Prophylaxis against ventricular arrhythmias during and after acute myocardial infarction
- Philip J Podrid, MD, FACC
Philip J Podrid, MD, FACC
- Professor of Medicine, Professor of Pharmacology and Experimental Therapeutics
- Boston University School of Medicine
- Lecturer, Harvard Medical School
- Leonard I Ganz, MD, FHRS, FACC
Leonard I Ganz, MD, FHRS, FACC
- Section Editor — Cardiac Arrhythmias
- Director of Cardiac Electrophysiology
- Heritage Valley Health System
- Section Editors
- Brian Olshansky, MD
Brian Olshansky, MD
- Section Editor — Cardiac Arrhythmias
- Adjunct Professor of Medicine
- Des Moines University
- Bernard J Gersh, MB, ChB, DPhil, FRCP, MACC
Bernard J Gersh, MB, ChB, DPhil, FRCP, MACC
- Editor-in-Chief — Cardiovascular Medicine
- Section Editor — Coronary Heart Disease; Myopericardial Disease
- Professor of Medicine
- Mayo Clinic College of Medicine
Sudden cardiac death (SCD) in the setting of an acute myocardial infarction (MI) is most frequently the result of a ventricular tachyarrhythmia. The appearance of a sustained ventricular tachyarrhythmia following a myocardial infarction, such as ventricular tachycardia (VT) or ventricular fibrillation (VF), in the early period post-MI may be the harbinger of ongoing myocardial ischemia, the development of pro-arrhythmic myocardial scar tissue, elevated sympathetic tone or increase in circulating catecholamines, or an electrolyte disturbance such as hypokalemia. In-hospital mortality approaches 20 percent or more in patients who develop VT or VF following a myocardial infarction. As such, rapid identification and treatment of these arrhythmias can be life-saving. (See "Clinical features and treatment of ventricular arrhythmias during acute myocardial infarction".)
Because of the marked increase in mortality associated with ventricular arrhythmias following a myocardial infarction, many researchers have focused on ways to prevent ventricular arrhythmias in the early post-MI period. This topic will focus on prophylaxis against ventricular arrhythmias following myocardial infarction (MI), primarily focusing on the appropriate use or non-use of antiarrhythmic medications. Treatment for established ventricular arrhythmias in the post-MI patient, using defibrillation with or without antiarrhythmic medications, is discussed separately. (See "Advanced cardiac life support (ACLS) in adults" and "Clinical features and treatment of ventricular arrhythmias during acute myocardial infarction", section on 'Sustained ventricular tachycardia' and "Clinical features and treatment of ventricular arrhythmias during acute myocardial infarction", section on 'Ventricular fibrillation' and "Role of antiarrhythmic drugs for ventricular arrhythmias in patients with a prior myocardial infarction".)
TYPES OF VENTRICULAR ARRHYTHMIAS
While many studies have evaluated the incidence of ventricular arrhythmias in the peri-infarct period, comparison of these studies is difficult due to differences in populations (percutaneous intervention therapy versus fibrinolytic therapy versus no therapy), type of infarct (ST elevation myocardial infarction (STEMI) versus non-STEMI versus both) and types of arrhythmia reported (eg, ventricular premature beats, ventricular tachycardia, ventricular fibrillation). The clinical significance of different types of ventricular ectopy following myocardial infarction also varies markedly.
Ventricular premature beats — Ventricular premature beats (VPBs), which are typically asymptomatic, are common after acute MI with a reported incidence as high as 93 percent . The early occurrence of VPBs does not predict short- or long-term mortality, but frequent and/or multiform VPBs that persist more than 48 to 72 hours after an MI may be associated with an increased long-term arrhythmic risk. Also of importance early after an acute MI are R-on-T VPBs. The pathogenesis of VPBs after MI and issues related to VPBs in patients with a prior MI are discussed separately. (See "Clinical features and treatment of ventricular arrhythmias during acute myocardial infarction", section on 'Ventricular premature beats'.)
Non-sustained ventricular tachycardia — The significance of non-sustained ventricular tachycardia (NSVT) following myocardial infarction (MI) or acute coronary syndrome (ACS) is dependent upon the proximity of the arrhythmia to the time of the MI. In the first 24 to 48 hours after MI, NSVT is usually due to transient abnormalities of automaticity or triggered activity in the region of ischemia or infarction; in comparison, NSVT that occurs later is more often due to reentry and permanent arrhythmic substrate. However, the incidence and prognostic significance of NSVT appear lower with contemporary primary percutaneous reperfusion therapies. (See "Pathogenesis of ventricular tachycardia and ventricular fibrillation during acute myocardial infarction" and "Incidence of and risk stratification for sudden cardiac death after acute myocardial infarction", section on 'NSVT on monitoring'.)
Subscribers log in hereLiterature review current through: Jul 2017. | This topic last updated: May 16, 2016.References
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- TYPES OF VENTRICULAR ARRHYTHMIAS
- Ventricular premature beats
- Non-sustained ventricular tachycardia
- Accelerated idioventricular rhythm
- Sustained ventricular tachycardia
- - Sustained monomorphic ventricular tachycardia
- - Polymorphic ventricular tachycardia
- Ventricular fibrillation
- Late arrhythmias
- Electrolyte supplementation
- - Potassium
- - Magnesium
- Beta blockers
- Antiarrhythmic drugs
- - Class Ic agents
- - Lidocaine
- - Amiodarone
- Device therapy
- SUMMARY AND RECOMMENDATIONS