Key result
Autonomic dysfunction during acute myocardial infarction is characterized by early vagal withdrawal and subsequent sympathetic activation, coinciding with peaks in ventricular tachyarrhythmias.
This review highlights the biphasic autonomic response (early vagal withdrawal, later sympathetic activation) as a key arrhythmogenic mechanism for ventricular tachyarrhythmias during acute myocardial infarction.
May inform arrhythmia risk timing in AMI; leaves open prospective trials of autonomic modulation.
Most cases of sudden cardiac death are attributed to sustained ventricular tachyarrhythmias (VTs), triggered by acute coronary occlusion. Autonomic dysfunction, an important arrhythmogenic mechanism in this setting, is being actively investigated, aiming at the advent of preventive strategies. Recent experimental studies have shown vagal withdrawal after anterior myocardial infarction, coinciding with high incidence of VTs, followed by more gradual sympathetic activation coinciding with a second arrhythmia peak. This article summarizes recent knowledge on this intriguing topic, generating hypotheses that can be investigated in future experimental and clinical studies.
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Theofilos M. Kolettis (2018) conducted a review in Acute myocardial infarction and ventricular tachyarrhythmias. Autonomic dysfunction was evaluated. Autonomic dysfunction during acute myocardial infarction is characterized by early vagal withdrawal and subsequent sympathetic activation, coinciding with peaks in ventricular tachyarrhythmias.
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