primary percutaneous angioplasty for ST-segment elevation myocardial infarction (STEMI).</AbstractText>The study included 2,486 patients (2,070 men, 416 women) who were treated with primary angioplasty for STEMI. Of these, 273 patients (11%) were found to have CKD (glomerular filtration rate <60 ml/min/1.73 m2) before the procedure. Patients with and without CKD were evaluated with respect to demographic and clinical features, primary angioplasty findings, and in-hospital clinical results.</AbstractText>Patients with CKD exhibited a higher mean age, Killip class, and higher frequencies of female gender, diabetes, hypertension, anemia, and previous myocardial infarction (p<0.05). Angioplasty showed higher rates of right coronary artery lesion, multivessel disease, contrast nephropathy, unsuccessful procedure, and increased stenosis rate and stent length in CKD patients (p<0.05). Cardiovascular mortality occurred in 11.7% and 1.4% of patients with and without CKD, respectively (p<0.001). Patients with CKD had significantly higher incidences of target vessel revascularization, major cardiac events, stroke, cardiopulmonary resuscitation, hemodialysis, ventricular tachycardia/fibrillation, severe heart failure, cardiogenic shock, and significant hemorrhage (p<0.05). Multivariate analysis showed that CKD was an independent predictor of mortality (OR=4.1, 95% CI 1.83-9.17; p=0.001).</AbstractText>Our findings show that CKD patients undergoing primary angioplasty for STEMI have an increased risk profile and poorer in-hospital results, and that CKD represents an independent risk factor for mortality.</AbstractText> |
15,131 | The prognostic value of atrial fibrillation on 30-day clinical outcome in patients with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention. | This study evaluated the association between atrial fibrillation (AF) and 30-day clinical outcome in patients with acute ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI). Between January 2005 and October 2009, 783 consecutive patients with acute STEMI undergoing primary PCI were enrolled. Of these patients, 85 (10.9%) with AF during admission were categorized into group 1, while the remaining 698 (89.1%) with sinus rhythm during admission served as group 2. The results demonstrated that the incidence of advanced Killip score (defined as ≥ score 3) and advanced congestive heart failure (defined as ≥ NYHA class 3) were significantly higher, whereas the left ventricular ejection fraction (LVEF) was notably lower in group 1 than in group 2 (all P < 0.003). Additionally, the normal blood flow in the infarct-related artery was notably lower in group 1 than in group 2 (P = 0.003). Moreover, the incidences of new-onset stroke and 30-day mortality were remarkably higher in group 1 than in group 2 (all P < 0.003). Furthermore, Kaplan-Meier analysis demonstrated that the 30-day survival rate was markedly lower in AF patients than in those with sinus rhythm. However, multivariate stepwise Cox regression analysis demonstrated that the advanced Killip score and low LVEF were significantly and independently predictive of 30-day mortality (all P < 0.004). In conclusion, AF was significantly associated with 30-day mortality. |
15,132 | Prediction of countershock success in patients using the autoregressive spectral estimation. | Ventricular fibrillation (VF) is a life-threatening cardiac arrhythmia and within of minutes of its occurrence, optimal timing of countershock therapy is highly warranted to improve the chance of survival. This study was designed to investigate whether the autoregressive (AR) estimation technique was capable to reliably predict countershock success in VF cardiac arrest patients.</AbstractText>ECG data of 1077 countershocks applied to 197 cardiac arrest patients with out-of-hospital and in-hospital cardiac arrest between March 2002 and July 2004 were retrospectively analyzed. The ECG from the 2.5 s interval of the precountershock VF ECG was used for computing the AR based features Spectral Pole Power (SPP) and Spectral Pole Power with Dominant Frequency weighing (SPPDF) and Centroid Frequency (CF) and Amplitude Spectrum Area (AMSA) based on Fast Fourier Transformation (FFT).</AbstractText>With ROC AUC values up to 84.1% and diagnostic odds ratio up to 19.12 AR based features SPP and SPPDF have better prediction power than the FFT based features CF (80.5%; 6.56) and AMSA (82.1%; 8.79).</AbstractText>AR estimation based features are promising alternatives to FFT based features for countershock outcome when analyzing human data.</AbstractText> |
15,133 | Targeting ryanodine receptors for anti-arrhythmic therapy. | Antiarrhythmic drugs are a group of pharmaceuticals that suppress or prevent abnormal heart rhythms, which are often associated with substantial morbidity and mortality. Current antiarrhythmic drugs that typically target plasma membrane ion channels have limited clinical success and in some cases have been described as being pro-arrhythmic. However, recent studies suggest that pathological release of calcium (Ca(2+)) from the sarcoplasmic reticulum via cardiac ryanodine receptors (RyR2) could represent a promising target for antiarrhythmic therapy. Diastolic SR Ca(2+) release has been linked to arrhythmogenesis in both the inherited arrhythmia syndrome 'catecholaminergic polymorphic ventricular tachycardia' and acquired forms of heart disease (eg, atrial fibrillation, heart failure). Several classes of pharmaceuticals have been shown to reduce abnormal RyR2 activity and may confer protection against triggered arrhythmias through reduction of SR Ca(2+) leak. In this review, we will evaluate the current pharmacological methods for stabilizing RyR2 and suggest treatment modalities based on current evidence of molecular mechanisms. |
15,134 | Mechanisms and management of the heart in myotonic dystrophy. | Myotonic dystrophy (DM) is the most common form of adult onset muscular dystrophy and is caused by expansion of short nucleotide repeats that, in turn, produce toxic RNA aggregates within cells. DM is multisystemic, and the heart is primary site of pathology. DM patients exhibit cardiac conduction disorders including atrial fibrillation, atrio-ventricular heart block and ventricular arrhythmias. DM patients are also at risk for cardiomyopathy and congestive heart failure. Myotonic dystrophy is also characterized by myotonia, muscle weakness, and profound fatigue. The management of these symptoms requires input from the cardiologist and a team approach to minimize the debilitating aspects of the disorder and optimize cardiac function. |
15,135 | Clinical and prognostic effects of atrial fibrillation in heart failure patients with reduced and preserved left ventricular ejection fraction. | Atrial fibrillation (AF) is common in heart failure (HF), but few data regarding the prognostic relevance of AF are available in HF patients with preserved left ventricular ejection fraction (HF-PEF). We aimed to study the clinical impact of AF vs. sinus rhythm (SR) in stabilized HF patients with reduced left ventricular ejection fraction (HF-REF) and in those with preserved left ventricular ejection fraction (HF-PEF).</AbstractText>We studied 927 patients with stable HF, of whom 336 (36%) had AF. N-terminal pro-B-type natriuretic peptide (NT-proBNP) concentrations were measured at baseline and patients were followed for 18 months. We compared time to first HF (re-)hospitalization or death between patients with AF and SR. Atrial fibrillation was present at baseline in 215 (35%) patients with HF-REF (mean LVEF 0.25 + 0.08) and in 121 (40%) patients with HF-PEF (mean LVEF 0.50 + 0.09). Plasma NT-proBNP levels were similar in AF and SR patients (median 2398 vs. 2532 pg/mL, P = 0.74). Atrial fibrillation was independently associated with elevated NT-proBNP levels in HF-PEF, but not in HF-REF patients (multivariable B = 0.33, P= 0.047 and B = 0.03; P = 0.89, respectively). After 18 months of follow-up, the presence of AF was an independent predictor of death or HF hospitalization in HF-PEF (multivariable hazard ratio 1.49 (95% CI 1.04-2.14), P = 0.03), but not in HF-REF patients (1.05 (CI 95% 0.80-1.38), P = 0.72).</AbstractText>Atrial fibrillation is equally common in patients with HF-PEF and HF-REF. In HF-PEF, but not in HF-REF patients, AF was associated with higher NT-proBNP levels and was independently related to death or HF hospitalization.</AbstractText> |
15,136 | Circadian rhythms and cardiovascular health. | The functional organization of the cardiovascular system shows clear circadian rhythmicity. These and other circadian rhythms at all levels of organization are orchestrated by a central biological clock, the suprachiasmatic nuclei of the hypothalamus. Preservation of the normal circadian time structure from the level of the cardiomyocyte to the organ system appears to be essential for cardiovascular health and cardiovascular disease prevention. Myocardial ischemia, acute myocardial infarct, and sudden cardiac death are much greater in incidence than expected in the morning. Moreover, supraventricular and ventricular cardiac arrhythmias of various types show specific day-night patterns, with atrial arrhythmias--premature beats, tachycardias, atrial fibrillation, and flutter - generally being of higher frequency during the day than night--and ventricular fibrillation and ventricular premature beats more common, respectively, in the morning and during the daytime activity than sleep span. Furthermore, different circadian patterns of blood pressure are found in arterial hypertension, in relation to different cardiovascular morbidity and mortality risk. Such temporal patterns result from circadian periodicity in pathophysiological mechanisms that give rise to predictable-in-time differences in susceptibility-resistance to cyclic environmental stressors that trigger these clinical events. Circadian rhythms also may affect the pharmacokinetics and pharmacodynamics of cardiovascular and other medications. Knowledge of 24-h patterns in the risk of cardiac arrhythmias and cardiovascular disease morbidity and mortality plus circadian rhythm-dependencies of underlying pathophysiologic mechanisms suggests the requirement for preventive and therapeutic interventions is not the same throughout the day and night, and should be tailored accordingly to improve outcomes. |
15,137 | ICU nurses' perceptions of potential constraints and anticipated support to practice defibrillation: a qualitative study. | The study examines the experience of intensive care nurses in caring for patients in cardiac arrest, and their perceptions of introducing nurse-led defibrillation.</AbstractText>This was a descriptive, exploratory and qualitative study at an intensive care unit (ICU) of an acute regional hospital in Hong Kong. Twelve registered nurses were purposefully selected for interview.</AbstractText>Although all the participants were trained in basic life support, only 50% were trained in advanced cardiac life support (ACLS), and those trained in ACLS described having limited opportunities to apply their defibrillation knowledge. Whilst participants believed that they were theoretically prepared to influence the patient's resuscitation outcomes, newly qualified nurses were reluctant to be accountable for defibrillation. In contrast, experienced nurses were more willing to perform nurse-led defibrillation. Support from management, cooperation between nurses and doctors, regular in-hospital 'real-drill' programmes, sponsorship for training, and the use of alternative defibrillation equipment should be considered to encourage nurse-led defibrillation in ICU settings.</AbstractText>Nurse-led defibrillation is an approach of delivering prompt care to critically ill patients, and a way ahead for intensive care nursing in Hong Kong. Emphasis on a consistent policy to promote nurse-led defibrillation practice is needed.</AbstractText>Copyright © 2011 Elsevier Ltd. All rights reserved.</CopyrightInformation> |
15,138 | Relationship between the hemoglobin level at hospital arrival and post-cardiac arrest neurologic outcome. | The hemoglobin (Hb) level is an essential determinant of oxygen delivery. The restoration of blood perfusion to vital organs and the capacity for oxygen delivery may be associated with ischemia and reperfusion injuries during cardiac arrest and after cardiac arrest. However, whether the Hb level is associated with neurologic outcome in post-cardiac arrest patients remains unclear.</AbstractText>Emergency medical service information and clinical demographics were compiled for witnessed out-of-hospital cardiac arrest patients with coma after the restoration of spontaneous circulation. The study end point was defined as a favorable neurologic outcome at 28 days. We evaluated the relationship between the Hb level at the time of hospital arrival and the neurologic outcome using univariate analyses and a multivariate logistic regression analysis.</AbstractText>There were 137 witnessed cardiac arrest patients: 49 (35.7%) survived and 34 (24.8%) achieved a favorable neurologic outcome. Univariate analyses showed that the favorable outcome group was characterized as having a higher Hb level, a younger age, a higher percentage of male patients, and ventricular fibrillation as the initial cardiac rhythm. In a multivariate analysis adjusting for potential confounding factors, the Hb level at the time of hospital arrival (odds ratio, 1.26; 95% confidence interval, 1.00-1.58) was an independent predictor of a favorable neurologic outcome.</AbstractText>A higher Hb level at the time of hospital arrival was associated with a favorable short-term neurologic outcome among post-cardiac arrest patients with a presumed cardiac etiology.</AbstractText>Copyright © 2012 Elsevier Inc. All rights reserved.</CopyrightInformation> |
15,139 | [Integration between cardiology and primary care: impact on clinical practice]. | To assess the impact of a program integrating cardiology and primary care in clinical practice, compared with usual care. The integrated care consists of a hospital cardiologist in each primary care clinic, shared clinical history, joint practice guidelines, consultation sessions, and other coordinating tools.</AbstractText>Observational, cross-sectional study of 2 series of chronic outpatients: conventional and integrated care. We analyzed patient distribution and the impact on good clinical practice indicators in patients with ischemic heart disease, heart failure and atrial fibrillation, along with primary care practitioner satisfaction and use of resources.</AbstractText>We included 3194 patients (1572 usual care, 1622 integrated care). Integrated care changed the patient distribution, allowing the cardiologist to focus on serious pathologies while cardiovascular risk factors and stable patients were monitored in primary care. In ischemic heart disease, improvement was observed in cholesterol management and blood pressure control; optimal medical treatment was more frequently prescribed and ventricular function evaluated more often. In heart failure, β-blockers treatment increased and functional class was assessed more often. In atrial fibrillation, an increase in anticoagulation prescription and echocardiography evaluation was observed. Satisfaction parameters improved with integrated care. The use of resources was not increased.</AbstractText>Using our integration model, follow-up and chronic treatment of patients with ischemic heart disease, heart failure, and atrial fibrillation were improved. Monitoring of chronic patients was redistributed between primary care and cardiology, and family physicians' satisfaction levels improved. There was no increase in use of resources. Full English text available from: www.revespcardiol.org.</AbstractText>Copyright © 2011 Sociedad Española de Cardiología. Published by Elsevier Espana. All rights reserved.</CopyrightInformation> |
15,140 | Rhythm disorders in isolated left ventricular noncompaction. | Both supraventricular and ventricular rhythm disorders are frequently observed in patients with isolated left ventricular noncompaction (IVNC). Most importantly, these patients are prone to develop life-threatening ventricular arrhythmias, which are amongst their most frequent causes of death. Data regarding risk stratification of ventricular arrhythmias, however, are scarce due to the rareness of the disease. Indeed, even invasive electrophysiological studies may be of limited value in this regard in the majority of patients. Implantable cardioverter defibrillators (ICDs) have been demonstrated to be highly effective for the prevention of sudden arrhythmic death in IVNC and should be considered in patients who are clinically judged to be at high risk for ventricular tachyarrhythmias. These include patients with a severely reduced ejection fraction as well as those with a prior history of sustained ventricular tachycardia or fibrillation, recurrent syncope of unknown etiology, or a family history of ventricular tachyarrhythmias or sudden cardiac death. This review summarizes the electrocardiographic and electrophysiological findings in patients with IVNC and discusses possibilities for risk stratification as well as the rationale for ICD implantation for the prevention of sudden cardiac death. |
15,141 | Spotlight on intravenous vernakalant in recent-onset atrial fibrillation. | Intravenous vernakalant (Brinavess®) is an atrial-repolarization-delaying agent that is currently approved in the EU for the rapid conversion of recent-onset atrial fibrillation to sinus rhythm. Vernakalant blocks atrial-specific potassium and sodium ion channels, prolonging atrial refractory periods and rate-dependently slowing atrial conduction, without promoting ventricular arrhythmia. In pivotal, randomized, phase III trials, intravenous vernakalant 3 mg /kg administered as a 10-minute infusion, followed by a 2 mg/kg 10-minute infusion after 15 minutes if atrial fibrillation persisted, was effective in the rapid termination of recent-onset atrial fibrillation in nonsurgical patients (≥ 3 hours' to ≤ 7 days' duration) and in those with postoperative atrial fibrillation (3-72 hours' duration) following cardiac surgery. Conversion to sinus rhythm occurred rapidly following infusion of vernakalant, with the majority of patients converting after the first dose, and conversion to sinus rhythm was generally associated with a rapid resolution of symptoms. These antiarrhythmic effects of vernakalant were durable, with most responders remaining in sinus rhythm 24 hours after treatment initiation. In nonsurgical patients with recent-onset atrial fibrillation of 3-48 hours' duration, vernakalant was more effective than intravenous amiodarone, with a significantly higher proportion of patients converting to sinus rhythm within the first 90 minutes of treatment. Vernakalant was generally well tolerated in clinical trials, with most adverse events being of mild or moderate severity and not treatment limiting. Increases in QRS or QT intervals were transient, and there was no increased incidence of ventricular arrhythmia observed with vernakalant compared with placebo. Therefore, intravenous vernakalant provides an effective option for the management of recent-onset atrial fibrillation. |
15,142 | Left ventricular noncompaction: analysis of a pediatric population. | Left ventricular noncompaction (LVNC) is a rare and potentially progressive cardiomyopathy, characterized by the persistence of multiple trabeculations and deep intratrabecular recesses in the ventricular myocardium. Although two-dimensional and color Doppler echocardiography are the most useful diagnostic modalities, cardiac magnetic resonance imaging has proved to have high sensitivity and specificity in the diagnosis of this anomaly.</AbstractText>To characterize the clinical and imaging features of LVNC in a pediatric population and to assess their evolution.</AbstractText>We performed a retrospective chart review of five pediatric patients with LVNC, followed at Coimbra Pediatric Hospital between January 1999 and December 2007. Median age at presentation was five months (ranging from one day to 13 years), and they were mainly male (1.5:1). Two of the children had a family history of sudden death. In one case the clinical presentation was cardiac arrest due to ventricular fibrillation and in three others, congestive cardiac failure. None of the five cases had associated congenital cardiac anomalies. Involvement of the ventricular apical region was found in all cases. Four children additionally had ventricular dysfunction which improved with diuretic and vasodilator therapy. Mean follow-up was 34 months, ranging from six months to seven years. In one case a change in the morphological phenotype was noted, from a dilated to a hypertrophic form. In this case and in the child's father a mutation in the MYBPC3 gene was identified, which is associated with hypertrophic cardiomyopathy. No thromboembolic phenomena or deaths occurred during the study period.</AbstractText>In the pediatric population, congestive cardiac failure is the most common clinical presentation of LVNC, which can coexist with other cardiomyopathies, particularly dilated and hypertrophic forms. The sample presented in this analysis is statistically non-significant due to its limited size and the authors highlight the need for larger prospective studies in the pediatric population in order to clarify this disease and its diagnostic criteria.</AbstractText> |
15,143 | Benefits of cardiac resynchronization therapy in "very dilated cardiomyopathy". | Recent clinical trials have studied parameters that could predict response to cardiac resynchronization therapy (CRT) in patients with advanced heart failure. Left ventricular end-diastolic dimension (LVEDD) is regarded as a possible predictor of response to CRT.</AbstractText>To study the response to CRT in patients with very dilated cardiomyopathy, i.e. those at a more advanced stage of the pathology, analyzing both the responder rate and reverse remodeling in two groups of patients classified according to LVEDD.</AbstractText>We performed a retrospective analysis of 71 patients who underwent CRT (aged 62 +/- 11 years; 65% male; 93% in NYHA functional class > or = III; 31% with ischemic cardiomyopathy; left ventricular ejection fraction [LVEF] 25.6 +/- 6.8%; 32% in atrial fibrillation; QRS 176 +/- 31 ms). Twenty-two (31%) patients with LVEDD > or = 45 mm/m2 (49.2 +/- 3.5 mm/m2) were considered to have very dilated cardiomyopathy (Group A) and 49 patients had LVEDD > 37 mm/m2 and < 45 mm/m2 (39.4 +/- 3.8 mm/m2) (Group B). All patients were assessed by two-dimensional echocardiography at baseline and six months after CRT. The following parameters were analyzed: NYHA functional class, LVEF and LVEDD. Responders were defined clinically (improvement of > or = 1 NYHA class) and by echocardiography, with a minimum 15% increase over baseline LVEF combined with a reduction in LVEDD (reverse remodeling).</AbstractText>There were no significant differences in baseline demographic characteristics between the two groups. At six-month followup, we observed an improvement in LVEF (delta 8.5 +/- 11.8%) and a reduction in LVEDD (delta 3.7 +/- 6.8 mm/m2), with fifty-seven (79%) patients being classified as clinical responders. The percentage of patients with reverse remodeling was similar in both groups (64% vs. 73%, p = NS), as were percentages of improved LVEF (delta 6.3 +/- 11% vs. delta 9.6 +/- 12%; p = NS) and decreased LVEDD (delta 3.7 +/- 5.5 mm/m2 vs. delta 3.7 +/- 7.4 mm/m2; p = NS). We found a higher percentage of clinical responders in patients with very dilated cardiomyopathy (96% vs. 72%, p < 0.05).</AbstractText>In this study, a significant number of responders showed reverse remodeling after CRT. Although a higher percentage of patients with very dilated cardiomyopathy showed improvement in functional class, the extent of reverse remodeling was similar in both groups.</AbstractText> |
15,144 | Prevention of cardioembolic stroke. | Cardiac causes of ischemic stroke lead to severe neurological deficits from large intracranial artery occlusion compared to small vessel ischemic stroke. The most common cause of cardioembolic stroke is atrial fibrillation (AF), which has an increasing incidence with age. AF stroke trials demonstrate that anti-coagulation is superior to anti-platelet therapy in terms of ischemic stroke prevention. Recently, warfarin was compared with dabigatran, an oral, direct thrombin inhibitor, and was found to be at least equally effective in reducing ischemic stroke with less intracranial bleeding risk. Future research is investigating other direct thrombin inhibitors as potential alternatives to warfarin, which has a narrow therapeutic index, requires frequent blood monitoring, has multiple drug interactions, and a higher rate of intracranial bleeding. Other causes of cardioembolic stroke include myocardial infarction, left ventricular thrombus, reduced ejection fraction, valvular abnormalities, and endocarditis. Patent foramen ovale is a common finding on echocardiograms in patients with and without stroke (up to 20% of the population), and it is a controversial source of cryptogenic stroke. The best way to prevent cardioembolic stroke remains early detection and treatment of AF, and treating the underlying stroke mechanism. Cardiac magnetic resonance imaging is an emerging technology and reveals some sources of cardiac embolism missed by echocardiography, and might provide an additional diagnostic tool in investigating cardioembolic stroke. |
15,145 | Frequency and timing of nonconvulsive status epilepticus in comatose post-cardiac arrest subjects treated with hypothermia. | Therapeutic hypothermia (TH) improves outcomes in comatose patients resuscitated from cardiac arrest. However, nonconvulsive status epilepticus (NCSE) may cause persistent coma. The frequency and timing of NCSE after cardiac arrest is unknown.</AbstractText>Review of consecutive subjects treated with TH and receiving continuous EEG (cEEG) monitoring between 8/1/2009 and 11/16/2010. Demographic data, survival, and functional outcome were prospectively recorded. Each cEEG file was analyzed using standard definitions to define NCSE. Data were analyzed using descriptive and nonparametric statistics.</AbstractText>Mean age of the 101 subjects was 57 years (SD 15) with most subjects being male (N = 55, 54%) and experiencing out-of-hospital cardiac arrest (N = 78; 77%). Ventricular fibrillation was the initial cardiac rhythm in 39 (38%). All subjects received TH. Thirty subjects (30%) awoke at a median of 41 h (IQR 30, 61) after cardiac arrest. A total of 29/30 (97%) subjects surviving to hospital discharge were awake. Median interval from arrest to placement of cEEG was 9 h (IQR 6, 12), at which time the mean temperature was 33.9°C. NCSE occurred in 12 (12%) subjects. In 3/12 (25%) subjects, NCSE was present when the cEEG recording began. In 4 subjects, NCSE occurred within 8 h of cEEG recording. One (8%) subject with NCSE survived in a vegetative state.</AbstractText>NCSE is common in comatose post-cardiac arrest subjects receiving TH. Most seizures occur within the first 8 h of cEEG recording and within the first 12 h after resuscitation from cardiac arrest. Outcomes are poor in those who experience NCSE.</AbstractText> |
15,146 | Effect of pseudoephedrine on cardiac rhythm of children with rhinitis. | To investigate the effect of pseudoephedrine on heart rhythm of children with rhinitis.</AbstractText>The study included 25 children diagnosed with rhinitis from March 2009 through February 2010 in the Department of Pediatrics. Holter records were obtained for 24 h before and at the fourth day of pseudoephedrine treatments.</AbstractText>Study group consisted of 18 girls (72%) and 7 boys (28%) with a mean age of 8.7 ± 3.4 (4-17.9 years). Common complaints of the patients were rhinorrhea (100%), cough (68%) fatigue (48%), sore throat (36%), and headache (28%). Of the 25 patients whose Holter recordings were evaluated, rare supraventricular extrasystoles were observed in one prior to the administration of pseudoephedrine, which were not repeated on this patient's follow-up recording on day four. There were two ventricular extrasystoles in the day four Holter recording of another patient. None of the patients complained of chest pain or palpitation. There were no observations of supraventricular tachycardia, ventricular tachycardia or ventricular fibrillation. No statistical differences could be found (p > 0.05) in the values before treatment and those on day four of treatment of either the time-dependent Heart rate variability (HRV) parameters SDNN, SDNN index, SDANN and RMSSD, or the frequency-dependent parameters (TP, HF, LF). No statistical difference could be determined between heart rate values of the patients before treatment and those on day four of treatment (p > 0.05).</AbstractText>This study has established that therapeutic doses of pseudoephedrine do not cause an additional dysrhythmia risk for children with no health problem except rhinitis.</AbstractText> |
15,147 | [Early repolarisation syndrome and idiopathic ventricular fibrillation]. | Syndrome of early repolarisation is a relatively not common electrocardiographic pattern with typically elevated J wave in most of the cases in lead II, III, aVF and V3-V6. There is increasing evidence that the early repolarisation might be associated with increased risk of sudden cardiac death in otherwise healthy individuals. Early repolarisation ECG pattern in inferolateral leads is associated with sudden death in younger otherwise healthy individuals. Identification of this risky group based on pure ECG criteria is still challenging but it must be considered in individuals with family history of sudden cardiac death or cardiac arrest. |
15,148 | A sternal accelerometer does not impair hemodynamics during piglet CPR. | To determine whether the residual weight of a 260 g sternal accelerometer/force feedback device (AFFD) adversely affects hemodynamics during cardiopulmonary resuscitation in a piglet model of ventricular fibrillation cardiac arrest.</AbstractText>After induction of ventricular fibrillation, cardiopulmonary resuscitation was provided to ten piglets (10.8 ± 1.9 kg) for 12 min while maintaining aortic systolic pressure of 80-90 mm Hg during four 3-min periods with or without an AFFD on the chest. Cardiac output and left ventricular myocardial blood flow were determined by neutron-microsphere technique.</AbstractText>Using a linear mixed-effect model with residual maximum likelihood estimation to control for changes in cardiopulmonary resuscitation hemodynamics over time, cardiac output and myocardial blood flow did not differ with AFFD versus without AFFD. During the first 6 min, mean (± SEM) cardiac outputs were 0.42 (± 0.05)L/min with AFFD versus 0.31 (± 0.04)L/min without AFFD, and median left ventricular myocardial blood flows were 40.5 (± 7.3)mL/min/100g with AFFD versus 40.4 (± 5.0)mL/min/100g without AFFD. The mean right atrial diastolic pressures and coronary perfusion pressures were also not different (8 ± 0.7 mm Hg versus 8 ± 0.9 mm Hg and 16 ± 2 mm Hg versus 16 ± 2 mm Hg, respectively, during the first 6 min of CPR).</AbstractText>The use of a 260 g accelerometer/force feedback device designed for real-time feedback to the rescuer during resuscitation efforts did not adversely affect cardiac output or left ventricular myocardial blood flow during 12 min of chest compressions in a piglet model of ventricular fibrillation cardiac arrest.</AbstractText>Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.</CopyrightInformation> |
15,149 | Application of impedance threshold devices during cardiopulmonary cerebral resuscitation. | To review the use of impedance threshold devices (ITD) during CPCR, their proposed mechanism of action, and their application in veterinary medicine.</AbstractText>Data sources include scientific reviews and original research publications using the PubMed search engine with the following keywords: 'impedance threshold device' and 'resuscitation' and the Veterinary Information Network search function using the keywords 'impedance threshold device.'</AbstractText>Studies in human medicine have demonstrated that the use of an ITD during CPCR in patients during out-of-hospital cardiac arrest improves coronary perfusion pressure and cerebral perfusion pressure. This improvement in vital organ blood flow results in increased cardiac output and faster return of spontaneous circulation. The use of an ITD has been studied in people and currently holds a class IIb level of recommendation according to the 2010 American Heart Association Guidelines for CPR and Emergency Cardiovascular Care. This device is recommended as a way to improve hemodynamics during CPCR by enhancing venous return and avoiding hyperventilation, thereby increasing the likelihood of a successful resuscitation.</AbstractText>Multiple controlled studies using pigs with ventricular fibrillation induced cardiopulmonary arrest have demonstrated increased myocardial and cerebral perfusion with the use of an ITD. These studies have emphasized the importance of decreasing intrathoracic pressures during the decompression phase of CPCR and avoiding hyperventilation in order to maximize vital organ blood flow.</AbstractText>Use of an ITD during CPCR in human and animal studies has demonstrated improved vital organ perfusion and faster return of spontaneous circulation. However, the majority of these studies have been carried out in people during out-of-hospital cardiac arrest and ventricular fibrillation cardiopulmonary arrest pig models. Further studies evaluating the use of an ITD during CPCR in the veterinary hospital setting are warranted.</AbstractText>© Veterinary Emergency and Critical Care Society 2011.</CopyrightInformation> |
15,150 | Fate of a modified fenestration of atrial septal occluder device after transcatheter closure of atrial septal defects in elderly patients. | Data on closure of atrial septal defects (ASD) in elderly patients with a fenestrated Amplatzer septal occluder (ASO) device is limited.</AbstractText>A hemodynamically significant ASD was closed with a fenestrated ASO in 3 patients with ages >62 years. Prior to implant a 4-mm fenestration was created by balloon dilatation without additional suture fixation just adjacent to the stent part of the device. Indications for fenestration were restrictive left ventricular physiology and/or pulmonary hypertension. Heparin had been administered during and for 48 hours after the procedure. Two patients were maintained on phenprocoumon because of chronic atrial fibrillation, the remaining patient on aspirin and clopidogrel for 3 months after implant. Transesophageal echocardiography (TEE) and hemodynamic evaluation were performed 4-18 months after ASD closure.</AbstractText>A trace or small fenestration through the ASO with left-to-right shunt was detected by TEE in all 3 patients without any hemodynamic significance. No thrombus formation was observed. Pulmonary hypertension improved in the affected patient. Pulmonary arterial wedge pressure and cardiac index improved in the second patient with improvement in heart failure symptoms and of quality of life in both. The third patient, after initial improvement for 6 months, developed significant comorbidities and clinical deterioration at 18 months follow-up.</AbstractText>The modified fenestration of the ASO decreased significantly in size at follow-up. Applying this technique to selected patients judged to be at risk for ASD closure avoids acute decompensation and allows gradual diminuition of right ventricular volume overload during mid-term follow-up. </AbstractText>©2011, Wiley Periodicals, Inc.</CopyrightInformation> |
15,151 | Atrial fibrillation in the aging heart: pharmacological therapy and catheter ablation in the elderly. | The majority of patients with atrial fibrillation (AF) seeking medical treatment are in the elderly age group and the management of these patients is often complicated by comorbidities, challenging the pharmacological management of these patients. Owing to hypertension, congestive heart failure, left ventricular hypertrophy and coronary artery disease, antiarrhythmic treatment often fails due to side effects, proarrhythmia or poor rhythm control. In recent years, radiofrequency catheter ablation has been widely performed as an effective treatment for recurrent, drug-refractory AF. However, few elderly patients were included in prior AF catheter ablation studies and the current guidelines for catheter ablation of AF recommend a conservative approach in the elderly population owing to the absence of clinical data. However, study results from our group and others suggest that catheter ablation is a safe and effective treatment for patients over the age of 65 years with symptomatic, drug-refractory AF and, therefore, patients should not be excluded from catheter ablation on the basis of age alone. In this article, we discuss the pharmacological (rhythm control, rate control and anticoagulation) and catheter management of AF in the elderly population. |
15,152 | Circulating KCNH2 current-activating factor in patients with heart failure and ventricular tachyarrhythmia. | It is estimated that approximately half of the deaths in patients with HF are sudden and that the most likely causes of sudden death are lethal ventricular tachyarrhythmias such as ventricular tachycardia (VT) or fibrillation (VF). However, the precise mechanism of ventricular tachyarrhythmias remains unknown. The KCNH2 channel conducting the delayed rectifier K(+) current (I(Kr)) is recognized as the most susceptible channel in acquired long QT syndrome. Recent findings have revealed that not only suppression but also enhancement of I(Kr) increase vulnerability to major arrhythmic events, as seen in short QT syndrome. Therefore, we investigated the existence of a circulating KCNH2 current-modifying factor in patients with HF.</AbstractText><AbstractText Label="METHODOLOGY/PRINCIPAL FINDINGS" NlmCategory="RESULTS">We examined the effects of serum of HF patients on recombinant I(Kr) recorded from HEK 293 cells stably expressing KCNH2 by using the whole-cell patch-clamp technique. Study subjects were 14 patients with non-ischemic HF and 6 normal controls. Seven patients had a history of documented ventricular tachyarrhythmias (VT: 7 and VF: 1). Overnight treatment with 2% serum obtained from HF patients with ventricular arrhythmia resulted in a significant enhancement in the peaks of I(Kr) tail currents compared to the serum from normal controls and HF patients without ventricular arrhythmia.</AbstractText><AbstractText Label="CONCLUSIONS/SIGNIFICANCE" NlmCategory="CONCLUSIONS">Here we provide the first evidence for the presence of a circulating KCNH2 channel activator in patients with HF and ventricular tachyarrhythmias. This factor may be responsible for arhythmogenesis in patients with HF.</AbstractText> |
15,153 | Acute cardiac arrhythmias following surgery for congenital heart disease: mechanisms, diagnostic tools, and management. | This article focuses on the management of those cardiac arrhythmias most commonly seen in the immediate postoperative period. They include ventricular tachycardia, ventricular fibrillation, atrial flutter, junctional ectopic tachycardia, bradycardia, and atrioventricular block. The mechanisms of cardiac arrhythmias are reviewed followed by a brief overview of the predominant acute arrhythmias, tools used for the diagnostic evaluation of these arrhythmias, management strategies, and, finally, nursing considerations. |
15,154 | [Non-drug treatment for hypertrophic obstructive cardiomyopathy in children]. | To retrospectively summarize the effect of non-medical therapies for pediatric patients with hypertrophic obstructive cardiomyopathy (HOCM).</AbstractText>From Nov. 2008 to Jun. 2010, 4 children with drug-refractory HOCM were admitted to our hospital. Their ages were 14, 7, 9 and 6 years old, respectively. Their body weights were 38, 17, 21.5 and 17 kg, respectively. Before operation, the pressure gradients over left ventricular outflow tract (LVOTG) were 60, 147, 58 and 114 mm Hg (1 mm Hg = 0.133 kPa), respectively. And mitral regurgitation (MR) areas were 2.2, 7.3 cm(2) and 2.9 cm(2), respectively, except that it was trivial in one case. Percutaneous transluminal septal myocardial ablation (PTSMA) was performed in case 1 and 2. Septal myectomy (SM) was performed in case 3 and 4. Follow-up was first performed right after operation or before discharge, then 1 month, 3 months, 6 months, and 12 months after operation, and then once a year. The follow-up period was 1 - 18 (9.3 ± 8.1) months.</AbstractText>All patients experienced relieved symptoms. Three of them had their NYHA functional class improved except case 2. Echocardiography revealed that LVOTGs right after operations were 38, 79, 20 and 0 mm Hg, respectively, suggesting significant improvement of left ventricular outflow tract obstruction (LVOTO) in all patients. During follow-up, case 2 suffered from recurrence of LVOTO, while the other 3 cases showed sustained relief. In the last follow-up, the LVOTGs of the four patients were 19, 168, 16 and 0 mm Hg, respectively. Echocardiography also revealed that MRs of all patients were significantly reduced, even in case 2 whose LVOTG rebounded, with no recurrence during follow-up. Severe complications were absent, such as ventricular septum perforation, cardiac tamponade, ventricular tachycardia or ventricular fibrillation. No one suffered from complete heart block. Transient complete right bundle branch block (CRBBB) was observed in case 1 after PTSMA and converted to intraventricular block after 1 month. Complete left bundle branch block (CLBBB) was present in both case 3 and 4, who received SM. In case 4, it converted to intraventricular block after 1 month while in case 3 CLBBB persisted.</AbstractText>The initial experience showed that PTSMA and SM were safe and effective for drug-refractory symptomatic HOCM children, with satisfactory short-term results. Further studies are needed to evaluate the long-term results and complications.</AbstractText> |
15,155 | Contribution of acquired factors to the pathogenesis of dilated cardiomyopathy. -The cause of dilated cardiomyopathy: genetic or acquired? (Acquired-Side)-. | Although genetic abnormalities play a pivotal role in the development of dilated cardiomyopathy (DCM), acquired infection and autoimmune abnormalities, or both, appear to be predominant underlying disorders. Of these, viral infection causes target organ damage via perforin produced by suppressor T cells. Thereafter, various antigens released from damaged myocytes are presented on the major histocompatibility complex II, which is expressed in antigen-presenting cells, resulting in activation of both cellular (Th1) and humoral (Th2) immunity. Various antimyocardial antibodies are detected in the serum of patients with DCM and recent findings suggest that at least some of them are directly related to the pathophysiology of DCM. An autoantibody targeting the β1-adrenergic receptor is related to the persistent myocardial damage resulting in DCM and provides the substrate for fatal ventricular arrhythmias. An antibody for the muscarinic M2 receptor is related to atrial fibrillation, an antibody targeting Na-K-ATPase is closely related to sudden cardiac death from fatal ventricular arrhythmias, and an autoantibody for troponin I increases the L-type calcium current and is related to myocardial damage. On the other hand, genetic factors are also involved in susceptibility to viral infection and aberrations of acquired immunity, including antigen presentation and autoantibody production. In conclusion, acquired factors are predominant causes of DCM, although the 2 predisposing factors are also linked to genetic abnormalities. |
15,156 | Characteristics and significance of very early recurrence of atrial fibrillation after catheter ablation. | Early restoration of sinus rhythm following ablation of atrial fibrillation (AF) facilitates reverse atrial remodeling and improves the long-term outcome. The purpose of this study was to determine the predictors and outcome in patients with very early AF recurrences (< 2 days).</AbstractText>Ablation was performed in 339 consecutive AF patients (paroxysmal AF = 262). Biatrial voltage was mapped during sinus rhythm. If recurrent AF occurred within 2 days following the ablation, electrical cardioversion was performed to restore sinus rhythm. Very early recurrences of AF occurred in 39 (15%) patients with paroxysmal AF and 26 (34%) with nonparoxysmal AF. Patients with very early recurrence had a higher incidence of nonparoxysmal AF (40% vs 18.6%, P< 0.001), requirement of electrical cardioversion during procedure, larger left atrial (LA) diameter (43 ± 7 vs 39 ± 6 mm, P< 0.001), lower left ventricular ejection fraction (54 ± 10% vs 59 ± 7, P< 0.001), longer procedural time, and lower LA voltage (1.5 ± 0.7 vs 1.9 ± 0.8 mV, P< 0.001). A multivariate analysis revealed that the independent predictors of a very early recurrence were a longer procedural time and lower LA voltage. During a follow-up of 13 ± 5 months, a very early recurrence did not predict the long-term outcome of a single procedure recurrence in the patients with paroxysmal AF, but was associated with a late recurrence in the nonparoxysmal AF patients.</AbstractText>Very early recurrence occurred in patients with paroxysmal AF is not associated with long-term recurrence. Nonparoxysmal AF is an independent predictor of late recurrence of AF in patients with very early recurrence.</AbstractText>© 2011 Wiley Periodicals, Inc.</CopyrightInformation> |
15,157 | Cardioprotective effects of pravastatin against lethal ventricular arrhythmias induced by reperfusion in the rat heart. | Statins are reported to reduce mortality in patients with coronary artery disease and that mortality benefit might be related to the drugs' antiarrhythmic properties.</AbstractText>Male rats were fed with or without pravastatin (0.1 mg·kg⁻¹·day⁻¹) for 7 days, and thereafter subjected to 10 min of ischemia by coronary artery ligation followed by 20 min reperfusion. Treatment with pravastatin reduced the frequency and duration of ventricular tachycardia and fibrillation (VT/VF) and improved the arrhythmia score after reperfusion. To investigate the rapid effects of pravastatin, isolated perfused rat hearts were subjected to 20 min of global ischemia followed by 30 or 60 min of reperfusion. Treatment with pravastatin (10 nmol/L) from 10 min before ischemia shortened the total duration of reperfusion-induced VT/VF. Interestingly, pravastatin administered from the beginning of reperfusion also exerted antiarrhythmic effects. These results indicate that pravastatin exerts antiarrhythmic effects not only with daily oral intake but also when administered just before ischemia or even after ischemia. Intracellular calcium ([Ca²⁺](i)) overload and collapse of mitochondrial inner membrane potential (Δψ(m)) are associated with the arrhythmogenesis during ischemia-reperfusion. In cultured cardiomyocytes, pretreatment with pravastatin (10 nmol/L) suppressed [Ca²⁺](i) overload and prevented Δψ(m) loss induced by H₂O₂.</AbstractText>Pravastatin attenuated reperfusion-induced lethal ventricular arrhythmias. Inhibition of [Ca²⁺](i) overload and preserving Δψ(m) may be the mechanisms of the observed antiarrhythmic effects of pravastatin.</AbstractText> |
15,158 | Pediatric cardiopulmonary resuscitation and stabilization. | Cardiopulmonary arrest refers to cessation of clinically detectable cardiac activity. In children, it usually results from progression of shock, respiratory failure or cardiac dysrhythmia. Early recognition and timely interventions in above group of patients is the key to prevent progression to cardiac arrest. The goal of resuscitation is to urgently re-establish oxygenation of vital organs by attention to Airway, Breathing and Circulation. Measures to restore airway patency include positioning, suctioning, continuous positive airway pressure, relieving a foreign-body airway obstruction and, endotracheal intubation, tracheotomy or laryngeal mask airway. Breathing is supported with O(2) and if needed, bag-mask ventilation, or endotracheal intubation and ventilation. Patients with absent or feeble central pulse are given cardiac compressions (CPR) at a rate of 100/ min synchronized with ventilation. In sudden witnessed collapse, immediate defibrillation is warranted, followed by CPR and administration of drugs. In unwitnessed collapse, CPR is performed for five cycles or 2 min before defibrillation. In patients with shock, a venous or an intraosseous access is rapidly established to administer 20 ml/kg saline bolus. Supraventricular tachycardia is treated with vagal maneuvers and adenosine, if the patient is stable and with synchronized cardioversion, if unstable. Ventricular tachycardia is treated with amiodarone or lidocaine, if stable, and cardioversion if unstable or if drugs fail. Ventricular fibrillation needs defibrillation. Aggressive supportive care is needed during the post-resuscitation phase. There is no definite marker to determine futility of CPR. Short duration of arrest, early initiation of CPR, hypothermia as the cause of arrest, and in-hospital arrest have better prognosis. |
15,159 | Entrance skin dose during radiofrequency catheter ablation for tachyarrhythmia: a multicenter study. | To assess the entrance skin dose (ESD) during radiofrequency catheter ablation procedures for tachyarrhythmia including atrial fibrillation (Af).</AbstractText>This study focused on 99 consecutive patients who underwent procedures for tachyarrhythmia (Af; n = 34, non-Af; n = 65) in three institutions. The non-Af group included atrial flutter, atrial tachycardia, paroxysmal supraventricular tachycardia, ventricular tachycardia, ventricular premature contraction, atrial premature contraction, atrioventricular nodal reentry tachycardia, and Wolff-Parkinson-White syndrome. In two of the three institutions, the procedures were performed for both Af and non-Af. The ESDs were measured using 100 radiosensitive indicators attached to the back of each patient's jacket at 5-cm intervals. For statistical analyses, multiple regression analysis (the dependent variable, Max-ESD; and the independent variables, dose area product [DAP], total fluoroscopic time [TFT], body mass index, etc.), Pearson's correlation test, and the Mann-Whitney test were employed.</AbstractText>The overall averages for the TFTs, the DAPs, and the Max-ESDs were 49.9 ± 28.2 minutes, 71.2 ± 73.7 Gy cm(2) , and 0.57 ± 0.51 Gy, respectively. DAP was positively related to the Max-ESD and was significant in stepwise multiple regression analysis (P < 0.0001). There was a significant association between TFT and Max-ESD in five of the six kinds of angiographic unit, and between DAP and Max-ESD in all three systems with available DAP measures. In one institution, TFT, DAP, and Max-ESD differed significantly between the Af and non-Af groups (P = 0.0002, P < 0.0001, and P < 0.0001).</AbstractText>During the cardiac catheter ablation, ESDs of only a few patients exceeded the thresholds of radiation skin injuries, and the DAP proved useful to estimate each patient's Max-ESD.</AbstractText>©2011, The Authors. Journal compilation ©2011 Wiley Periodicals, Inc.</CopyrightInformation> |
15,160 | [Effect of tongxinluo capsule on platelet activities and vascular endothelial functions as well as prognosis in patients with acute coronary syndrome undergoing percutaneous coronary intervention]. | To observe the effect of Tongxinluo Capsule on platelet activities and vascular endothelial functions as well as prognosis in patients with acute coronary syndrome (ACS) after percutaneous coronary intervention (PCI) at different stages.</AbstractText>160 patients with acute coronary syndrome were randomly assigned to Tongxinluo (TXL) group (80 patients) and the conventional treatment group (80 patients). And 50 healthy subjects were set up as the health control group. Patients' plasma platelet activating factors (CD62p, CD63), and glucose protein (GP) IIb/IIIa, and endothelium-1 (ET-1), von Willebrand factor (vWF), nitric oxide (NO) levels, and endothelium dependent flow-mediated dilatation (FMD) were detected respectively. Patients in the TXL group orally took TXLC for six months. The aforesaid indices were re-detected in all patients after two months and six months. Comparison between before and after treatment in the same group and inter-group comparison were performed in the two groups.</AbstractText>Compared with the health control group, CD62p, CD63, GPIIb/IIIa, vWF, and ET-1 levels increased significantly in ACS patients after PCI (all P<0.01), NO and FMD significantly decreased (P<0.01). CD62p, CD63, GPIIb/IIIa and, vWF also increased, and FMD decreased after PCI (all P<0.05), but insignificant difference was found in ET-1 and NO (P>0.05). In the TXL group and the conventional treatment group, the levels of CD62p, CD63, GPIIb/IIIa, vWF and ET-1 decreased significantly (P<0.05, P<0.01), NO and FMD increased (P<0.05, P<0. 01) when compared with before treatment. Compared with the conventional treatment group, the decrement of CD62p, CD63, GPIIb/IIIa and vWF (P<0.05, P<0.01), and the increment of FMD and NO (both P<0.05) were more obvious in the TXL group. The aforesaid indices were more obviously different between 6-month treatment and 2-month treatment in the TXL group and the conventional treatment group (P<0.05, P<0.01). Seven patients suffered from angina, six from heart failure, three from ventricular tachycardiac (VT)/ventricular fibrillation (VF), and two died suddenly in the conventional treatment group after six months of treatment, while only one suffered from angina, one from heart failure, and none from VT/VF or died suddenly in the TXL treatment group after 6 months of treatment.</AbstractText>TXL could be used in the prevention and treatment of coronary thrombosis, protect the vascular endothelial functions, as well as improve the prognosis of ACS patients after PCI.</AbstractText> |
15,161 | Validity of claims-based definitions of left ventricular systolic dysfunction in Medicare patients. | Ejection fraction (EF) is crucial information when studying the use and effectiveness of therapies in patients with heart failure (HF) and myocardial infarction (MI). We aimed to assess the validity of claims data-based definitions of systolic dysfunction (SD).</AbstractText>We identified 1072 patients with EF recorded for an HF/MI hospitalization in Medicare linked with pharmacy data and national HF/MI registries in 1999-2006. Thirteen claims-based definitions for SD were developed using a single or combination of ICD-9 diagnosis codes and cardiovascular medications use. We calculated sensitivity, specificity, and positive predictive values (PPVs) using recorded EFs as the gold standard.</AbstractText>Using an EF cutoff of 45%, the definitions based on digoxin use and no atrial fibrillation or flutter had the highest PPVs (76% to 84%) and specificity (>97%) but low sensitivity (6%-14%). As we varied the EF cutoff between 50% and 25%, the specificity decreased by 3%, but the PPVs decreased by 52%. We observed potential differences in the PPVs by patients' characteristics. In a hypothetical study assessing implantable defibrillator effectiveness, using our definition to identify patients with SD would underestimate the effectiveness by 3% to 24%. In another hypothetical study comparing two classes of angiotensin system blockers where SD was considered confounding, our definition introduced ~43% misclassification bias.</AbstractText>Claims-based definitions for SD had excellent specificity and good PPV but low sensitivity. The definitions with good PPV could be used for cohort identification or confounding adjustment by restriction and would result in relatively small misclassification bias albeit limited generalizability.</AbstractText>Copyright © 2011 John Wiley & Sons, Ltd.</CopyrightInformation> |
15,162 | Association between plaque thickness of the thoracic aorta and recurrence of atrial fibrillation after ablation. | Several predictors of recurrence of atrial fibrillation (AF) after ablation have been identified, including age, type of AF, hypertension, left atrial diameter and impaired left ventricular ejection fraction. The aim of this study was to investigate whether the atherosclerotic plaque thickness of the thoracic aorta is associated with a recurrence of AF after circumferential pulmonary vein ablation (CPVA).</AbstractText>Among patients with drug-refractory paroxysmal or persistent AF, 105 consecutive (mean age 58±11 years, male : female=76 : 29) patients who underwent transesophageal echocardiography and CPVA were studied. The relationships between the recurrence of AF and variables, including clinical characteristics, plaque thickness of the thoracic aorta, laboratory findings and echocardiographic parameters were evaluated.</AbstractText>A univariate analysis showed that the presence of diabetes {hazard ratio (HR)=3.425; 95% confidence interval (CI), 1.422-8.249, p=0.006}, ischemic heart disease (HR=4.549; 95% CI, 1.679-12.322, p=0.003), duration of AF (HR=1.010; 95% CI, 1.001-1.018, p=0.025), type of AF (HR=2.412, 95% CI=1.042-5.584, p=0.040) and aortic plaque thickness with ≥4 mm (HR=9.514; 95% CI, 3.419-26.105, p<0.001) were significantly associated with the recurrence of AF after ablation. In Cox multivariate regression analysis, only the aortic plaque thickness (with ≥4 mm) was an independent predictor of recurrence of AF after ablation (HR=7.250, 95% CI=1.906-27.580, p=0.004).</AbstractText>Significantly increased aortic plaque thickness can be a predictable marker of recurrence of AF after CPVA.</AbstractText> |
15,163 | Bolus fluorouracil induced syncope and pulseless ventricular tachycardia: a case report. | 5-fluorouracil is an anti-cancer drug commonly used in oncology practice. Typical side effects are myelosupression, nausea, vomiting, diarrhea and stomatitis. Cardiotoxicity is the other toxicity. Cardiac side effects are ST segment changes, rhythm abnormalities, supraventricular and ventricular dysrhytmias. Pulseless ventricular tachycardia and ventricular fibrillation releated with bolus fluorouracil were not detected in the literature. Here we discussed a 46 year-old male patient that has no known cardiac history. After bolus fluorouracil administration, syncope and pulseless ventricular tachycardia developed in this patient. There are a few explanations about the cardiotoxicity of fluorouracil. One of these is the effect on nitric oxide. It causes a reduction in the levels of endothelial NO and this leads coronary vasospasm. Another explanation is protein kinase C mediated vasospasm. In animal studies toxic myocarditis like lesions were detected with fluorouracil infusions. Finally both myocardit and vasospasm may lead cardiac problems like sudden cardiac deaths. Bolus 5-fluorouracil is as cardiotoxic as 5-fluorouracil infusion and we must be careful about the arrhytmia after the bolus administration. |
15,164 | Large blood transfusion as a rare cause of ventricular fibrillation. | Large blood transfusions are common in clinical practice. Though several complications have been described with this procedure, cardiac arrhythmias occur uncommonly in this setting. We describe a case of a previously healthy 17-year-old girl who developed wide-complex ventricular tachycardia rapidly culminating in a ventricular fibrillation cardiac arrest several hours following an uneventful large-volume blood transfusion. Hypomagnesemia was detected on postcardiac arrest investigations. A review of this life-threatening complication and discussion on the ways to prevent it are presented. |
15,165 | Effect of ZP123, a gap junction modifier, on prolonged ventricular fibrillation in swine. | It was the aim of this study to investigate the effect of ZP123 on prolonged ventricular fibrillation (VF) in swine.</AbstractText>VF was electrically induced in 20 pigs. The animals randomly received either ZP123 or saline control infusion before VF. After 8 min of untreated VF, cardiopulmonary resuscitation and biphasic defibrillation shocks were applied. VF mean frequency (VF(mf)) and mean amplitude (VF(ma)), hemodynamics, outcome of defibrillation and the rate of return of spontaneous circulation (ROSC) were analyzed.</AbstractText>Compared with the control group, VF(mf) was higher but VF(ma) lower during the 8 min of VF in the drug group (11.8 ± 2.1 vs. 10.4 ± 2.0 Hz and 0.24 ± 0.10 vs. 0.31 ± 0.16 mV, respectively; p < 0.05). Hemodynamic variables in the 2 groups were comparable (p > 0.05). The defibrillation threshold was lower and the rate of successful defibrillation was higher in the drug group compared with the control group (92.2 ± 26.4 vs. 133.3 ± 28.9 J and 90 vs. 30%, respectively; p < 0.05). The rate of ROSC was not different between the 2 groups (40 vs. 30%; p > 0.05).</AbstractText>In prolonged VF, ZP123 could decrease the defibrillation threshold and improve the rate of successful defibrillation. However, it could not improve the rate of ROSC - which may be due to its side effect of decreasing VF(ma).</AbstractText>Copyright © 2011 S. Karger AG, Basel.</CopyrightInformation> |
15,166 | Circumstances and outcomes of sudden unexpected death in patients with high-risk myocardial infarction: implications for prevention. | Sudden death (SD) is a frequent catastrophic complication in patients after myocardial infarction. Circumstances of SD may affect strategies for prevention.</AbstractText>We reviewed source documentation for 1067 patients who had SD in the Valsartan in Acute Myocardial Infarction Trial (VALIANT) trial. We determined the circumstances of these events and assessed long-term mortality in patients who were resuscitated. Location of the SD event was available in 978 of 1067 patients, with 226 events occurring within the first 40 days. Although SD was more likely to occur at home (645 of 978, 66%) than in hospital (204 of 978, 21%), the proportion of in-hospital events was higher early on (99 of 226, 44%). Home events were less likely to be witnessed regardless of time frame. Preceding activity was known for 42% of patients with home arrest; of these, 52% were determined to be asleep at time of event, and these deaths were more likely to be unwitnessed. A majority of patients for whom initial ECG rhythm was reported had ventricular tachycardia/ventricular fibrillation (189 of 283, 67%). Of the 155 patients successfully resuscitated, 24% subsequently received an implantable cardioverter-defibrillator. Nineteen percent of those who received an implantable cardioverter-defibrillator subsequently died compared with 49% of patients who did not receive an implantable cardioverter-defibrillator (hazard ratio, 0.36; 95% confidence interval, 0.14 to 0.93; P=0.04).</AbstractText>A high proportion of SD events after high-risk myocardial infarction occurred at home, but in-hospital events were more common early on. Patients who were asleep were more likely to have unwitnessed arrests. Alternative strategies for the prevention of SD in patients who are not candidates for implantable cardioverter-defibrillator will need to take into account the circumstances of SD events.</AbstractText> |
15,167 | Arrhythmogenic right ventricular dysplasia/cardiomyopathy: pathogenic desmosome mutations in index-patients predict outcome of family screening: Dutch arrhythmogenic right ventricular dysplasia/cardiomyopathy genotype-phenotype follow-up study. | Arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) is an autosomal dominant inherited disease with incomplete penetrance and variable expression. Causative mutations in genes encoding 5 desmosomal proteins are found in ≈50% of ARVD/C index patients. Previous genotype-phenotype relation studies involved mainly overt ARVD/C index patients, so follow-up data on relatives are scarce.</AbstractText>One hundred forty-nine ARVD/C index patients (111 male patients; age, 49±13 years) according to 2010 Task Force criteria and 302 relatives from 93 families (282 asymptomatic; 135 male patients; age, 44±13 years) were clinically and genetically characterized. DNA analysis comprised sequencing of plakophilin-2 (PKP2), desmocollin-2, desmoglein-2, desmoplakin, and plakoglobin and multiplex ligation-dependent probe amplification to identify large deletions in PKP2. Pathogenic mutations were found in 87 index patients (58%), mainly truncating PKP2 mutations, including 3 cases with multiple mutations. Multiplex ligation-dependent probe amplification revealed 3 PKP2 exon deletions. ARVD/C was diagnosed in 31% of initially asymptomatic mutation-carrying relatives and 5% of initially asymptomatic relatives of index patients without mutation. Prolonged terminal activation duration was observed more than negative T waves in V(1) to V(3), especially in mutation-carrying relatives <20 years of age. In 45% of screened families, ≥1 affected relatives were identified (90% with mutations).</AbstractText>Pathogenic desmosomal gene mutations, mainly truncating PKP2 mutations, underlie ARVD/C in the majority (58%) of Dutch index patients and even 90% of familial cases. Additional multiplex ligation-dependent probe amplification analysis contributed to discovering pathogenic mutations underlying ARVD/C. Discovering pathogenic mutations in index patients enables those relatives who have a 6-fold increased risk of ARVD/C diagnosis to be identified. Prolonged terminal activation duration seems to be a first sign of ARVD/C in young asymptomatic relatives.</AbstractText> |
15,168 | Cardiac resynchronization therapy in patients undergoing atrioventricular junction ablation for permanent atrial fibrillation: a randomized trial. | On the basis of the current knowledge, cardiac resynchronization therapy (CRT) cannot be recommended as a first-line treatment for patients with severely symptomatic permanent atrial fibrillation undergoing atrioventricular (AV) junction ablation. We examined whether CRT was superior to conventional right ventricular (RV) pacing in reducing heart failure (HF) events.</AbstractText>In this prospective, multi-centre study, we randomly assigned 186 patients, in whom AV junction ablation and CRT device implantation had been successfully performed, to receive optimized echo-guided CRT (97 patients) or RV apical pacing (89 patients). The data were analysed according to the intention-to-treat principle. During a median follow-up of 20 months (interquartile range 11-24), the primary composite endpoint of death from HF, hospitalization due to HF, or worsening HF occurred in 11 (11%) patients in the CRT group and 23 (26%) patients in the RV group [CRT vs. RV group: sub-hazard ratio (SHR) 0.37 ( 95% CI 0.18-0.73), P = 0.005]. In the CRT group, compared with the RV group, fewer patients had worsening HF [SHR 0.27 (95% CI 0.12-0.58), P = 0.001] and hospitalizations for HF [SHR 0.20 (95% CI 0.06-0.72), P = 0.013]. Total mortality was similar in both groups [hazard ratio (HR) 1.57 (95% CI 0.58-4.27), P = 0.372]. The beneficial effects of CRT were consistent in patients who had ejection fraction ≤35%, New York Heart Association Class ≥III and QRS width ≥120 and in those who did not. At multi-variable Cox regression, only CRT mode remained an independent predictor of absence of clinical failure during the follow-up [HR = 0.23 (95% CI 0.08-0.66), P = 0.007].</AbstractText>In patients undergoing 'Ablate and Pace' therapy for severely symptomatic permanent atrial fibrillation, CRT is superior to RV apical pacing in reducing the clinical manifestations of HF. (ClinicalTrials.gov number: NCT00111527).</AbstractText> |
15,169 | Beneficial effects of l-leucine and l-valine on arrhythmias, hemodynamics and myocardial morphology in rats. | Branched chain amino acids (BCAA) have been shown to have a general protective effect on the heart in different animal models as well as in humans. However, so far no attempt has been made to specifically elucidate their influence on arrhythmias. Our study was performed to evaluate whether an infusion of either l-leucine or l-valine in a dose of 1mgkg(-1)h(-1) 10min before a 7-min period of left anterior descending artery occlusion followed by 15min of reperfusion, had an effect on arrhythmias measured during the reperfusion phase in the ischemia- and reperfusion-induced arrhythmias model in rats in vivo. The effect of the infusion of these substances on mean arterial blood pressure was monitored throughout the experiment. Both of the tested amino acids exhibited significant antiarrhythmic properties. l-Leucine reduced the duration of ventricular fibrillation (P<0.05) and l-valine decreased the duration of ventricular fibrillation (P<0.001) and ventricular tachycardia (P<0.05). The two amino acids were generally hypotensive. l-Valine lowered blood pressure in all phases of the experiment (P<0.05) while l-leucine lowered this parameter mainly towards the end of occlusion and reperfusion (P<0.05). In addition, 30min infusion of the amino acids in the used dose did not produce any apparent adverse histological changes that were remarkably different from control. In summary, the results of our study suggest that l-leucine and l-valine in the dose that was used attenuates arrhythmias and are hypotensive in their influence. Our findings lend support to the many ongoing investigations into the benefit of the application of l-leucine and l-valine in cardiology like their addition to cardioplegic solutions. |
15,170 | Prognostic significance of atrial arrhythmias in a primary prevention ICD population. | We investigated whether primary prevention implantable cardioverter defibrillator (ICD) patients with atrial arrhythmias are at higher risk for ICD shocks and mortality compared to patients without atrial arrhythmias in a subanalysis of the PREPARE study.</AbstractText>Details of the PREPARE study design and results have been previously reported. We now included 537 of the 700 patients enrolled in PREPARE. These patients had a dual or biventricular device and at least one device follow-up after implantation. Continuously collected device diagnostics data were used to classify patients into two groups during follow-up: with (n = 133) or without (n = 404) atrial tachycardia/atrial fibrillation (AT/AF). The primary outcomes were ICD shocks and mortality. Subjects were followed for a mean of 333 ± 73 (range 5-365) days. During a follow-up of 1 year, ICD shocks occurred in 44 (8%) patients. Significantly, more patients with AT/AF received a shock (13.0% vs 6.9%, P = 0.03), with inappropriate shocks accounting for the majority of the difference (6.9% vs 2.6%, P = 0.02). There was no difference in prevalence of shocks between patients with and without a history of AF. Mortality was similar in patients with and without AT/AF, whether detected during the study or prior to the study. In addition, the 34 subjects with high average ventricular rate (≥110 beats per minute) during AT/AF had a higher risk of an inappropriate shock (21.0% vs 2.1%, P < 0.01).</AbstractText>Primary prevention ICD patients with AT/AF are more likely to receive shocks, especially inappropriate shocks. Mortality was not higher in AT/AF patients. (PACE 2011; 34:1070-1079).</AbstractText>©2011, The Authors. Journal compilation ©2011 Wiley Periodicals, Inc.</CopyrightInformation> |
15,171 | Postanesthetic torsade de pointes in a patient with unrecognized long QT syndrome -A case report-. | Torsade de pointes (TdP) is a devastating form of polymorphic ventricular arrhythmia associated with corrected QT (QTc) interval prolongation. TdP usually terminates spontaneously but frequently recurs and may degenerate to ventricular fibrillation. The present report describes a case of TdP in a patient being transferred to the postanesthetic care unit following an emergency laparoscopic appendectomy. The patient had undergone open heart surgery 1 week before. Retrospective electrocardiogram analysis revealed the patient had QTc and Tpeak-Tend interval prolongation that had gone unrecognized. We believe TdP may have been induced by accentuation of sympathetic nervous system during emergence from general anesthesia. |
15,172 | New and emerging drugs and device therapies for chronic heart failure in patients with systolic ventricular dysfunction. | Chronic heart failure remains a common end product of cardiovascular diseases and, despite significant advances in therapy, continues to be accompanied by significant morbidity and mortality. Attenuation of neurohumoral overactivation with blockers of the renin-angiotensin-aldosterone system and β-blockers has improved outcome and helped reverse or halt disease progression in many patients; however, despite this, morbidity and mortality have remained elevated, and only marginal advances have occurred over the last few years. How best to combine these various agents continue to be tested but, apart from the addition of aldosterone receptor blockers and reduction of heart rate with ivabradine, advances have been few. Implantable defibrillators and cardiac resynchronization devices have proved to be very beneficial, and the limits of their use are presently still being tested. How best to handle atrial fibrillation in patients with heart failure remains unanswered, but for now, rate control appears to be appropriate in many patients. Surgical ventricular restoration of the left ventricle has not proved to generally be useful, and although the role of coronary artery bypass graft surgery (CABG) is well established in some patients, its use in others is being reevaluated. The use of biomarkers in patients with heart failure has stimulated great interest; however, much work remains before its full potential can be realized. As the complexity of the use of pharmacogenomics in clinical practice becomes clearer, research in the area is intensifying, but much work remains to be done before its use can be clearly outlined in patients with heart failure. |
15,173 | [A rare cause of sudden cardiac failure: histiocytoid cardiomyopathy]. | Histiocytoid cardiomyopathy is a rare disease which occurs predominantly in the first two years of life, with a female preponderance. We report the cases of two girls (11 and 15-month-old) which were respectively referred to our institution for ventricular tachycardia and ventricular fibrillation without prodroma. Etiologic findings only showed mild cardiomyopathy. Autopsy and histologic examination led to the diagnosis of histiocytoid cardiomyopathy. Furthermore, in the first observation, agenesis of the corpus callosum was found. |
15,174 | Digoxin therapy in the elderly: pharmacokinetic considerations in nursing. | Digoxin is effective in controlling ventricular rhythm in atrial fibrillation and is used in heart failure when angiotensin converting enzyme inhibitors and diuretics are ineffective. Because use of more than 1 drug is often required with these conditions, pharmacokinetic considerations, including those related to complementary medicine, are important. Increased awareness of drug action in the elderly is important because there is often an increase in body fat and leaner muscle mass as well as changes in organ function, such as that of the kidney, which alters drug activity. Nurses have an important role to play in the safe administration of digoxin. |
15,175 | Relation between preoperative mild increased in serum creatinine level and early outcomes after coronary artery bypass grafting. | This study evaluates the effect of preoperative increased level of serum creatinine (Cr) on early outcomes after coronary artery bypass graft surgery (CABG). 1140 patients who underwent CABG in our center were studied. Patients with Cr >2.25 mg/dl or preoperative dialysis and who had off-pump operations were excluded. Group 1 consisted of 892 patients with normal Cr (0.5-1.2 mg/dl) and group 2 consisted of 248 (21.8%) patients with mild increased level of serum Cr (1.3-2.2 mg/dl). Patients in group 1 were younger than group 2. There were more patients with hypertension in group 2, but there were not statistically significant difference between two groups in terms of the frequency of diabetes, smoking, cerebrovascular disease and New York Heart Association (NYHA) class. Left ventricular ejection fraction (LVEF) was lower in group 2. Cardiopulmonary bypass time (CPB) was longer in group 2. Early mortality was 3.2% in group 1 and 8.4% in group 2 (P<0.001). Prolonged ICU stay, low cardiac output, prolonged mechanical ventilation, postoperative atrial fibrillation, postoperative re-exploration and sepsis were more frequent in group 2. Mild increase in serum Cr level preoperatively is a marker of increased early mortality and outcome after CABG. |
15,176 | Emerging genomic applications in coronary artery disease. | Over the last 4 years, an unprecedented number of studies illuminating the genomic underpinnings of common "polygenic" diseases including coronary artery disease have been published. Notably, these studies have established numerous deoxyribonucleic acid (DNA) variants within or near chromosome 9p21.3, the LPA, CXADR, and APOE genes, to name a few, as key coronary artery disease and sudden cardiac death susceptibility markers. Most importantly, many of these DNA variants confer over a 2-fold increase in risk for coronary artery disease, myocardial infarction, and ventricular fibrillation. Additionally, loss-of-function variants in the hepatic cytochrome 2C19 system have now been found to be the predominant genetic mediators of clopidogrel antiplatelet response, with variant carriers having a >3-fold increase in risk for stent thrombosis. In the near future, many additional rare polymorphisms, structural variants, and tissue-specific epigenetic features of the human genome including DNA methylation, histone modifications, and chromatin state will emerge as significant contributors to disease pathogenesis and drug response. In aggregate, these findings will have the potential to radically change the practice of cardiovascular medicine. However, only the individual clinician can ultimately enable the translation of these important discoveries to systematic implementation in clinical practice. |
15,177 | SCN5A mutations associate with arrhythmic dilated cardiomyopathy and commonly localize to the voltage-sensing mechanism. | The aim of this study was to discern the role of the cardiac voltage-gated sodium ion channel SCN5A in the etiology of dilated cardiomyopathy (DCM).</AbstractText>Dilated cardiomyopathy associates with mutations in the SCN5A gene, but the frequency, phenotype, and causative nature of these associations remain the focus of ongoing investigation.</AbstractText>Since 1991, DCM probands and family members have been enrolled in the Familial Cardiomyopathy Registry and extensively evaluated by clinical phenotype. Genomic deoxyribonucleic acid samples from 338 individuals among 289 DCM families were obtained and screened for SCN5A mutations by denaturing high-performance liquid chromatography and sequence analysis.</AbstractText>We identified 5 missense SCN5A mutations among our DCM families, including novel mutations E446K, F1520L, and V1279I, as well as previously reported mutations D1275N and R222Q. Of 15 SCN5A mutation carriers in our study, 14 (93%) manifested arrhythmia: supraventricular arrhythmia (13 of 15), including sick sinus syndrome (5 of 15) and atrial fibrillation (9 of 15), ventricular tachycardia (5 of 15), and conduction disease (9 of 15).</AbstractText>Mutations in SCN5A were detected in 1.7% of DCM families. Two-thirds (6 of 9) of all reported DCM mutations in SCN5A localize to the highly conserved homologous S3 and S4 transmembrane segments, suggesting a shared mechanism of disruption of the voltage-sensing mechanism of this channel leading to DCM. Not surprisingly, SCN5A mutation carriers show a strong arrhythmic pattern that has clinical and diagnostic implications.</AbstractText>2011 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.</CopyrightInformation> |
15,178 | Comment accompanying: obstructive sleep apnoea: a stand-alone risk factor for chronic kidney disease by Chou Yu-Ting. | Sleep apnoea (SA) is a high priority health problem because it disrupts sleep and reduces quality of life, it is associated with obesity, hypertension, especially resistant hypertension, congestive heart failure, diabetes and it engenders cardiovascular (CV) complications and death. The following types of apnoea can be distinguished: (i) obstructive, (ii) central (i.e. neurally mediated) and (iii) mixed. Obstructive SA (OSA) is characterized by a cessation of airflow caused by occlusion of the oropharyngeal tract and central SA by a transient abolition of the neural drive to respiratory muscles. Mixed apnoea represents a combination of the two forms. SA is one of the most important triggers of high sympathetic activity and it is perhaps the most important non-traditional risk factor underlying the high CV risk of chronic kidney disease (CKD). The high sympathetic activity engenders three intermediate mechanisms, chronic hypertension, left ventricular hypertrophy and arrhythmias, particularly atrial fibrillation, which eventually leads to CV complications and death. SA is common in end-stage renal disease and studies in haemodialysis and peritoneal dialysis patients coherently show that intensive dialysis improves SA in patients with severe sleep disordered breathing. Renal transplantation is in theory the ideal way of correcting SA, because a restored renal function abrogates the uraemic toxicity. In a case-control study, the prevalence of mild and severe SA was almost identical in renal transplant patients as compared to age-, sex- and body mass index-matched healthy subjects, supporting the contention that renal transplantation reverses SA. A study published in this issue of Nephrology, Dialysis Transplantation assesses the association between CKD and SA in symptomatic (snorers) patients, excluding by protocol those with hypertension and diabetes, which are well-known risk factors for SA and CKD. The primary hypothesis tested in this study, i.e. whether snorers are at a higher risk for renal dysfunction, is a sensible one. |
15,179 | Early selective trans-nasal cooling during CPR improves success of resuscitation in a porcine model of prolonged pulseless electrical activity cardiac arrest. | In the present study, we investigated trans-nasal cooling in settings of pulseless electrical activity (PEA). We hypothesized that early trans-nasal cooling during CPR improves outcomes when cardiac arrest is associated with PEA.</AbstractText>Ventricular fibrillation (VF) was electrically induced in 16 domestic male pigs weighing 40±3 kg. After 14 min of untreated VF, PEA was induced following delivery of one or more electrical shocks. One min after onset of PEA, CPR was started, including chest compression and ventilation. Each animal received 5 min of CPR prior to defibrillation attempt. CPR and resuscitation efforts were discontinued at 15 min unless return to spontaneous circulation was achieved. In 8 animals, selective trans-nasal cooling was begun coincident with start of CPR and 8 randomized controls were identically treated except for trans-nasal cooling. Mean aortic pressure was continuously measured together with aortic and right atrial pressure and nasal, body and right jugular vein temperatures. Coronary perfusion pressure (CPP) was computed from measured data.</AbstractText>Six of eight animals were resuscitated after early trans-nasal cooling, while only one untreated control was resuscitated (p=0.012). Nasal, body and jugular vein temperatures decreased after cooling. At PC (precordial compression) 5 min, the cooled group recorded a higher CPP (25±5 mmHg) than the non-cooled group (15±4 mmHg, p=0.001).</AbstractText>When selective trans-nasal cooling was initiated during CPR in the animal model of prolonged cardiac arrest with PEA, CPP was higher and the likelihood of return of spontaneous circulation was improved.</AbstractText>Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.</CopyrightInformation> |
15,180 | Implantable cardioverter/defibrillator interventions in primary prevention: do current implantation criteria really predict ICD interventions? | Randomized controlled trials have proven the efficacy of implantable cardioverter/defibrillators (ICDs) to prevent sudden cardiac death (SCD) in primary prevention. However,long-term data on the incidence of appropriate and inappropriate interventions in real life and on the predictive value of commonly used clinical variables to guide patient selection are scarce.</AbstractText>We retrospectively studied 101 patients who received an ICD for primary prophylaxis of SCD: 63.4% with ischaemic heart disease (IHD) and 36.6% with idiopathic dilated cardiomyopathy (IDCM). The mean follow-up period was 26.2 (+/- 14.8; median 27.8; range 5.6-70.5) months. Age, left ventricular ejection fraction (LVEF), QRS duration, NYHA class and electrophysiological study (EPS) outcome were evaluated as predictors of ICD intervention.</AbstractText>At 2 years the cumulative incidence of appropriate (17.5% in IHD; 28% in IDCM; P= 0.63) and inappropriate (12.8% in IHD, 15.4% in IDCM; P = 0.62) interventions was similar in both groups. Atrial fibrillation was the most common cause of inappropriate interventions in the IHD group, sinus tachycardia in the IDCM group. Advanced age was associated with less inappropriate interventions (HR: 0.96 (95% confidence interval (CI) 0.94-0.98); P < 0.01), and a better LVEF with less appropriate interventions (HR: 0.97 (95% Cl 0.94-0.99); P < 0.01). This amounted in a significant absolute difference in the number of appropriate interventions between the group with a LVEF < 25% and 25-34% after 3 years of follow-up of 42% in IHD (48% vs 6%). A prolonged QRS duration was associated with a slightly elevated risk for appropriate interventions only in the IHD group (HR: 1.01 (95% CI 1.00-1.03); P = 0.04). On the other hand, increased NYHA class was only associated with increased risk for appropriate interventions in the IDCM group (HR: 5.24 (95% CI1.11-24.74); P= 0.04). No significant statistical association was found between a positive EPS and appropriate or inappropriate interventions.</AbstractText>In primary prevention, during a mean follow-up of 2 years, one in five patients had a possibly live-saving appropriate intervention. However, the incidence of inappropriate interventions was substantial. Predictors for appropriate interventions were: (i) LVEF in the total study group, (ii) NYHA class in the IDCM group and (iii) QRS duration in the IHD group.</AbstractText> |
15,181 | [Statistics concerning patients of out-of-hospital cardiac arrests in Japan]. | The Fire and Disaster Management Agency (FDMA) of Japan started a nationwide, population-based, cohort study in 2005 and keeps collecting the ambulance transportation records of out-of-hospital cardiac arrests in Japan based on the standardized Utstein style. By analyzing the outcomes of bystander-witnessed arrests among patients who had ventricular fibrillation and arrests, the rate of survival at 1 month is 11.4% and the rate of survival with minimal neurologic impairment at 1 month is 7.1%. The rate of survival at 1 month and the rate of survival with minimal neurologic impairment at 1 month are improved by bystander (family member or other) CPR, early CPR by EMS personnel, and the administration of a shock with the use of a public-access AED. It is important to improvement the ambulance service system by using these statistical data. |
15,182 | [Usage of a defibrillator]. | Guideline 2010 for cardiopulmonary resuscitation was released the other day. There is no big change in the use of a defibrillator. Asynchronous defibrillation is used as a therapy for VF and pulseless VT. When you find a patient, start CPR immediately and prepare a defibrillator. About the value of energy, comply a recommended value of defibrillator's manufacturer with biphasic waveform, on the other hand, deliver 360J shock with monophasic waveform. Cardioversion is used as a therapy for supraventricular arrhythmia like atrial fibrillation. It is important to synchronize with QRS complex on ECG surely and deliver a shock. If it is not synchronized surely, there is a possibility to occur VF. Transcutaneous pacing is used as a therapy for bradycardia. It produces a depolarization of myocardium by giving current stimulus from a surface of a body, and force a heart to contract. It is usually carried out at demand mode, and confirmed that a heart contracts certainly. Defibrillator is an only device to terminate VF and pulseless VT and it is important to test defibrillator usually so that it can be used any time it is necessary. |
15,183 | [Percutaneous cardiopulmonary support (PCPS)]. | The percutaneous cardiopulmonary support (PCPS) allows maintaining the patient's cardiac and pulmonary status with low cardiac or pulmonary performance due to acute myocardial infarction, pulmonary thromboembolism, postoperative phase of great blood vessels/open heart surgery or percutaneous coronary intervention, and so on. This system consists of a centrifugal pump with its control system, membrane oxygenator, measure devices for blood flow and pressure and a heating system for temperature conditioning of blood. The potential effectiveness is suggested using PCPS for cardiopulmonary resuscitation(CPR), so called extracorporeal cardiopulmonary resuscitation(ECPR). The single center studies suggesting the utility of ECPR appear, but ECPR is contents to have possibilities to improve prognosis in limited adaptation because there is not yet enough evidence in CoSTR 2010 by ILCOR. However, multicenter study about the utility of ECPR used PCPS for the out-of-hospital cardiac arrest(Study of Advanced life support for Ventricular fibrillation with Extracorporeal circulation in Japan: SAVE-J) is started in April 2007, and it is said that ECPR may improve neurological outcome comparing with that of the conventional CPR by the interim report. Further studies will determine its efficacy and adequate criteria. |
15,184 | Effects of KATP channel openers diazoxide and pinacidil in coronary-perfused atria and ventricles from failing and non-failing human hearts. | This study compared the effects of ATP-regulated potassium channel (K(ATP)) openers, diazoxide and pinacidil, on diseased and normal human atria and ventricles. We optically mapped the endocardium of coronary-perfused right (n=11) or left (n=2) posterior atrial-ventricular free wall preparations from human hearts with congestive heart failure (CHF, n=8) and non-failing human hearts without (NF, n=3) or with (INF, n=2) infarction. We also analyzed the mRNA expression of the K(ATP) targets K(ir)6.1, K(ir)6.2, SUR1, and SUR2 in the left atria and ventricles of NF (n=8) and CHF (n=4) hearts. In both CHF and INF hearts, diazoxide significantly decreased action potential durations (APDs) in atria (by -21±3% and -27±13%, p<0.01) and ventricles (by -28±7% and -28±4%, p<0.01). Diazoxide did not change APD (0±5%) in NF atria. Pinacidil significantly decreased APDs in both atria (-46 to -80%, p<0.01) and ventricles (-65 to -93%, p<0.01) in all hearts studied. The effect of pinacidil on APD was significantly higher than that of diazoxide in both atria and ventricles of all groups (p<0.05). During pinacidil perfusion, burst pacing induced flutter/fibrillation in all atrial and ventricular preparations with dominant frequencies of 14.4±6.1 Hz and 17.5±5.1 Hz, respectively. Glibenclamide (10 μM) terminated these arrhythmias and restored APDs to control values. Relative mRNA expression levels of K(ATP) targets were correlated to functional observations. Remodeling in response to CHF and/or previous infarct potentiated diazoxide-induced APD shortening. The activation of atrial and ventricular K(ATP) channels enhances arrhythmogenicity, suggesting that such activation may contribute to reentrant arrhythmias in ischemic hearts. |
15,185 | Steady-state B-type natriuretic peptide levels in patients with atrial fibrillation of various clinical backgrounds. | B-type natriuretic peptide level is increased in patients with atrial fibrillation. The aim of the present study was to present the distribution of steady-state B-type natriuretic peptide levels of various clinical backgrounds and to elucidate the usefulness of measuring them in patients with atrial fibrillation. B-type natriuretic peptide was measured in stable conditions in patients with atrial fibrillation (74 ± 10 y/o, n = 473). The average B-type natriuretic peptide level was 161 ± 202 (median 101) pg/ml. Multiple regression analysis showed that age, left ventricular ejection fraction, left atrial diameter, structural heart disease, chronic atrial fibrillation, and heart failure symptoms were independently associated with elevated B-type natriuretic peptide levels. However, in chronic atrial fibrillation patients without structural heart disease, B-type natriuretic peptide levels did not differ between those with and without heart failure symptoms. Notably, B-type natriuretic peptide levels were high (≥ 150 pg/ml) in 41% of asymptomatic chronic atrial fibrillation without structural heart disease. Steady-state B-type natriuretic peptide levels of various clinical backgrounds were presented. Contributions of BNP elevation by clinical variables were somewhat different in different population. B-type natriuretic peptide was elevated in substantial percentage of asymptomatic chronic atrial fibrillation even without structural heart disease. |
15,186 | Effect of tumor necrosis factor-α on neutralization of ventricular fibrillation in rats with acute myocardial infarction. | The purpose of this study was to explore the effects of tumor necrosis factor-α (TNF-α) on ventricular fibrillation (VF) in rats with acute myocardial infarction (AMI). Rats were randomly classified into AMI group, sham operation group and recombinant human tumor necrosis factor receptor:Fc fusion protein (rhTNFR:Fc) group. Spontaneous and induced VFs were recorded. Monophasic action potentials (MAPs) among different zones of myocardium were recorded at eight time points before and after ligation and MAP duration dispersions (MAPDds) were calculated. Then expression of TNF-α among different myocardial zones was detected. After ligation of the left anterior descending coronary artery, total TNF-α expression in AMI group began to markedly increase at 10 min, reached a climax at 20-30 min, and then gradually decreased. The time-windows of VFs and MAPDds in the border zone performed in a similar way. At the same time-point, the expression of TNF-α in the ischemia zone was greater than that in the border zone, and little in the non-ischemia zone. Although the time windows of TNF-α expression, the MAPDds in the border zone and the occurrence of VFs in the rhTNFR:Fc group were similar to those in the AMI group, they all decreased in the rhTNFR:Fc group. Our findings demonstrate that TNF-α could enlarge the MAPDds in the border zone, and promote the onset of VFs. |
15,187 | Pharmacological management of atrial fibrillation: one, none, one hundred thousand. | atrial fibrillation (AF) is associated with a significant burden of morbidity and increased risk of mortality. Antiarrhythmic drug therapy remains a cornerstone to restore and maintain sinus rhythm for patients with paroxysmal and persistent AF based on current guidelines. However, conventional drugs have limited efficacy, present problematic risks of proarrhythmia and cause significant noncardiac organ toxicity. Thus, inadequacies in current therapies for atrial fibrillation have made new drug development crucial. New antiarrhythmic drugs and new anticoagulant agents have changed the current management of AF. This paper summarizes the available evidence regarding the efficacy of medications used for acute management of AF, rhythm and ventricular rate control, and stroke prevention in patients with atrial fibrillation and focuses on the current pharmacological agents. |
15,188 | Vagus nerve stimulation protects against ventricular fibrillation independent of muscarinic receptor activation. | The role of the vagus in the ventricle is controversial, although the vagus can protect against ventricular fibrillation (VF) via nitric oxide (NO). This study aims to determine whether the mechanisms involved are dependent on post-ganglionic release and muscarinic receptor activation. For this purpose, NO release and electrophysiological effects of vagus nerve stimulation (VNS) were evaluated in relation to acetylcholine and vasoactive intestinal peptide (VIP). In addition, the role of the coronary endothelium and afferent nerves was tested.</AbstractText>Using the isolated innervated rabbit heart, we measured ventricular NO release using 4,5-diaminofluorescein (DAF-2) fluorescence and ventricular fibrillation threshold (VFT) during VNS after muscarinic, ganglionic, and VIP inhibition [atropine, hexamethonium, and VIP (6-28), respectively] and after Triton-X endothelial functional dysfunction. The vagal-mediated increases in NO and VFT were not significantly affected (P> 0.05) during (i) atropine perfusion [increase in NO: 196.8 ± 35.2 mV (control) vs. 156.1 ± 20.3 mV (atropine) and VFT 3.1 ± 0.5 mA (control) vs. 2.7 ± 0.4 mA (atropine)], (ii) VIP inhibition-increase in NO: 243.0 ± 42.4 mV (control) vs. 203.9 ± 28.5 mV [VIP(6-28)] and VFT 3.3 ± 0.3 mA (control) vs. 3.9 ± 0.6 mA [VIP(6-28)], or (iii) after endothelial functional dysfunction [increase in NO: 127.7 ± 31.7 mV (control) vs. 172.1 ± 31.5 mV (Triton-X) and VFT 2.6 ± 0.4 mA (control) vs. 2.5 ± 0.5 mA (Triton-X)]. However, the vagal effects were inhibited during ganglionic blockade [increase in NO: 175.1 ± 38.1 mV (control) vs. 0.6 ± 25.3 mV (hexamethonium) and VFT 3.3 ± 0.5 mA (control) vs. -0.3 ± 0.3 mA (hexamethonium)].</AbstractText>We show that the vagal anti-fibrillatory action in the rabbit ventricle occurs via post-ganglionic efferent nerve fibres, independent of muscarinic receptor activation, VIP, and the endothelium. Together with our previous publications, our data support the possibility of a novel ventricular nitrergic parasympathetic innervation and highlight potential for new therapeutic targets to treat ventricular dysrhythmias.</AbstractText> |
15,189 | Increased dispersion of atrial repolarization in Brugada syndrome. | Patients with Brugada syndrome (BS) often experience atrial fibrillation (AF) and atrial vulnerability, as measured by increased atrial conduction time. To date, however, dispersion of atrial repolarization has not been reported in these patients.</AbstractText>Monophasic action potentials (MAPs) recorded from four sites of the right atrium were analysed in 11 patients (10 men, 1 woman; mean age, 40 ± 9 years) with BS and in 10 controls (8 men, 2 women; mean age, 35 ± 8 years). None of these patients had a history of AF. Monophasic action potentials were recorded during right atrial pacing at a drive cycle length of 600 ms after continuous pacing. Dispersion of MAP duration (D-MAPD90) was defined as the difference between the maximum and minimum MAP duration measured at 90% repolarization (MAPD90). Inducibility of AF and repetitive atrial firing were also determined. The MAPD90 did not differ significantly between the BS and control groups (245 ± 42 vs. 228 ± 24 ms, P = ns), but D-MAPD90 was significantly higher in the BS group (69.1 ± 35.0 vs. 41.4 ± 10.3 ms, P < 0.05). Atrial fibrillation was induced in six BS patients and repetitive atrial firing in four, but neither was induced in any of the control subjects.</AbstractText>The significantly increased dispersion of MAPD90 observed in patients with BS suggests that the heterogeneity of atrial repolarization may contribute to the development of atrial fibrillation in patients with BS.</AbstractText> |
15,190 | No evidence for an association between the rs2824292 variant at chromosome 21q21 and ventricular fibrillation during acute myocardial infarction in a German population. | In a recently published genome-wide association study (GWAS), three single nucleotide polymorphisms (SNPs) (rs2824292, rs1353342, rs12090554) were significantly associated with increased susceptibility for ventricular fibrillation (VF) during acute myocardial infarction (AMI). The association of rs2824292 could be confirmed in a second cohort. Both cohorts were from the Netherlands. We aimed to replicate this association in a German cohort of AMI patients with or without VF.</AbstractText>We included a German cohort of 90 individuals with AMI and VF (cases) and 167 AMI individuals without VF and used Taqman assays for SNP typing.</AbstractText>None of the loci showed evidence for a statistically significant association with VF. The observed genotype frequencies of the three loci were in Hardy-Weinberg equilibrium, which essentially excludes genotyping errors.</AbstractText>In contrast to the data from the Netherlands, we could not detect a significant association of the rs2824292 locus and risk of VF during AMI in our German cohort. Differences in recruitment and clinical phenotypes between the Dutch and German cohorts may underlie different genotype associations.</AbstractText> |
15,191 | Cardiac arrest in Greek primary health care and willingness of general practitioners to use automatic external defibrillator. | The aim of this study was to calculate the incidence of out-of-hospital cardiac arrest (OHCA) in primary health care in Greece and assess general practitioners' (GPs) willingness towards the use of automatic external defibrillator (AED).</AbstractText>We conducted a survey in GPs working in both private and public sectors. The survey consisted of 32 questions and was distributed via email in 180 randomly selected GPs. To estimate OHCA incidence, data concerning the number of examined patients and the number of cardiac arrests were used.</AbstractText>Based on the population of our study, the incidence of OHCA in primary health care in Greece is 15.3/100,000 population per year. Most of the arrests occur in health centers, while ventricular fibrillation/ventricular tachycardia are the first monitored rhythms. Almost all GPs were willing to use an AED even though some of them did not know how to use it.</AbstractText>The incidence of OHCA in primary health care in Greece is 15.3/100,000 population per year. Greek GPs may have an important role in managing OHCA victims and are willing to use an AED. This is the first study estimating OHCA in primary health care in Greece.</AbstractText>Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.</CopyrightInformation> |
15,192 | Rapid induction of hypothermia with a small volume aortic flush during cardiac arrest in pigs. | The induction of deep cerebral hypothermia (15°C) via large-volume cold (4°C) saline aortic flush during cardiac arrest and resuscitation with cardiopulmonary bypass improves neurologic outcome in pigs. We hypothesized that induction of mild cerebral hypothermia (33°C) via smaller volume and resuscitation without bypass will improve survival and neurologic outcome after 15 minutes of cardiac arrest as compared with conventional resuscitation attempts.</AbstractText>Twenty-four pigs (29-38 kg) underwent ventricular fibrillation cardiac arrest for 15 minutes. Conventional resuscitation (n=8) was compared with hypothermic (4°C, n=8) and normothermic (38.5°C, n=8) aortic flush (30 mL/kg) at the beginning of resuscitation efforts, with defibrillation attempts 2 minutes later. Outcomes after 9 days were compared.</AbstractText>In the hypothermic flush group, brain temperature decreased from 38.3°C±0.5°C to 33°C±0.5°C within 277±112 seconds. We observed considerably higher mean coronary perfusion pressures in the normothermic and hypothermic flush groups (hypothermic vs conventional, P=.023; normothermic vs conventional, P=.041). Three animals of each flush group, compared with none of the conventional group, achieved restoration of spontaneous circulation (P=.2); and 3 pigs of the hypothermic flush group and 2 pigs of the normothermic flush group survived to 9 days without differences in neurologic outcome.</AbstractText>A smaller volume, cold saline aortic flush during prolonged cardiac arrest rapidly induces mild cerebral hypothermia to 33°C and improves coronary perfusion pressure but does not result in a significant improvement in outcome as compared with conventional resuscitation attempts.</AbstractText>Copyright © 2012 Elsevier Inc. All rights reserved.</CopyrightInformation> |
15,193 | Ebstein anomaly in an adult presenting with wide QRS tachycardia: diagnostic and therapeutic dilemmas. | A 51-year-old man presented to the emergency department with sustained hemodynamically unstable wide QRS tachycardia and was revived successfully by immediate direct current (DC) cardioversion. There was evidence of previous open heart surgery, possibly atrial septal defect closure. Transthoracic echocardiography showed severe Ebstein anomaly with severe tricuspid regurgitation, no residual atrial septal defect, but with severe right ventricular dysfunction. Subsequent electrocardiograms showed transient atrial fibrillation with no manifest Wolff-Parkinson-White (WPW) accessory pathway during sinus rhythm. The cause of wide QRS tachycardia in this patient may be WPW related or ventricular tachycardia. This case illustrates the diagnostic and therapeutic dilemmas in patients with wide QRS tachycardia and suspected WPW syndrome. In addition, this case demonstrates that unoperated Ebstein anomaly can present in late adult life with tachyarrhythmias. |
15,194 | A link between emergency dispatch and public access AEDs: potential implications for early defibrillation. | Public access defibrillation can improve survival but is involved in only a small fraction of out-of-hospital cardiac arrest. One approach to increase involvement is to couple emergency dispatch with mapping technology to identify public access automated external defibrillators (AEDs) that are on-site or nearby.</AbstractText>We conducted a retrospective observational cohort investigation of out-of-hospital cardiac arrest who received dispatch by a community dispatch center between January 1, 2007 and December 31, 2009. The dispatch system is linked to the public access AED registry. The technology enables dispatcher alert of an on-site AED and the potential to alert for an AED within 0.1 mile. We report the observed and potential frequency of AED involvement.</AbstractText>Of the 763 cardiac arrest events, 4.2% (32/763) had an AED applied by non-EMS persons, 1.3% (10/763) by police and 2.9% (22/763) in layperson settings. Among the remaining 731 where an AED was not applied, 8.1% (59/731) had an AED identified through dispatch; 18 with an AED on-site and an additional 41 with an AED within 0.1 mile. When restricting to ventricular fibrillation arrests, 8.9% (16/179) had an AED applied by non-EMS persons, 2.8% (5/179) by police and 6.1% (11/179) in layperson settings. Among the remaining 163 where an AED was not applied, 11.7% (19/163) had an AED identified through dispatch; 9 with an AED on-site and an additional 10 with an AED within 0.1 mile.</AbstractText>A working link between emergency dispatch and an AED registry may provide an opportunity to improve resuscitation.</AbstractText>Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.</CopyrightInformation> |
15,195 | Incidence of atrial fibrillation in patients with either heart failure or acute myocardial infarction and left ventricular dysfunction: a cohort study. | We examined the incidence of new-onset atrial fibrillation in patients with left ventricular dysfunction. Patients either had a recent myocardial infarction (with or without clinical heart failure) or symptomatic heart failure (without a recent MI). Patients were with and without treatment with the class III antiarrhythmic drug dofetilide over 36 months.</AbstractText>The Danish Investigations of Arrhythmia and Mortality ON Dofetilide (DIAMOND) studies included 2627 patients without atrial fibrillation at baseline, who were randomised to treatment with either dofetilide or placebo.</AbstractText>The competing risk analyses estimated the cumulative incidences of atrial fibrillation during the 42 months of follow-up to be 9.6% in the placebo-treated heart failure-group, and 2.9% in the placebo-treated myocardial infarction-group. Cox proportional hazard regression found a 42% significant reduction in the incidence of new-onset AF when assigned to dofetilide compared to placebo (hazard ratio 0.58, 95% confidence interval 0.40-0.82) and there was no interaction with study (p = 0.89). In the heart failure-group, the incidence of atrial fibrillation was significantly reduced to 5.6% in the dofetilide-treated patients (hazard ratio 0.57, 95% confidence interval 0.38-0.86). In the myocardial infarction-group the incidence of atrial fibrillation was reduced to 1.7% with the administration of dofetilide. This reduction was however not significant (hazard ratio 0.61, 95% confidence interval 0.30-1.24).</AbstractText>In patients with left ventricular dysfunction the incidence of AF in 42 months was 9.6% in patients with heart failure and 2.9% in patients with a recent MI. Dofetilide significantly reduced the risk of developing atrial fibrillation compared to placebo in the entire study group and in the subgroup of patients with heart failure. The reduction in the subgroup with recent MI was not statistically significant, but the hazard ratio was similar to the hazard ratio for the heart failure patients, and there was no difference between the effect in the two studies (p = 0.89 for interaction).</AbstractText> |
15,196 | Impact of routine percutaneous coronary intervention after out-of-hospital cardiac arrest due to ventricular fibrillation. | Since 2003, we have routinely used percutaneous coronary intervention (PCI) and mild therapeutic hypothermia (MTH) to treat patients < 80 years of age after out-of-hospital cardiac arrest (OHCA) related to ventricular fibrillation. The aim of our study was to evaluate the prognostic impact of routine PCI in association with MTH and the potential influence of age.</AbstractText>We studied 111 consecutive patients resuscitated successfully following OHCA related to shock-sensitive rhythm. They were divided into five groups according to age: < 45 years (n = 22, group 1), 45 to 54 years (n = 27, group 2), 55 to 64 years (n = 22, group 3), 65 to 74 years (n = 23, group 4) and ≥75 years (n = 17, group 5). Emergency coronary angiography was performed in hemodynamically stable patients < 80 years old, regardless of the electrocardiogram pattern. MTH was targeted to a core temperature of 32°C to 34°C for 24 hours.</AbstractText>Most patients (73%) had coronary heart disease, although its incidence in group 1 was lower than in other groups (41% versus 81%; P = 0.01). In group 1, all patients but one underwent coronary angiography, and 33% of them underwent associated PCI. In group 5, only 53% of patients underwent a coronary angiography and 44% underwent PCI. Overall in-hospital survival was 54%, ranging between 52% and 64% in groups 1 to 4 and 24% in group 5. Time from collapse to return of spontaneous circulation was associated with mortality (odds ratio (OR) = 1.05 (25th to 75th percentile range, 1.03 to 1.08); P < 0.001), whereas PCI was associated with survival (OR = 0.30 (25th to 75th percentile range, 0.11 to 0.79); P = 0.01).</AbstractText>We suggest that routine coronary angiography with potentially associated PCI may favorably alter the prognosis of resuscitated patients with stable hemodynamics who are treated with MTH after OHCA related to ventricular fibrillation. Although age was not an independent cause of death, the clinical relevance of this therapeutic strategy remains to be determined in older people.</AbstractText> |
15,197 | Early repolarization in Wolff-Parkinson-White syndrome: prevalence and clinical significance. | Idiopathic ventricular fibrillation (IVF) with early repolarization (ER) has recently been reported; however, ER is a common finding in healthy subjects and is also found sporadically in patients with Wolff-Parkinson-White (WPW) syndrome. The present study was designed to evaluate the prevalence and clinical significance of ER in patients with WPW syndrome.</AbstractText>One hundred and eleven patients with WPW syndrome were studied retrospectively. Early repolarization was defined as QRS slurring or notching with J-point elevation ≥ 1 mm. The prevalence of ER was determined before and after successful catheter ablation. Before ablation, ER was found in 35 of 75 patients with a left free wall, 6 of 23 with a right free wall, and 7 of 13 with a septal accessory pathway (48 of 111, 43% as a whole). Early repolarization was always observed in leads with positive deflection of the initial part of the delta wave. After successful ablation of accessory pathways, ER was preserved in 28 (25%), disappeared in 20 (18%), and newly developed in 8 (7%) patients. In the remaining 55 (50%) patients, ER was not observed either before or after ablation. In patients with persistent ER, the amplitude and width of ER were significantly decreased 3-7 days after the ablation (1.7 ± 0.7 vs. 1.4 ± 0.6 mm, P < 0.005 and 42 ± 11 vs. 34 ± 9 ms, P < 0.001, respectively).</AbstractText>In patients with WPW syndrome, ER could be partly related to early depolarization through the accessory pathway. However, persistent ER and new ER appearing after the ablation were frequently found. Therefore, in these patients, mechanisms other than early depolarization may be involved in the genesis of ER.</AbstractText> |
15,198 | Investigation of myocardial stunning after cardiopulmonary resuscitation in pigs. | To investigate cardiac function and myocardial perfusion during 48 h after cardiopulmonary resuscitation (CPR), further to test myocardial stunning and seek indicators for long-term survival after CPR.</AbstractText>After 4 min of untreated ventricular fibrillation, fifteen anesthetized pigs were studied at baseline and 2 h, 4 h, 24 h, and 48 h after restoration of spontaneous circulation (ROSC). Hemodynamic data, echocardiography and gated-single photon emission computed tomography myocardial perfusion images were carried out.</AbstractText>Mean arterial pressure (MAP), coronary perfusion pressure (CPP) and cardiac troponin I (CTNI) showed significant differences between eventual survival animals and non-survival animals at 4 h after ROSC (109.2 ± 10.7 mmHg vs. 94.8 ± 12.3 mmHg, P=0.048; 100.8 ± 6.9 mmHg vs. 84.4±12.6 mmHg, P=0.011; 1.60 ± 0.13 ug/L vs. 1.75 ± 0.10 ug/L, P=0.046). Mitral valve early-to-late diastolic peak velocity ratio, mitral valve deceleration time recovered 24 h; ejection faction and the summed rest score recovered 48 h after ROSC.</AbstractText>Cardiac systolic and early active relaxation dysfunctions were reversible within survival animals; cardiac stunning might be potentially adaptive and protective after CPR. The recovery of MAP, CPP, and CTNI could be the indicators for long-term survival after CPR.</AbstractText>Copyright © 2011 The Editorial Board of Biomedical and Environmental Sciences. Published by Elsevier B.V. All rights reserved.</CopyrightInformation> |
15,199 | Congenitally corrected transposition of the great arteries ventricular function at the time of systemic atrioventricular valve replacement predicts long-term ventricular function. | The objective was to evaluate the systemic ventricular ejection fraction (SVEF) at the time of systemic atrioventricular valve (SAVV) replacement as a predictor of SVEF ≥1 year after surgery in patients with congenitally corrected transposition of the great arteries (CCTGA).</AbstractText>Progressive SAVV regurgitation causes systemic ventricular failure in CCTGA patients, who are commonly referred late for intervention. Survival after surgery is poor when the pre-operative SVEF is <44%.</AbstractText>We retrospectively reviewed 46 patients (pre-operative SVEF ≥ 40% in 27 patients and <40% in 19 patients) with 2 good-sized ventricles, a morphologically right systemic ventricle, and SAVV regurgitation requiring surgery. Median follow-up was not different in patients with a pre-operative SVEF ≥ 40% (8.8 years) or <40% (7.7 years, p = 0.36).</AbstractText>Pre-operative SVEF was the only independent predictor of ≥ 1-year post-operative SVEF (p < 0.0001). The late SVEF was preserved (defined as ≥ 40%) in 63% of patients who underwent surgery with an SVEF ≥ 40% compared with 10.5% of patients who underwent surgery with an SVEF <40%. Pre-operative variables associated with late mortality were an SVEF ≤ 40%, a subpulmonary ventricular systolic pressure ≥ 50 mm Hg, atrial fibrillation, and New York Heart Association functional class III to IV.</AbstractText>Post-operative systemic ventricular function after SAVV replacement can be predicted from the pre-operative SVEF. For best results, operation should be considered at an earlier stage, before the SVEF falls below 40% and the subpulmonary ventricular systolic pressure rises above 50 mm Hg.</AbstractText>Copyright © 2011 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.</CopyrightInformation> |
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