Myocardial Fibrosis as a Pathway of Prediction of Ventricular Arrhythmias and Sudden Cardiac Death in Patients With Nonischemic Dilated Cardiomyopathy

Abstract

The mechanism of sudden cardiac death (SCD) in patients with nonischemic dilated cardiomyopathy (NIDCM) is mostly due to sustained ventricular tachycardia and ventricular fibrillation. The clinical guidelines for the therapeutic management of this set of patients are mostly based on left ventricular ejection fraction value which has a low specificity to differentiate the risk of SCD from the risk of mortality associated with heart failure or other comorbidities. Moreover, since SCD can occur in patients with normal or mildly depressed ejection fraction, it is necessary to identify new markers to improve the prognostic stratification of SCD. Several studies that analyzed the ventricular arrhythmia substrate found that myocardial fibrosis plays an important role in the genesis of ventricular arrhythmias in patients with NIDCM. The surrounding zone of the area of fibrosis is a heterogeneous medium, where tissue with different levels of fibrosis coexists, resulting in both viable and nonviable myocardium. This myocardial fibrosis may constitute a substrate for ventricular arrhythmias, where slow and heterogeneous conduction may favor the genesis of reentry mechanism increasing the chance to develop sustained ventricular tachycardia or ventricular fibrillation. Therefore, the evaluation of ventricular fibrosis by late gadolinium enhancement (LGE) cardiac magnetic resonance imaging has been suggested as an indicator for SCD risk stratification. Indeed, LGE in patients with NIDCM is associated with increased risk of all-cause mortality, heart failure hospitalization, and SCD. Detection of myocardial fibrosis as LGE by cardiac magnetic resonance imaging can be considered as a useful pathway of prediction of malignant ventricular arrhythmias since it has excellent prognostic characteristics and may help guide risk stratification and management in patients with NIDCM.

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“…Its presence suggests more severe heart disease and is associated with a more reserved prognosis, due to accelerated heart dysfunction [ 26 ]. Additionally, myocardial fibrosis plays an important role in the genesis of ventricular arrhythmia, through reentry mechanisms, increasing the risk of sustained ventricular tachycardia or ventricular fibrillation [ 27 ]. The relationship between galectin-3 values and myocardial fibrosis in patients with nonischemic dilated cardiomyopathy was first described by Vergano and collaborators.…”

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“…Diffuse myocardial fibrosis may lead to left ventricular dysfunction and heart failure [ 172 ]. Ongoing myocardial injury, pericardial inflammation, microvascular ischemia, and fibrosis related to SARS-CoV-2 infection are associated with ventricular tachycardia [ 160 , 173 ] and atrial fibrillation (AF) [ 174 ]. In a similar manner, inflammatory processes provoked by SARS-CoV2 may induce long-term vascular damage and accelerate the formation of atherosclerotic plaques in the coronary arteries and the aorta, which is a theme yet to be investigated in long-term follow-up studies [ 175 ].…”

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“…[5][6][7] Myocardial fibrosis plays a key role in the maintenance of arrhythmia, which can cause cardiac remodeling, affect the diastolic and contractile functions of the heart, and even cause malignant arrhythmias and sudden cardiac death. 8,9) The content and distribution of cardiac fibrotic tissue in patients with AF are related to the mechanism of AF, the risk of complications, and the effect of treatment. 10) Myocardial fibrosis is a key pathological feature of AF that leads to the excessive deposition of extracellular matrix, causing myocardial remodeling and even heart failure, including increased myocardial interstitial collagen deposition and abnormal distribution and excessive proliferation of myocardial fibroblasts.…”