Tale of two hearts: a TNNT2 hypertrophic cardiomyopathy case report

Figures

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  Figure 1. Targeted family pedigree. Family members with a confirmed diagnosis of HCM are denoted by solid dark shapes. Patient A and patient B are denoted by the letters A and B, respectively. Deceased family members are denoted with a diagonal line. Diamonds represent the presence of additional family members within a generation who have not been diagnosed with HCM.

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  Figure 2. Imaging of patient A. Parasternal long axis echocardiogram prior to septal myectomy (A). The interventricular septum has reverse curve morphology, with a septal thickness measurement of 33 mm (red line) during diastole and a patent left ventricular outflow tract. Right anterior oblique caudal angiogram with prominent myocardial bridging of the large first and second septal perforators (B). Parasternal long axis echocardiogram, status-post septal myectomy (C). Four-chamber echocardiogram, with increased apical cavity size following septal myectomy (D).

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  Figure 3. Imaging of patient B. Parasternal long axis echocardiogram, with an interventricular septal thickness measurement of 11 mm during diastole, and a patent left ventricular outflow tract (A). Right anterior oblique caudal angiogram demonstrating a diminutive left anterior descending artery (B). Images (C–F): cardiac magnetic resonance imaging of patient B. Near-transmural delayed gadolinium enhancement of the mid inferior and inferoseptal wall segments, short-axis view (C). Near-transmural delayed gadolinium enhancement of the mid inferior and inferoseptal wall segments, four-chamber view (D). Focus of mid-myocardial delayed gadolinium enhancement in the mid anteroseptal wall segment, short-axis view (E). Near-transmural septal hypoperfusion, short-axis view (F).

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  Figure 4. Recommended diagnostic paradigm for TNNT2 HCM.