International medical case reports journal · 2026
Apical Hypertrophic Cardiomyopathy Misdiagnosed as Hypertensive Heart Disease Due to Anchoring Bias in an African Man: A Case Report.
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Okema James Nelson, Chukwuocha Chigozie, Danvictor Ebirim, Uche Clinton Nwanaga, Ekengwu Chigozie Charles, Egharevba Jovita Eghe, Ebunoluwa Esther Oniagba, Bongomin Felix
Аннотация
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.
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.