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Multimodality cardiac imaging aids differentiation between hypertrophic cardiomyopathy and cardiac amyloidosis

Multimodality cardiac imaging aids differentiation between hypertrophic cardiomyopathy and cardiac a…
Photo by Marek Studzinski / Unsplash
Key Takeaway
Consider multimodality imaging patterns to help differentiate HCM from CA, but confirm diagnosis clinically.

This narrative review synthesizes evidence on the use of multimodality cardiac imaging—specifically echocardiography and cardiac MRI—to differentiate hypertrophic cardiomyopathy (HCM) from cardiac amyloidosis (CA) in patients presenting with myocardial thickening. The review does not report a specific sample size, study setting, or comparator, and it is based on a synthesis of existing literature rather than new patient data.

The review describes characteristic echocardiographic features for each condition. For HCM, these include asymmetric septal hypertrophy, dynamic left ventricular outflow tract obstruction, and systolic anterior motion of the mitral valve. For CA, features include concentric wall thickening, biatrial enlargement, restrictive filling, and an "apical sparing" strain pattern. On cardiac MRI, HCM is associated with patchy mid-wall or junctional fibrosis on late gadolinium enhancement (LGE), while CA shows diffuse LGE involving the subendocardium or full wall thickness. Mapping parameters show mildly elevated native T1 and extracellular volume (ECV) in HCM versus markedly increased values in CA. No quantitative effect sizes, absolute numbers, or statistical measures are reported for these findings.

Safety and tolerability data for the imaging modalities are not reported. Key limitations include the descriptive nature of the review, the lack of reported quantitative data or comparative performance metrics, and the absence of information on funding or conflicts of interest. The practice relevance is that differentiating HCM from CA is clinically crucial due to differing management strategies and prognoses, but this review provides a qualitative summary of imaging patterns rather than definitive diagnostic criteria.

Study Details

Study typeSystematic review
EvidenceLevel 1
PublishedMar 2026
View Original 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.
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