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Sympathetic Activation and Arrhythmogenesis after Myocardial Infarction: Where Do We Stand?

Journal

Publisher

MDPI
DOI: 10.3390/jcdd8050057

Keywords

myocardial infarction; ventricular tachyarrhythmias; sympathetic activation

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Myocardial infarction leads to structural and electrophysiologic remodeling of the left ventricle, causing high morbidity and mortality from ventricular tachyarrhythmias. Research has shown alterations in sympathetic nerve endings post-infarction, creating an arrhythmogenic environment and sparking interest in neuromodulation therapy.
Myocardial infarction often leads to progressive structural and electrophysiologic remodeling of the left ventricle. Despite the widespread use of beta-adrenergic blockade and implantable defibrillators, morbidity and mortality from chronic-phase ventricular tachyarrhythmias remains high, calling for further investigation on the underlying pathophysiology. Histological and functional studies have demonstrated extensive alterations of sympathetic nerve endings at the peri-infarct area and flow-innervation mismatches that create a highly arrhythmogenic milieu. Such accumulated evidence, along with the previously well-documented autonomic dysfunction as an important contributing factor, has stirred intense research interest for pharmacologic and non-pharmacologic neuromodulation in post-infarction heart failure. In this regard, aldosterone inhibitors, sacubitril/valsartan and sodium-glucose cotransporter type 2 inhibitors have shown antiarrhythmic effects. Non-pharmacologic modalities, currently tested in pre-clinical and clinical trials, include transcutaneous vagal stimulation, stellate ganglion modulation and renal sympathetic denervation. In this review, we provide insights on the pathophysiology of ventricular arrhythmogenesis post-myocardial infarction, focusing on sympathetic activation.

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