ArticleESC heart failure2024
Intramyocardial calcification in apical hypertrophic cardiomyopathy assessed using multimodality imaging: a case series.
Article in ESC heart failure, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Multimodality imaging of a rare case of apical hypertrophic cardiomyopathy with endomyocardial fibrosis and myocardial calcification: case report and literature review.Frontiers in cardiovascular medicine · 2026Article
- Precision management of severe coronary artery calcification with concomitant left ventricular outflow tract obstruction: a case report.Frontiers in medicine · 2026Article
- Heart Failure in the Modern Era: A Narrative Overview of Recent Research from 2022-2025.Journal of cardiovascular development and disease · 2025Review
- Apical Hypertrophic Cardiomyopathy With Endomyocardial Calcification: A Multimodality Imaging-Based Case Report.Cureus · 2025Article
- Intramyocardial calcification in apical hypertrophic cardiomyopathy assessed using multimodality imaging: a case series.ESC heart failure · 2024Article
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apical hypertrophic cardiomyopathy (ApHCM) is an HCM variant, affecting frequently males in midlife. It is characterized by apical obliteration and persistent diastolic contraction, often resulting in microvascular ischaemia. We report five cases of ApHCM, with evidence of intramyocardial calcification on echocardiogram. On cardiac magnetic imaging (MRI), a hypointense component at early gadolinium enhancement (EGE) sequences, compatible with calcium, and a deep layer, with hyperintensity at late gadolinium enhancement (LGE) sequences, referable to fibrosis, suggest an endomyocardial fibrosis (EMF) diagnosis. EMF pathologic hallmark is endocardium and myocardium scarring, evolving to dystrophic calcification. It is found only in few ApHCM patients. Our series is the largest one described until now. Analysing patients' history, coexistent inflammatory triggers were evident in all of them, so their co-morbidities could represent a further cause of small vessel disease, in the context of ischaemic microvascular stress due to hypertrophy, leading to fibrosis and dystrophic calcification. This series could demonstrate the relation between apical fibrosis/calcification and microvascular ischaemia due to hypertrophy and inflammatory triggers.
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