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Zekios KC, Mouchtouri ET, Lekkas P, et al. Sympathetic Activation and Arrhythmogenesis after Myocardial Infarction: Where Do We Stand?. J Cardiovasc Dev Dis. 2021;8(5)doi: 10.3390/jcdd8050057.
Zekios, K. C., Mouchtouri, E. T., Lekkas, P., Nikas, D. N., & Kolettis, T. M. (2021). Sympathetic Activation and Arrhythmogenesis after Myocardial Infarction: Where Do We Stand?. Journal of cardiovascular development and disease, 8(5), . https://doi.org/10.3390/jcdd8050057
Zekios, Konstantinos C, et al. "Sympathetic Activation and Arrhythmogenesis after Myocardial Infarction: Where Do We Stand?." Journal of cardiovascular development and disease vol. 8,5 (2021). doi: https://doi.org/10.3390/jcdd8050057
Zekios KC, Mouchtouri ET, Lekkas P, Nikas DN, Kolettis TM. Sympathetic Activation and Arrhythmogenesis after Myocardial Infarction: Where Do We Stand?. J Cardiovasc Dev Dis. 2021 May 15;8(5). doi: 10.3390/jcdd8050057. PMID: 34063477; PMCID: PMC8156099.
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J Cardiovasc Dev Dis. 2021 May 15;8(5). doi: 10.3390/jcdd8050057.

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

Journal of cardiovascular development and disease

Konstantinos C Zekios, Eleni-Taxiarchia Mouchtouri, Panagiotis Lekkas, Dimitrios N Nikas, Theofilos M Kolettis

Affiliations

  1. 1st Department of Cardiology, University Hospital of Ioannina, 1 St. Niarxou Avenue, 45500 Ioannina, Greece.
  2. Department of Cardiology, University of Ioannina, 1 St. Niarxou Avenue, 45500 Ioannina, Greece.
  3. Cardiovascular Research Institute, 1 St. Niarxou Avenue, 45500 Ioannina, Greece.

PMID: 34063477 PMCID: PMC8156099 DOI: 10.3390/jcdd8050057

Abstract

Myocardial infarction often leads to progressive structural and electrophysiologic remodeling of the left ventricle. Despite the widespread use of β-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.

Keywords: myocardial infarction; sympathetic activation; ventricular tachyarrhythmias

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