The Research http://bit.ly/2qwV33U Group on Cardiovascular Diseases of the Vall d'Hebron Research Institute (VHIR), a member group of http://bit.ly/2qwZbB0 CIBERCV and led by Dr. David Gacía-Dorado, has carried out a study with rats in which they have shown for the first time that the chronic inhibition of the calpain (enzymes activated by the increase of intracellular calcium) is possible through an oral treatment and could become a therapeutic strategy to mitigate damage to the heart after acute myocardial infarction.Previous studies have shown that the activation of calpain plays an important role in the death of myocardial cells during reperfusion and that its inhibition decreases the size of the infarct.In the present study, published in the journal http://bit.ly/2rQDy2k Cardiovascular Research, using a transient coronary occlusion infarction model in rats, Dr. Javier Inserte et al. show that calpains persist overactivated during the weeks following an infarct and that overactivation plays a key role in the development of adverse ventricular remodeling (a series of changes that affect the heart after the infarction favouring the appearance of arrhythmias)."Daily oral administration of a novel calpain inhibitor - with specific properties that make it absorbable orally - prevents this overactivation, reduces ventricular remodeling, and improves contractile function at 21 days of infarction, even if treatment is started one day after the coronary occlusion episode, decreasing hypertrophy, fibrosis and inflammation in the non-infarcted myocardium," explains Dr. Javier Inserte, principal investigator of the Research Group on Cardiovascular Diseases of the VHIR. The results suggest that this protective effect of calpain inhibition is due to the prevention of the effect of calpain on regulatory molecules of gene expression.This study demonstrates for the first time that chronic inhibition of calpain is possible by oral treatment and may represent a therapeutic strategy aimed at attenuating adverse remodeling and heart failure in patients who survive acute myocardial infarction," highlights Dr . García-Dorado. Given the importance of post-infarction adverse remodeling as a cause of heart failure and the absence of treatments capable of effectively preventing it, these results are very promising.Myocardial infarctionMyocardial infarction, a condition usually caused by thrombotic occlusion of a coronary artery, is one of the main manifestations of ischemic heart disease.Although the acute reopening of the occluded artery by primary angioplasty (with a catheter) or with thrombolytic agents has markedly reduced mortality in the acute phase of the infarction, many patients survive with significant myocardial damage and subsequently develop heart failure, a situation increasingly more prevalent, with high mortality and with a huge personal, social and economic impact.The mechanism by which survivors of an infarct develop heart failure is adverse ventricular remodeling, a series of changes that affect not only the infarcted area but the entire heart producing progressive ventricular dilation, fibrosis on the myocardium, decrease of the contractile function and alterations of the propagation of the electric impulse that favour the appearance of serious, potentially fatal arrhythmias.Therefore, the development of effective and clinically applicable treatments that interfere with the cellular and molecular mechanisms involved in adverse ventricular remodeling is a priority objective in the fight to reduce the socio-health impact of ischemic heart disease.