Arrhythmic risk stratification of post–myocardial infarction patients

Abstract

Post-myocardial infarction risk stratification, especially arrhythmic risk stratification, is an issue that has still not been wholly addressed in modern clinical cardiology. In the past 10 years, arrhythmic risk stratification has been approached mainly by evaluating frequency and complexity of premature ventricular contractions, detected on Holter monitoring, often in association with determination of percent ejection fraction. This methodology has been proven to be limited and fallacious according to the Cardiac Arrhythmia Suppression Trial I and II (CAST I,II) results, in which suppression of premature ventricular contractions or premature ventricular beats throughout by antiarrhythmic drugs resulted in an increase in both cardiac and arrhythmic mortality. Only amiodarone as an antiarrhythmic drug, as proven in the recent European Myocardial Infarct Amiodarone Trial (EMIAT) and Canadian Amiodarone Myocardial Infarction Trial (CAMIAT), was effective in reducing arrhythmic mortality without affecting cardiac mortality, in patients selected mainly because of a reduced ejection fraction, with and without premature ventricular contractions. Conversely, it is well known that beta-blockers are effective in preventing sudden death in post-acute myocardial infarction (AMI) patients, thus reducing cardiac and arrhythmic mortality. Conversely, in other institutions, risk stratification in post-AMI patients has been performed by electrophysiologic study obtained, without any previous noninvasive arrhythmic risk stratification, in all post-AMI patients. In recent years, many other noninvasive electrocardiology parameters, such as late potentials (signal-averaged electrocardiography), heart rate variability, baroreflex sensitivity, and, more recently, T-wave alternance, have been shown to be useful, but they are associated with a low specificity in the noninvasive identification of patients at high risk for arrhythmic mortality. Conversely, in the Multicenter Automatic Defibrillation Implantation Trial (MADIT), electrophysiology confirmed that inducibility of ventricular tachycardia shows high specificity and a high predictive value for arrhythmic events. Nevertheless, the MADIT study population is not comparable to a cohort of consecutive patients who have recently had a myocardial infarction. In this setting, the highest risk of arrhythmic events can be observed in patients with depressed percent ejection fraction (< 35%) and in the first 6 months after AMI. Today, the most convincing approach seems to be the one combining both noninvasive risk stratification parameters (e.g., premature ventricular beats > 10/h or reduced heart rate variability < 70 ms or a positive signal-averaged electrocardiogram) followed by a further arrhythmic risk stratification, obtained through electrophysiologic study. Several published and ongoing trials that utilize various arrhythmic risk stratification techniques as part of their protocol are reviewed.

Prognostic value of heterogeneity of ventricular repolarization in survivors of acute myocardial infarction

“…The following cut-off values were predefined for risk stratification: EF < 35%. 19 tQRS > 114 ms, 20 > 10 VE/h, 21,22 HRV < 20 U, 23 HRT < 2.5 mm/RR. 18 The method of calculating TCRT has been described previously.…”

Mechanically induced potentials in atrial fibroblasts from rat hearts are sensitive to hypoxia/reoxygenation

“…Contractile dysfunction of the heart due to arrhythmia is a major cause of cardiovascular mortality after myocardial infarction (reviewed in [18,23]). The molecular mechanisms that underlie the rhythm disturbances in the ischemic heart are beginning to emerge.…”

Impact of anemia in patients with acute myocardial infarction undergoing primary percutaneous coronary intervention

“…Early and late prognosis of patients with acute myocardial infarction (AMI) is principally dependent on three major variables: left ventricular function, susceptibility to ventricular arrhythmias, and residual ischemia after reperfusion (1)(2)(3). Reduction in the hemoglobin concentration may compromise oxygen supply to infarcted or ischemic myocardium, which may promote arrhythmias, worsen hypotension, and increase infarct size (4 -6).…”