25-Year Evolution of Apical Hypertrophic Cardiomyopathy in a Professional Athlete

Figures

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  Visual Summary. Evolution of the Disease and of the Guidelines Twenty-five-year clinical course of a professional athlete with HCM showing progression from subclinical disease to apical HCM with fibrosis and late apical aneurysm formation across evolving guideline eras. AHA/ACC = American Heart Association/American College of Cardiology; ESC = European Society of Cardiology; HCM = hypertrophic cardiomyopathy.

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  Figure 1. Initial Electrocardiographic and Echocardiographic Evaluation (A) 2001: Baseline 12-lead ECG showing sinus rhythm with minor inferolateral T-wave inversion. (B) 2002: Follow-up ECG demonstrating progression of repolarization abnormalities. (C) 2001: Baseline apical 4-chamber echocardiographic view during a contrast echocardiogram study demonstrating normal left ventricular wall thickness. ECG = electrocardiogram.

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  Figure 2. Follow-Up Investigations (2005) Electrocardiogram showing extreme left ventricular (LV) hypertrophy and giant negative T waves with ST-segment depression in the lateral and inferior leads. Echocardiogram showing apical LV hypertrophy with a maximal wall thickness of 14 to 15 mm.

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  Figure 3. Evolution of the Electrocardiogram During Follow-Up (2017) QRS voltage and T-wave depth are decreased.

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  Figure 4. Late Gadolinium Enhancement Cardiac Magnetic Resonance Images (2017) Circumferential subendocardial fibrosis at the mid-segment to the apical segments. Late gadolinium enhancement becomes almost transmural at the lateral apical wall.

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  Figure 5. Cardiac Magnetic Resonance (2021) Akinesia of the true apex and of the lateral apical wall. Transmural scar of the lateral apical left ventricular wall.