Worsening Thoracic Impedance as a Ventricular Tachyarrhythmia Risk
Bernard Abi‐SalehChristopher MalozziEdriss CharafBassam OmarClara V. MasseyMaurice KhourySumit Verma
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Abstract:
The use of heart failure classification to identify patients with systolic dysfunction who are at risk for ventricular tachyarrhythmias (VAs), sudden cardiac death, and shocks from implantable cardioverter defibrillators (ICDs) is limited by its subjectivity. Measurement of thoracic impedance offers a more objective tool for assessing worsening of heart failure. We sought to look at the correlation between ventricular arrhythmia and heart failure as assessed objectively by thoracic impedance. We reviewed device interrogation data on thoracic impedance from ICD with Medtronic's OptiVol® feature (Medtronic Inc., Minneapolis, MN) at two medical centers. Data from the last two interrogations of the same device separated by at least 2 months were included. An OptiVol fluid index threshold of 60 represented early heart failure prior to appearance of symptoms. VAs included were ventricular fibrillation and/or ventricular tachycardia lasting more than 16 beats. Chi square distribution test was used in statistical data analysis. There were 24 VAs identified among the 322 interrogations reviewed (7.5%). Elevated OptiVol fluid index was seen in 71% (17/24), whereas normal OptiVol index was seen in the remaining 29% (7/24) of these interrogations with VA (P < .05). Our review shows that heart failure patients who have VA are approximately 2.5 times as likely to have worsening thoracic impedance as assessed objectively by the OptiVol fluid index. Careful monitoring of the OptiVol fluid index may identify a population at high risk of VA that merits more intense attention.Keywords:
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Identification of subsets of patients with coronary artery disease (CAD) who are prone to ventricular tachycardia or fibrillation (VT/VF) and to sudden arrhythmic death still represents one of the major problems in clinical cardiology today. Ninety-two patients with CAD were included in this prospective study, which was designed to assess the prognostic significance of ventricular late potentials (VLP) detected non-invasively using high-gain electrocardiography and signal averaging. The results clearly demonstrate that the presence of VLP increases the risk of VT/VF and the risk of sudden arrhythmic death in CAD patients. Because of its high sensitivity and non-invasiveness, high-gain electrocardiography should be included among the various electrophysiological investigations used to assess prognosis in CAD patients.
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This chapter contains sections titled: Epidemiology of ventricular tachycardia and ventricular fibrillation Classification of ventricular tachycardia and ventricular fibrillation Classification according to the duration of ventricular arrhythmias Classification according to QRS morphologies Classification according to clinical characteristics of ventricular tachycardia Conditions associated with ventricular tachycardia/ventricular fibrillation Coronary heart disease as the most frequent cause of ventricular tachycardia/ventricular fibrillation and sudden cardiac death Natural history of patients with sustained ventricular arrhythmias and ischemic and nonischemic cardiomyopathy Mechanisms of ventricular arrhythmias in ischemic cardiomyopathy Mechanisms of ventricular arrhythmias in nonischemic dilated cardiomyopathy Impact of sudden cardiac death in the natural history of ischemic and nonischemic dilated cardiomyopathy with a history of heart failure The different natural history of ischemic and nonischemic dilated cardiomyopathy patients Arrhythmogenic right ventricular cardiomyopathy: its role in sudden cardiac death and mechanisms of ventricular arrhythmias related to this entity Hypertrophic cardiomyopathy and sudden cardiac death with special emphasis on athletes Congenital heart disease Catecholaminergic polymorphic ventricular tachycardia The Brugada syndrome The long QT syndrome Drug-induced ventricular arrhythmias Ventricular tachycardia/ventricular fibrillation clinical presentation: hemodynamically stable and hemodynamically unstable References
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BACKGROUND Death during the first year after myocardial infarction is most commonly due to spontaneous ventricular tachycardia (VT) or fibrillation (VF). The purpose of this study was to compare, in a single cohort of patients, the values of inducible VT, delayed ventricular activation, low left ventricular ejection fraction, high-grade ventricular ectopy, and ST segment displacement on exercise in predicting electrical events (witnessed instantaneous death and spontaneous VT or VF) during the first year after myocardial infarction. METHODS AND RESULTS Three hundred sixty one patients aged less than 71 years underwent electrophysiological study, signal-averaged electrocardiogram, gated blood-pool scan, 24 hour ambulatory electrocardiographic monitoring, and exercise testing 1-2 weeks after myocardial infarction and were then followed up for at least 1 year. There were 34 deaths (eight witnessed instantaneous, 26 other), and nine patients survived one or more episodes of spontaneous VF or VT. Patients with inducible VT were 15.2 times more likely to suffer electrical events than patients without inducible VT. No proportional-hazards model excluding inducible VT was as good a predictor of electrical events as was inducible VT alone. CONCLUSIONS Inducible VT at electrophysiological study was the single best predictor of spontaneous VT and sudden death after myocardial infarction.
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Previous studies have suggested that coronary artery bypass surgery is sufficient to prevent recurrence of sudden death in patients with critical coronary artery stenosis presenting with ventricular fibrillation or polymorphic ventricular tachycardia. We present our experience in patients with one or more episodes of sudden death associated with documented ventricular fibrillation or polymorphic ventricular tachycardia and severe operable coronary artery disease who underwent defibrillator implant at the time of bypass surgery.Fifty-eight consecutive patients (age 63 +/- 8 years) were included in this study. Eighteen of the 58 patients had no evidence of previous myocardial infarction. The mean ejection fraction was 37 +/- 13%. All patients underwent electrophysiologic study before and after revascularization. At the time of first defibrillator discharge, each patient was reevaluated to exclude the presence of ischemia. The benefits of defibrillator implant were estimated comparing the projected survival based upon defibrillator discharge preceded by syncope or presyncope with survival curves generated including total death and sudden plus cardiac death. After a mean follow-up of 4.6 +/- 2 years, 22 patients received appropriate shocks preceded by syncope or presyncope, and an additional 19 patients received asymptomatic shocks. At 4 years, survival free of total death was 71.2%, and the projected survival was 58.8% (P < 0.05). Multivariate analysis showed that ejection fraction lower than 30% and induction of arrhythmia with one or two extrastimuli (S2, S3) were independent predictors for defibrillator discharge. None of the remaining variables including age, gender, number of bypasses, history of myocardial infarction, and type of arrhythmias induced were predictive for death and occurrence of shocks.In patients with ventricular fibrillation and polymorphic ventricular tachycardia, bypass surgery does not protect from recurrence of life-threatening arrhythmias, and, as in our population, defibrillator implant may have significant impact on survival.
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Atrial fibrillation and congestive heart failure are two distinct clinical entities that are responsible for significant morbidity and mortality in the Western world. Hypertension, coronary artery disease, and nonischemic cardiomyopathy represent the most prevalent underlying pathologies of both diseases, implying a coincidence of both in many patients. The prevalence of atrial fibrillation with a progressive degree of congestive heart failure is increasing, as judged by New York Heart Association functional class. Moreover, the presence of congestive heart failure has been identified as one of the most powerful independent predictors of atrial fibrillation, with a sixfold increase in relative risk of its development. On the other hand, atrial fibrillation can cause or significantly aggravate symptoms of congestive heart failure in previously asymptomatic or well-compensated patients. In some patients, symptomatic dilated cardiomyopathy may develop over time entirely due to atrial fibrillation with rapid ventricular rates. Upon restoration of sinus rhythm, this type of “tachymyopathy” has been shown to be often reversible. Recent investigations of the physiologic and structural changes of the atrial myocardium (“electrical and structural remodeling”) have shown that neurohumoral activation, fibrosis, and apoptosis are demonstrable with both diseases. On the other hand, experimental data suggest that the substrates of atrial fibrillation in congestive heart failure are different from those of pure atrial tachycardia-related forms of atrial fibrillation. This review highlights the clinical and pathophysiologic similarities and differences of atrial fibrillation and congestive heart failure relevant to the understanding, treatment, and prevention of these diseases in the population at risk.
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