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Left Ventricular Apical Thrombus in Apical Hypertrophic Cardiomyopathy Without Aneurysm or Arrhythmia: A Case Report
Ibrahim Antoun1,2, Jeffrey Khoo1, Sanjay S Bhandari1
1Department of Cardiology, University Hospitals of Leicester NHS Turst, Leicester, UK.
Insights
A rare case of apical hypertrophic cardiomyopathy (ApHCM) presented with a large left ventricular thrombus despite preserved function. This highlights the risk of thrombotic complications in ApHCM, even without typical risk factors.
Area of Science:
- Cardiology
- Cardiovascular Imaging
- Internal Medicine
Background:
- Apical hypertrophic cardiomyopathy (ApHCM) is a rare variant of hypertrophic cardiomyopathy, usually with a benign prognosis.
- Complications like arrhythmias, apical aneurysms, and thrombus formation can occur.
- Left ventricular (LV) thrombus is uncommon in ApHCM, particularly with preserved systolic function and normal sinus rhythm.
Abstract:
Apical hypertrophic cardiomyopathy (ApHCM) is a rare variant of hypertrophic cardiomyopathy, typically associated with a benign course. However, complications such as ventricular arrhythmias, apical aneurysms, and thrombus formation may occur. Left ventricular (LV) thrombus is an unusual finding in ApHCM, especially in patients with preserved systolic function and normal sinus rhythm. A 54-year-old male with a history of pulmonary embolism and ApHCM was under routine surveillance. He remained asymptomatic with a normal sinus rhythm. Transthoracic echocardiography (TTE) identified an echogenic mass in the LV apex. Cardiac magnetic resonance imaging (CMR) confirmed severe apical hypertrophy, preserved LV systolic function, and a large apical mass measuring 24 × 19 mm. The mass showed no contrast uptake on early or late gadolinium enhancement sequences, consistent with thrombus. Native T1 mapping was mildly elevated, suggesting diffuse interstitial fibrosis, and focal non-ischaemic replacement fibrosis was noted. There was no evidence of apical aneurysm or mid-ventricular obstruction. The patient was anticoagulated with warfarin and remains under close follow-up. This case represents a rare occurrence of a large LV thrombus in ApHCM without associated apical aneurysm or impaired LV function. The findings suggest that regional fibrosis and altered apical flow dynamics may contribute to thrombus formation even in hypercontractile ventricles. Multimodal imaging, particularly CMR, is essential for accurate diagnosis and risk assessment. Clinicians should maintain vigilance for thrombotic complications in ApHCM, even in the absence of classical risk factors, as subtle fibrosis or flow abnormalities may predispose to thrombus formation.
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