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Arrhythmias in acute coronary syndrome
Published in K Sarat Chandra, AJ Swamy, Acute Coronary Syndromes, 2020
Ventricular premature complexes (VPCs) are common in patients with ACS and constitute the most common arrhythmias in this substrate. They may occur during the acute phase as well as during reperfusion. Before the advent of modern reperfusion therapy, certain configurations of VPCs were considered to predict ventricular fibrillation (VF) and sudden death, namely frequent VPCs, multiform VPCs, ‘R-on-T’ phenomenon, couplets and salvos. It was expected that suppression of these VPCs would reduce the risk of sudden death. However, the Cardiac Arrhythmia Suppression Trial (CAST) conclusively demonstrated increased mortality in patients prophylactically treated with class I anti-arrhythmic agents [3]. Current data shows that VPCs are very unreliable predictors of occurrence of significant ventricular arrhythmias [1].
Impotent drug regulation
Published in Peter C. Gøtzsche, Richard Smith, Drummond Rennie, Deadly Medicines and Organised Crime, 2019
Peter C. Gøtzsche, Richard Smith, Drummond Rennie
Similar stories can be told from other therapeutic areas.100 A cardiac arrhythmia suppression trial (CAST)was stopped prematurely because the two active drugs, encainide and flecainide, killed the patients. This trial was originally designed as one-sided, which means that the drug can only be beneficial or neutral, since the cardiologists couldn’t imagine that the treatments could be harmful.101 At the peak of their use in the late 1980s, anti-arrhythmic drugs were likely causing about 50 000 deaths every year in the United States alone, which is of the same order of magnitude as the total number of Americans who died in the Vietnam War.102 The drugs were widely used because they had an effect on a surrogate outcome, the ECG, and although the FDA had serious safety concerns, they gave in to the pressures of the companies, which – quite predictably – led to the drugs being used in many completely healthy people with benign rhythm disturbances that many of us have.
Ventricular arrhythmias in the elderly
Published in Wilbert S. Aronow, Jerome L. Fleg, Michael W. Rich, Tresch and Aronow’s Cardiovascular Disease in the Elderly, 2019
Jason T. Jacobson, Sei Iwai, Wilbert S. Aronow
The Cardiac Arrhythmia Suppression Trial (CAST) I was a prospective, double-blind, randomized study in survivors of MI with asymptomatic or mildly symptomatic VA in which 730 patients, of whom 38% were 66–79 years of age, were randomized to class Ic agents encainide or flecainide and 725 patients to placebo (59). The prevalence of nonsustained VT was 21%. Mean LV ejection fraction was 40%. Adequate suppression of VA by encainide or flecainide was required before randomization. Despite adequate suppression of VA, at 10-month follow-up, encainide and flecainide significantly increased mortality from arrhythmia or cardiac arrest (relative risk = 3.6; 95% confidence interval [CI] 1.7–8.5) and significantly increased total mortality (relative risk = 2.5; 95% CI 1.6–4.5) (57). Older age increased the likelihood of adverse events, including death, in patients receiving encainide and flecainide (60).
Precision medicine in cardiac electrophysiology: where we are and where we need to go
Published in Expert Review of Precision Medicine and Drug Development, 2020
Ashish Correa, Syed Waqas Haider, Wilbert S. Aronow
From the 1960s through the 1980s, arrhythmia management rested on anti-arrhythmic drugs. However, over time, there was gradual recognition that any putative benefits brought on by these drugs were counterbalanced by various adverse effects, particularly pro-arrhythmic effects. The first major trial to demonstrate this was the Cardiac Arrhythmia Suppression Trial I (CAST I) in 1989 which randomized post-myocardial infarction patients to either antiarrhythmic therapy (with Class I agents flecainide, encainide, and/or moricizine) or placebo to analyze reduction sudden cardiac death (SCD) by malignant arrhythmias [1]. The trial had to be stopped early, because while the drugs did reduce premature ventricular contractions (PVCs) and non-sustained ventricular tachycardias (NSVT), they demonstrated a significant increase in mortality, primarily by pro-arrhythmic effects. This trial was followed by several other trials assessing anti-arrhythmics for the primary prevention of SCD, particularly in heart failure (HF) and post-myocardial infarction patients. These largely demonstrated no benefit, and sometimes even harm [2–4]. For atrial fibrillation (AF) and atrial flutter, apart from beta-blockers, calcium channel blockers, and the Class III agent amiodarone, very few anti-arrhythmic agents have shown long-term benefits. One notable exception is dofetilide, which was shown to be effective in cardioverting patients, both with and without concomitant HF, to sinus rhythm and in maintaining sinus rhythm [5,6].
Association of QRS duration with left ventricular volume and ejection fraction after anterior myocardial infarction assessed by gated single photon emission computed tomography
Published in Acta Cardiologica, 2018
Satoshi Kurisu, Yoji Sumimoto, Hiroki Ikenaga, Ken Ishibashi, Yukihiro Fukuda, Yasuki Kihara
ECG is an universally available, non-invasive and inexpensive examination. Several studies have assessed the effects of QRS duration on the prognosis after MI. Capone et al. [6] showed that QRS prolongation as well as high NYHA functional class or low LVEF was associated with mortality in placebo-treated patients after MI in the Cardiac Arrhythmia Suppression Trial. Jordaens et al. [5] also revealed that NYHA functional class > I and filtered QRS duration ≥110 ms were important predictive variables for sudden death in patients after MI. However, few studies have examined the effects of intermediate QRS duration on LV volume and ejection fraction [14]. Murkofsky et al. [14] revealed that prolonged QRS duration was a specific, but relatively insensitive indicator of decreased LVEF using radionuclide ventriculography. Their study did not assess the status of myocardial perfusion, and possibly consisted of ischaemic and nonischemic heart diseases. Also, end-diastolic and end-systolic counts were used simply for estimating LVEDV and LVESV. In the present study, we included patients with prior anterior MI, and assigned patients with QRS duration ≥100 ms to intermediate QRS prolongation group because the upper limit of normal QRS duration is generally considered <100 ms, and this criterion has been used in previous studies [7,8]. We demonstrated that patients with intermediate QRS prolongation had larger LVEDV and lower LVEF compared to those with normal QRS. Furthermore, QRS duration was positively associated with LVEDV, and was inversely associated with LVEF. Possible mechanisms for intermediate QRS prolongation associated with larger LV volume include the longer time required to activate dilated LV, decreased conduction velocity in dilated LV and changes in the relative conductivity of fibrotic spaces after MI as previously discussed by Okin et al. [15–18] in hypertrophied LV. Our results suggested that intermediate QRS prolongation was a simple ECG maker for LV dilatation after anterior MI.
Current pharmacotherapeutic strategies for cardiac arrhythmias in heart failure
Published in Expert Opinion on Pharmacotherapy, 2020
Ashish Correa, Yogita Rochlani, Wilbert S. Aronow
The Cardiac Arrhythmia Suppression Trial (CAST I) showed the marked pro-arrhythmic effects of class I antiarrhythmics (flecainide, encainide, propafenone) in the post-myocardial infarction population [61]. Extrapolating this information to the HF population, these agents are generally avoided in patients with HF.