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Indexed/Abstracted in: BIOSIS Previews, EMBASE, Scopus, Emerging Sources Citation Index
Online ISSN 1827-1812
Incardona V. M., Dato E., Dato A. G.
Centro di Diagnostica Cardiovascolare del Dott. Dato Achille Giuseppe & C., Paternò, Catania, Italia
Cardiac hypertrophy is a major determinant of mortality and morbidity including the risk of sudden cardiac death in patients with hypertrophic cardiomyopathy (HCM). The conventionally used pharmacological agents in treatment of patients with HCM have not been shown to reverse or attenuate established cardiac hypertrophy and fibrosis. An effective treatment of HCM has to target the molecular mechanisms that are involved in the pathogenesis of the phenotype. Severus studies suggest that cardiac hypertrophy in HCM is secondary to activation of various hypertrophic signaling molecules and is potentially reversible. The results have shown potential beneficial effects of angiotensin II receptor blocker losartan, mineralocorticoid receptor blocker spironolactone, HMG-CoA reductase inhibitors simvastatin and atorvastatin, and most recently, N-acetylcysteine (NAC) on reversal or prevention of hypertrophy and fibrosis in HCM. The most promising results have been obtained with NAC. The results in animal models have established the reversibility of cardiac hypertrophy and fibrosis in HCM.