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Pathogenesis of ventricular tachycardia and ventricular fibrillation during acute myocardial infarction

INTRODUCTION

Life-threatening ventricular arrhythmias — ventricular tachycardia (VT) and ventricular fibrillation (VF) — are infrequent but serious complications of an acute ST-elevation myocardial infarction (MI). The largest experience on the incidence of VT and VF during an acute ST elevation MI comes from the GUSTO-1 trial of 40,895 patients who were treated with thrombolytic therapy [1]. The overall incidence of sustained VT or VF was 10.2 percent: 3.5 percent developed VT, 4.1 percent VF, and 2.7 percent both VT and VF. Approximately 80 to 85 percent of these arrhythmias occurred in the first 48 hours.

Sustained ventricular arrhythmias are less common in patients with an acute non-ST elevation MI or unstable angina, as illustrated in a pooled analysis of four major trials of over 25,000 such patients [2]. The overall incidence of VT or VF was 2.1 percent, lower than the 10.2 percent incidence in GUSTO-1 in STEMI [3]. VT occurred in 0.8 percent, VF in 1 percent, and VT and VF in 0.3 percent. The median time to arrhythmia was 78 hours.

Sustained VT and VF in the setting of myocardial infarction result from the complex interaction of multiple factors, including myocardial ischemia (with resulting local electrolyte abnormalities), necrosis, reperfusion, healing, and scar formation. In addition, there are autonomic changes resulting from the infarction that have an important impact. These events produce the mechanisms that initiate arrhythmias and the substrate for arrhythmia perpetuation. Arrhythmia pathogenesis varies at different stages in this process. For ventricular arrhythmias occurring more than 48 to 72 hours after an acute myocardial infarction (MI), scar formation is of primary importance.

Ventricular arrhythmias during acute MI are typically classified based upon their time of onset. This scheme is useful clinically because VT and VF occurring early (≤24 to 48 hours) have been thought to be epiphenomena of the MI and do not require long-term therapy because they are not associated with a worse prognosis after hospital discharge. In contrast, VT or VF occurring later is generally thought to reflect the development of arrhythmic substrate, and require chronic therapy because of an increased risk of sudden cardiac death. (See "Clinical features and treatment of ventricular arrhythmias during acute myocardial infarction".)

This topic will review the mechanisms of arrhythmogenesis during acute MI, with particular attention to serious ventricular arrhythmias occurring in the first 48 to 72 hours. The clinical features and management of these arrhythmias are discussed separately. (See "Clinical features and treatment of ventricular arrhythmias during acute myocardial infarction".)

                 

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Literature review current through: Sep 2014. | This topic last updated: May 1, 2014.
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