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Although the claim is commonly made that age-associated physiological changes predispose older adults to develop heart failure with normal EF, the aetiology of diastolic heart failure is unknown. More than 50% of patients with heart failure have normal or near normal EF and the incidence and prevalence of this condition increases with age. The aging myopathy typically manifests itself with diastolic dysfunction and preserved ejection fraction (EF) 1. Thus, I NaL offers inotropic support, but negatively interferes with cellular and ventricular compliance, providing a new perspective of the biology of myocardial aging and the aetiology of the defective cardiac performance in the elderly. Similarly, repolarization and diastolic tension of the senescent myocardium are partly restored. Inhibition of I NaL shortens the AP and corrects dynamics of Ca 2+ transient, cell contraction and relaxation. These alterations increase force development and passive tension. Here we show that an increase in the late Na + current ( I NaL) in aging cardiomyocytes prolongs the action potential (AP) and influences temporal kinetics of Ca 2+ cycling and contractility. We raised the possibility that, in a mouse model of physiological aging, defects in electromechanical properties of cardiomyocytes are important determinants of the diastolic characteristics of the myocardium, independently from changes in structural composition of the muscle and collagen framework. The aging myopathy manifests itself with diastolic dysfunction and preserved ejection fraction.