Intramyocardial calcification in apical hypertrophic cardiomyopathy assessed using multimodality imaging: a case series.

Autor: Radano I; Department of Cardiology, Mauriziano Hospital, Torino, Italy., Mabritto B; Department of Cardiology, Mauriziano Hospital, Torino, Italy., Luceri S; Department of Cardiology, Mauriziano Hospital, Torino, Italy., Bongioanni S; Department of Cardiology, Mauriziano Hospital, Torino, Italy., Maiellaro F; Department of Cardiology, Santa Croce e Carle Hospital, Cuneo, Italy., Zappia L; Department of Cardiology, Mauriziano Hospital, Torino, Italy., Lario C; Department of Radiology, Mauriziano Hospital, Torino, Italy., Macera A; Department of Radiology, Mauriziano Hospital, Torino, Italy., Cirillo S; Department of Radiology, Mauriziano Hospital, Torino, Italy., Pizzuti A; Department of Cardiology, Mauriziano Hospital, Torino, Italy., Citro R; Department of Cardiology, University Hospital San Giovanni di Dio e Ruggi d'Aragona, Salerno, Italy., Galasso G; Department of Cardiology, University Hospital San Giovanni di Dio e Ruggi d'Aragona, Salerno, Italy., Musumeci G; Department of Cardiology, Mauriziano Hospital, Torino, Italy.
Jazyk: angličtina
Zdroj: ESC heart failure [ESC Heart Fail] 2024 Aug; Vol. 11 (4), pp. 2415-2420. Date of Electronic Publication: 2024 Apr 17.
DOI: 10.1002/ehf2.14775
Abstrakt: 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.
(© 2024 The Authors. ESC Heart Failure published by John Wiley & Sons Ltd on behalf of European Society of Cardiology.)
Databáze: MEDLINE
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