Cardiac mitochondria and Heart Failure: the chicken or the egg?

Current medical therapies for heart failure are aimed at suppressing the neurohormonal activation (e.g., angiotensin converting enzyme [ACE] inhibitors, angiotensin II receptor antagonists, beta-adrenergic receptor antagonists, aldosterone receptor antagonists) and/or treating fluid volume overload and hemodynamic symptoms (diuretics, digoxin, inotropic agents). Evidence suggests that intense suppression of the neurohormonal systems does not provide further benefit compared with more modest therapy. There is a need for novel therapies for heart failure that are independent of the neurohormonal axis and can improve cardiac performance and prevent the progression of heart failure and heart remodeling. Modulation of mitochondrial metabolism and the oxidative status of the myocardium may represent a new approach to the treatment of heart failure and could work additively with standard medical therapy while not exerting negative hemodynamic effects.