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7,800 | Aged male and female spontaneously hypertensive rats benefit from n-3 polyunsaturated fatty acids supplementation. | Hypertension-induced myocardial metabolic, structural and electrophysiological remodeling deteriorates with aging and contributes to both heart failure and occurrence of malignant arrhythmias. It has been shown in clinical trials that n-3 polyunsaturated fatty acids (n-3 PUFA) reduce the incidence of cardiovascular diseases and sudden cardiac death. We investigated the cardioprotective effects of n-3 PUFA in aged spontaneously hypertensive rats (SHR) and possible cellular mechanisms involved. Male and female 14-moth-old SHR were fed with n-3 PUFA (Vesteralens, Norway, 20 mg/day for two months) and compared with untreated SHR. Results showed that n-3 PUFA supplementation led to 1) significant decline of blood pressure; 2) suppression of inducible ventricular fibrillation (VF) by 57 % (male) and 67 % (female), although the arrhythmogenic substrates, like fibrosis, hypertrophy and abnormal gap junctions distribution were not eliminated; 3) preservation of the cardiomyocytes and the integrity of their junctions; 4) enhancement of energetic metabolism enzyme activity; 5) augmentation of capillary density associated with increased alkaline phosphatase and decreased dipeptidyl peptidase-4 (DPP4) activity and 6/ increase in gap junction channel connexin-43 expression. Thus, aged male as well as female SHR benefit from n-3 PUFA supplementation that results in decrease in VF susceptibility, partly due to an improvement of myocardial metabolic state, cardiomyocyte and cell-to-cell junctions integrity and Cx43 up-regulation. |
7,801 | Thyroid hormones modulate occurrence and termination of ventricular fibrillation by both long-term and acute actions. | Thyroid hormones (TH) are powerful modulators of heart function, but their arrhythmogenic effects are less elucidated. We have examined both acute and long-term action of TH on the heart susceptibility to the ventricular fibrillation (VF) and on the heart ability to terminate VF and restore a sinus rhythm. Triiodothyronine (T3) was applied in the range of 10(-9)-10(-6) mol/l in acute experiments using isolated perfused aged (14-month-old) guinea pig hearts. L-thyroxine (T4) was applied in the dose of 50 microg/100g/day to young (3-month-old) and aged (20-month-old) rats for 2 weeks. The T4 treatment resulted in an increased susceptibility of young, but not adult rat hearts to a hypokalemia-induced VF and facilitated a spontaneous sinus rhythm (SSR) restoration in the latter group. The acute T3 administration in the range of 10(-9)-10(-7) mol/l significantly decreased the susceptibility of an isolated heart to an electrically induced VF and also facilitated the sinus rhythm restoration. The SSR restoration was, however, not affected by 10(-6) mol/l concentration of T3, which also led to an increased VF susceptibility. Results indicate that TH can affect the susceptibility of the heart to VF and its ability to restore the sinus rhythm via acute (non-genomic) and long-term (genomic) actions. Furthermore, an anti- and pro-arrhythmic potential of TH appears to be age- and dose-dependent. |
7,802 | Apical hypertrophic cardiomyopathy might lead to misdiagnosis of ischaemic heart disease. | In this study, demographic, clinic, electrocardiographic and angiographic properties of patients, on whom coronary angiography was performed with the pre-diagnosis of coronary artery disease (CAD) and whose ventriculography demonstrated typical apical hypertrophic cardiomyopathy (AHCM), were investigated.</AbstractText>Seventeen patients (mean age 58 +/- 10 years, 10 male) with CAD pre-diagnosis, on whom coronary angiography was performed and had typical spade-like appearance on left ventriculography, were included in the study between January 2000 and May 2005.</AbstractText>As risk factor for CAD, 8 (47%) patients had hypertension, 8 (47%) patients had dyslipidaemia, 2 (11%) patients had type 2 diabetes mellitus, 13 (77%) patients had a history of smoking, and 2 (11%) patients had family history. Seven (42%) patients presented unstable angina pectoris, 8 (47%) patients presented stable angina pectoris and 2 (11%) patients were asymptomatic. On coronary angiography, it was determined that 10 (58%) patients had normal coronary arteries, 3 (17%) patients had non-significant stenosis and 4 (25%) patients had myocardial bridging. Five (30%) patients revealed mid-ventricular obstruction and intraventricular gradient was 25 +/- 5 mmHg by the catheterization. All patients showed ''giant'' negative (> or = 10 mm) T waves in the precordial leads, whereas 2 patients had atrial fibrillation. Maximum wall thickness was measured as 18 +/- 4 mm in the apical region by transthoracic echocardiography. One patient (5%) who had mid-ventricular obstruction developed atrial fibrillation during 2 years follow-up, though any other events did not occur during hospitalization or follow-up period.</AbstractText>Physicians caring for patients with chest pain should consider AHCM in their differential diagnosis in case of a patient with chest pain and electrocardiographic changes suggestive of CAD.</AbstractText> |
7,803 | Diagnostic value of stored electrograms in pacemaker patients. | Stored electrograms (EGMs) are diagnostic tools in modern pacemakers, providing data concerning arrhythmia occurrence and device function. We sought to validate the impact of stored EGMs on diagnosis and verification of arrhythmias presented after pacemaker implantation.</AbstractText>We enrolled 71 consecutive patients (mean age 64 +/- 8 years, 51 men) with a standard indication for pacemaker implantation. The following pacemaker devices were implanted: DDDR = 57, VDDR = 5, VVIR = 9. EGM triggers were atrial tachycardia (AT), non-sustained ventricular tachycardia (NSVT) and ventricular tachycardia (VT). We retrieved and analysed 362 EGMs at 3 and 6 months after implantation. The EGMs were triggered by AT in 260 EGMs (72%), by NSVT in 80 (22%) and by VT in 22 (6%). In total, 243 episodes (67%) confirmed the arrhythmic events, while 119 episodes (33%) were classified as false-positive. They were divided into false-positive AT in 85 EGMs (33%), false-positive NSVT in 28 (35%) and false-positive VT in 6 EGMs (27%). The false-positive AT cases were caused by ventricular far-field sensing from the atrial channel in 34 EGMs (40%) and noise or myopotentials in 51 EGMs (60%). Most of the false-positive VT and NSVT episodes were due to atrial fibrillation or atrial tachycardias in 21 EGMs (62%), while the rest were caused by noise in 11 EGMs (32%) or ventricular T wave oversensing in 2 EGMs (6%).</AbstractText>Stored EGMs in pacemaker patients were diagnostic in two thirds of arrhythmic episodes. They are useful tools to diagnose arrhythmias and identify sensing problems, and they contribute to optimal device programming and patient management.</AbstractText> |
7,804 | Appropriate and inappropriate implantable cardioverter defibrillator interventions during secondary prevention. | ICD therapy is established therapy for secondary prevention after aborted sudden death or ventricular tachycardia. Long-term data on the incidence of appropriate and inappropriate interventions are scarce.</AbstractText>We retrospectively studied 391 patients with an ICD for secondary prophylaxis: 247 (63%) with ischaemic heart disease (IHD) and 144 without IHD (37%). Fifty-four patients were free from left ventricular structural disease. Mean follow-up was 30.8 months. Kaplan-Meier methodology was used for survival analysis. The use of beta-blockers was high and similar in both groups (85% IHD; 88% non-IHD; P = 0.36). The incidence of appropriate interventions was identical in IHD and non-IHD (42.7% and 47.8% at 4 y; HR 1.0, P = 0.99). There was a yearly rate of first intervention around 5% even in the fourth and fifth year after implantation. The incidence of inappropriate interventions was about half that of appropriate ICD interventions (21.4% at 4 y). It was higher in patients who also had received appropriate therapy (HR: 2.73 in the IHD group, 1.61 in the non-IHD group, P < 0.001 for both). Atrial fibrillation was the most common cause of inappropriate interventions in IHD, and sinus tachycardia in those without LV disease. The incidence of inappropriate interventions was not dependent on the type of ICD (VVI vs. DDD), in any group.</AbstractText>Patients with an ICD for secondary prophylaxis have a high rate of appropriate interventions, and remain at risk for developing a first intervention several years after implantation. Inappropriate interventions constitute a significant burden. Taking preventive measures (AV nodal slowing drugs, device selection and programming, patient counseling regarding allowable physical activity) is required to optimize the quality-of-life adjusted life-saving potential of ICDs.</AbstractText> |
7,805 | QT and TdP. QT: an unreliable predictor of proarrhythmia. | When triangulation, reverse use dependence, instability and dispersion (TRIaD) of the action potential are associated with drug-induced prolongation of the QT interval, then proarrhythmia in the form of torsade de pointes is most likely. However, as the QT interval is shortened, TRIaD increasingly leads to ventricular fibrillation (VF). Thus, use of QT prolongation by itself may not recognize drug-induced VF (false negatives) and in the absence of TRIaD may erroneously incriminate valuable and safe agents (false positives). In patients,TRIaD equivalents in the ECG may likewise be more important than QT interval. |
7,806 | An update on cardioembolic stroke. | About one-fifth of all ischaemic strokes are cardioembolic. Recent years have seen considerable progress in our understanding of atrial fibrillation, the most important cause of cardioembolism, and evidence-based treatment strategies have emerged. Progress in relation to other cardioembolic disorders has been more limited and here stroke prevention strategies remain less certain and subject to debate. This article briefly reviews the methods currently used to identify and investigate cardioembolic stroke and then provides an update on stroke prevention in relation to atrial fibrillation, valvular heart disease, patent foramen ovale and left ventricular dysfunction (after myocardial infarction and chronic failure). |
7,807 | Effect of drugs on defibrillation capacity. | Over 300,000 people die of sudden cardiac death (SCD) in the US annually. Implantable cardioverter-defibrillators (ICDs) have been shown to be more effective than antiarrhythmic drugs for the prevention of SCD in specific susceptible populations. Many patients in whom ICDs have been implanted receive concomitant therapy with antiarrhythmic drugs, for the purpose of reducing the frequency of appropriate and inappropriate defibrillation shocks. Drugs may influence defibrillation capacity and therefore influence the function of ICDs. The objective of this article is to review and update the literature regarding the effects of drugs on defibrillation capacity.A literature search was performed using PubMed (1966 to December 2007) to identify clinical studies, case reports and animal studies describing the effects of drugs on defibrillation capacity. Search terms included: antiarrhythmic drugs; cardiovascular drugs; amiodarone; sotalol; flecainide; propafenone; dofetilide; ibutilide; beta-blockers; lidocaine; procainamide; N-acetylprocainamide; mexiletine; disopyramide; moricizine; calcium channel blockers; defibrillation threshold; defibrillation energy requirements; defibrillation energy changes; defibrillation efficacy; implantable cardioverter defibrillators; and external defibrillators. Evidence from clinical studies indicates that amiodarone may increase defibrillation threshold (DFT). In addition, some data indicate that drugs including lidocaine, mexiletine, moracizine (moricizine), verapamil, venlafaxine and anaesthetic agents may increase DFT. In contrast, agents including sotalol, dofetilide and beta-adrenergic receptor antagonists (beta-blockers) may reduce DFT. Propafenone and procainamide appear to have minimal effect on DFT. For those antiarrhythmic drugs with both sodium and potassium channel blockade (e.g. amiodarone), the effect of sodium channel blockade predominates, resulting in an increase in DFT. Numerous drugs may affect defibrillation capacity. These effects must be considered when managing patients who have an ICD and require concomitant pharmacotherapy. |
7,808 | WPW and preexcitation syndromes. | Wolff-Parkinson-White syndrome is a disorder characterized by presence of an accessory pathway which predisposes patients to tachyarrhythmias and sudden death. Among patients with WPW syndrome, atrioventricular reentrant tachycardia (AVRT) is the most common arrhythmia, accounting for 95% of re-entrant tachycardias. It has been estimated that one-third of patients with WPW syndrome have atrial fibrillation (AF). AF is a potentially life-threatening arrhythmia. If an accessory pathway has a short anterograde refractory period, then rapid repetitive conduction to the ventricles during AF can result in a rapid ventricular response with subsequent degeneration to ventricular fibrillation (VF). The accessory pathway may be located anywhere along the atrioventricular valve Most of the patients are young and do not have structural heart disease hence it is important to risk stratify these patients so as to prevent the sudden death. Management of asymptomatic patients with WPW syndrome has always remained controversial Catheter ablation of accessory pathways has become an established mode of therapy for symptomatic patients and asymptomatic patients employed in high-risk professions. |
7,809 | Sudden cardiac death complicating newly diagnosed atrial fibrillation in the setting of subclinical hyperthyroidism. | Atrial fibrillation (AF) is the most common arrhythmia in clinical practice and a predictor of all-cause mortality. Subclinical hyperthyroidism is an independent risk factor for developing AF but its clinical significance in younger patients has not been established. We describe a clinical case of a 44-year-old female with newly diagnosed AF, degenerating to ventricular fibrillation in the setting of subclinical hyperthyroidism. |
7,810 | Propofol infusion syndrome: an overview of a perplexing disease. | Propofol (2, 6-diisopropylphenol) is a potent intravenous hypnotic agent that is widely used in adults and children for sedation and the induction and maintenance of anaesthesia. Propofol has gained popularity for its rapid onset and rapid recovery even after prolonged use, and for the neuroprotection conferred. However, a review of the literature reveals multiple instances in which prolonged propofol administration (>48 hours) at high doses (>4 mg/kg/h) may cause a rare, but frequently fatal complication known as propofol infusion syndrome (PRIS). PRIS is characterized by metabolic acidosis, rhabdomyolysis of both skeletal and cardiac muscle, arrhythmias (bradycardia, atrial fibrillation, ventricular and supraventricular tachycardia, bundle branch block and asystole), myocardial failure, renal failure, hepatomegaly and death. PRIS has been described as an 'all or none' syndrome with sudden onset and probable death. The literature does not provide evidence of degrees of symptoms, nor of mildness or severity of signs in the clinical course of the syndrome. Recently, a fatal case of PRIS at a low infusion rate (1.9-2.6 mg/kg/h) has been reported. Common laboratory and instrumental findings in PRIS are myoglobinuria, downsloping ST-segment elevation, an increase in plasma creatine kinase, troponin I, potassium, creatinine, azotaemia, malonylcarnitine and C5-acylcarnitine, whereas in the mitochondrial respiratory electron transport chain, the activity of complex IV and cytochrome oxidase ratio is reduced. Propofol should be used with caution for sedation in critically ill children and adults, as well as for long-term anesthesia in otherwise healthy patients, and doses exceeding 4-5 mg/kg/h for long periods (>48 h) should be avoided. If PRIS is suspected, propofol must be stopped immediately and cardiocirculatory stabilization and correction of metabolic acidosis initiated. So, PRIS must be kept in mind as a rare, but highly lethal, complication of propofol use, not necessarily confined to its prolonged use. Furthermore, the safe dosage of propofol may need re-evaluation, and new studies are needed. |
7,811 | Long-term follow-up of patients treated with ICD: benefit in patients with preserved left ventricular function. | Most major defibrillator trials have short follow-up and may neither capture the benefit for those with preserved function nor the progressive nature of advanced heart disease. We intended to investigate the long-term outcome in an unselected population of patients treated with ICD.</AbstractText>We followed 124 consecutive patients that received an ICD during 1993-2002 at our institution for a median of 6.1 years. Information about heart disease, index arrhythmia, follow-up and death was extracted from medical records.</AbstractText>The crude mortality was 26% (32/124). One- and two-year mortality was 6% and 12%, estimated 5- and 10-year mortality 20% and 33%. The cause of death was heart failure in 75% of deaths. The ejection fraction was below 35% in 91% of the 32 patients who died. We estimated that 28% of the patients received lifesaving therapy. The relative number of saved lives and complications was not related to the ejection fraction.</AbstractText>Patients with preserved left ventricular function are excellent candidates for ICD, with life-saving ICD therapies in a substantial proportion, low mortality and good quality of life.</AbstractText> |
7,812 | [Specific bradycardic drug zatebradin: cardiac rhythm variability, antifibrillatory, and antiischemic effects]. | The results of experiments on narcotized cats and rats showed that the drug zatebradin produces a specific bradycardic action by reducing the heart rate and the double product, while virtually not influencing vitally important parameters of the heart activity such as the cardiac output and the mean acceleration of the aorta blood flow. The drug reduced the rise of ST segment recorded in multiple epicardial ECG leads made in narcotized cats during a 5-min occlusion of the anterior descending branch of the left coronary artery. Zatebradin was found to increase the cardiac rhythm variability in narcotized rats and decrease the rate of ventricular fibrillations during a 7-min occlusion with the subsequent 3-min coronary artery reperfusion. |
7,813 | The prevalence of supraventricular arrhythmias with regard to the type and degree of left ventricular hypertrophy in patients with hypertensive heart disease. | We investigated the correlation between the type and degree of left ventricular hypertrophy and the prevalence of supraventricular arrhythmias in patients with hypertensive heart disease.</AbstractText>The study included 179 patients (79 men, 100 women, aged 43-80 years, median 68 years) with left ventricular hypertrophy. Patients were classified into three groups (concentric, eccentric and asymmetric types of hypertrophy) and into three subgroups (mild, moderate and severe hypertrophy). After discontinuation of all medication for 48 h, blood pressure was measured, electrocardiography and echocardiography performed and the prevalence of supraventricular arrhythmias assessed using Holter monitoring and bicycle ergometry. Antihypertensive drugs and duration of previous treatment were taken into consideration.</AbstractText>Atrial fibrillation or paroxysmal supraventricular tachycardia were found in 43% of patients. The analysis showed no significant correlation between the prevalence of atrial fibrillation and/or paroxysmal supraventricular tachycardia and the degree (P = 0.607) and type of left ventricular hypertrophy (P = 0.455). However, the frequency of supraventricular premature beats was higher in the concentric and eccentric types than in the asymmetric type (P = 0.048) and increased with the degree of hypertrophy (significantly in men with the concentric type, P = 0.015).</AbstractText>Concentric and eccentric types of left ventricular hypertrophy have a greater impact on the frequency of atrial arrhythmias. In the concentric type the prevalence of supraventricular premature beats correlates with the degree of left ventricular hypertrophy. Patients with moderate and severe concentric and eccentric left ventricular hypertrophy should be always tested using Holter monitoring and bicycle ergometry and treated with the maximum tolerable doses of antihypertensives, particularly with angiotensin-converting enzyme inhibitors/angiotensin receptor blockers.</AbstractText> |
7,814 | [Drug induced QT prolongation]. | Prolongation of the ventricular repolarisation manifests itself as a prolongation of the QT intervall on the surface ECG and represents a major risk for a special form of ventricular tachycardia called "torsades de pointes". Torsades de pointes are often self limited and are associated with palpitations, dizziness or syncope. Degeneration into ventricular fibrillation and sudden cardiac death can occur. In addition to the various forms of the congenital long QT syndrome many drugs, such as antiarrhythmic drugs class IA and III, antibiotics, antihistamines, antidepressants, and methadone are known to prolong the QT interval. Most of these drugs block a specific potassium channel substantially involved in the ventricular repolarisation. In addition, drug interaction or disturbances of drug metabolism may play a major role in the acquired form of the long QT syndrome. The individual risk and the potential of a pharmacologic substance to prolong the QT interval are not predictable. Certain risk factors identify patients at higher risk for drug-induced prolongation of the QT interval. Correctable factors include electrolyte disorders (e.g. hypokalemia) and concomitant administration of different QT prolonging drugs. External defibrillation is the therapy of choice in the hemodynamic unstable patient presenting torsades de pointes. In hemodynamic more stable patients application of intravenous magnesium can terminate torsades de pointes (membrane stabilizing properties). Temporary external or transvenous pacing at high heart rate might terminate incessant torsades de pointes by decreasing QT interval. Repeated ECG controls during therapy with QT prolonging drugs are mandatory, especially when drug doses are changed, additional drugs are prescribed, or in case of vomiting and diarrhea. QT prolongation in individual medical therapy is not always predictable. Therefore, updated lists of drugs with the potential of QT prolongation are available on the Internet (e.g. www.qtdrugs.org ). |
7,815 | [Effect of streptomycin on stretch-induced change in myocardial activation during ventricular fibrillation]. | The aim of this study was to determine whether the changes in myocardial activation pattern resulting from acute stretching during ventricular fibrillation can be counteracted by administering a compound that blocks receptors sensitive to stretch. The study involved 16 isolated rabbit hearts, in which refractoriness and activation frequency during ventricular fibrillation were measured before, during and after localized acute stretching of the left ventricular free wall, either without (series A, n=8) or with (series B, n=8) the presence of streptomycin, 200 micromol. At baseline and during and after stretching, ventricular fibrillation was slower with streptomycin perfusion in series B than in series A (dominant frequency at baseline, 13+/-2 Hz vs. 16+/-2 Hz, respectively; P< .005; dominant frequency with stretching, 14+/-2 Hz vs. 19+/-3 Hz, respectively; P< .005). Streptomycin attenuated the electrophysiological changes produced by stretching and had a direct effect on refractoriness and activation frequency during ventricular fibrillation. |
7,816 | [Non-invasive characterization of atrial activity immediately prior to termination of paroxysmal atrial fibrillation (corrected)]. | Atrial activity characterization with a high degree of detail can be reached by analyzing invasive recordings. Nevertheless, electrocardiographic signal processing tools can nowadays obtain equivalent information in some cases. The aim of this work is to study the electrocardiographic alterations produced during the last instants prior to spontaneous AF termination.</AbstractText>Fifty patients in paroxysmal AF with an episode lasting more than two hours were selected. The last minute prior to spontaneous AF termination (group S) and the central minute (group N) from each episode were analyzed. Ventricular response, f waves morphology, and atrial activity spectral and organization were studied through the use of signal processing tools.</AbstractText>RR intervals variability was a discriminative parameter (group S 630+/-200 ms vs. group N 740+/-100 ms; P=.034), although a low specificity was obtained (54.2%). Significative differences between both groups were not reported by the f waves morphological study. Group S presented a significative low dominant atrial frequency mean value than group N (group S 5.010+/-0.671 Hz vs. group N 6.514+/-0.804 Hz, P=4.55x10(-9)). Finally, group N showed a considerable low atrial activity organization degree than group S (group S 0.071+/-0.012 vs. group N 0.103+/-0.013, P=6.73x10(-12)).</AbstractText>The analysis of the electrocardiographic interval prior to spontaneous AF termination has revealed an atrial activity organization process, which cannot be observed by visual inspection of f waves morphology, but can be successfully quantified through signal processing.</AbstractText> |
7,817 | The proarrhythmic effect of incomplete pulmotricuspid isthmus ablation in a patient with sarcoid-related ventricular tachycardia? | Proarrhythmia is relatively common after extensive atrial ablation for atrial fibrillation, but has not been frequently documented after catheter ablation of ventricular tachycardia (VT). In theory, this phenomenon could occur if an incomplete ablation line is created between two nonconducting structures, such as dense scar or valvular annuli. This report illustrates the possible proarrhythmic effect of ablation in a patient with sarcoid-related VT and extensive right ventricular (RV) myopathy who presented with slow incessant VT one month after an ablation procedure including ablation at the pulmotricuspid isthmus (PTI). The extensive preexisting RV myopathy appeared to be an important substrate in the pathogenesis of this patient's incessant VT. This case suggests that the PTI region may serve as a critical tachycardia isthmus if sufficiently modified with an incomplete ablation line in the setting of significant myocardial scarring. |
7,818 | Clinical profile, prognosis and treatment of patients with infective endocarditis--a 14-year follow-up study. | Poor prognosis of infective endocarditis (IE) is not only attributable to high morbidity and mortality during an active phase of the disease, but also to late complications and relapses occurring after eradication of the infection. Identification of unfavorable prognostic factors allows to optimize therapeutic modalities in patients with particularly poor prognosis.</AbstractText>To determine clinical features and long-term prognosis among patients with IE.</AbstractText>The study group consisted of 69 IE patients hospitalized in our center between 1992 and 2005. The diagnosis of IE was based on the Duke University criteria. The mean age was 52 +/- 12 years. Surgical treatment was performed in 48 (70%) cases.</AbstractText>The etiology of IE was Staphylococcus sp. in 32% of patients, Streptococcus sp. in 16% of patients, in 41% of cases blood cultures were negative. The infection was located on the aortic (43%), mitral (26%), tricuspid (8%) and multiple valves (20%). During 1-14 years of follow-up, 27 patients died (39%). Prognostic factors included NYHA class of heart failure (p = 0.031), lower left ventricular ejection fraction (p = 0.017), kidney failure (p = 0.012), atrial fibrillation (p = 0.006), a history of rheumatic valve disease (p = 0.046). In multivariate logistic analysis the only significant parameter related to poor prognosis after IE was atrial fibrillation. The analysis of receiver operating characteristic curve showed that patients with atrial fibrillation were significantly associated with higher mortality (HR 5.35, 95% CI 1.47-19.56, p = 0.011).</AbstractText>Regardless of the mode of treatment (medical or combined medical-surgical), the mortality of patients with infective endocarditis remains relatively high. In this study atrial fibrillation seems to be the most important risk factor of death.</AbstractText> |
7,819 | Signal-averaged P-wave ECG as a marker of atrial electrical instability in patients with right ventricular dysfunction. | Severe pulmonary hypertension (PAH) leads to right ventricular dysfunction and is associated with different atrial arrhythmias. In PAH patients, the echocardiographic Tei-index is used for monitoring right heart function. The P-wave signal-averaged ECG (SA-ECG) has been shown to have a potential role in identifying patients at risk of developing paroxysmal atrial fibrillation and those likely to change from paroxysmal to chronic atrial fibrillation. The aim of the present study was to define the correlation of the Tei-Index with parameters of P-wave triggered and bidirectional P-wave SA-ECG. A total of 18 patients (14 men, 4 women) with normal sinus rhythm and a mean age of 67+/-10 years (BMI 27.6+/-5.1 kg/m2) were included into the study. Right ventricular (RV) Tei-index was calculated from the sum of isovolumetric contraction time and relaxation time divided by ejection time. Furthermore, P-wave triggered P-wave signal averaged ECG was performed from an X, Y, and Z lead system. The results show that there was a statistically significant correlation between Tei-index and filtered P-wave duration (r=0.53; P=0.023). Teiindex did not correlate with the root mean square voltage of the last 20 ms of the P wave (r=-0.16; P=0.52). In conclusion, a correlation of RV Tei index with P-wave duration indicates that this echocardiographic measurement is not only a marker of right heart function, but also an indicator of electrical instability that could be useful to detect patients at risk for atrial arrhythmias. |
7,820 | Cibenzoline intoxication: effect of combined hemoperfusion-hemodialysis on plasma clearance. | Cibenzoline is an antiarrhythmic drug used to treat patients with supraventricular or ventricular arrhythmias. Cibenzoline overdose is associated with proarrhythmic and hemodynamic effects such as hypotension and congestive heart failure.</AbstractText>We report a case of cardiogenic shock due to cibenzoline overdose in a patient with progressive renal insufficiency.</AbstractText>The standard treatment of a cibenzoline intoxication is symptomatic, but we used combined hemoperfusion-hemodialysis to treat our patient.</AbstractText>This was associated with a rapid decline in plasma cibenzoline concentration and improvement of the clinical condition. However, only 28.98 mg of an estimated body pool of cibenzoline (447.2 to 806.6 mg) was removed during the 8 hours of treatment.</AbstractText> |
7,821 | Regenerative therapies in electrophysiology and pacing. | The prevention and treatment of cardiac arrhythmias conferring major morbidity and mortality is far from optimal, and relies heavily on devices and drugs for the partial successes that have been seen. The greatest success has been in the use of electronic pacemakers to drive the hearts of patients having high degree heart block. Recent years have seen the beginnings of attempts to use novel approaches available through gene and cell therapies to treat both brady- and tachyarrhythmias. By far the most successful approaches to date have been seen in the development of biological pacemakers. However, the far more difficult problems posed by atrial fibrillation and ventricular tachycardia are now being addressed. In the following pages we review the approaches now in progress as well as the specific methodologic demands that must be met if these therapies are to be successful. |
7,822 | Inappropriate analyses of automated external defibrillators used during in-hospital ventricular fibrillation. | The use of automated external defibrillators (AEDs) has increased the number of survivors of out-of-hospital cardiac arrest. The AED has a high specificity and moderately high sensitivity in detecting rhythms appropriately treated by defibrillation. However, a few shockable rhythms are misdiagnosed by the AED. Two cases of inappropriate analyses by AEDs in patients with in-hospital ventricular fibrillation are presented. In the first case, the AED failed to recognize ventricular fibrillation because of the presence of pacemaker spikes. In the second case, the fine ventricular fibrillation and the presence of artifacts were suspected as the causes of inappropriate analysis by the AED. Both patients were resuscitated by advanced cardiovascular life support with a manual defibrillator. Trained healthcare providers should be aware of the limitations of AED in specific situations. |
7,823 | Atria are more susceptible to electroporation than ventricles: implications for atrial stunning, shock-induced arrhythmia and defibrillation failure. | Defibrillation shock is known to induce atrial stunning, which is electrical and mechanical dysfunction.</AbstractText>We hypothesized that atrial stunning is caused by higher atrial susceptibility to electroporation vs ventricles. We also hypothesize that electroporation may be responsible for early recurrence of atrial fibrillation.</AbstractText>We investigated electroporation induced by 10-ms epicardial high-intensity shocks applied locally in atria and ventricles of Langendorff-perfused rabbit hearts (n = 12) using optical mapping.</AbstractText>Electroporation was centered at the electrode and was evident from transient diastolic depolarization and reduction of action potential amplitude and maximum upstroke derivative. Electroporation was voltage-dependent and polarity-dependent and was significantly more pronounced in the atria vs ventricles (P <.01), with a summary 50% of Effective Dose (ED50) for main measured parameters of 9.2 +/- 3.6 V/cm and 13.6 +/- 3.2 V/cm in the atria vs 37.4 +/- 1.5 V/cm and 48.4 +/- 2.8 V/cm in the ventricles, for anodal and cathodal stimuli, respectively. In atria (n = 5), shocks of both polarities (27.2 +/- 1.1 V/cm) transiently induced conduction block and reentry around the inexcitable area. Electroporation-induced ectopic activity was a possible trigger for reentry. However, in the thicker ventricles, electroporation and resulting conduction slowing and block were restricted to the surface only, preventing complete block and arrhythmia. The upstroke morphology revealed that the wave front dived below the electroporated region and resurfaced into unaffected epicardial tissue.</AbstractText>We showed that the atria are more vulnerable to electroporation and resulting block and arrhythmia than the ventricles.</AbstractText> |
7,824 | Excito-oscillatory dynamics as a mechanism of ventricular fibrillation. | The instabilities associated with reentrant spiral waves are of paramount importance to the initiation and maintenance of tachyarrhythmias, especially ventricular fibrillation (VF). In addition to tissue heterogeneities, there are only a few basic purported mechanisms of spiral wave breakup, most notably restitution.</AbstractText>We test the hypothesis that oscillatory membrane properties act to destabilize spiral waves.</AbstractText>We recorded transmembrane potential (V(m)) from isolated rabbit myocytes using a constant current stimulation protocol. We developed a mathematical model that included both the stable excitable equilibrium point at resting V(m) (-80 mV) and the unstable oscillatory equilibrium point at elevated V(m) (-10 mV). Spiral wave dynamics were studied in 2-dimensional grids using variants of the model.</AbstractText>All models showed restitution and reproduced the experimental values of transmembrane resistance at rest and during the action potential plateau. Stable spiral waves were observed when the model showed only 1 equilibrium point. However, spatio-temporal complexity was observed if the model showed both excitable and oscillatory equilibrium points (i.e., excito-oscillatory models). The initial wave breaks resulted from oscillatory waves expanding in all directions; after a few beats, the patterns were characterized by a combination of unstable spiral waves and target patterns consistent with the patterns observed on the heart surface during VF. In our model, this VF-like activity only occurred when the single cell period of V(m) oscillations was within a specific range.</AbstractText>The VF-like patterns observed in our excito-oscillatory models could not be explained by the existing proposed instability mechanisms. Our results introduce the important suggestion that membrane dynamics responsible for V(m) oscillations at elevated V(m) levels can destabilize spiral waves and thus may be a novel therapeutic target for preventing VF.</AbstractText> |
7,825 | Association between statin use and mortality in patients with implantable cardioverter-defibrillators and left ventricular systolic dysfunction. | A few previous nested cohort trials have evaluated the use of statins on survival and the occurrence of ventricular tachycardia or fibrillation (VT/VF). While the studies generally agreed on the survival effects, they disagreed on the magnitude of the mortality benefit and on the effect on VT/VF.</AbstractText>The purpose of this study was to determine in a large, long-term follow-up cohort whether statin therapy could reduce mortality and the occurrence of VT/VF in a mixed population receiving an implantable cardioverter-defibrillator (ICD) for primary or secondary prevention and either ischemic or nonischemic cardiomyopathy.</AbstractText>Cohort evaluation of all patients undergoing implantation of an ICD with a left ventricular ejection fraction <40% at an urban U.S. teaching hospital from December 1997 through January 2007. Multivariable analysis of predictors of mortality and VT/VF were conducted.</AbstractText>There were 314 deaths among the 1204 patients (26.1%). The use of statin therapy (n = 642) was associated with an adjusted hazard ratio of 0.67 (95% confidence interval [CI] 0.53-0.85; P<.001) for mortality as compared with the no-statin group (n = 562). The use of statin therapy was not associated with a reduction in the adjusted hazard ratio for VT/VF (0.85; 95% CI 0.68-1.06; P = .14).</AbstractText>Statin therapy is associated with a reduction in overall mortality in patients with ischemic or nonischemic cardiomyopathy with an ICD implanted for either primary or secondary prevention. The magnitude of survival benefit might have been underestimated given our inability to use statin as a time-dependent covariate.</AbstractText> |
7,826 | The role of fish oil in arrhythmia prevention. | Numerous epidemiological studies, case-control series, and randomized trials have demonstrated the ability of fish oil to reduce major cardiovascular events, particularly sudden cardiac death and all-cause mortality. We discuss the potential benefits of fish oil therapy to improve overall autonomic tone and potentially reduce the risk of major ventricular and atrial arrhythmias. Specifically, this review focuses on how fish oil therapy has performed in 3 primary prevention trials in patients with implantable cardioverter defibrillators, reviews the effects that fish oil has on the autonomic nervous system, focuses on the use of fish oil as a novel therapy for atrial fibrillation, and revisits other beneficial properties of fish oil (ie, ability to lower serum triglycerides, anti-inflammatory effects, and possible improvements in arterial pressure/diastolic function). We also discuss the safety profile of fish oil, including effects on bleeding time and bleeding complications as well as provide commentary regarding fish oil supplementation in light of increasing contaminants contained in fish. In summary, any patient with documented coronary heart disease and those with risk factors for sudden cardiac death, such as left ventricular dysfunction, left ventricular hypertrophy, prior myocardial infarction, or high-grade ventricular dysrhythmias, should consider fish oil supplementation. The American Heart Association recommends four 3-ounce servings of oily fish weekly. For those who cannot eat fish or do not have access to fish, as well as those who would prefer not to eat fish regularly, capsules of fish oil are readily available in various concentrations. At the present time, we recommend doses of eicosapentanoic acid and docosahexanoic acid in the combined range of 800 to 1000 mg/day for primary and secondary prevention of cardiovascular disease. |
7,827 | Effect on treatment delay of prehospital teletransmission of 12-lead electrocardiogram to a cardiologist for immediate triage and direct referral of patients with ST-segment elevation acute myocardial infarction to primary percutaneous coronary intervention. | Prehospital electrocardiogram (ECG) transmission to hospitals was shown to reduce time to treatment in patients with acute myocardial infarction. However, new technologies allow transmission directly to a mobile unit so an attending physician can respond irrespective of presence within or outside the hospital. The primary study purpose was to determine whether delays could be decreased in an urban area by transmitting a prehospital 12-lead ECG directly to the attending cardiologist's mobile telephone for rapid triage and transport to a primary percutaneous coronary intervention (PCI) center, bypassing local hospitals and emergency departments. A secondary purpose was to describe whether transport would be safe despite longer transport times. During a 2-year period, patients with acute nontraumatic chest pain had their prehospital ECG transmitted directly to a cardiologist's mobile telephone. Time to treatment was compared with historic controls. After ECG evaluation, 168 patients (30%) were referred directly for PCI, and 146 of these (87%) underwent emergent catheterization. In referred patients, median time from 911 call to PCI was significantly shorter than in the control group (74 vs 127 minutes; p <0.001). Accordingly, door-to-PCI time was 63 minutes shorter for referred patients versus controls (34 vs 97 minutes; p <0.001). During transport, 7 patients (4%) experienced ventricular fibrillation; 3 patients (2%), ventricular tachycardia; and 1 patient (0.5%), pulseless electrical activity, including 2 deaths (1%) caused by treatment-resistant arrhythmia. In conclusion, transmission of a prehospital 12-lead ECG directly to the attending cardiologist's mobile telephone decreased door-to-PCI time by >1 hour when patients were transported directly to PCI centers, bypassing local hospitals. Ambulance transport seems safe despite longer transport times. |
7,828 | Myocardial cytokine IL-8 and nitric oxide synthase activity during and after resuscitation: preliminary observations in regards to post-resuscitation myocardial dysfunction. | Increases in serum cytokines have been reported after successful resuscitation from prolonged ventricular fibrillation (VF). Pro-inflammatory cytokines can stimulate inducible nitric oxide synthase (iNOS) to produce excessive levels of nitric oxide (NO). High levels of both myocardial inflammatory cytokines and nitric oxide levels can depress myocardial contractile function. We hypothesized that myocardial pro-inflammatory cytokines and iNOS activity would increase following successful resuscitation from prolonged ventricular fibrillation cardiac arrest, and that such increases would parallel the development of post-resuscitation myocardial dysfunction.</AbstractText>Ventricular fibrillation cardiac arrest was induced in seven domestic swine (25+/-5 kg). After 10 min of untreated VF, the animals were defibrillated and resuscitated. Left ventricular (LV) systolic and diastolic function measurements, serum samples (arterial and coronary sinus) for IL-8 cytokine quantification, and LV myocardial biopsies were collected before, during, and after resuscitation. Quantification of myocardial endothelial (eNOS) and inducible (iNOS) nitric oxide synthase protein levels were determined using immunoblot analyses and protein localization was examined using immunohistochemistry.</AbstractText>Post-resuscitation LV systolic and diastolic functions were depressed while increases in both coronary sinus IL-8 levels and myocardial iNOS activity were found. Compared to pre-arrest baseline, levels of iNOS protein increased during VF (p < or = 0.05) and continued to increase throughout the post-resuscitation study period of 6 h (p < or = 0.05).</AbstractText>Myocardial inflammatory cytokines and iNOS activity increase during and after prolonged cardiac arrest and successful resuscitation. These increases correspond to the well described decrease in LV function post-resuscitation.</AbstractText> |
7,829 | Mechanical modulation of atrial flutter cycle length. | Although atrial flutter (AFL) is considered a highly regular rhythm, small fluctuations in cycle length have been described. The mechanisms responsible for these interval oscillations have been investigated by recent studies in humans which have shown that cyclic variations in atrial volume and pressure following ventricular contraction may account for the spontaneous variability of AFL. Other studies have shown that variations in the dimensions of the atria, caused by hemodynamical alterations due to imposed manoeuvres, directly modify the rate of AFL. All this evidence has led to the development of the mechano-electrical feedback (MEF) hypothesis, which assumes that changes in atrial volume directly affect AFL cycle length variability by modifying the conduction properties of the circulating impulse in the atrium. In the present study, we re-examined the variability pattern of typical AFL by spectral analysis aiming to support the MEF hypothesis for AFL cycle length variability. In a study population of 30 patients with typical AFL, we observed that AFL cycle length presented a spontaneous beat-to-beat variability, composed of two oscillations: a main oscillation at the frequency of ventricular contraction (1.70+/-0.48 Hz, spectral power: 15.4+/-17.6 ms2) and a second oscillation at the frequency of respiration (0.32+/-0.07 Hz, spectral power: 2.9+/-2.6 ms2). Both ventricular and respiratory oscillations persisted after pharmacologic autonomic blockade (ventricular spectral power: 17.7+/-14.7 ms2 (before block) vs 20.2+/-18.3 ms2 (after block), p=NS; respiratory spectral power: 6.0+/-3.8 ms2 (before block) vs 5.0+/-3.4 ms2 (after block), p=NS), suggesting a non-neurally mediated underlying mechanism. Contrary to respiratory modulation of heart rate during sinus rhythm, respiratory AFL cycle length oscillations displayed a reverse pattern, with longer cycle lengths during inspiration and shorter during expiration (AA insp=223.2+/-28.6 ms vs AA exp=221.1+/-28.2 ms, p<0.0005), which was consistent with a mechanical modulation of AFL reentry. The use of spectral analysis techniques applied to ventricular interval series and combined with computer simulations of atrioventricular conduction showed that the respiratory oscillation of atrial cycle length determined an oscillation in ventricular intervals with longer intervals during inspiration and shorter during expiration (VV insp=639.9+/-186.0 ms vs VV exp=634.8+/-182.9 ms, p<0.05). Ventricular interval oscillations resulted amplified by a factor 1.8 with respect to corresponding atrial cycle length oscillations. Thus, the mechanical fluctuations in AFL cycle length, although of small amplitude, might become clinically relevant through a magnified effect on ventricular variability. |
7,830 | Headache angina. | The initial recognition of acute myocardial infarction at the time of the emergency department (ED) visit may be difficult in the absence of typical presentations such as chest pain, diaphoresis, and radiation tenderness. Headache angina, although reported in several instances in the past with variable patient outcomes, is still an uncommon phenomenon in patients with acute myocardial infarction. We report a patient with inferior myocardial infarction who presented to the ED with a complaint of severe headache and subsequent cardiogenic shock secondary to ventricular fibrillation. |
7,831 | Double-dose external cardioversion for refractory unstable atrial fibrillation in the ED. | A 45-year-old man with dilated cardiomyopathy, atrial fibrillation, and hypertension presented to the emergency department with palpitations and shortness of breath for 2 days after running out of his medications. An electrocardiogram disclosed atrial fibrillation with rapid ventricular response. The patient was hemodynamically unstable and failed multiple cardioversion attempts up to 360 J. A second defibrillator was then attached and the patient successfully cardioverted once both defibrillators were set to their maximum levels, thus delivering a total of 720 J. Double-dose external cardioversion with 2 defibrillators is an important alternative method that the emergency physician should be aware of when treating refractory atrial fibrillation in the hemodynamically unstable patient. |
7,832 | Efficacy of transesophageal defibrillation in ventricular fibrillation of long duration. | Increasing duration of ventricular fibrillation (VF) is associated with a higher risk of ineffective resuscitation. In addition, precountershock chest compression can influence defibrillation success. Transesophageal defibrillation may increase defibrillation success because of the proximity of the esophagus to the heart. We evaluated the efficacy of transesophageal defibrillation compared with standard transthoracic defibrillation after long episodes of VF.</AbstractText>Defibrillation success after 10 minutes of untreated VF was evaluated in 12 sheep randomized into 2 groups: (group A) in 6 sheep, up to 3 transthoracic shocks were applied, followed by up to 3 transesophageal shocks (first shock: 150 J, second and third shocks: 200 J). (group B) In 6 sheep, 2 minutes of precountershock chest compression preceded the defibrillation shocks. Truncated biphasic shocks were delivered between a sternal and an apical patch electrode for transthoracic defibrillation and between an esophageal and a cutaneous patch electrode for transesophageal defibrillation.</AbstractText>In group A with no precountershock chest compression, external defibrillation failed despite shocks with maximum energy (200 J) in all 6 sheep. Transesophageal defibrillation was successful in 3 sheep (50%). In group B with precountershock chest compression, external defibrillation failed in all 6 sheep. Transesophageal defibrillation was successful with the first shock in all 6 sheep.</AbstractText>Transesophageal defibrillation may terminate VF of long duration that is refractory to standard defibrillation. Precountershock chest compression may increase transesophageal defibrillation success.</AbstractText> |
7,833 | The role of concomitant arrhythmia surgery in patients undergoing repair of congenital heart disease. | Long-term survival after repair of complex congenital heart lesions is associated with the late development of arrhythmias as well as residual hemodynamic abnormalities. Understanding arrhythmias as electromechanical problems provides the basis for surgical intervention to correct the arrhythmia as well as anatomical disturbances. Operative techniques are highly effective in treating atrial reentry tachycardia and atrial fibrillation. Surgery for ventricular tachycardia is less effective: the arrhythmia may be reduced by improving hemodynamics, but a defibrillator may be required. Integration of device therapy into surgery may improve outcomes by preventing bradycardia as a precursor to tachycardia, and optimizing ventricular synchrony. |
7,834 | Antifibrillatory properties of mivacurium in a canine model of atrial fibrillation. | The electrophysiologic actions of the competitive neuromuscular blocker mivacurium (0.05-0.8 mg/kg IV; N = 10) and atropine sulfate [0.01-0.16 mg/Kg intravenously (IV), N = 6] were determined under control conditions, during right vagus nerve stimulation, and during anterior right ganglionated plexus stimulation. Both drugs suppressed shortening of right atrial monophasic action potential (MAP) duration, right atrial refractoriness, and right superior pulmonary vein sleeve refractoriness produced by vagus nerve or ganglionated plexus stimulation and suppressed the induction of atrial fibrillation. Suppression of atrial fibrillation by atropine was accompanied by improved sinus and atrioventricular (AV) nodal function, increasing the ventricular heart rate observed during sinus rhythm and atrial fibrillation and eliminating the depressant actions of vagus nerve stimulation on sinoatrial (SA) and AV nodal function. Unlike atropine, mivacurium selectively antagonized the effects of vagus nerve and ganglionated plexus stimulation on atrial and pulmonary vein sleeve myocardium (shortening of action potential duration/refractoriness and increased atrial vulnerability) without altering sinus or AV nodal function under control conditions or during vagus nerve stimulation. The selective inhibition of parasympathetic nervous system effects in atrium versus sinus and AV nodes by mivacurium may represent a selective mechanism for the suppression of atrial fibrillation without altering SA and AV nodal function. |
7,835 | Piperazine protects the rat heart against sudden cardiac death from barium chloride-induced ventricular fibrillation. | Fifteen of 20 Wistar albino rats were treated with various doses of the anthelmintic agent piperazine citrate (15, 30, and 60 mg/kg body weight). All 20 rats were subsequently given barium chloride, 20 mg/kg. The 5 rats (25%) that did not receive piperazine citrate developed ventricular fibrillations after barium chloride was administered to them, via one of the external jugular veins, and died shortly thereafter. The remaining 75% of the rats were fully protected by all the doses of piperazine citrate employed for the study. Barium chloride did not produce any dysrhythmic phenomenon in the piperazine-protected rats. Conversely, sinus rhythm was maintained in the electrocardiogram of all the rats, with every P wave followed by a normal QRS-T complex. This may portend a novel application for an old drug. |
7,836 | Sudden death in an Emery-Dreifuss muscular dystrophy patient with an implantable defibrillator. | We report the first case of witnessed sudden death of an Emery-Dreifuss muscular dystrophy (EDMD) patient with a properly functioning implantable cardioverter-defibrillator (ICD). This 38-yr-old woman with normal left ventricular function had a history of recurrent syncope and nonsustained ventricular tachycardia, for which a single-chamber ventricular ICD was implanted. She later collapsed suddenly and unexpectedly while at home, with witnesses present, and was found cyanotic with pulseless electrical activity by the emergency squad. This event took place in the setting of previously documented hypercapnic ventilatory insufficiency, for which she had refused the use of respiratory muscle aids to normalize alveolar ventilation. Subsequent interrogation of the ICD demonstrated normal function, with no evidence of ventricular tachycardia or ventricular fibrillation. In the hospital, her myocardial function was found to be normal by echocardiography. Further workup revealed that the patient had severe anoxic encephalopathy. She was eventually made "do not resuscitate," and she died on the sixth day of hospitalization. An autopsy was performed, and no obvious cause for the sudden death could be established. Review of the clinical presentation, with all the data available, suggests acute respiratory failure as the likely primary cause of this patient's sudden death, which then secondarily led to the observed pulseless electrical activity of the heart. The use of respiratory muscle aids--in particular, noninvasive mechanical ventilation to prevent chronic hypercapnia and cor pulmonale--is crucial for EDMD patients with symptomatic ventilatory insufficiency, for whom sudden deaths may not necessarily be of primarily cardiac origin. |
7,837 | Cardiac resynchronization therapy in patients with heart failure and atrial fibrillation: importance of new-onset atrial fibrillation and total atrial conduction time. | Cardiac resynchronization therapy (CRT) is an established therapy for patients with heart failure and sinus rhythm (SR), but its value in atrial fibrillation (AF) remains unclear. Furthermore, response to CRT may be difficult to predict in these patients. The aim of our study was to investigate whether predictors for CRT success differ between patients with AF and SR and to study the influence of present or developing AF on response to CRT.</AbstractText>We examined consecutive patients in whom CRT was implanted disregarding the atrial rhythm. Atrial fibrillation was defined as either current or earlier AF, response to CRT was defined as a decrease in the left ventricular end-systolic volume of > or = 10% after 6 months. Total atrial conduction time (TACT), a measure to predict the risk of developing AF, was determined by echocardiography. We included 114 patients, of whom 56 (49%) were known with AF (23 current AF and 33 earlier AF). The other 58 patients had no history of AF. After 6 months, response in current and earlier AF and that in SR patients was comparable (56, 58 and 55%, respectively). In AF patients, multivariate analysis revealed a shorter TACT at baseline [odds ratio (OR) 16.7 (1.5-185.3), P = 0.02] and an interventricular mechanical delay (IVMD) > 40 ms [OR 10.4 (1.0-110.9), P = 0.05] as predictors for response. Non-responders more frequently suffered from new-onset AF (P = 0.02).</AbstractText>Failure to CRT is associated with new-onset AF. Total atrial activation time may be a parameter to predict response in AF patients.</AbstractText> |
7,838 | Atrial fibrillation in patients with Brugada syndrome relationships of gene mutation, electrophysiology, and clinical backgrounds. | The goal of our work was to examine the relationships of atrial fibrillation (AF) with genetic, clinical, and electrophysiological backgrounds in Brugada syndrome (BrS).</AbstractText>Atrial fibrillation is often observed in patients with BrS and indicates that electrical abnormality might exist in the atrium as well as in the ventricle. SCN5A, a gene encoding the cardiac sodium channel, has been reported to be causally related to BrS. However, little is known about the relationships of atrial arrhythmias with genetic, clinical, and electrophysiological backgrounds of BrS.</AbstractText>Seventy-three BrS patients (49 +/- 12 years of age, men/women = 72/1) were studied. The existence of SCN5A mutation and clinical variables (syncopal episode, documented ventricular fibrillation [VF], and family history of sudden death) were compared with spontaneous AF episodes. Genetic and clinical variables were also compared with electrophysiologic (EP) parameters: atrial refractory period, interatrial conduction time (CT), repetitive atrial firing, and AF induction by atrial extra-stimulus testing.</AbstractText>Spontaneous AF occurred in 10 (13.7%) of the BrS patients and SCN5A mutation was detected in 15 patients. Spontaneous AF was associated with higher incidence of syncopal episodes (60.0% vs. 22.2%, p < 0.03) and documented VF (40.0% vs. 14.3%, p < 0.05). SCN5A mutation was associated with prolonged CT (p < 0.03) and AF induction (p < 0.05) in EP study, but not related to the spontaneous AF episode and other clinical variables. In patients with documented VF, higher incidence of spontaneous AF (30.8% vs. 10.0%, p < 0.05), AF induction (53.8% vs. 20.0%, p < 0.03), and prolonged CT was observed.</AbstractText>Spontaneous AF and VF are closely linked clinically and electrophysiologically in BrS patients. Patients with spontaneous AF have more severe clinical backgrounds in BrS. SCN5A mutation is associated with electrical abnormality but not disease severity.</AbstractText> |
7,839 | Ventricular repolarization restitution properties in patients exhibiting type 1 Brugada electrocardiogram with and without inducible ventricular fibrillation. | This study aimed to elucidate the contribution of the repolarization restitution property to the sustained ventricular fibrillation (VF) in Brugada syndrome.</AbstractText>Although phase 2 re-entry develops as the trigger of VF, the other precipitating factors have remained unclear.</AbstractText>Twenty-one patients with a type 1 Brugada electrocardiogram underwent programmed electrical stimulation. Before the VF induction, single extrastimuli were delivered at 3 basic drive cycle lengths (BCLs) (400 ms, 600 ms, and 750 ms) from the right ventricular apex (RVA) and outflow tract (RVOT), and the activation recovery interval (ARI) was measured at 5-mm vicinity of the pacing site. The maximum ARI restitution slope was determined using the overlapping least-squares linear segments.</AbstractText>We found that VF was inducible in 10 patients. A repeated-measure analysis of variance revealed that the slope in the RVA was steeper in patients with inducible VF than in those without but that in the RVOT was similar. The slope was steeper at longer BCLs and also steeper in the RVA than RVOT at BCLs of 600 and 750 ms. In patients with inducible VF, the percentage of patients exhibiting a slope >1 was 0%, 20%, and 75% in the RVA and 0%, 0%, and 14% in the RVOT at BCLs of 400 ms, 600 ms, and 750 ms, respectively. No patients without inducible VF had a slope >1.</AbstractText>These results suggest the repolarization restitution property is a contributing factor to the propensity for VF in Brugada syndrome and, regarding this property, the RVA plays more important role than the RVOT.</AbstractText> |
7,840 | Atrial fibrillation and Brugada syndrome. | Brugada syndrome is characterized by right bundle branch block pattern with ST-segment elevation in leads V(1) to V(3) and a propensity for sudden cardiac death due to ventricular arrhythmias. The arrhythmogenic substrate in Brugada syndrome may not be restricted to the ventricles, and atrial arrhythmias are being increasingly reported. Incidences of spontaneous atrial arrhythmias vary from 6% to 38% and those of inducible atrial arrhythmias from 3% to 100%. Atrial fibrillation (AF) is the most common atrial arrhythmia found in Brugada syndrome. Enhanced duration of atrial action potential and increased intra-atrial conduction time may contribute to the genesis of atrial arrhythmias in Brugada syndrome. Atrial arrhythmias are an important cause of inappropriate discharge of implantable defibrillators in patients with Brugada syndrome. Hence, implantation of dual-chamber defibrillators and careful programming of single-chamber devices have been recommended. Atrial fibrillation has been associated with mutations in both the sodium and calcium channels of the heart, as well as with cases of Brugada syndrome that could not genotyped to any of the known genes associated with the disease. This observation suggests that the substrate responsible for the development of ventricular arrhythmias also may contribute to arrhythmogenesis in the atria of the heart. The presence of a prominent transient outward current in atria and the observation that episodes of AF are triggered by closely coupled atrial extrasystoles point to the possibility that a substrate similar to that responsible for ventricular arrhythmogenesis underlies the development of AF in patients with Brugada syndrome. |
7,841 | Early and late survival after surgical revascularization for ischemic ventricular fibrillation/tachycardia. | Ischemic ventricular fibrillation/tachycardia (VF/VT) treated by myocardial revascularization, often with an implanted cardioverter defibrillator, prevents sudden cardiac death. Early series have suggested that recurrent VF/VT threatens survival even after treatment. As late outcome is unknown, we sought to determine if the early survival benefit is sustained.</AbstractText>From January 1999 through January 2007, 93 consecutive patients (75 male, 81%) presented with ischemic VF/VT; 21% survived cardiac arrest and underwent coronary artery bypass graft surgery at our institution. We analyzed their early and late survival.</AbstractText>Median age was 66 years (range, 44 to 88). Clinical presentation included class III/IV angina (46%), controlled heart failure (43%), prior myocardial infarction (68%), left ventricular ejection fraction less than 0.30 (23%) and 0.30 to 0.50 (35%), left main stem disease (24%), and triple-vessel disease (67%). Surgical revascularization, mostly nonelective (urgent 73%, emergency 7%), was combined with aortic valve replacement in 5 patients and left ventricular pseudoaneurysm repair in 3. Ischemic territories and mean number of diseased coronaries (2.6) corresponded to the grafted territories and average number of grafts (2.5). Operative mortality was 6.5% (n = 6, median EuroSCORE [European System for Cardiac Operative Risk Evaluation] predicted mortality 9). Recurrent VF/VT occurred early postoperatively in 21 patients (24%). All patients had electrophysiologic studies postoperatively and 40% received an implanted cardioverter defibrillator. Of 12 late deaths (16%) at follow-up extending to 8 years, 4 (33%) were due to cardiac causes. Five-year survival was 88%, equivalent to that (83% to 85%) reported for patients with sinus rhythm preoperatively.</AbstractText>Complete myocardial revascularization for ischemic VF/VT yields excellent early and late results; 5-year survival is comparable to that of patients with preoperative sinus rhythm.</AbstractText> |
7,842 | [Arrhythmias in patients with obstructive sleep apnea]. | The authors summarize the current knowledge on the types, prevalence, reasons, diagnosis and current therapy of arrhythmias occurring in patients with obstructive sleep apnea. Most of the patients with obstructive sleep apnea have nocturnal bradycardia (5-50%), paroxysmal tachyarrhythmia (atrial 35%; ventricular 0-15%), or both. The frequency of rhythm disturbances associated with the severity of the sleeping disorder. It is important to recognize the factors predisposing to arrhythmias and the early appropriate therapy of patients is essential, in order to protect patients from life threatening arrhythmias which may worsen the clinical outcome. |
7,843 | Chronic heart failure, selected risk factors and co-morbidities among adults treated for hypertension in a cardiac referral hospital in Cameroon. | Information on clinical characteristics of heart failure (HF) among Africans with hypertension is needed to help define the burden of hypertension in this population, but currently there is little data available.</AbstractText>To determine the clinical characteristics of HF, related risk factors and co-morbidities among adult Cameroonians treated for hypertension.</AbstractText>Medical files of 1218 patients with hypertension followed at the cardiac clinic of Yaounde General Hospital were evaluated over a 10-year period from 1995 to 2005. One hundred and forty (11.5%) patients with clinical HF or asymptomatic left ventricular dysfunction were included in the present analysis. Ages ranged from 26 to 84 years (mean 54.9 years) and 86 (61.4%) were men. Systolic dysfunction and isolated diastolic HF were found in 64% and 23% of patients, respectively. Seventy nine (56.4%) patients had at least one co-morbidity and 43 (30.7%) had multiple co-morbidities. Co-morbidities included: renal impairment (24.3%), overweight and obesity (20.7%), chronic obstructive pulmonary disease (17.1%), gout (16.4%), anaemia (15.7), diabetes mellitus (13.5%), atrial fibrillation (12.9%), stroke (9.3%), and ischaemic heart disease (5.7%).</AbstractText>HF is frequent among Cameroonian patients treated for hypertension and is regularly associated with co-morbidities. Efforts are needed to improve the control of hypertension and enhance early detection of these co-morbidities in this context.</AbstractText> |
7,844 | Overexpression of junctate induces cardiac hypertrophy and arrhythmia via altered calcium handling. | Junctate-1 is a newly identified integral endoplasmic/sarcoplasmic reticulum Ca2+ binding protein. However, its functional role in the heart is unknown. In the present study, the consequences of constitutively overexpressed junctate in cardiomyocytes were investigated using transgenic (TG) mice overexpressing junctate-1. TG mice (8 weeks old) showed cardiac remodeling such as marked bi-atrial enlargement with intra-atrial thrombus and biventricular hypertrophy. The TG mice also showed bradycardia with atrial fibrillation, reduced amplitude and elongated decay time of Ca2+ transients, increased L-type Ca2+ current and prolonged action potential durations. Time-course study (2-8 weeks) showed an initially reduced SR function due to down-regulation of SERCA2 and calsequestrin followed by sarcolemmal protein expression and cardiac hypertrophy at later age. These sequential changes could well be correlated with the physiological changes. Adrenergic agonist treatment and subsequent biochemical study showed that junctate-1 TG mice (8 weeks old) were under local PKA signaling that could cause increased L-type Ca2+ current and reduced SR function. Junctate-1 in the heart is closely linked to the homeostasis of E-C coupling proteins and a sustained increase of junctate-1 expression leads to a severe cardiac remodeling and arrhythmias. |
7,845 | Electromagnetic interference produced by a hearing aid device on electrocardiogram recording. | An 85-year-old male was implanted with a single-chamber permanent pacemaker because of atrial fibrillation with slow ventricular response. The patient had a chronic hearing impairment and decided to buy a hearing aid device. The MyLink device (MyLink, Phonak, Stafa, Switzerland) is a multifrequency FM transmitter/receiver (169.40-176.00 MHz and 214.00-220.00 MHz) with a neck-loop antenna that is designed to be used in combination with a second FM transmitter, which detects sound, produced by an audio source or person, and transmits this information to the MyLink wearer. These transmissions are subsequently converted by the MyLink and sent to the patient's existing hearing aids wirelessly. Given the proximity of the receiver to the left-sided pacemaker pocket, a concern about possible interaction was brought to our attention. Normal functioning of the pacemaker was observed during the test. However, potent electromagnetic interference on electrocardiogram (ECG) recording was induced when the MyLink loop antenna was placed on top or near the ECG electrodes. |
7,846 | The current prevalence of sleep disordered breathing in congestive heart failure patients treated with beta-blockers. | Although sleep disordered breathing is thought to be common in patients with systolic heart failure, prior studies are difficult to interpret due to a variety of factors including small sample sizes, referral bias to sleep laboratories among participants, lack of modern medical therapy for congestive heart failure, and the failure to use modern techniques to assess breathing such as nasal pressure. Our objective was to determine the current prevalence of sleep disordered breathing in a state-of-the-art congestive heart failure clinic.</AbstractText>We conducted a prospective study of consecutive patients who visited our heart failure clinic to assess the prevalence of sleep apnea in all eligible patients on maximal medical therapy. We used 4-channel recording equipment and modified Chicago criteria for scoring respiratory events (using heart rate response as a surrogate for arousal from sleep).</AbstractText>We observed that among the 108 participants, 61% had some form of sleep disordered breathing (31% central apnea with Cheyne Stokes respiration and 30% obstructive sleep apnea). Sleep disordered breathing was significantly associated with atrial fibrillation (OR = 11.56, p = 0.02) and worse functional heart failure class (OR = 2.77, p = 0.02), after adjusting for male sex, age over 60 years, body mass index, and left ventricular ejection fraction.</AbstractText>We conclude that both obstructive and central sleep apnea remain common in congestive heart failure patients despite advances in medical therapy, and that the previously reported high prevalence values are unlikely to be explained by referral bias or participation bias in prior studies. These data have important clinical implications for practitioners providing CHE therapy.</AbstractText> |
7,847 | Ablation of atrial fibrillation in patients with heart failure: reversal of atrial and ventricular remodelling. | The management of patients with heart failure and atrial fibrillation (AF) is a medical challenge, especially in the case of patients in whom sinus rhythm or rate control cannot be achieved with optimal pharmaceutical treatment.</AbstractText>Thirteen consecutive patients (11 men and 2 women, 35-70 years old, median age 55 +/- 23 years) with heart failure (NYHA I-IV, median ejection fraction 35 +/- 5%, range 25-40%) and symptomatic persistent (10 patients, 76.9%) or permanent (3 patients, 23.1%) AF, underwent circumferential ablation using a system of electroanatomic mapping with contact. Circumferential ablation, encircling the pulmonary veins in pairs, and linear ablation between the left and right superior pulmonary vein and along the mitral isthmus were performed. Follow up included 24-hour Holter monitoring and transthoracic echocardiogram at 1, 3, 6, 9 and 12 months.</AbstractText>Eight patients (62%) remained in sinus rhythm at the end of the follow up and had achieved a statistically significant improvement in ejection fraction (from 37.5 8.75% to 60.0 +/- 3.75%, p = 0.011), reduction of left ventricular end-diastolic diameter (from 63.0 +/- 3.25 mm to 56.5 +/- 1.75 mm, p = 0.011) and reduction of left atrial diameter (from 49.0 +/- 5.5 mm to 44.5 +/- 4.25 mm, p = 0.011). In contrast, patients with relapse of AF had none of the above changes (p > 0.05). Prognostic indexes of AF recurrence appeared to be the failure to improve ejection fraction (p = 0.003), non-reversal of left ventricular (p = 0.002) and left atrial (p = 0.006) remodelling, a shorter energy application time (p = 0.030) and the presence of coronary artery disease (p = 0.035). None of the patients suffered any complication from the procedure.</AbstractText>AF ablation in selected patients with heart failure and low ejection fraction is a relatively effective method of maintaining sinus rhythm, improving left ventricular systolic function and reversing atrial and ventricular remodelling.</AbstractText> |
7,848 | Effects of chronic exercise on myocardial refractoriness: a study on isolated rabbit heart. | To determine whether chronic physical training increases atrial and ventricular refractoriness in isolated rabbit heart.</AbstractText>Trained rabbits were submitted to a protocol of treadmill running. The electrophysiological parameters of refractoriness investigated in an isolated heart preparation were: (1) atrial effective refractory period (AERP) and atrial functional refractory period and ventricular effective and functional refractory periods (VERP and VFRP) using the extrastimulus technique at four different pacing cycle lengths; (2) the dominant frequency (DF) of ventricular fibrillation (VF). A multi-electrode plaque containing 256 electrodes and a spectral method were used to obtain the mean, maximum and minimum DF of VF. Sinus cycle length of the isolated hearts was determined as an electrophysiological parameter of training. In vivo heart rate, myocardial heat shock proteins (HSP60) and inducible nitric oxide synthase were also determined in some animals as electrophysiological and biochemical markers of training respectively.</AbstractText>VERP and VFRP were longer in the trained group than in the control group. The mean DF of VF was lower in the trained group than in the control group. Despite the fact that training did not significantly modify the AERP, it tended to be longer in the trained group (P = 0.09).</AbstractText>Training seems to increase the electrical stability of ventricular myocardium. As the electrophysiological modifications were exhibited in hearts not submitted to extrinsic nervous system or humoral influences, they are, at least in part, intrinsic modifications. These electrophysiological data also suggest that training could protect against reentrant ventricular arrhythmias.</AbstractText> |
7,849 | [Vasopressin for treatment of hemodynamic disorders]. | Vasopressin is a 9-amino acid peptide synthesized by magnocellular neurons of the hypothalamus and released from posterior pituitary gland. The primary physiological role of vasopressin is the maintenance of fluid homeostasis. In this review, the classification of vasopressin receptors, namely V1 vascular, V2 renal, V3 pituitary, oxytocin receptors, and purinergic receptors, and the effects of vasopressin on vascular smooth muscles, the heart, and the kidneys are discussed. Mortality rates of vasodilatory (or distributive), for example septic shock, are high. The use of vasopressin is an alternative therapy for vasodilatory shock with better outcome. Vasopressin is effective in resuscitation of adults after ventricular fibrillation or pulseless tachycardia, when epinephrine is not effective. |
7,850 | [Right ventricular desynchronization in patients with pacemaker syndrome]. | To observe the incidence of ventricular desynchronization in patients with or without pacemaker syndrome (PMS).</AbstractText>The systolic peak velocity, the acceleration and the time to peak velocity of the interventricular septum (IVS), left ventricular (LV) and right ventricular (RV) lateral wall were detected by tissue Doppler imaging (TDI) in 14 atrial fibrillation patients without pacemaker implantation (control), 18 atrial fibrillation patients without PMS and 16 atrial fibrillation patients with PMS. All patients were free of valve disease, myocardial infarction, severe pulmonary hypertension, low left ventricular eject fraction (< or = 50%), significant segmental hypokinesis of ventricular wall or complete bundle branch block.</AbstractText>Compared to the control patients, the systolic peak velocity and the accelerations on lateral walls of the LV and RV reduced significantly in patients with implanted pacemakers (P < 0.05). The intervals to peak velocity of the IVS and LV lateral walls were significantly prolonged [PMS group (80.13 +/- 26.92) ms vs. (25.60 +/- 4.30) ms, P < 0.01; without PMS group (76.22 +/- 23.32) ms vs. (25.60 +/- 4.30) ms, P < 0.01] and the intervals to peak velocity of the IVS and RV lateral walls significantly shortened [PMS group (16.33 +/- 6.85) ms vs. (40.70 +/- 7.60) ms, P < 0.01; without PMS group (21.20 +/- 7.34) ms vs. (40.70 +/- 7.60) ms, P < 0.01]. The systolic peak velocities, the accelerations of the IVS and bilateral walls and the intervals to peak velocity of the IVS and LV lateral wall were similar in patients with and without PMS (P > 0.05), however, the intervals to peak velocity of the IVS and RV lateral wall was significant shorter in patients with PMS compared to that of patients without PMS [(16.33 +/- 6.85) ms vs. (21.20 +/- 7.34) ms, P < 0.01].</AbstractText>RV desynchronization but not LV desynchronization might play an important role in patients with PMS.</AbstractText> |
7,851 | [Factors associated with efficacy of cardiac resynchronization therapy for patients with congestive heart failure]. | The efficacy of cardiac resynchronization therapy (CRT) in patients with congestive heart failure and the potential factors associated with responder or nonresponder were investigated.</AbstractText>Fifty three patients with congestive heart failure (42 with sinus rhythm and 11 with atrial fibrillation) underwent CRT were enrolled in this study. Conventional echocardiography and tissue Doppler imaging were performed in each patient before implantation and 6 month post implantation. Clinical response was defined as improvement of one NYHA functional class and echocardiographic response was defined as a reduction in LV end-systolic volume by > 15% or an increase of absolute value of LVEF > 5%.</AbstractText>The clinical response rate was 75% and echocardiographic response rate was 69.8% during 6 month follow-up. The echocardiographic response rate for patients with atrial fibrillation was lower than that for patients with sinus rhythm (45.5% vs. 76.2%, P < 0.05). In patients with sinus rhythm, higher response rate was seen in patients with widen QRS duration, lower pulmonary systolic pressure and prolonged left ventricular pre-ejection time (LVPT) while response rate was not affected by LVEF, left ventricular volume, NYHA functional class and intra-ventricular dyssynchrony.</AbstractText>Response rate to CRT was lower in patients with atrial fibrillation compared to patients with sinus rhythm. In patients with sinus rhythm, QRS duration, LVPT and pulmonary systolic pressure were useful parameters to predict the response to CRT.</AbstractText> |
7,852 | [Efficacy of cardiac resynchronization therapy-defibrillator for treating patients with chronic heart disease]. | To observed the clinical efficacy of cardiac resynchronization therapy-defibrillator (CRT-D) in selected patients with chronic heart failure one year after implantation.</AbstractText>Seventeen patients with drug-refractory heart failure received CRT-D implantation (6 patients were implanted with InSync Sentry). The underlying heart diseases were dilated cardiomyopathy in 12 patients and ischemic heart disease in 5 patients. There were 13 patients with a history of ventricular tachycardia/ventricular fibrillation.</AbstractText>CRT-D were successfully implanted in all patients without complication. The mean left ventricular pacing threshold was 1.6 V. The defibrillation threshold was no more than 20 J. During a mean follow-up of 13 months, no death occurred and LV function was improved. The shock induced by ventricular tachycardia was delivered in 5 patients and alarming due to heart failure occurred twice in 1 patient.</AbstractText>The implantation of CRT-D for treating refractory heart failure patients is feasible and safe. The application of CRT-D was associated with an improved cardiac function and a reduced risk of sudden cardiac death.</AbstractText> |
7,853 | A case of appropriate inappropriate device therapy: hyperkalemia-induced ventricular oversensing. | The present case describes a patient who received inappropriate, but potentially life-saving, therapy from her implantable cardioverter defibrillator (ICD) in the setting of acute hyperkalemia (plasma potassium concentration = 8 mM). Hyperkalemia was associated with the development of a slow sinusoidal ventricular tachycardia, at a rate of 100 beats/min to 125 beats/min (610 ms to 480 ms) in a patient who is pacemaker-dependent. There was associated fractionation of the ICD electrogram and T wave oversensing, leading to ventricular oversensing with resultant detection in the ventricular fibrillation rate zone. This was followed by shock therapy, even though the ventricular tachycardia rate was below the programmed detection rate of the ICD. The subsequent emergency treatment of the hyperkalemia normalized the electrogram, corrected the ventricular oversensing and arrhythmia, and restored rate-adaptive single-chamber ventricular pacing.</Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Oudit</LastName><ForeName>Gavin Y</ForeName><Initials>GY</Initials><AffiliationInfo><Affiliation>Division of Cardiology, Toronto General Hospital, University of Toronto, Ontario. gavin.oudit@utoronto.ca</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cameron</LastName><ForeName>Doug</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Harris</LastName><ForeName>Louise</ForeName><Initials>L</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D002363">Case Reports</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Can J Cardiol</MedlineTA><NlmUniqueID>8510280</NlmUniqueID><ISSNLinking>0828-282X</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D017147" MajorTopicYN="Y">Defibrillators, Implantable</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004562" MajorTopicYN="N">Electrocardiography</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006947" MajorTopicYN="N">Hyperkalemia</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="Y">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013616" MajorTopicYN="N">Tachycardia, Sinus</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="Y">etiology</QualifierName><QualifierName UI="Q000628" MajorTopicYN="Y">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016896" MajorTopicYN="N">Treatment Outcome</DescriptorName></MeshHeading></MeshHeadingList><OtherAbstract Type="Publisher" Language="fre">Le présent cas décrit une patiente qui a reçu un traitement inapproprié, mais qui lui a peut-être sauvé la vie, déclenché par son défibrillateur à synchronisation automatique (DSA) en raison d’une hyperkaliémie aiguë (concentration de potassium plasmatique = 8 mM). L’hyperkaliémie s’associait au développement d’une lente tachycardie ventriculaire sinusoïdale, à un taux de 100 battements/minute à 125 battements/minute (610 ms à 480 ms) chez une patiente dépendante d’un stimulateur. Un fractionnement de l’électrogramme du DSA et une surdétection des ondes T en ont découlé, ce qui a provoqué une surdétection ventriculaire à un taux dans la zone de fibrillation ventriculaire. Un traitement de choc s’est ensuivi, même si le taux de tachycardie ventriculaire était inférieur au taux de détection programmé du DSA. Le traitement d’urgence subséquent de l’hyperkaliémie a normalisé l’électrogramme, corrigé la surdétection ventriculaire et l’arythmie et rétabli la stimulation ventriculaire monochambre à fréquence asservie. |
7,854 | Influence of atrial fibrillation on plasma von willebrand factor, soluble E-selectin, and N-terminal pro B-type natriuretic peptide levels in systolic heart failure. | Endothelial dysfunction is present in patients with heart failure (HF) due to left ventricular systolic dysfunction, as well as in patients with atrial fibrillation (AF) who have normal cardiac function. It is unknown whether AF influences the degree of endothelial dysfunction in patients with systolic HF.</AbstractText>We measured levels of plasma von Willebrand factor (vWF) and E-selectin (as indexes of endothelial damage/dysfunction and endothelial activation, respectively; both enzyme-linked immunosorbent assay) in patients with AF and HF (AF-HF), who were compared to patients with sinus rhythm and HF (SR-HF), as well as in age-matched, healthy, control subjects. We also assessed the relationship of vWF and E-selectin to plasma N-terminal pro B-type natriuretic peptide (NTpro-BNP), a marker for HF severity and prognosis.</AbstractText>One hundred ninety patients (73% men; mean age, 69.0 +/- 10.1 years [+/- SD]) with systolic HF were studied, who were compared to 117 healthy control subjects: 52 subjects (27%) were in AF, while 138 subjects (73%) were in sinus rhythm. AF-HF patients were older than SR-HF patients (p = 0.046), but left ventricular ejection fraction and New York Heart Association class were similar. There were significant differences in NT-proBNP (p < 0.0001) and plasma vWF (p = 0.003) between patients and control subjects. On Tukey post hoc analysis, AF-HF patients had significantly increased NT-proBNP (p < 0.001) and vWF (p = 0.0183) but not E-selectin (p = 0.071) levels when compared to SR-HF patients. On multivariate analysis, the presence of AF was related to plasma vWF levels (p = 0.018). Plasma vWF was also significantly correlated with NT-proBNP levels (Spearman r = 0.139; p = 0.017).</AbstractText>There is evidence of greater endothelial damage/dysfunction in AF-HF patients when compared to SR-HF patients. The clinical significance of this is unclear but may have prognostic value.</AbstractText> |
7,855 | Vasopressin and epinephrine in the treatment of cardiac arrest: an experimental study. | Epinephrine remains the drug of choice for cardiopulmonary resuscitation. The aim of the present study is to assess whether the combination of vasopressin and epinephrine, given their different mechanisms of action, provides better results than epinephrine alone in cardiopulmonary resuscitation.</AbstractText>Ventricular fibrillation was induced in 22 Landrace/Large-White piglets, which were left untreated for 8 minutes before attempted resuscitation with precordial compression, mechanical ventilation and electrical defibrillation. Animals were randomized into 2 groups during cardiopulmonary resuscitation: 11 animals who received saline as placebo (20 ml dilution, bolus) + epinephrine (0.02 mg/kg) (Epi group); and 11 animals who received vasopressin (0.4 IU/kg/20 ml dilution, bolus) + epinephrine (0.02 mg/kg) (Vaso-Epi group). Electrical defibrillation was attempted after 10 minutes of ventricular fibrillation.</AbstractText>Ten of 11 animals in the Vaso-Epi group restored spontaneous circulation in comparison to only 4 of 11 in the Epi group (p = 0.02). Aortic diastolic pressure, as well as, coronary perfusion pressure were significantly increased (p < 0.05) during cardiopulmonary resuscitation in the Vaso-Epi group.</AbstractText>The administration of vasopressin in combination with epinephrine during cardiopulmonary resuscitation results in a drastic improvement in the hemodynamic parameters necessary for the return of spontaneous circulation.</AbstractText> |
7,856 | A fatal case of venlafaxine overdose. | Based on its primary action of serotonin reuptake inhibition, venlafaxine overdose would be expected to result in serotonergic effects.</AbstractText>A 40 year old male ingested venlafaxine without co-ingestants in a suicide attempt. The patient developed refractory ventricular fibrillation and expired approximately 9 hours post-ingestion. ECG monitoring revealed significant QRS and QTC interval prolongation prior to his demise.</AbstractText>A literature review of venlafaxine overdose cases and investigation into its mechanism of action was conducted. The potential for sodium channel blockade and implications for therapy are discussed.</AbstractText> |
7,857 | [Predictive value of NT-pro-BNP for the non-cardiologist. A study on 573 hospitalized patients with cardiovascular disease]. | B-type natriuretic peptides are excellent markers of cardiac function and are strong prognostic parameters in patients with coronary heart disease and heart failure. We examined the diagnostic and prognostic value of natriuretic peptides in a heterogeneous group of patients of a cardiological university hospital.</AbstractText>NT-pro-BNP was assessed in 573 inpatients (66 % male, median age 66 years) and association with demographic and cardiological parameters, in-hospital course as well as the combined endpoint of death, heart failure hospitalization and stroke was analyzed during a median follow-up time of 1117 days.</AbstractText>NT-pro-BNP was significantly associated with age, diastolic blood pressure, renal function, previous myocardial infarction, arterial occlusive disease, atrial fibrillation, NYHA class and left-ventricular dysfunction. Differentiation of distinct cardiac diseases by NT-pro-BNP was not possible. NT-pro-BNP identified patients with a length of hospital stay of more than 12 days with a sensitivity of 88,2 % and a negative predictive value of 97 %. Supramedian NT-pro-BNP values (> 300 pg/ml) indicated a relative risk for the combined endpoint of 7,5 (95 % CI 4,1 - 13,8) compared to inframedian NT-pro-BNP values. Prognostic value of NT-pro-BNP was independent of and stronger than demographic and cardiological risk markers.</AbstractText>NT-pro-BNP is a strong and independent predictor of in-hospital course and long-term outcome in inpatients with cardiovascular disease. NT-pro-BNP assessment allows a risk-adapted patient management for non-cardiologists.</AbstractText> |
7,858 | Impact of acute renal failure following percutaneous coronary intervention on long-term mortality. | Acute renal failure (ARF) following percutaneous coronary intervention (PCI) has been shown to be associated with a worse outcome. Whether this event should be considered as a marker of disease severity or an independent contributor to mortality is still unclear.</AbstractText>In a multicenter, prospective cohort study we investigated the predictive variables and the impact of postprocedural ARF on 2-year all-cause mortality in 2860 consecutive patients (50% with stable angina and 50% with non-ST-elevation acute coronary syndromes) undergoing PCI. Serum creatinine determinations were made immediately before and 24 h after PCI. ARF was defined as an increase in serum creatinine of > or =0.5 mg/dl over baseline.</AbstractText>One hundred and six patients (3.7%) experienced ARF. At logistic regression analysis, ARF was associated with pre-existing low values of estimated glomerular filtration rate, reduced left ventricular ejection fraction, hypertension, and prior coronary bypass surgery. Mortality data at 2 years were available for all patients: 119 patients (4.16%) had died, 3.9% of those without and 11.3% of those with ARF (univariate hazard ratio 3.16; 95% confidence interval 1.68-5.94; P = 0.0004). At Cox regression analysis, the significant predictors of mortality were age, ejection fraction, preprocedural estimated glomerular filtration rate, PCI failure, atrial fibrillation, diabetes mellitus, and fluoroscopy time. In this comprehensive mortality model, ARF maintained a borderline statistical significance (hazard ratio 1.83, 95% confidence interval 0.98-3.44; P = 0.06).</AbstractText>ARF following PCI occurs almost exclusively in patients with chronic kidney disease or left ventricular dysfunction. These risk factors are also among the most powerful predictors of long-term mortality and are likely to explain most of the association between postprocedural ARF and long-term mortality. After correction for clinical determinants, however, postprocedural ARF maintains a clinically significant impact on mortality that must be taken into account for benefit vs. risk evaluation of PCI in individual patients.</AbstractText> |
7,859 | Minimally interrupted cardiac resuscitation by emergency medical services for out-of-hospital cardiac arrest. | Out-of-hospital cardiac arrest is a major public health problem.</AbstractText>To investigate whether the survival of patients with out-of-hospital cardiac arrest would improve with minimally interrupted cardiac resuscitation (MICR), an alternate emergency medical services (EMS) protocol.</AbstractText><AbstractText Label="DESIGN, SETTING, AND PATIENTS" NlmCategory="METHODS">A prospective study of survival-to-hospital discharge between January 1, 2005, and November 22, 2007. Patients with out-of-hospital cardiac arrests in 2 metropolitan cities in Arizona before and after MICR training of fire department emergency medical personnel were assessed. In a second analysis of protocol compliance, patients from the 2 metropolitan cities and 60 additional fire departments in Arizona who actually received MICR were compared with patients who did not receive MICR but received standard advanced life support.</AbstractText>Instruction for EMS personnel in MICR, an approach that includes an initial series of 200 uninterrupted chest compressions, rhythm analysis with a single shock, 200 immediate postshock chest compressions before pulse check or rhythm reanalysis, early administration of epinephrine, and delayed endotracheal intubation.</AbstractText>Survival-to-hospital discharge.</AbstractText>Among the 886 patients in the 2 metropolitan cities, survival-to-hospital discharge increased from 1.8% (4/218) before MICR training to 5.4% (36/668) after MICR training (odds ratio [OR], 3.0; 95% confidence interval [CI], 1.1-8.9). In the subgroup of 174 patients with witnessed cardiac arrest and ventricular fibrillation, survival increased from 4.7% (2/43) before MICR training to 17.6% (23/131) after MICR training (OR, 8.6; 95% CI, 1.8-42.0). In the analysis of MICR protocol compliance involving 2460 patients with cardiac arrest, survival was significantly better among patients who received MICR than those who did not (9.1% [60/661] vs 3.8% [69/1799]; OR, 2.7; 95% CI, 1.9-4.1), as well as patients with witnessed ventricular fibrillation (28.4% [40/141] vs 11.9% [46/387]; OR, 3.4; 95% CI, 2.0-5.8).</AbstractText>Survival-to-hospital discharge of patients with out-of-hospital cardiac arrest increased after implementation of MICR as an alternate EMS protocol. These results need to be confirmed in a randomized trial.</AbstractText> |
7,860 | A detector for a chronic implantable atrial tachyarrhythmia monitor. | Continuous long-term monitoring of atrial fibrillation (AF) and tachycardia (AT) is an unmet clinical need, which could be met with a chronically-implanted monitor. Improved therapeutic decisions based on accurate monitoring of parameters, such as daily AF/AT burden (hours/ day) may lead to improvements in clinical outcomes such as reduction in hospitalizations, symptoms, and strokes. This paper describes an AF/AT detector that detects AF as well as AT with an irregular ventricular response, and a supplementary AT detector for AT with more regular ventricular response. Seven databases with significant durations of AF, AT, and sinus rhythm were used to evaluate the performance of the detectors. All patient records with AF (N = 124) were detected by the AF/AT detector to have AF/AT burden with a mean, median, and 75 percentile of absolute error in burden detection of 8.8, 0, and 4 min, respectively. In patients having AF burden (= or > 10 min), the AF/AT detector was found to have burden accuracy within 20% of true burden in 96% of patients. The specificity was 94%, defined as follows: in patient records without AF/AT (N = 174), the percentage with AF/AT burden = or < 10 min in the 24-h recordings. The AF/AT detector underestimatesAT burden, thus degrading performance, in patients with significant amounts of AT with more regular ventricular response. The supplementary AT detector reduces the underestimation of AT while overestimating burden in patients without a significant amount of AT. The detectors described here could be implemented in an implantable monitor for accurate long-term AF/AT monitoring. |
7,861 | Ranolazine: a new antiarrhythmic agent for patients with non-ST-segment elevation acute coronary syndromes? | Ranolazine is a novel antianginal agent that has also been shown to have electrophysiological properties in laboratory models. This is the first clinical evaluation of the antiarrythmic effects of ranolazine.</AbstractText>To compare the incidence of cardiac arrhythmias in patients with non-ST-segment elevation acute coronary syndromes (NSTE ACS) receiving ranolazine with that in patients receiving placebo.</AbstractText>This was a subanalysis of the international, randomized, double-blind, placebo-controlled MERLIN-TIMI 36 trial, which was conducted from 8 October 2004 to 24 May 2006. Patients with NSTE ACS and at moderate to high cardiovascular risk were enrolled within 48 h of their last ischemic symptoms. A detailed description of the inclusion and exclusion criteria has previously been published. Patients were randomized to receive ranolazine (intravenous followed by oral administration) or matching placebo, alongside standard medication and interventional therapy. All patients underwent continuous electro cardiographic (cECG; Holter) monitoring for the first 7 days after randomization.</AbstractText>The primary end point was the incidence of clinically significant arrhythmia (supraventricular tachycardia >120 beats per min lasting at least four beats, ventricular tachycardia of at least three beats, ventricular pause >2.5 s, new-onset atrial fibrillation [AF], or complete heart block).</AbstractText>A total of 6,560 patients were enrolled in the trial, of whom 6,351 (97%) had interpretable cECG recordings (ranolazine = 3,162; placebo = 3,189). The baseline characteristics were similar in both groups. The mean age was 63 years and around a third of patients were female. Approximately 4% of patients in each group had a prior ventricular arrhythmia, approximately 34% in each had a prior myocardial infarction, and the majority of patients had a Thrombolysis in Myocardial Infarction (TIMI) risk score of 3−4. The median time from symptom onset to randomization was 23.9 h in the ranolazine group and 23.3 h in the placebo group. Overall, the mean duration of cECG monitoring was 6.8 days, after which time significantly fewer patients in the ranolazine group than in the placebo group had experienced ventricular tachycardia lasting for more than three (52.1% vs 60.6%, risk ratio [RR] 0.86, 95% CI 0.82−0.90; P</i> <0.001), four (20.9% vs 29.5%, RR 0.71, 95% CI 0.60−0.78; P</i> <0.001), or eight (5.3% vs 8.3%, RR 0.63, 95% CI 0.52−0.76; P</i> <0.001) beats. Similarly, ranolazine was associated with a lower incidence of supraventricular tachycardias than was placebo (44.7% vs 55.0%, RR 0.81, 95% CI 0.77−0.85; P</i> <0.001). There were only two cases of torsade de pointes, one in each group. There was also a trend towards a lower rate of new-onset AF in the ranolazine group, although the difference was not significant (P</i> = 0.08).</AbstractText>Ranolazine is associated with reduced incidences of ventricular and supraventricular arrhythmia in moderate-to-high-risk patients with NSTE ACS.</AbstractText> |
7,862 | MURC, a muscle-restricted coiled-coil protein that modulates the Rho/ROCK pathway, induces cardiac dysfunction and conduction disturbance. | We identified a novel muscle-restricted putative coiled-coil protein, MURC, which is evolutionarily conserved from frog to human. MURC was localized to the cytoplasm with accumulation in the Z-line of the sarcomere in the murine adult heart. MURC mRNA expression in the heart increased during the developmental process from the embryonic stage to adulthood. In response to pressure overload, MURC mRNA expression increased in the hypertrophied heart. Using the yeast two-hybrid system, we identified the serum deprivation response (SDPR) protein, a phosphatidylserine-binding protein, as a MURC-binding protein. MURC induced activation of the RhoA/ROCK pathway, which modulated serum response factor-mediated atrial natriuretic peptide (ANP) expression and myofibrillar organization. SDPR augmented MURC-induced transactivation of the ANP promoter in cardiomyocytes, and RNA interference of SDPR attenuated the action of MURC on the ANP promoter. Transgenic mice expressing cardiac-specific MURC (Tg-MURC) exhibited cardiac contractile dysfunction and atrioventricular (AV) conduction disturbances with atrial chamber enlargement, reduced thickness of the ventricular wall, and interstitial fibrosis. Spontaneous episodes of atrial fibrillation and AV block were observed in Tg-MURC mice. These findings indicate that MURC modulates RhoA signaling and that MURC plays an important role in the development of cardiac dysfunction and conduction disturbance with increased vulnerability to atrial arrhythmias. |
7,863 | BNP and NT-proBNP predict echocardiographic severity of diastolic dysfunction. | To evaluate the best combination of clinical parameters and brain natriuretic peptide (BNP) or N-terminal pro-BNP (NT-proBNP), to predict diastolic dysfunction (DD) in heart failure with preserved left ventricular ejection fraction (HF-PLEF) as determined by Doppler-echocardiography.</AbstractText>HF patients with EF >40% in the CHARM Echocardiographic Substudy were included and classified to have normal diastolic function, or mild, moderate or severe diastolic dysfunction. Plasma BNP and NT-proBNP levels were measured and relevant clinical characteristics recorded. 181 participants were included in this analysis, 72 (40%) had moderate to severe DD. A model including age, sex, BNP, body mass index, history of atrial fibrillation, coronary artery disease, diabetes mellitus, hypertension and left atrial volume was highly predictive of moderate to severe DD; AUC 0.81 (0.73-0.88; p<0.0001). Similarly, substitution of BNP with NT-proBNP resulted in an AUC 0.79 (0.72-0.87; p<0.0001). In these models; BNP>100 pg/ml (OR 6.24 CI 2.42-16.09, p=0.0002), history of diabetes (OR 3.52 CI 1.43-8.70, p=0.006) and NT-proBNP >600 pg/ml (OR 5.93 CI 2.21-15.92, p=0.0004), history of diabetes mellitus (OR 2.75 CI 1.12-6.76, p=0.03) respectively remained independent predictors of DD in HF-PLEF.</AbstractText>Natriuretic peptides were the strongest independent predictors of DD, as determined by Doppler-echocardiography, in HF-PLEF.</AbstractText> |
7,864 | New concepts in understanding and modulating atrial repolarisation in patients with atrial fibrillation. | Atrial fibrillation is the most frequent cardiac arrhythmia in clinical practice. Although much has been learned, the underlying mechanisms are incompletely understood. Clinically used antiarrhythmic drugs are limited in their efficacy to terminate atrial fibrillation or to maintain sinus rhythm and were associated with substantial toxicity including life-threatening ventricular arrhythmias. Novel therapeutic approaches suggest targeting of atrium-selective ion channels and pathology-specific alterations in atrial repolarisation and arrhythmogenesis as promising drug targets for patients with atrial fibrillation. This article focuses on novel aspects of altered atrial repolarisation and discusses atrium-selective (I(Kur), I(K,ACh)) and pathology-specific (I(K,ACh)) ion channels as potential targets for safe and effective treatment of atrial fibrillation. |
7,865 | [Avoidance of ventricular pacing in patients with sinus node disease or intermittent AV block]. | In patients with frequent right ventricular stimulation, worsening of heart failure and atrial fibrillation may occur. Avoidance of unnecessary right ventricular pacing is a major requirement for pacemaker selection and programming in patients with sinus node disease or intermittent AV block. In dual chamber pacemakers this goal can be achieved by programming a long AV delay or an AV delay hysteresis. Algorithms that allow AAI pacing in a dual chamber pacing mode and change to DDD mode in case of high degree AV block are a new attempt to avoid unnecessary right ventricular pacing. The article describes various strategies to avoid unnecessary ventricular pacing and discusses their advantages and disadvantages. |
7,866 | Electrical restitution determined by epicardial contact mapping and surface electrocardiogram: its role in ventricular fibrillation inducibility in swine. | The roles of electrical restitution determined by epicardial contact mapping and surface electrocardiogram (ECG) in the inducibility of ventricular fibrillation (VF) were evaluated.</AbstractText>Ten epicardial unipolar electrograms using contact mapping and the surface ECGs were simultaneously recorded in 7 swine. Activation-recovery interval (ARI) and QT-interval restitution curves were constructed. Steady-state pacing protocol was performed to induce VF. Ventricular fibrillation threshold was defined as the longest pacing interval for inducing VF. Statistical correlation analysis was performed to determine the relationship between local ARI restitutions, QT-interval restitution, and ventricular fibrillation threshold.</AbstractText>One hundred thirteen restitution curves were constructed (50 in left ventricular sites, 52 in right ventricular sites, and 11 in surface ECG lead II) from 11 steady-state pacing procedures. Statistical correlation between the slopes of the QT restitution curve and the slopes of regional ARI restitution curves was noted in several mapping sites. Ventricular fibrillation threshold significantly related to the local ARI restitution curve slope for the right ventricular apex (R = 0.752, P = .019) and the QT-interval restitution curve slope (R = 0.802, P = .005).</AbstractText>There is a significant correlation between the local ARI restitutions and the QT-interval restitutions, both of which were associated with VF inducibility.</AbstractText> |
7,867 | Antiarrhythmic effects of growth hormone--in vivo evidence from small-animal models of acute myocardial infarction and invasive electrophysiology. | A growing body of evidence suggests a possible role for growth hormone (GH) in the treatment of congestive heart failure (CHF) and myocardial infarction (MI). The aim of this study was to investigate in vivo the effects of GH treatment on incidence and severity of ventricular arrhythmias normal and MI rats.</AbstractText>Male Sprague-Dawley rats weighing approximately 350 g were randomized into 3 groups. Growth hormone-treated rats (n = 6) received 6 mg/kg of human GH. The placebo group (n = 10) received 1 mL of saline. Amiodarone-treated rats (n = 10) were injected with 25 mg/kg and served as positive controls. All animals received a single intraperitoneal injection 6 hours before induction of MI. Myocardial infarction was induced by ligation of the left coronary artery, resulting in a large (approximately 40%) anterolateral MI. A computerized electrocardiographic tracing was obtained continuously before induction of MI and up to 1 hour postinfarction. Invasive hemodynamics including intraventricular and arterial pressure were registered for 60 minutes post-MI. Qualitative as well as quantitative variables of ventricular arrhythmias were analyzed. Invasive electrophysiology with pacing in right atrium and ventricle was performed in normal rats (control, n = 13; GH, n = 6; amiodarone, n = 6) to asses inducibility of supraventricular and ventricular arrhythmias.</AbstractText>Growth hormone- and amiodarone-treated rats had lower resting heart rate at baseline before induction of MI. The arrhythmia scores in the GH- (3.8 +/- 1) and amiodarone-treated (3.9 +/- 0.5) animals were significant lower than in the placebo group (5.9 +/- 0.5, P < .05). There was no significant difference in arrhythmia score between the GH and amiodarone groups. The incident of inducible ventricular arrhythmias was lower in the GH (2/6, 33%) and amiodarone (2/6, 33%) groups compared with controls (13/16, 81%; P = .05). There was no difference in inducibility of atrial fibrillation between the GH (5/6, 83%) and control (13/14, 93%) groups, whereas the inducibility of atrial fibrillation was significantly lower in the amiodarone group (2/6, 33%; P < .05).</AbstractText>Pretreatment with GH reduces the burden of ventricular arrhythmias in rats with postinfarction CHF due to acute MI. Growth hormone may be useful in the treatment of CHF and acute MI.</AbstractText> |
7,868 | Persistent atrial fibrillation worsens heart rate variability, activity and heart rate, as shown by a continuous monitoring by implantable biventricular pacemakers in heart failure patients. | Atrial fibrillation (AF) induces loss of atrial contribution, heart rate irregularity, and fast ventricular rate.</AbstractText>The objectives of the study were to accurately measure AF incidence and to investigate the mutual temporal patterns of AF and heart failure (HF) in patients indicated to cardiac resynchronization therapy.</AbstractText>Four hundred ten consecutive patients (70% male, age 69 +/- 11) with advanced HF (NYHA = 3.0 +/- 0.6), low ejection fraction (EF = 27 +/- 9%), and ventricular conduction delay (QRS = 165 +/- 29 ms) received a biventricular pacemaker. Enrolled patients were divided into two groups: G1 = 249 patients with no AF history, G2 = 161 patients with history of paroxysmal/persistent AF.</AbstractText>In a median follow-up of 13 months, AF episodes longer than 5 minutes occurred in 105 of 249 (42.2%) G1 patients and 76 of 161 (47.2%) G2 patients, while AF episodes longer than one day occurred in 14 of 249 (5.6%) G1 patients and in 36 of 161 (22.4%) G2 patients. Device diagnostics monitored daily values of patient activity, night heart rate (NHR), and heart rate variability (HRV). Comparing 30-day periods before AF onset and during persistent AF, significant (P < 0.0001) changes were observed in patient activity, which decreased from 221 +/- 13 to 162 +/- 12 minutes, and in NHR, which increased from 68 +/- 3 to 94 +/- 7 bpm. HRV significantly decreased (from 75 +/- 5 ms before AF onset to 60 +/- 6 ms after AF termination). NHR during AF was significantly (P < 0.01) and inversely correlated (R(2)= 0.73) with activity, with a significant lower activity associated with NHR >or= 88 bpm.</AbstractText>AF is frequent in HF patients. Persistent AF is associated with statistically significant decrease in patient activity and HRV and NHR increase.</AbstractText> |
7,869 | The role of surface ECG and transthoracic echocardiography for predicting postoperative atrial fibrillation after coronary artery bypass surgery. | To evaluate the roles of surface electrocardiogram (ECG) and transthoracic echocardiography (ECHO) for prediction of atrial fibrillation (AF) after coronary artery bypass grafting (CABG).</AbstractText>This study was conducted from 2002-2004 at the Cardiovascular Department of Hacettepe University, Ankara, Turkey. Seventy consecutive patients were enrolled in this study that underwent elective CABG. A 12-lead ECG was recorded one day before cardiac surgery and was repeated during the 5 days after CABG. P-wave dispersion (PWD) was defined as the difference between maximum and minimum P-wave duration. Differences in P-wave duration were compared between the pre- and postoperative 12-lead ECG measurements.</AbstractText>Postoperative AF developed in 17 (24%) cases of 70 patients. The PWD was found to be significantly higher in patients with AF preoperatively (60+/-19 versus 47+/-13, p=0.003), postoperative first day (56+/-12 versus 44+/-11, p<0.002) and fifth day (51+/-29 versus 41+/-11, p<0.001). Patients with AF were significantly older, the mean age of the AF group was (68+/-7) years and of the sinus rhythm (SR) group was (59+/-10 years) (p<0.001). The AF group had left ventricular systolic dysfunction (56+/-13% versus 56+/-8%, p=0.042, preoperatively; 49+/-8% versus 60+/-10%, p=0.001, postoperatively) and a larger left atrium (46+/-5 versus 39+/-5 mm, p<0.001, preoperatively and 44+/-7 versus 39+/-5 mm, p=0.046, postoperatively) than the SR group.</AbstractText>This prospective study demonstrated that PWD on surface ECG and additional echocardiographic parameters are simple and reliable indexes to predict the development of AF after CABG.</AbstractText> |
7,870 | Association between hypertensive urgencies and subsequent cardiovascular events in patients with hypertension. | To determine whether patients with hypertensive urgency have a higher risk for subsequent cardiovascular events compared with hypertensive patients without this event.</AbstractText>Overall, 384 patients with hypertensive urgency and 295 control patients were followed up for at least 2 years. Hypertensive urgency was defined as a systolic blood pressure above 220 mmHg and/or a diastolic blood pressure above 120 mmHg without any evidence of acute end-organ damage. The control group consisted of patients admitted to the emergency department with a systolic blood pressure between 135 to 180 mmHg and a diastolic blood pressure between 85-110 mmHg. The number of cardiovascular events defined as acute coronary syndrome, acute stroke, atrial fibrillation, acute left ventricular failure and aortic aneurysm were consecutively analyzed during follow-up. The median follow-up time was 4.2 years (interquartile range 2.9-5.7 years). Twenty-six patients of the urgency group and 23 patients of the control group were lost for follow-up.</AbstractText>Overall, 117 (17%) patients had nonfatal clinical cardiovascular events and 13 had (2%) fatal cardiovascular events. The frequency of cardiovascular events was significantly higher in patients with hypertensive urgencies (88 vs. 42; P = 0.005). The Cox regression analysis identified age (P < 0.001) and hypertensive urgencies (P = 0.035) as independent predictors for subsequent cardiovascular events.</AbstractText>Hypertensive urgencies are associated with an increased risk for subsequent cardiovascular events in patients with arterial hypertension.</AbstractText> |
7,871 | Pericardial delivery of omega-3 fatty acid: a novel approach to reducing myocardial infarct sizes and arrhythmias. | Basic and clinical evidence suggests that omega-3 (n-3) polyunsaturated fatty acids (PUFAs) decrease fatal arrhythmias and infarct sizes. This study investigated if pericardial delivery of n-3 PUFAs would protect the myocardium from ischemic damages and arrhythmias. Acute myocardial infarctions were induced in 23 pigs with either 45 min balloon inflations or clamp occlusions of the left anterior descending coronary arteries and 180 min reperfusion. Docosahexaenoic acid (C22:6n-3, DHA, 45 mg), one of the main n-3 PUFAs in fish oil, was infused within the pericardial space only during the 40-min stabilizing phase, 45 min ischemia and initial 5 min reperfusion. Hemodynamics and cardiac functions were very similar between the DHA-treated and control groups. However, DHA therapy significantly reduced infarct sizes from 56.8 +/- 4.9% for controls (n = 12) to 28.8 +/- 7.9% (P < 0.01) for DHA-treated animals (n = 11). Compared with controls, DHA-treated animals significantly decreased heart rates and reduced ventricular arrhythmia scores during ischemia. Furthermore, three (25%) control animals experienced eight episodes of ventricular fibrillation (VF), and two died subsequent to unsuccessful defibrillation. In contrast, only 1 (9%) of 11 DHA-treated pigs elicited one episode of VF that was successfully converted via defibrillation to normal rhythm; thus, mortality was reduced from 17% in the controls to 0% in the DHA-treated animals. These data demonstrate that pericardial infusion of n-3 PUFA DHA can significantly reduce both malignant arrhythmias and infarct sizes in a porcine infarct model. Pericardial administration of n-3 PUFAs could represent a novel approach to treating or preventing myocardial infarctions. |
7,872 | [Differential diagnosis in patients with suspected anoxic-ischaemic coma]. | Three case studies illustrate that suspected anoxic-ischaemic coma often requires careful differential diagnosis to detect treatable conditions. A 47-year-old man underwent cardiopulmonary resuscitation for ventricular fibrillation caused by myocardial ischaemia. He exhibited rhythmic eyelid movements while in a coma. Epilepsy was suspected, and the patient regained consciousness after being treated with antiepileptic drugs. A 34-year-old man underwent cardiopulmonary resuscitation for multiple episodes of ventricular fibrillation. Treatment was directed toward myocardial ischaemia and included anticoagulants. The patient had bilateral, fixed dilated pupils. A CT of the brain showed traumatic contrecoup haemorrhage in the left temporal lobe with signs of transtentorial herniation. The patient died. A 74-year-old woman was found unconscious at home. An ECG performed by the paramedics showed ST segment elevation in the precordial leads. Anoxic-ischaemic coma following cardiac arrest was suspected. However, a coronary angiogram was normal and a CT of the brain revealed subarachnoid haemorrhage caused by a ruptured intracranial aneurysm. She recovered after cranial surgery. |
7,873 | [Nibentan in arresting acute atrial fibrillation: risk or benefit?]. | To study efficacy and safety of using a domestic anti-arrhythmic drug nibentan for arresting acute atrial fibrillation.</AbstractText>A total of 210 patients received nibentan in a dose 0.125 mg/kg dissolved in 20.0 ml of 0.9% sodium chloride solution by intravenous slow jet 3-min injection. In no response, the injection was repeated 20 min later. Nibentan injection was accompanied with continuous ECG monitoring, measurements of QT interval, arterial pressure. The criterion of efficacy was atrial fibrillation conversion into the sinus rhythm within 24 hours after injection of a total nibentan dose.</AbstractText>Nibentan in a dose 0.125 mg/kg demonstrated high efficacy (91.9%) and sufficient safety (incidence of polymorphic ventricular tachycardia 2.4%) including patients taking other antiarrhythmic drugs. A basic marker of an electrophysiological effect of nibentan on the myocardium is a dynamic change in the interval QT which may serve a predictor of sinus rhythm reestablishment (in QT > or =480 ms) and of a risk to develop proarrhythmogenic complications (in QT > or =640 ms).</AbstractText> |
7,874 | Prediction of successful defibrillation in human victims of out-of-hospital cardiac arrest: a retrospective electrocardiographic analysis. | In the present study we sought to examine the efficacy of an electrocardiographic parameter, 'amplitude spectrum area' (AMSA), to predict the likelihood that any one electrical shock would restore a perfusing rhythm during cardiopulmonary resuscitation in human victims of out-of-hospital cardiac arrest. AMSA analysis is not invalidated by artefacts produced by chest compression and thus it can be performed during CPR, avoiding detrimental interruptions of chest compression and ventilation. We hypothesised that a threshold value of AMSA could be identified as an indicator of successful defibrillation in human victims of cardiac arrest. Analysis was performed on a database of electrocardiographic records, representing lead 2 equivalent recordings from automated external defibrillators including 210 defibrillation attempts from 90 victims of out-of-hospital cardiac arrest. A 4.1 second interval of ventricular fibrillation or ventricular tachycardia, recorded immediately preceding the delivery of the shock, was analysed using the AMSA algorithm. AMSA represents a numerical value based on the sum of the magnitude of the weighted frequency spectrum between two and 48 Hz. AMSA values were significantly greater in successful defibrillation (restoration of a perfusing rhythm), compared to unsuccessful defibrillation (P < 0.0001). An AMSA value of 12 mV-Hz was able to predict the success of each defibrillation attempt with a sensitivity of 0.91 and a specificity of 0.97. In conclusion, AMSA analysis represents a clinically applicable method, which provides a real-time prediction of the success of defibrillation attempts. AMSA may minimise the delivery of futile and detrimental electrical shocks, reducing thereby post-resuscitation myocardial injury. |
7,875 | Treatment options for patients with coronary artery disease identified as high risk by T-wave alternans testing. | Risk stratification for primary prevention of sudden cardiac death (SCD) remains a major challenge in cardiology. The utility of T-wave alternans (TWA) as a marker of risk of life-threatening ventricular tachycardia and fibrillation is supported by two decades of basic and clinical research. Both frequency- and time-domain methods have been developed, validated, and made available in clinical practice. A principal application of TWA testing has been to improve assessment of patients with depressed left ventricular ejection fraction (EF; </= 40%) who are considered for implantable cardioverter-defibrillator (ICD) implantation for primary prevention of SCD. TWA has been most useful in identifying patients who are unlikely to benefit from ICD therapy. Although patients with low EF should remain an important focus, the absolute number of SCD events is far greater among post-myocardial infarction patients with relatively preserved EF, even though the incidence of SCD in this population is low. Recent studies suggest that TWA testing is predictive in this population as well. Absolute quantification of TWA rather than binary classification into "normal" or "abnormal" appears to be valuable in more finely stratifying the magnitude of arrhythmic risk. Longitudinal testing may be warranted in certain populations, although the optimum interval remains to be determined. Combining TWA with noninvasive markers of autonomic function, such as heart rate turbulence, may further increase predictive accuracy. Future development will likely expand the role of TWA testing with routine exercise and ambulatory electrocardiographic monitoring to screen lower-risk populations and to guide medical and device-based therapy. |
7,876 | Medium- and long-term survival after pacemaker implant: Improved survival with right ventricular outflow tract pacing. | Long-term prognosis after pacemaker implant depends on numerous variables, particularly structural heart disease. There is evidence that apical stimulation could favor the development of heart failure and, therefore, influence mortality. Other right ventricular pacing sites have been studied, for example the outflow tract, but no reports regarding long-term clinical outcome are available.</AbstractText>Compare all-cause mortality between two different sites of stimulation in the right ventricle.</AbstractText>We retrospectively analyzed 150 consecutive patients who underwent pacemaker implantation because of complete AV block (spontaneous or after AV node ablation), symptomatic second-degree AV block, and symptomatic atrial fibrillation with slow ventricular response. All patients were implanted at the same institution with the standard technique. Apical stimulation was performed with a passive or active fixation lead and outflow tract pacing with an active fixation lead. Data collection period began in July 1999 and ended on December 2004. All patients included were greater than 70% ventricular paced during pacemaker follow-up. Patients older than 85 years were excluded from the analysis. Age, pacemaker mode, sex, ejection fraction, diabetes, and structural cardiac disease were analyzed. Mean age was 72+/-7 years (median 74 years, range 27-85 years), 101 (67%) were male, 56 had implanted a VVI PM, and 94 patients a DDD PM. Patients were divided into two groups: outflow tract (55 patients) and apical pacing (95 patients). Mean follow-up was 1,231+/-642 days (median 1,158 days, range 9 to 2,694 days), which ended on July 2007. Total mortality was examined with the Kaplan-Meier method to construct overall survival curves. Multivariate Cox proportional hazards regression models were performed.</AbstractText>All patients or relatives were contacted personally or by phone. There were no major statistical differences in patient background between the two groups. During follow-up, 18 patients (32%) died in the outflow tract group and 49 (51%) in the apical group (log-rank p=0.02). Cox regression multivariate analysis showed that outflow tract pacing and a low left ventricular ejection fraction (<40%) were the only independent variables with significant correlation with survival (p=0.006 and 0.003, respectively).</AbstractText>Outflow tract pacing appears to improve medium- and long-term survival. Prospective randomized trials with a greater amount of patients are necessary to confirm the findings of this study.</AbstractText> |
7,877 | [Surgical cryoablation and left ventriculoplasty for electrical storm after acute myocardial infarction]. | A 65-year-old man was referred to our hospital to treat recent anterior myocardial infarction. Coronary artery angiography showed acute occlusion of left anterior descending coronary artery (LAD) and chronic occlusion of right coronary artery. After emergent percutaneous coronary intervention for LAD, drug-refractory electrical storm necessitating frequent electrical defibrillating cardioversion occurred. This patient successfully underwent surgical cryoablation, left ventriculoplasty and coronary revascularization. At 2 years and 10th month after the operation, he is well without limitation of daily activities and any evidence of myocardial ischemia and ventricular tachycardia. |
7,878 | Regulatory mechanisms of atrial fibrotic remodeling in atrial fibrillation. | Electrical, contractile and structural remodeling have been characterized in atrial fibrillation (AF), and the latter is considered to be the major contributor to AF persistence. Recent data show that interstitial fibrosis can predispose to atrial conduction impairment and AF induction. The interplay between cardiac matrix metalloproteinases (MMPs) and their endogenous inhibitors, tissue inhibitors of MMPs (TIMPs), is thought to be critical in atrial extracellular matrix (ECM) metabolism. At the molecular level, angiotensin II, transforming growth factor-beta1, inflammation and oxidative stress are particularly important for ECM dysregulation and atrial fibrotic remodeling in AF. Therefore, we review recent advances in the understanding of the atrial fibrotic process, the major downstream components in this remodeling process, and the expression and regulation of MMPs and TIMPs. We also describe the activation of bioactive molecules in both clinical studies and animal models to modulate MMPs and TIMPs and their effects on atrial fibrosis in AF. |
7,879 | Electrocardiographic abnormalities in patients with heart failure. | The morbidity and mortality from heart failure (HF) differ between patients with reduced (< 50%) and with preserved ( >or= 50%) left ventricular ejection fraction (LVEF) on account of many factors, including abnormalities detected in the electrocardiogram (ECG). The aim of this study was to determine and compare the ECG abnormalities between HF patients with reduced and with preserved LVEF.</AbstractText>The study was cross-sectional in design and carried out in Aminu Kano teaching hospital and Murtala Mohammed specialist hospital, Kano, Nigeria, from April 2005 to June 2006. We studied the resting electrocardiograms of all HF patients aged 15 years and older who were referred to the two centres for echocardiography.</AbstractText>A total of 113 patients were studied and 98.2% of them had abnormal ECGs. Forty-two patients (37.2%) had preserved LVEF while the remaining 71 (62.8%) had reduced LVEF. Left ventricular hypertrophy (LVH) was the commonest ECG abnormality, found among 55 patients (77.5%) with reduced LVEF, and 21 patients (50%) with preserved LVEF (p = 0.0026). The commonest arrhythmia was atrial fibrillation, found among 10 patients (14.1%) with reduced LVEF and eight patients (19.1%) with preserved LVEF (p = 0.486). Prolonged corrected QT interval was found among 30 (71.4%) and 56 patients (78.9%) with preserved and reduced LVEF, respectively (p 5 0.370).</AbstractText>Most of the patients with heart failure studied in Kano, Nigeria had abnormal electrocardiograms, and the most common abnormality was LVH.</AbstractText> |
7,880 | Postaortic valve replacement bradycardia induced torsades de pointes. | The authors present an unusual case of torsades de pointes (Tdp) in an elderly woman with a history of aortic stenosis, status post aortic valve replacement. She was admitted for atrial fibrillation with a slow ventricular response. At the time of admission, the patient was asymptomatic and not taking any medications known to be associated with QT prolongation. During hospitalization, she developed episodes of Tdp without any provocable cause. This case highlights the occurrence of Tdp secondary to conduction disturbance caused by aortic valve surgery. |
7,881 | Echocardiographic parameters and all-cause mortality: the Rotterdam Study. | Even when heart failure has not yet become clinically manifest, preclinical ventricular dysfunction may be present, and therapeutic interventions introduced at this time may reduce morbidity and mortality. However, data on the predictive value of echocardiographic characteristics in the general population remain relatively scarce.</AbstractText>The Rotterdam Study is a population-based cohort study in men and women aged >or=55 years. Participants with prevalent heart failure, myocardial infarction and atrial fibrillation and flutter at the time of echocardiography were excluded. Structural, systolic and diastolic parameters were assessed using two-dimensional, M-mode and Doppler echocardiography. Echocardiograms were available in 4425 participants.</AbstractText>During a mean follow-up of 3.0 years, 226 participants died. Increased left ventricular mass was an independent risk factor for all-cause mortality, particularly in men (hazard ratio per standard deviation of natural log transformed left ventricular mass, 1.20 (95% CI, 1.01-1.43)). Fractional shortening and left ventricular systolic function did not show a clear association with mortality. E/A ratio <0.75 was an independent risk factor in men (age-adjusted hazard ratio 1.82 (95% CI 1.23-2.69)). This was further reflected by diastolic function: impaired relaxation was a risk factor in men, but not in women.</AbstractText>Structural and diastolic echocardiographic parameters are associated with all-cause mortality in an asymptomatic population. However, the evidence is still inadequate to support the usefulness of echocardiography for screening to identify asymptomatic individuals with preclinical ventricular dysfunction.</AbstractText> |
7,882 | Pioglitazone, a peroxisome proliferator-activated receptor-gamma activator, attenuates atrial fibrosis and atrial fibrillation promotion in rabbits with congestive heart failure. | The peroxisome proliferator-activated receptor-gamma (PPAR-gamma) activator pioglitazone antagonizes angiotensin II actions and possesses anti-inflammatory and antioxidant properties in vitro. There is evidence that pioglitazone improves ventricular remodeling in some experimental models.</AbstractText>The purpose of this study was to assess the effects of pioglitazone on arrhythmogenic atrial structural remodeling versus the effects of the angiotensin II type 1 receptor blocker candesartan in a rabbit model of congestive heart failure.</AbstractText>Rabbits subjected to ventricular tachypacing at 380 to 400 bpm for 4 weeks in the absence and presence of treatment with pioglitazone, candesartan, and combined pioglitazone and candesartan were assessed by electrophysiologic study, atrial fibrosis measurements, and cytokine expression analyses.</AbstractText>Atrial fibrillation (AF) lasting longer than 2 seconds was induced in no nonpaced controls but in all ventricular tachypacing-only rabbits (mean duration of AF: 8.0 +/- 1.4 seconds). Pioglitazone reduced the duration of AF (3.5 +/- 0.2 seconds, P <.05) and attenuated atrial structural remodeling, with significant reductions in interatrial activation time (50 +/- 2 ms vs 41 +/- 2 ms, P <.05) and atrial fibrosis (16.8% +/- 0.8% vs 10.9% +/- 0.7%, P <.05; control 1.6% +/- 0.2%), effects comparable to those of candesartan (duration of AF: 3.0 +/- 0.2 seconds; activation time 44 +/- 2 ms; fibrosis: 9.4% +/- 0.6%). Both pioglitazone and candesartan reduced transforming growth factor-beta1, tumor necrosis factor-alpha, and activated extracellular signal-regulated kinase expression similarly, but neither affected p38-kinase or c-Jun N-terminal kinase activation. The effects of combined pioglitazone and candesartan therapy were not significantly different from the effects of pioglitazone or candesartan alone.</AbstractText>Pioglitazone can attenuate congestive heart failure-induced atrial structural remodeling and AF promotion, with effects similar to those of candesartan. PPAR-gamma may be a potential therapeutic target for human AF.</AbstractText> |
7,883 | Optimization of superior vena cava coil position and usage for transvenous defibrillation. | Prior studies of active pectoral implantable defibrillator (ICD) lead systems demonstrated a lowering of defibrillation thresholds (DFTs) with the addition of a superior vena cava (SVC) coil. These studies were done on fixed-tilt waveforms where a large reduction in impedance leads to large phase duration changes.</AbstractText>The present study was designed to evaluate the SVC coil benefit and intercoil spacing on DFTs with a "tuned" waveform.</AbstractText>This prospective, multicenter study included 113 patients randomized at implant to a 17-cm and a 21-cm intercoil spacing ICD lead. DFTs were measured with SVC coil turned ON versus OFF in a random order, using an optimized binary search method.</AbstractText>DFT voltage (423 +/- 120 vs. 438 +/- 118 V; P = .042) and stored energy (9.8 +/- 5.6 vs. 10.2 +/- 5.8 J; P = .043) were significantly reduced with the SVC coil ON. However, intercoil distance had no significant effect on DFT voltage (437.3 +/- 115.1 vs. 407.7 +/- 123.8 V; P = .19) or stored energy (10.3 +/- 5.4 vs. 9.2 +/- 5.8 J; P = .31). Subgroup analyses showed that the dual-coil leads were most effective when placed in the high position (innominate vein-SVC junction) or when the single-coil shock impedance was > or =58 Omega, regardless of intercoil spacing.</AbstractText>With a tuned waveform, the addition of an SVC coil to the shocking pathway reduces DFTs, although this difference was smaller than reported previously. Intercoil distance had no significant effect on the defibrillation parameters.</AbstractText> |
7,884 | Mitral valve surgery in emergency for severe acute regurgitation: analysis of postoperative results from a multicentre study. | To evaluate postoperative outcome of emergency surgery for acute severe mitral regurgitation (ASMR) from a multicentre experience.</AbstractText>In six centres, 279 patients (mean age 62+/-14 years, 62% female) undergoing emergency surgery for ASMR from December 1986 to March 2007 were analysed and followed up. Aetiology included acute myocardial infarction (AMI) in 126 patients (group 1, 45%), degenerative mitral valve disease in 74 (group 2, 26%), and acute endocarditis (AE) in 79 (group 3, 28%). Preoperatively, all patients were in haemodynamic instability, with 185 patients in cardiogenic shock (66%), 184 (66%) intubated, and 61 (22%) on IABP, respectively. Valve repair was performed in 76 (27%), whereas 203 (73%) underwent valve replacement. Median follow-up (98% complete) was 70.8 months (inter-quartile range 59.8-86.66 months).</AbstractText>Overall 30-day mortality was 22.5% (63/279). Early death was significantly lower in group 2 (p<0.001 and p=0.005 vs group 1 and 3, respectively) whereas no difference was detected between group 1 and 3. At logistic regression analysis AMI, AE, shock, left ventricular dysfunction, and coronary artery disease were predictors of early death. Overall 15-year survival was 67+/-10%. Survival was lower in group 1 (39+/-11%) than in group 2 (75+/-9%) and group 3 (77+/-10%). Cox regression found AMI, and associated coronary artery disease to be predictors of late death. Overall 15-year actuarial and actual freedom from cardiac-related events were 44+/-9% and 28+/-10%, respectively, with the worst outcome in the presence of AE. Associated coronary artery disease, AE, AMI, preoperative atrial fibrillation, and chronic renal failure were independent predictors of cardiac-related events.</AbstractText>Emergency surgery for ASMR remains a surgical challenge for high incidence of early and late cardiac-related events, particularly in patients with associated coronary artery disease and acute endocarditis. Apparently, type of mitral valve surgical approaches (repair or replacement) did not provide any influence on postoperative outcome.</AbstractText> |
7,885 | Anticoagulants, antiplatelets, and statins in heart failure. | The existing guidelines for the treatment of patients who have heart failure limit the administration of antiplatelet and anticoagulant agents to patients who have specific comorbidities, including coronary artery disease, atrial fibrillation, history of thromboembolic events, and left ventricular mural thrombus. Retrospective analyses of large clinical trials or smaller nonrandomized studies indicate that the use of statins may be beneficial both in ischemic and idiopathic dilated cardiomyopathy. This article outlines the current knowledge regarding the use of antiplatelet and anticoagulant agents and statins in patients who have heart failure. |
7,886 | Sudden cardiac arrest in hypertrophic cardiomyopathy in the absence of conventional criteria for high risk status. | Two patients with hypertrophic cardiomyopathy are reported from the recent experience of the Hypertrophic Cardiomyopathy Center of the Minneapolis Heart Institute Foundation, demonstrating limitations in the risk stratification algorithm currently used for this disease. One patient, an asymptomatic 21-year-old male college student, was prophylactically implanted with a cardioverter-defibrillator. This decision was based largely on the presence of apparent extensive myocardial fibrosis identified by contrast-enhanced cardiovascular magnetic resonance imaging, currently not considered a risk factor in this disease. Fifteen months later, ventricular fibrillation was interrupted by an appropriate defibrillator shock. The other patient, an asymptomatic 15-year-old male subject without any apparent high-risk markers, died suddenly at home. Necropsy examination of the heart identified scarring confined to portions of both left ventricular papillary muscles, possibly representing a substrate for ventricular tachyarrhythmias. In conclusion, these 2 cases demonstrate that present strategies for assessing high-risk status in hypertrophic cardiomyopathy are inadequate to identify all such patients. However, while the anecdotal nature of these observations cannot yet justify altering the general guidelines for implantation of defibrillators for the primary prevention of sudden death related to hypertrophic cardiomyopathy, 1 of our 2 cases suggests a future role for contrast-enhanced cardiovascular magnetic resonance in the risk stratification of this complex disease. |
7,887 | Meta-analysis comparing reported frequency of atrial fibrillation after acute coronary syndromes in Asians versus whites. | The development of atrial fibrillation (AF) in cardiac patients is multifactorial, including not well defined genetic factors. To determine if Asian ethnicity is associated with the development of AF in patients with coronary disease, a meta-analysis was conducted of patient-level data from 7 prospective randomized clinical trials that prospectively collected information on the development of AF: 3 trials in patients with ST-elevation myocardial infarction (Global Use of Strategies to Open Occluded Coronary Arteries [GUSTO] I, GUSTO III, and GUSTO V), 3 trials in patients with non-ST-elevation acute coronary syndromes (Platelet Glycoprotein IIb/IIIa in Unstable Angina: Receptor Suppression Using Integrilin Therapy [PURSUIT], Integrilin to Minimize Platelet Aggregation and Coronary Thrombosis-II [IMPACT II], and Platelet IIb/IIIa Antagonist for the Reduction of Acute Coronary Syndrome Events in a Global Organization Network [PARAGON A]), and 1 trial in patients with both conditions (GUSTO IIb). A total of 94,785 patients were identified (93,050 white, 1,735 Asian). At baseline, Asian patients were younger; had lower body mass indexes; had a lower prevalence of female gender, previous angioplasty, and previous coronary artery bypass grafting; and had a greater prevalence of diabetes compared with white patients. The development of AF was lower in Asian than in white patients (4.7% vs 7.6%, p <0.001), while rates of ventricular tachycardia and fibrillation were similar in the 2 groups. In multivariate logistic regression analysis, Asian ethnicity was associated with significantly lower rates of AF (odds ratio 0.65, 95% confidence interval 0.50 to 0.84, p = 0.001) compared with white ethnicity. In conclusion, similar to previous studies showing a lower incidence of AF in non-Caucasian populations, Asians experiencing acute ischemic syndromes have a significantly lower frequency of AF compared with whites. Further study is needed to investigate the mechanisms and potential genetic underpinnings behind this association. |
7,888 | Mild hypothermia during advanced life support: a preliminary study in out-of-hospital cardiac arrest. | Induction of mild hypothermia after cardiac arrest may confer neuroprotection. We assessed the feasibility, safety and effectiveness of therapeutic infusion of 2 l of normal saline at 4 degrees C before return of spontaneous circulation during cardiopulmonary resuscitation after out of hospital cardiac arrest.</AbstractText>This was a prospective, observational, multicenter clinical trial conducted in Emergency Medical Services units and in a medical intensive care unit at Caen University Hospital, Cen, France.</AbstractText>In patients who had suffered out of hospital cardiac arrest, hypothermia was induced by infusing 2 l of 4 degrees C NaCl 0.9% over 30 minutes during advanced life support prior to arrival at the hospital. A total of 33 patients were included in the study. Eight patients presented with ventricular fibrillation as the initial cardiac rhythm. Mild hypothermia was achieved after a median of 16 minutes (interquartile range 11.5 to 25.0 minutes) after return of spontaneous circulation. After intravenous cooling, the temperature decreased by 2.1 degrees C (P < 0.0001) to a mean body temperature of 33.3 degrees C (interquartile range 32.3 to 34.3 degrees C). The only observed adverse event was pulmonary oedema, which occurred in one patient.</AbstractText>We concluded that prehospital induction of therapeutic hypothermia using infusion of 2 l of 4 degrees C normal saline during advanced life support was feasible, effective and safe. Larger studies are required to assess the impact that this early cooling has on neurological outcomes after cardiac arrest.</AbstractText> |
7,889 | Moderate hypothermia increases the chance of spiral wave collision in favor of self-termination of ventricular tachycardia/fibrillation. | In cardiac arrest due to ventricular fibrillation (VF), moderate hypothermia (MH, 33 degrees C) has been shown to improve defibrillation success compared with normothermia (NR, 37 degrees C) and severe hypothermia (SH, 30 degrees C). The underlying mechanisms remain unclear. We hypothesized that MH might prevent reentrant excitations rotating around functional obstacles (rotors) that are responsible for the genesis of VF. In two-dimensional Langendorff-perfused rabbit hearts prepared by cryoablation (n = 13), action potential signals were recorded by a high-resolution optical mapping system. During basic stimulation (2.5-5.0 Hz), MH and SH caused significant prolongation of action potential duration and significant reduction of conduction velocity. Wavelength was unchanged at MH, whereas it was shortened significantly at SH at higher stimulation frequencies (4.0-5.0 Hz). The duration of direct current stimulation-induced ventricular tachycardia (VT)/VF was reduced dramatically at MH compared with NR and SH. The spiral wave (SW) excitations documented during VT at NR were by and large organized, whereas those during VT/VF at MH and SH were characterized by disorganization with frequent breakup. Phase maps during VT/VF at MH showed a higher incidence of SW collision (mutual annihilation or exit from the anatomical boundaries), which caused a temporal disappearance of phase singularity points (PS-0), compared with that at NR and SH. There was an inverse relation between PS-0 period in the observation area and VT/VF duration. MH data points were located in a longer PS-0 period and a shorter VT/VF duration zone compared with SH. MH causes a modification of SW dynamics, leading to an increase in the chance of SW collision in favor of self-termination of VT/VF. |
7,890 | [Trichosporon asahii an emerging etiologic agent of fungal infection and colonization in heart failure patients in intensive care unit: case report and literature review]. | Infection with the non-Candida yeast species Trichosporon have been recognized with increasing frequency over the last two decades. Invasive disease due to trichosporonosis has been reported from neutropenic patients with cancer and the mortality is high. Recently, others groups of patients have become susceptible to this rare fungi. We report the emerging of infection with pathogenic Trichosporon asahii in severely ill heart failure patients in a tertiary cardiological intensive care unit (CICU). We describe our data, and report a fatal case of disseminated trichosporonosis in a patient with heart failure. We also review literature pertaining to T. asahii infections.</AbstractText>An 85 year-old woman with a history of hypertension, heart failure (ejection fraction (EJ): 30%) and pulmonary embolism was admitted to a medical cardiological ICU after cardiac arrest (ventricular fibrillation) resuscitated during a routine consultation. There were no neurological sequelae and the echocardiogram revels no changes, neither the cardiac biomarkers. Ventricular fibrillation was considered secondary to heart failure. The patient had extubation failure and difficult weaning needing long term mechanical ventilation even after tracheostomy. Her hospital course was complicated by acute renal failure and recurrent respiratory, urinary and systemic bacterial infections, which responded to broad-spectrum antibiotics. After a temporary improvement she developed urinary infection and subsequent septic shock. Cultures of urine and blood specimens grew T. asahii. Treatment with liposome amphotericin B (5 mg/kg/day) was started. Despite receiving vancomycin and imipenem, the clinical condition of the patient deteriorates. Blood taken for culture on the seventh day of amphotericin B therapy were negative but urine specimen still grew T. asahii. On the eighteenth day of antifungal therapy, the patient died with multiorgan failure.</AbstractText>The increasing of severely ill patients, and the use of broad spectrum antibiotics, has predisposed the emerging of invasive infections by rare and new opportunistic fungal pathogens. Severe infection related to T. asahii, until recently restricted to neutropenic patients with cancer, has been frequently identified in heart failure patients with advanced age. The mortality is high. These data highlights the importance of considering this group of patients as a risk group for T. asahii infection.</AbstractText> |
7,891 | Improvement in cardiac sympathetic nerve activity in responders to resynchronization therapy. | To assess changes in cardiac adrenergic activity with cardiac resynchronization therapy (CRT), and to investigate whether these changes are related to improvement in left ventricular ejection fraction (LVEF).</AbstractText>Sixteen patients (13 males, age 66 +/- 7 years) were studied at baseline and after > or =6 months of CRT (mean follow-up 9.2 +/- 3.2 months). LVEF was assessed by nuclear angiography. Responders were defined as patients showing > or =5% absolute increase in LVEF + improvement in > or =1 NYHA class + absence of heart failure hospitalization. Cardiac sympathetic nerve activity was studied by (123)I-metaiodobenzyl-guanidine ((123)I-MIBG) scintigraphy. Responders (n = 8) showed lower (123)I-MIBG washout at follow-up when compared with non-responders (P = 0.002), indicating lower cardiac sympathetic nerve activity. The decrease in (123)I-MIBG washout at follow-up when compared with baseline was only seen in the responder group (P = 0.036). There was a moderate correlation between increase in LVEF and decrease in (123)I-MIBG washout (r = 0.52, P = 0.04).</AbstractText>CRT induces a reduction in cardiac sympathetic nerve activity in responders, that parallels an improvement in LVEF, whereas non-responders do not show any significant changes.</AbstractText> |
7,892 | Right ventricular pacing is an independent predictor for ventricular tachycardia/ventricular fibrillation occurrence and heart failure events in patients with an implantable cardioverter-defibrillator. | There is increasing evidence that right ventricular (RV) pacing may have detrimental effects by increasing morbidity and mortality for heart failure in implantable cardioverter-defibrillator (ICD) patients. In this study we prospectively tested the hypothesis that cumulative RV pacing increases ventricular tachycardia/ventricular fibrillation (VT/VF) occurrence (primary endpoint) and hospitalization and mortality for heart failure (secondary endpoint) in a predominantly secondary prophylactic ICD patient population.</AbstractText>Two hundred and fifty patients were divided into two groups according to the median of cumulative RV pacing (< or =2 vs. >2%) and prospectively followed-up for occurrence of primary and secondary endpoints for 18 +/- 4 months. Established predictors for VT/VF occurrence and heart failure events such as age, left ventricular ejection fraction (EF), QRS duration, history of atrial fibrillation, and NT-proBNP were collected at enrollment. Multivariate Cox regression analysis revealed that cumulative RV pacing > 2% and EF < 40% were independent predictors for VT/VF occurrence and heart failure events. Kaplan-Meier analysis showed that patients with >2% cumulative RV pacing more frequently suffered from VT/VF occurrence and heart failure hospitalization.</AbstractText>Cumulative RV pacing > 2% and EF < 40% are independent predictors for VT/VF occurrence and mortality and hospitalization for heart failure in predominantly secondary prophylactic ICD patients. Our data show that algorithms capable of reducing cumulative RV pacing should be used more frequently in clinical practice.</AbstractText> |
7,893 | High defibrillation energy requirements are encountered rarely with modern dual-chamber implantable cardioverter-defibrillator systems. | Defibrillation conversion testing to assure a 10 J safety margin is a standard practice during implantable cardioverter-defibrillator (ICD) implantation. Little data are available on the number of patients who do not have a 10 J margin initially and therefore require system revisions, further testing, or a higher energy output device.</AbstractText>The INTRINSIC RV study enrolled 1530 new ICD recipients who were not in permanent atrial fibrillation who received a VITALITY AVT (Guidant, St Paul, MN, USA) standard energy (31 J maximum) ICD and underwent defibrillation conversion testing at the time of implantation from 108 centres. Among enrolled patients, 59 (3.9%) did not initially meet the 10 J safety margin criterion. In these 59 patients, a 10 J safety margin was achieved by making at least one system revision: reversing shocking polarity (n = 33, 56%), right ventricular lead repositioning (n = 19, 32%), repeat testing at a later date (n = 1, 2%), adding a subcutaneous array (n = 1, 2%), or other means (n = 10, 17%). Only New York Heart Association class (P = 0.001) and no previous myocardial infarction (P = 0.044) predicted a failed initial conversion test. There were no reported complications from ICD shock testing.</AbstractText>Successful defibrillation conversion criteria with the first configuration tested with a standard energy device is almost always met with modern dual-chamber ICD systems. The need for revising the initial ICD shock configuration to achieve a 10 J safety margin appears extremely low and of low risk.</AbstractText> |
7,894 | Mechanisms for the genesis of paroxysmal atrial fibrillation in the Wolff Parkinson-White syndrome: intrinsic atrial muscle vulnerability vs. electrophysiological properties of the accessory pathway. | Paroxysmal atrial fibrillation (PAF) develops in up to one-third of patients with the Wolff Parkinson-White syndrome (WPW). The reason for this high incidence of PAF in the WPW syndrome is not yet clearly understood. When PAF appears in patients with WPW syndrome who have anterograde conduction via the accessory pathway (AP), it may be life-threatening if an extremely rapid ventricular response develops degenerating into ventricular fibrillation.</AbstractText>Several mechanisms responsible for the genesis of PAF in WPW patients were hypothesized, namely, spontaneous degeneration of atrioventricular reciprocating tachycardia into atrial fibrillation (AF), electrical properties of the APs, effects of APs on atrial architecture, and intrinsic atrial muscle vulnerability. Focal activity, multiple reentrant wavelets, and macroreentry have all been implicated in AF, perhaps under the further influence of the autonomic nervous system. AF can also be initiated by ectopic beats originating from the pulmonary veins, and elsewhere. Several studies demonstrated a decrease incidence of PAF after successful elimination of the AP, suggesting that the AP itself may play an important role in the initiation of PAF. However, PAF still occurs in some patients with the WPW syndrome even after successful elimination of the AP. There is an important evidence of an underlying atrial disease in patients with the WPW syndrome.</AbstractText>Atrial vulnerability has been studied performing an atrial endocardial catheter mapping and analysing abnormal atrial electrograms. Other studies evaluated atrial refractoriness and intraatrial conduction times, suggesting an intrinsic atrial vulnerability as the mechanism of PAF and considering the AP as an innocent bystander. It is our intention to analyse the available data on this particular and interesting topic since AF has a singular prognostic significance in patients with the WPW syndrome, and its incidence is unusually high in the absence of any clinical evidence of cardiac organic disease.</AbstractText> |
7,895 | Association of body weight with total mortality and with ICD shocks among survivors of ventricular fibrillation in out-of-hospital cardiac arrest. | Studies have shown an association between obesity and total mortality among people with and without coronary artery disease. This study reviews outcomes among obese survivors of ventricular fibrillation in out-of-hospital cardiac arrest.</AbstractText>All survivors of ventricular fibrillation in out-of-hospital cardiac arrest who presented in Rochester, MN from November 1990 to September 2006 were included and classified by body weight. Implantable cardioverter defibrillator shocks administered were determined by review of subsequent device interrogations.</AbstractText>Among a study population of 226, 99 (44%) survived to hospital discharge with neurological recovery. Data to calculate body mass index were available in 213 cases (95%). There was no significant difference in the relative distribution of body weight between hospital survivors and non-survivors, nor in cardioverter defibrillator implantation rates. Mean follow-up was 5.8+/-4.4 years; 5-year survival was 80+/-5%, lower among underweight and normal compared with heavier individuals. The 5-year survival free of implantable cardioverter defibrillator shocks was 61+/-7%, with no weight-based difference in shocks.</AbstractText>There was no apparent weight-based influence on resuscitation survival after ventricular fibrillation in out-of-hospital cardiac arrest. People of normal or low weight had a lower long-term survival and represent at population high risk from primarily non-cardiac diseases.</AbstractText> |
7,896 | A blinded, randomized controlled evaluation of an impedance threshold device during cardiopulmonary resuscitation in swine. | An impedance threshold device (ITD) has been designed to enhance circulation during CPR. A recent study suggests that the ITD does not improve hemodynamics and that it may actually worsen outcomes. We sought to independently assess the effect of the ITD on coronary perfusion pressure (CPP) and passive ventilation (PaCO(2) and PaO(2)) during standard CPR (S-CPR), and its impact on the return of spontaneous circulation (ROSC) and short-term survival in a blinded fashion.</AbstractText>Thirty male swine were instrumented under anesthesia. Ventricular fibrillation (VF) was electrically induced. CPP was continuously recorded. After 8 min of untreated VF, baseline characteristics were documented and S-CPR initiated. After 3 cycles of S-CPR, an ABG was drawn and drugs were given. Following 6 additional cycles of S-CPR, an ABG was drawn and the first rescue shock was delivered. Group comparisons were assessed using descriptive statistics. Proportions with 95% confidence intervals were calculated for outcomes.</AbstractText>Baseline characteristics between the two groups were the same. The mean CPP in the ITD group was 51.2 mmHg [95% CI: 37.7, 64.7] compared to 50.2 mmHg [95% CI: 37.0, 63.4] in the sham group. The PaCO(2) and PaO(2) were 68 Torr [95% CI: 55.7, 79.5] and 103 Torr [95% CI: 76, 129] in the ITD group and 59 Torr [95% CI: 49.1, 68.5] and 137 Torr [95% CI: 83, 191] in the sham group. The rate of ROSC was 14/15 in both groups and 13 animals in each groups survived.</AbstractText>In this independent blinded study, use of the active ITD had no significant impact on CPP, passive ventilation, or outcomes compared to the sham device.</AbstractText> |
7,897 | Usefulness of emergency medical teams in sport stadiums. | In August 2006, the new AZ Alkmaar soccer stadium (capacity 17,000) opened. To provide adequate emergency support, medical teams of Red Cross volunteers and coronary care unit and emergency room nurses were formed, and facilities including automated external defibrillators were made available at the stadium. During every match, 3 teams are placed among the spectators. All patients who had cardiac events were stabilized by the teams and transported to the hospital. They formed the study group. From August 2006 to May 2007, >800,000 individuals attended soccer matches at the new stadium. Four cardiac events (3 out-of-hospital-resuscitations for ventricular fibrillation, 1 patient with chest pain) requiring emergency medical support occurred. On-site resuscitations using defibrillators were successful. Two patients with triple-vessel disease subsequently underwent coronary bypass surgery and implantable cardioverter-defibrillator implantation. One patient had single-vessel disease of the circumflex branch, for which he received a coronary stent. All had uneventful recoveries. An acute coronary syndrome was ruled out in the patient presenting with chest pain. In conclusion, the presence of emergency medical teams at a large sport stadium was of vital importance in the immediate care of critically ill patients. On-site resuscitation using automated external defibrillators was lifesaving in all cases. The presence of medical teams equipped with defibrillators and emergency action plans is recommended at large venues that host sports and other activities. |
7,898 | Predictors of atrial arrhythmias after device closure of secundum type atrial septal defects in adults. | Atrial tachyarrhythmias (ATs) contribute substantially to morbidity in adult patients with secundum atrial septal defects (ASDs). The purpose of this study was to prospectively determine the incidence of AT in adults with an ASD and identify predictors of AT occurrence after closure. This was a prospective study of 200 adult patients undergoing closure of a secundum ASD. Arrhythmic events were defined as sustained or symptomatic AT requiring treatment. Twenty percent of patients (mean age 50 +/- 17 years; 26% men) referred for ASD closure had a history of AT. Early follow-up was available for 90% of patients, and the prevalence of AT was 17%. Of 171 patients with late follow-up (mean 1.9 +/- 0.9 years), data were available for 90%. AT was detected in 16% of these patients. Closure resulted in alleviation of symptoms (p <0.001), but symptoms alone did not identify patients at risk of recurrent AT. After closure of the ASD, the likelihood of remaining arrhythmia free was highest in patients without a history of AT (p = 0.001) and those <40 years at closure (p = 0.04). In conclusion, transcatheter ASD closure in patients without a history of arrhythmias and those <40 years of age conferred the highest likelihood of a patient remaining arrhythmia free in follow-up. An arrhythmia-specific treatment strategy should be considered for patients with documented established AT before ASD closure, in addition to shunt relief. |
7,899 | Atrial fibrillation associated with a thyroid stimulating hormone-secreting adenoma of the pituitary gland leading to a presentation of acute cardiac decompensation: a case report. | Hyperthyroidism is a well established cause of atrial fibrillation (AF). Thyroid Stimulating Hormone-secreting pituitary tumours are rare causes of pituitary hyperthyroidism. Whilst pituitary causes of hyperthyroidism are much less common than primary thyroid pathology, establishing a clear aetiology is critical in minimising complications and providing appropriate treatment. Measuring Thyroid Stimulating Hormone (TSH) alone to screen for hyperthyroidism may be insufficient to appropriately evaluate the thyroid status in such cases.</AbstractText>A 63-year-old Caucasian man, previously fit and well, presented with a five-day history of shortness of breath associated with wheeze and dry cough. He denied symptoms of hyperthyroidism and his family, social and past history were unremarkable. Initial investigation was in keeping with a diagnosis of atrial fibrillation (AF) with fast ventricular response leading to cardiac decompensation.TSH 6.2 (Normal Range = 0.40 - 4.00 mU/L), Free T3 of 12.5 (4.00 - 6.8 pmol/L) and Free T4 51(10-30 pmol/L). Heterophilic antibodies were ruled out. Testosterone was elevated at 43.10 (Normal range: 10.00 - 31.00 nmol/L) with an elevated FSH, 18.1 (1.0-7.0 U/L) and elevated LH, 12.4 (1.0-8.0 U/L). Growth Hormone, IGF-1 and prolactin were normal. MRI showed a 2.4 cm pituitary macroadenoma. Visual field tests showed a right inferotemporal defect.While awaiting neurosurgical removal of the tumour, the patient was commenced on antithyroid medication (carbimazole) and maintained on this until successful trans-sphenoidal excision of the macroadenoma had been performed. AF persisted post-operatively, but was electrically cardioverted subsequently and he remains in sinus rhythm at twelve months follow-up off all treatment.</AbstractText>This case reiterates the need to evaluate thyroid function in all patients presenting with atrial fibrillation. TSH-secreting pituitary adenomas must be considered when evaluating the cause of hyperthyroidism. Early diagnosis and treatment of such adenomas is critical in reducing neurological and endocrine complications.</AbstractText> |
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