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Intramyocardial calcification in apical hypertrophic cardiomyopathy assessed using multimodality imaging: a case
Ilaria Radano1, Barbara Mabritto1, Stefania Luceri1
1Department of Cardiology, Mauriziano Hospital, Torino, Italy.
Insights
Apical hypertrophic cardiomyopathy (ApHCM) can involve intramyocardial calcification, potentially mimicking endomyocardial fibrosis (EMF). Inflammatory triggers may contribute to fibrosis and calcification in ApHCM patients.
Area of Science:
- Cardiology
- Cardiovascular Imaging
- Pathology
Background:
- Apical hypertrophic cardiomyopathy (ApHCM) is a variant of hypertrophic cardiomyopathy characterized by apical obliteration and diastolic dysfunction.
- It frequently affects middle-aged males and can lead to microvascular ischemia.
Observation:
- This study reports five cases of ApHCM with evidence of intramyocardial calcification on echocardiography.
- Cardiac MRI revealed hypointensity on early gadolinium enhancement (EGE) sequences (suggesting calcium) and hyperintensity on late gadolinium enhancement (LGE) sequences (suggesting fibrosis).
Findings:
- The imaging findings suggest a potential diagnosis of endomyocardial fibrosis (EMF), characterized by scarring and dystrophic calcification.
- This series represents the largest description of ApHCM with these features to date.
- Coexistent inflammatory triggers were identified in all patients, suggesting a role in the development of small vessel disease.
Implications:
- The findings suggest a link between apical fibrosis/calcification and microvascular ischemia in ApHCM.
- Inflammatory comorbidities may exacerbate microvascular stress in the context of cardiac hypertrophy.
- This research highlights a potential pathway involving inflammation, hypertrophy, fibrosis, and calcification in ApHCM.
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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