Cellular and Molecular Mechanisms of Heart Failure and Sudden Cardiac Death in Hypertrophic Cardiomyopathy and Methods Used for Their Pathogenetic Correction

<b>Background/Objectives:</b> This paper provides a review of the literature data concerning the cellular and molecular mechanisms of heart failure and sudden cardiac death in hypertrophic cardiomyopathy (HCM), and explores approaches used for their pathogenetic correction. <b>Methods</b>: This study highlights genetically determined targets of primary damage to the cardiomyocyte ultra-structure-the actomyosin complex of sarcomeres and mitochondria. <b>Results/Conclusions</b>: Damage to these structures leads to heart failure and an increased risk of sudden cardiac death, manifesting against a background of phenotypic features such as cardiac remodeling, asymmetric hypertrophy, left ventricular outflow tract obstruction, myofiber disarray, and atrial fibrillation. Both invasive and non-invasive approaches for the pathogenetic management of these fatal complications are characterized.

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Publication Details

Journal
Biomedicines
Published
2025-11-28
DOI
https://doi.org/10.3390/biomedicines13122926
Primary Topic
Cardiomyopathy and Myosin Studies
Type
article
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article

Cellular and Molecular Mechanisms of Heart Failure and Sudden Cardiac Death in Hypertrophic Cardiomyopathy and Methods Used for Their Pathogenetic Correction

N.A. Gutyrchik, Н. Б. Тихонова, Yu. V. Belov, Л.М. Михалева et al.
Biomedicines
Cardiomyopathy and Myosin Studies
article

Cellular and Molecular Mechanisms of Heart Failure and Sudden Cardiac Death in Hypertrophic Cardiomyopathy and Methods Used for Their Pathogenetic Correction

N.A. Gutyrchik, Н. Б. Тихонова, Yu. V. Belov, Л.М. Михалева, Z.V. Gioeva, Lev Kakturskiy, A.B. Lysenko
article en

Abstract

<b>Background/Objectives:</b> This paper provides a review of the literature data concerning the cellular and molecular mechanisms of heart failure and sudden cardiac death in hypertrophic cardiomyopathy (HCM), and explores approaches used for their pathogenetic correction. <b>Methods</b>: This study highlights genetically determined targets of primary damage to the cardiomyocyte ultra-structure-the actomyosin complex of sarcomeres and mitochondria. <b>Results/Conclusions</b>: Damage to these structures leads to heart failure and an increased risk of sudden cardiac death, manifesting against a background of phenotypic features such as cardiac remodeling, asymmetric hypertrophy, left ventricular outflow tract obstruction, myofiber disarray, and atrial fibrillation. Both invasive and non-invasive approaches for the pathogenetic management of these fatal complications are characterized.

BiomedicinesVol. 13(12)
Peoples' Friendship University of Russia (RU), Research Institute of Human Morphology (RU)
Openalex Percentile: Top 45%
Cardiomyopathy and Myosin Studies
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