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Arrhythmias and Hypertrophic Cardiomyopathy: Unravelling the Connection
Kanishk Aggarwal1, Sri Pranvi Boyapati2, Jayesh Valecha3
1Dayanand Medical College & Hospital, Punjab, India.
Insights
Hypertrophic cardiomyopathy (HCM) causes heart muscle thickening due to gene mutations. This review covers HCM
Area of Science:
- Cardiology
- Genetics
- Electrophysiology
Background:
- Hypertrophic cardiomyopathy (HCM) is a genetic heart disease affecting 1:200-1:500 individuals.
- Characterized by left ventricular hypertrophy, HCM involves sarcomeric gene mutations and autosomal dominant inheritance.
- HCM increases risks of heart failure, thromboembolism, and sudden cardiac death due to arrhythmias.
Purpose of the Study:
- To discuss the pathophysiology of arrhythmias in hypertrophic cardiomyopathy.
- To review clinical recommendations for managing atrial and ventricular arrhythmias in HCM patients.
- To highlight risk stratification for sudden cardiac death in HCM.
Main Methods:
- Literature review of HCM pathophysiology and arrhythmia mechanisms.
- Analysis of clinical guidelines for managing arrhythmias in HCM.
- Discussion of diagnostic and therapeutic strategies for HCM-related arrhythmias.
Main Results:
- HCM pathophysiology involves myocardial structural changes and triggers like exertion, leading to reentry and arrhythmias.
- Atrial fibrillation (AF) is common in HCM, necessitating anticoagulation and antiarrhythmic drugs.
- Ventricular arrhythmias, including sudden cardiac death, require risk assessment and interventions like ICDs.
Conclusions:
- Comprehensive analysis of clinical, anatomical, hemodynamic, functional, and genetic factors is crucial for risk stratification.
- Management strategies include long-term anticoagulation, antiarrhythmic drugs, catheter ablation, and implantable cardioverter-defibrillators (ICDs).
- Understanding arrhythmia mechanisms in HCM guides personalized treatment approaches to reduce mortality.
Abstract:
Hypertrophic cardiomyopathy (HCM) results from gene mutations affecting cardiac sarcomeres and is inherited in an autosomal dominant manner. With a prevalence of 1:200-1:500 in the general population, HCM is characterised by a hypertrophied and non-dilated left ventricle with predominant involvement of the interventricular septum. The myocardium's structural and intracellular factors, combined with triggers such as physical exertion, autonomic dysfunction, and ischemia, can lead to reentry events, and atrial and ventricular arrhythmias, including atrial fibrillation (AF) which is common among HCM patients. To manage the increased risk of mortality arising from congestive heart failure and thromboembolism, in patients with AF long-term anticoagulation and antiarrhythmic drugs are employed. HCM patients may also encounter supraventricular and ventricular arrhythmias, such as nonsustained ventricular tachycardia and ventricular premature beats, which can potentially lead to sudden cardiac death and necessitate treatment with implanted defibrillators. Physicians must comprehensively analyse clinical, anatomical, hemodynamic, rhythmic, functional, and genetic characteristics to identify HCM patients at high risk of sudden death. This article aims to discuss the pathophysiology of arrhythmia in HCM and clinical recommendations for various ventricular and atrial fibrillation including catheter ablation and implantable cardioverter-defibrillator (ICD).
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