# The Role of Cardiac Magnetic Resonance Imaging in the Management of Hypertrophic Cardiomyopathy

## TL;DR

This paper discusses how cardiac MRI helps diagnose and manage hypertrophic cardiomyopathy, a heart condition with varied symptoms and genetic causes.

## Contribution

The paper highlights the growing role of contrast-enhanced cardiac MRI in diagnosing and managing hypertrophic cardiomyopathy.

## Key findings

- CMR provides detailed cardiac morphology and function information in HCM patients.
- CMR detects hypertrophy in areas not visible via echocardiogram and identifies myocardial fibrosis.
- CMR aids in evaluating LV outflow tract obstruction and assessing LV function in advanced HCM.

## Abstract

Hypertrophic cardiomyopathy (HCM) is the most common genetic cardiomyopathy, caused by either sarcomere protein or other gene mutations. It is a complex and highly heterogeneous disorder, with phenotypes ranging from asymptomatic to severe disease, characterized by asymmetric left ventricular (LV) hypertrophy unexplained by loading conditions, which is also associated with myocardial fiber disarray, and preserved or increased ejection fraction without LV dilation. Comprehensive personal and family history, physical examination, and ECG testing raise suspicion of HCM, and echocardiogram represents the first-line imaging modality for confirming a diagnosis. Moreover, contrast-enhanced cardiac magnetic resonance (CMR) imaging has increasingly emerged as a fundamental diagnostic and prognostic tool in HCM management. This article reviews the role of CMR in HCM identification and differentiation from phenotypic mimics, characterization of HCM phenotypes, monitoring of disease progression, evaluation of pre- and post-septal reduction treatments, and selection of candidates for implantable cardioverter-defibrillator. By providing information on cardiac morphology and function and tissue characterization, CMR is particularly helpful in the quantification of myocardial wall thickness, the detection of hypertrophy in areas blind to echocardiogram, subtle morphologic features in the absence of LV hypertrophy, myocardial fibrosis, and apical aneurysm, the evaluation of LV outflow tract obstruction, and the assessment of LV function in end-stage dilated HCM.