Front Cardiovasc Med. 2026 Mar 26;13:1752135. doi: 10.3389/fcvm.2026.1752135. eCollection 2026.
ABSTRACT
Hypertrophic cardiomyopathy (HCM) and cardiac amyloidosis (CA) are major causes of myocardial thickening, yet they arise from distinct genetic, structural, and pathophysiological mechanisms. Differentiating these entities is clinically crucial, as management strategies and prognostic implications differ substantially. However, overlapping phenotypic features, particularly left ventricular hypertrophy, frequently complicate diagnosis. Recent advances in multimodality cardiac imaging have markedly improved the ability to distinguish HCM from CA through refined anatomical assessment and non-invasive tissue characterization. Echocardiography helps evaluate ventricular structure, diastolic function, and flow patterns. Asymmetric septal hypertrophy, dynamic left ventricular outflow tract (LVOT) obstruction, and systolic anterior motion (SAM) of the mitral valve are characteristic of HCM, while concentric wall thickening, biatrial enlargement, restrictive filling, and the "apical sparing" strain pattern point toward CA. Cardiac MRI adds further diagnostic value through tissue characterization. In HCM, late gadolinium enhancement (LGE) typically appears as patchy mid-wall or junctional fibrosis, whereas in CA it is diffuse, involving the subendocardium or the full wall thickness. Mapping parameters also help differentiate the two conditions: native T1 and ECV are mildly elevated in HCM but markedly increased in CA due to extensive extracellular amyloid deposition.
PMID:41969688 | PMC:PMC13062188 | DOI:10.3389/fcvm.2026.1752135