| Summary: | <p>Abstract</p> <p>Originally described by Brock and Teare, today hypertrophic cardiomyopathy is clinically defined as left (or right) ventricular hypertrophy without a known cardiac or systemic cause, such as systemic hypertension, Fabry's disease or aortic stenosis.</p> <p>Also appreciated today is the enormous genotypic and phenotypic heterogeneity of this disease with more than 300 mutations over more than 24 genes, encoding various sarcomeric, mitochondrial and calcium-handling proteins, all as genetic causes for hypertrophic cardiomyopathy.</p> <p>Phenotypically, the disease can vary from negligible to extreme hypertrophy, affecting either the left and/or right ventricle in an apical, midventricular or subaortic location.</p> <p>Left ventricular false tendons are thin, fibrous or fibromuscular structures that traverse the left ventricular cavity. Recently, a case report was presented where it was shown that such a false tendon, originating from a subaortic location, was responsible for striking ST-segment elevation on the surface electrocardiogram.</p> <p>In this case report, a case is presented where such a subaortic tendon led to the classic echocardiographic appearance of hypertrophic cardiomyopathy, thus in the assessment of hypertrophic cardiomyopathy, this entity needs to be excluded in order to prevent a false positive diagnosis of hypertrophic cardiomyopathy.</p>
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