Abstract
This editorial refers to ‘Augmentation of left ventricularmechanics by recirculation-mediated AAV2/1-SERCA2agene delivery in experimental heart failure’ by JustinMariani et al. published in this issue on page 247–253.Therapy of congestive heart failure was revolutionized more than20 years ago by the introduction of angiotensin-convertingenzyme inhibitors and b-adrenoceptor blocking agents. Bothhave resulted in the improvement of symptoms and prognosis ofpatients with chronic heart failure. In the meantime, device-basedtherapies have been added to the therapeutic armamentarium.However, all attempts to directly address molecular alterations rel-evant to heart failure pathophysiology as treatment strategies havefailed. Because morbidity and mortality of heart failure patients arestill unacceptably high, there is an urgent need for new treatmentstrategies. Alterations of calcium cycling have been identified as asignificant contributor to heart failure pathophysiology, and there-fore, therapeutic strategies addressing calcium homeostasis seemlogical.
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