Abstract
Early pharmacological interventions on transgenic models of hypertrophic cardiomyopathy (HCM) using angiotensin receptor blockers (ARBs) may be effective in preventing development of clinical phenotype or causing phenotype regression in early stages of disease. In the clinical setting, however, the effects of ARBs on HCM phenotype have been less consistent. INHERIT (INHibition of the renin angiotensin system in hypertrophic cardiomyopathy and the Effect on hypertrophy—a Randomised Intervention Trial with losartan) was designed to assess the effect of 100 mg of losartan in promoting the regression of LV hypertrophy in HCM. The primary end-point of the study was the reduction in LV mass assessed by MRI or computed tomography. After 12 months, no reduction in LV mass was observed in the losartan arm, and there was no difference in LV mass change with the placebo arm. The same was true for all secondary endpoints. The implications of these findings are discussed in the light of further, ongoing study targeting the HCM phenotype.
Highlights
Hypertrophic cardiomyopathy (HCM) is caused by mutations in genes coding cardiac sarcomere proteins such as myosin binding protein C and beta-myosin heavy chain, generating complex pathophysiological manifestations, which translate into a heterogeneous spectrum of morphological and clinical phenotypes.[3]
While the disease is defined by the presence of asymmetric left ventricular (LV) hypertrophy, features such as impaired cardiomyocyte energetics, increased calcium sensitivity, microvascular ischemia, myocardial fibrosis, diastolic dysfunction, dynamic LV outflow obstruction, atrial fibrillation and ventricular arrhythmias are all part of the disease spectrum, representing established or potential targets for treatment.[2,4]
Pharmacological interventions in patients with HCM are often necessary for control of symptoms, arrhythmias and obstruction
Summary
Hypertrophic cardiomyopathy (HCM) is the most common genetic heart disease, with prevalence in the general population of 1:500, and represents an important cause of cardiovascular morbidity and sudden cardiac death in young individuals.[1,2] HCM is caused by mutations in genes coding cardiac sarcomere proteins such as myosin binding protein C and beta-myosin heavy chain, generating complex pathophysiological manifestations, which translate into a heterogeneous spectrum of morphological and clinical phenotypes.[3].
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