Key result
Neural modulation, including left stellectomy or beta-blocker therapy, is highlighted as an effective strategy for preventing ventricular tachyarrhythmias and sudden cardiac death after myocardial infarction.
Why the study?
Does neural modulation reduce ventricular arrhythmias and sudden cardiac death after myocardial infarction?
Does neural modulation reduce ventricular arrhythmias and sudden cardiac death after myocardial infarction?
This review highlights the molecular mechanisms of cardiac sympathetic hyperinnervation post-MI and the therapeutic potential of neural modulation to prevent malignant ventricular arrhythmias.
Should not yet alter post-MI arrhythmia management; leaves open the role of neural modulation pending randomized evidence.
Ventricular arrhythmogenesis is thought to be a common cause of sudden cardiac death following myocardial infarction (MI). Nerve remodeling as a result of MI is known to be an important genesis of life-threatening arrhythmias. It is hypothesized that neural modulation might serve as a therapeutic option of malignant arrhythmias. In fact, left stellectomy or β-blocker therapy is shown to be effective in the prevention of ventricular tachyarrhythmias (VT), ventricular fibrillation (VF), and sudden cardiac death (SCD) after MI both in patients and in animal models. Results from decades of research already evidenced a positive relationship between abnormal nerve density and ventricular arrhythmias after MI. In this review, we summarized the molecular mechanisms involved in cardiac sympathetic rejuvenation and mechanisms related to sympathetic hyperinnervation and arrhythmogenesis after MI and analyzed the potential therapeutic implications of nerve sprouting modification for ventricular arrhythmias and SCD control.
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Li et al. (2015) conducted a review in Myocardial Infarction and Ventricular Arrhythmias. Neural modulation (left stellectomy or β-blocker therapy) was evaluated. Neural modulation, including left stellectomy or beta-blocker therapy, is highlighted as an effective strategy for preventing ventricular tachyarrhythmias and sudden cardiac death after myocardial infarction.
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