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Arrhythmic Risk (arrhythmic + risk)
Selected AbstractsCardiac side effects of psychiatric drugs,HUMAN PSYCHOPHARMACOLOGY: CLINICAL AND EXPERIMENTAL, Issue S1 2008Paul Mackin Abstract This review describes the common effects of psychotropic drugs on the cardiovascular system and offers guidance for practical management. Selected reports from the literature describing common side effects associated with psychotropic drugs are reviewed, and suggestions for further reading are given throughout the text. Orthostatic hypotension is the most common adverse autonomic side effect of antipsychotic drugs. Among the atypical antipsychotics the risk of orthostatic hypotension is highest with clozapine and among the conventional drugs the risk is highest with low potency agents. Rarely, orthostatic hypotension may result in neurocardiogenic syncope. QTc prolongation can occur with all antipsychotics but an increased risk is seen with pimozide, thioridazine, sertindole and zotepine. QTc prolongation is a marker of arrhythmic risk. Torsade de pointe, a specific arrhythmia, may lead to syncope, dizziness or ventricular fibrillation and sudden death. Heart muscle disease presents most commonly in the elderly as chronic heart failure, but myocarditis and cardiomyopathy, although relatively rare, are devastating, but potentially reversible complications of psychotropic drug therapy have been particularly linked to clozapine treatment. Patients with severe mental illness (SMI) are a ,high risk' population with regard to cardiovascular morbidity and mortality. It is probable that many patients accumulate an excess of ,traditional' risk factors for the development of cardiovascular disease, but other mechanisms including psychotropic drugs may also be influential in increasing risk in this vulnerable group. These risks need to be seen in the context of the undoubted therapeutic efficacy of the psychotropic armamentarium and the relief that these drugs bring to those suffering from mental disorder. Copyright © 2007 John Wiley & Sons, Ltd. [source] To Replace or Not to Replace: A Systematic Approach to Respond to Device AdvisoriesJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 2 2009Ph.D., SILVIA G. PRIORI M.D. Aim: The decision of whether and when to replace a device in response to an "advisory" letter requires careful consideration, because device replacement carries related risks and is influenced by the clinical characteristics of the patient. Methods and Results: The risk/benefit of device replacement depends on four parameters: expected annual sudden cardiac death rate; residual device life; difference in failure rate between the device listed on the advisory letter and the replacement device; and the replacement procedure mortality risk. Using these four factors, we have developed an equation that provides the "number needed to replace" (NNR) to save one life. Per our model, patients implanted with a device with a failure rate approaching 1% and a probability of requiring device intervention ,25% per year,in particular, pacemaker-dependent patients,have an NNR <250. Pacemaker-dependent patients, with devices having three or more years longevity, but with device failure rates ,0.5%, have an NNR <100. Patients with arrhythmic risk ,2.5% per year and those with devices having failure rates <0.1% have a high NNR and stand more risk to be harmed than benefited from device replacement. Conclusions: Pacemaker-dependent patients and those with high arrhythmic risk (,25% annually) when having "advisory" devices with high failure rate (,1%) have an NNR <250 and, hence, could be considered for device replacement. Conversely, patients with arrhythmic risk ,2.5% per year and those with devices having failure rates ,0.1% have a high NNR or even risk of "harm" from device replacement. In all the intermediate cases, the NNR will quantify the benefit/risk ratio of replacement, thus helping physicians and patients decide on the preferred approach. The NNR methodology proposed here is also applicable to advisory notices issued to leads, but the high morbidity associated with lead replacement will generally rule out interventions to replace leads. [source] Cigarette Smoking and the Risk of Supraventricular and Ventricular Tachyarrhythmias in High-Risk Cardiac Patients with Implantable Cardioverter DefibrillatorsJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 9 2006ILAN GOLDENBERG M.D. Introduction: Nicotine elevates serum catecholamine concentration and is therefore potentially arrhythmogenic. However, the effect of cigarette smoking on arrhythmic risk in coronary heart disease patients is not well established. Methods and Results: The risk of appropriate and inappropriate defibrillator therapy by smoking status was analyzed in 717 patients who received an implantable cardioverter defibrillator (ICD) in the Multicenter Automatic Defibrillator Implantation Trial-II. Compared with patients who had quit smoking before study entry (past smokers) and patients who had never smoked (never smokers), patients who continued smoking (current smokers) were significantly younger and generally had more favorable baseline clinical characteristics. Despite this, the adjusted hazard ratio (HR) for appropriate ICD therapy for fast ventricular tachycardia (at heart rates ,180 b.p.m) or ventricular fibrillation was highest among current smokers (HR = 2.11 [95% CI 1.11,3.99]) and intermediate among past smokers (HR = 1.57 [95% CI 0.95,2.58]), as compared with never smokers (P for trend = 0.02). Current smokers also exhibited a higher risk of inappropriate ICD shocks (HR = 2.93 [95% CI 1.30,6.63]) than past (HR = 1.91 [95% CI 0.97,3.77]) and never smokers (P for trend = 0.008). Conclusions: In patients with ischemic left ventricular dysfunction, continued cigarette smoking is associated with a significant increase in the risk of life-threatening ventricular tachyarrhythmias and inappropriate ICD shocks induced by rapid supraventricular arrhythmias. Our findings stress the importance of complete smoking cessation in this high-risk population. [source] Heterogeneous Regional Endocardial Repolarization is Associated with Increased Risk for Ischemia-Dependent Ventricular Fibrillation after Myocardial InfarctionJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 8 2003Michael H. Swann M.SC. Introduction: The aim of this study was to investigate whether the characteristics of endocardial ventricular repolarization are associated with differential risk for sudden death. Prolonged surface QT interval is associated with increased arrhythmic risk after myocardial infarction (MI), but the underlying mechanism of QT prolongation and its relation to lethal arrhythmias are unclear. Methods and Results: Ventricular fibrillation (VF) risk was assessed in 12 dogs 1 month after anterior MI during an exercise test coupled with brief circumflex coronary occlusion. Susceptible dogs (n = 5) developed VF during the brief ischemic episode, whereas resistant dogs did not (n = 7). Surface QT interval was measured at rest. Endocardial electroanatomic catheter maps of left ventricular repolarization were obtained in four unique regions identified by echocardiography and compared between groups. Compared to resistant dogs, susceptible dogs were characterized by prolonged surface QT intervals (240 ± 10 msec vs 222 ± 7 msec, P = 0.04). In addition, they had lower baroreflex sensitivity (9.7 ± 1.5 msec/mmHg vs 28 ± 9.8 msec/mmHg, P < 0.01) and a tachycardic response to acute ischemia suggesting higher propensity for stronger sympathetic reflexes. Surface QT interval prolongation in susceptible dogs was due to a marked heterogeneity of endocardial left ventricular repolarization (239 ± 42 msec, basal anterior wall vs 197 ± 35, lateral wall; P < 0.001). Resistant animals had no regional differences in endocardial repolarization. Conclusion: Sympathetic activation following MI not only produces adverse structural remodeling but also contributes to adverse electrophysiologic remodeling resulting in heterogeneous ventricular repolarization and in a myocardial substrate conducive to lethal reentrant arrhythmias. (J Cardiovasc Electrophysiol, Vol. 14, pp. 873-879, August 2003) [source] Prolonged QRS Duration Increases QT Dispersion But Does Not Relate to Arrhythmias in Survivors of Acute Myocardial InfarctionPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 5 2001PAULUS KIRCHHOF KIRCHHOF P., et al.: Prolonged QRS Duration Increases QT Dispersion But Does Not Relate to Arrhythmias in Survivors of Acute Myocardial Infarction. QT dispersion has been suggested and disputed as a risk marker for ventricular arrhythmias after myocardial infarction. Delayed ventricular activation after myocardial infarction may affect arrhythmic risk and QT intervals. This study determined if delayed activation as assessed by (1) QRS duration in the 12-lead ECG and by (2) late potentials in the signal-averaged ECG affects QT dispersion and its ability to assess arrhythmic risk after myocardial infarction. QT duration, JT duration, QT dispersion, and JT dispersion were compared to QRS duration in the 12-lead ECG and to late potentials in the signal-averaged ECG recorded in 724 patients 2,3 weeks after myocardial infarction. Prolonged QRS duration (> 110 ms) and high QRS dispersion increased QT and JT dispersion by 12%,15% (P < 0.05). Presence of late potentials, in contrast, did not change QT dispersion. Only the presence of late potentials (n = 113) was related to arrhythmic events during 6-month follow-up. QT dispersion, JT dispersion, QRS duration, and QRS dispersion were equal in patients with (n = 29) and without arrhythmic events (QT disp 80 ± 7 vs 78 ± 1 ms, JT disp 80 ± 6 vs 79 ± 2 ms, mean ± SEM, P > 0.2). In conclusion, prolonged QRS duration increases QT dispersion irrespective of arrhythmic events in survivors of myocardial infarction. Presence of late potentials, in contrast, relates to arrhythmic events but does not affect QT dispersion. Therefore, QT dispersion may not be an adequate parameter to assess arrhythmic risk in survivors of myocardial infarction. [source] | ||||||||||