Clinical, angiographic, and electrophysiologic findings in patients with aborted sudden death as compared with patients with sustained ventricular tachycardia after myocardial infarction.

Abstract

After the acute phase of myocardial infarction, patients who develop sustained ventricular arrhythmias present with either sudden death or ventricular tachycardia (VT). Although current evidence suggests that VT frequently precedes ventricular fibrillation (VF) in patients presenting with sudden death, the factors resulting in rapid deterioration of VT to VF have not been delineated in humans. To determine whether left ventricular function, coronary anatomy, or electrophysiologic characteristics could differentiate patients with sudden death from those with VT without sudden death, we compared results of cardiac angiography and programmed electrical stimulation in 42 patients referred for evaluation of sustained VT or surviving "aborted" sudden death for more than 9 days after myocardial infarction. By univariate analysis there were no differences between patients with sudden death and those with VT in age, time from myocardial infarction to VT or sudden death, ejection fraction (0.31 0.12 vs 0.29 + 0.09), or the number of patients with a major area of contracting myocardium supplied by an artery with a 50% or greater or a 70% or greater stenosis (84% vs 64% and 68% vs 41 %). Thirty-six percent of patients with sudden death but no patient with VT had two separate areas of infarction. During programmed electrical stimulation, a sustained ventricular arrhythmia was initiated in 100% of patients with VT and 73% of patients with sudden death and rapidly produced syncope in 67% of patients with sudden death but in only 5% of those with VT. This difference was due to the more frequent initiation of rapid polymorphic VT or VF (27% of patients) and to the shorter VT cycle length (242 + 31 vs 319 ± 69 msec) when monomorphic VT was induced in the group with sudden death. No difference was found in the number of extrastimuli required for initiation of a sustained ventricular arrhythmia. We conclude that (1) resting ventricular function and the potential for ischemia remote from the infarct fail to distinguish patients with sudden death from those with VT without sudden death, (2) electrophysiologic properties determining VT rate and stability are major determinants of the clinical presentation of VT after myocardial infarction, and (3) two separate areas of infarction may predispose to sudden death.

Effect of Nonuniform Muscle Contraction on Sustainability and Frequency of Triggered Arrhythmias in Rat Cardiac Muscle

“…Among these mechanisms, delayed afterdepolarizations (DADs) play an important role, especially in arrhythmias associated with catecholamine-excess,10, 11 heart failure,12-14 and mutations of the ryanodine receptor or calsequestrin 15. These arrhythmias can be benign or lethal in nature depending on their hemodynamic consequence, which is regulated by various factors, including their duration and ventricular rate, that is, sustainability and frequency 16, 17. While it has been reported that the sustainability and frequency of re-entrant arrhythmias are at least in part determined by the wavelength of re-entering impulse and the circuit path,18 what determines the sustainability and frequency of triggered arrhythmias remains to be established 19, 20…”

Life-Threatening Ventricular Arrhythmias: Current Role of Imaging in Diagnosis and Risk Assessment

“…Electrophysiological studies have suggested a greater risk for SCA among those with ischemic cardiomyopathy who have multiple areas of transmural infarction when compared to those with less extensive scars(36). In nonischemic cardiomyopathy the presence of midwall fibrosis has been reported to predict those at risk SCA(37).…”

Exploring susceptibility to atrial and ventricular arrhythmias resulting from remodeling of the passive electrical properties in the heart: a simulation approach

“…Ischemic cardiomyopathy (i.e., infarct-related) VT is the most frequent clinical ventricular arrhythmia, present in 64% of patients with ventricular rhythm disorder and in 89% of patients with sudden cardiac death (Stevenson et al, 1985). Recently, the peri-infarct (border) zone surrounding the necrotic scar, also known as GZs, as indicated above, based on its appearance as a region of intermediate intensity in the LGE-MRI scans, has been shown to correlate with post-MI mortality (Yan et al, 2006), clinical VT (Roes et al, 2009), and VT inducibility (Schmidt et al, 2007).…”