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A sparkling case of familial, cardiac‐specific amyloidosis

In a 74-year-old black man referred for worsening dyspnea, electrocardiogram showed atrial fibrillation, inferior infarction pattern, and low voltage (Fig. 1A). Echocardiogram revealed severe bi-atrial enlargement, valvular thickening without doming, and severe concentric left ventricular hypertrophy with a uniform, sparkling appearance of all ventricular walls (Figs. 1B, C). Bone marrow and fat pad biopsies were negative for immunoglobulin or systemic amyloidosis. Spot planar 99technetium-pyrophosphate uptake scintigraphy showed diffuse myocardial uptake consistent with cardiac amyloidosis (Fig. 1D). Genetic testing revealed a heterozygous isoleucine (Ile 122) mutation in the transthyretin gene (TTR) known to result in nonimmunoglobulin, cardiac-specific amyloidosis. Transthyretin Ile 122 mutation is present in up to 4% of black Americans and may be a cause of increased prevalence of heart failure among older black Americans.1