Abstract
Familial hypertrophic cardiomyopathy is caused by mutations in cardiac sarcomere proteins. Along with distinct histopathological features, it is also associated with a high risk of ventricular arrhythmias and sudden cardiac death during exercise. β1--adrenergic receptor blockers are administered as therapy in patients with hypertrophic cardiomyopathy because the drug improves diastolic function and reduces outflow-obstruction but its role as an antiarrhythmic during increased sympathetic stimulation has not been clarified.
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