Key result
Echo and strain imaging correctly identify apical HCM to guide symptom-resolving therapy in a misdiagnosed patient.
Why the study?
ApHCM is frequently misdiagnosed as hypertensive heart disease in African patients with longstanding hypertension, especially in resource-limited settings where CMR is unavailable, often driven by anchoring bias.
Case Report (n=1)
Answers are grounded in this paper and cite their sources.
Anchoring bias may drive ApHCM misdiagnosis as hypertensive heart disease in African patients; case report leaves open need for improved diagnostics where CMR is unavailable.
Background: Apical hypertrophic cardiomyopathy (ApHCM) is an uncommon variant of hypertrophic cardiomyopathy, accounting for approximately 5– 10% of all cases. It is frequently misdiagnosed as hypertensive heart disease in African patients with longstanding hypertension, particularly in resource-limited settings where cardiac magnetic resonance imaging (CMR) is unavailable. Anchoring bias, the tendency to adhere to an initial diagnosis despite contradictory evidence is a well-recognized contributor to this diagnostic error. Case Presentation: A 60-year-old African man with a 15-year history of hypertension presented with exertional dyspnea and palpitations. Initial differentials included hypertensive heart disease, coronary artery disease, and dilated cardiomyopathy. Troponin I was negative. Electrocardiography revealed deep symmetric T-wave inversions (7– 9 mm) in anterolateral leads without voltage criteria for left ventricular hypertrophy. Transthoracic echocardiography demonstrated apical-predominant hypertrophy (apical wall 18 mm, posterior wall 11 mm; ratio 1.6), preserved ejection fraction (55– 60%), and classic systolic apical cavity obliteration with an ace-of-spades configuration. Speckle-tracking echocardiography showed selective apical longitudinal strain reduction (− 12%) with preserved basal strain (− 18%). These findings established ApHCM. Dual renin-angiotensin system blockade and unindicated clopidogrel were discontinued, bisoprolol was optimized, and symptoms resolved completely within two weeks. Conclusion: Deep T-wave inversions without voltage criteria for left ventricular hypertrophy should prompt focused apical echocardiographic assessment, even in patients with longstanding hypertension. An apical-to-posterior wall thickness ratio of at least 1.5 with systolic apical cavity obliteration permits ApHCM diagnosis without CMR. Selective apical strain reduction distinguishes ApHCM from hypertensive heart disease. Recognizing anchoring bias is essential to avoid diagnostic delay when electrocardiographic and echocardiographic findings are discordant.
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Okema et al. (2026) conducted a case report in Apical Hypertrophic Cardiomyopathy (n=1). Diagnostic reassessment and medication optimization was evaluated on Symptom resolution. Echocardiography and strain imaging correctly identified apical hypertrophic cardiomyopathy in a misdiagnosed hypertensive patient, leading to complete symptom resolution after medication optimization.
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