Prevention of Sudden Cardiac Death After a First Myocardial Infarction by Pharmacologic or Surgical Antiadrenergic Interventions

Abstract

Introduction: Growing evidence points to sympathetic hyperactivity as one critical trigger for life-threatening arrhythmias among postmyocardial infarction patients.Methods and Results: We have evaluated, in a placebo-controlled multicenter study, the efficacy of a /3-adrenergic blocking agent (oxprenolol 160 mg) and of a selective left cardiac sympathetic denervation in preventing sudden death in patients with a first and anterior myocardial infarction. Two patient groups were studied. The high-risk group included 144 patients who survived a myocardial infarction complicated by either ventricular tachycardia or fibrillation. The relatively low-risk group included 869 patients whose myocardial infarction did not have these complications; they were allocated only to placebo or oxprenolol. Randomization took place 30 days postmyocardial infarction; mean follow-up was 22 months. In the high-risk group the sudden cardiac death (crude rate) in the placebo subgroup was indeed high (21.3%), and was strikingly reduced to 2.7% and to 3.6% by oxprenolol and by left cardiac sympathetic denervation, respectively (P < 0.05). In the low-risk group the sudden cardiac death (crude rate) in the placebo subgroup was 5.2% and was still reduced by oxprenolol to 1.6% (P < 0.05). The results for total mortality were quite similar to those for sudden death iu both groups.Conclusion: This study, unique for the populations studied and for one of the treatments used, demonstrates that pharmacologic and surgical antiadrenergic interventions significantly reduce sudden cardiac death in postmyocardial infarction patients at high and at low risk. With due consideration to the relatively small size of the high-risk group, it seems reasonable to suggest that left cardiac sympathetic denervatiou may be considered as a possible alternative for high-risk patients with contraindications to beta hlockers. (

Clinical Management of Catecholaminergic Polymorphic Ventricular Tachycardia

“…The results are based on a strong rationale 21 and match those already observed in other arrhythmogenic conditions. 18,[22][23][24] These findings should therefore have an important impact on the approach to managing CPVT.…”

Left Cardiac Sympathetic Denervation in the Management of High-Risk Patients Affected by the Long-QT Syndrome

“…20,21 Clinically, the only randomized study with LCSD has demonstrated a significant reduction (from 22% to 3.5% during a 21-month follow-up) of SD among high-risk postmyocardial infarction patients. 22 Thus, there is a strong experimental and clinical rationale fostering the expectation that, especially in the setting of augmented sympathetic activity, life-threatening arrhythmias might be prevented or reduced by LCSD.…”

Focal myocardial infarction induces global remodeling of cardiac sympathetic innervation: neural remodeling in a spatial context

“…autonomic nervous system; sympathetic nerves; cardiac innervation; neural remodeling REMODELING of the cardiac sympathetic nervous system after myocardial infarction (MI) has been linked to ventricular arrhythmias in animal models (29) and in humans (4,12,24). Modulation of cardiac sympathetic signaling is a major therapeutic strategy to prevent and treat ventricular arrhythmias (1,8,22). Despite its importance, the global electrophysiological consequences of postinfarct neural remodeling from a focal infarct remain poorly characterized.…”