Left ventricular noncompaction shares a molecular etiology with other cardiomyopathic phenotypes through sarcomere protein gene defects.
Consider sarcomere gene testing in LVNC; extends the cardiomyopathy spectrum but remains hypothesis-generating.
We conclude that left ventricular noncompaction is within the diverse spectrum of cardiac morphologies triggered by sarcomere protein gene defects. Our findings support the hypothesis that there is a shared molecular etiology of different cardiomyopathic phenotypes.
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Klaassen et al. (2008) studied this question.
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