Therapeutic Strategies for Diastolic Dysfunction: A Clinical Perspective

Abstract

I In nt tr ro od du uc ct ti io on nDespite the fact that up to 50% of heart failure patients have preserved left ventricular (LV) systolic function, treatment of diastolic heart failure remains largely empiric because there have been no large scale randomized trials evaluating the effects of specific pharmacological agents. Nonpharmacologic, pharmacologic and surgical approaches are available, although its efficacy has not been proven. Treatment should target the underlying pathological condition that causes the diastolic heart failure. For example, coronary artery disease, hypertensive heart disease, hypertrophic obstructive cardiomyopathy, and constrictive pericarditis provide relatively specific therapeutic targets, such as lowering of blood pressure, regression of hypertrophy and fibrosis, and treatment of ischemia, and a complete removal of constricting pericardium. Theoretically, pharmacological agents that facilitate myocardial relaxation and improve LV compliance would be ideal for the treatment of diastolic dysfunction. As a shortterm therapeutic goal, manipulation of the loading conditions (preload, afterload) and control of the heart rate will be crucial. The treatment of underlying condition (e.g. hypertension) should be the ultimate goal for the treatment of LV diastolic dysfunction. Many of the drugs used for the treatment of symptoms of heart failure due to diastolic dysfunction are similar to those of systolic dysfunction, although the rationale for their use, the pathophysiological process that is being altered by the drug, and the dosing regimen may be entirely different. In this review, several therapeutic modalities including pharmacologic, nonpharmacologic, and surgical approaches for primary diastolic heart failure will be discussed. P Ph ha ar rm ma ac co ol lo og gi ic c T Th he er ra ap py y Angiotensin converting enzyme (ACE) inhibitors and angiotensin II receptor blockersACE-inhibitors and angiotensin II receptor blockers show not only an effect on blood pressure but elicit a direct effect on the myocardium via the local renin-angiotensin system. These effects are essential for the regression of LV hypertrophy, and the improvement in the elastic properties of the myocardium. 1)2) Several studies have documented that LV hypertrophy is more effectively reduced by ACE inhibitors than by other antihypertensive drugs, 3)4) suggesting an effect on myocardial structure beyond that provided by the reduction of pressure overload. Experimental and clinical studies suggest that the interaction of angiotensin II with its type 1 (AT1) receptors plays a critical role in alterations of collagen type I metabolism and development of myocardial fibrosis in arterial hypertension. Myocardial fibrosis is responsible for an increase in intrinsic myocardial stiffness that may alter the LV diastolic properties. Chronic activation of the reninangiotensin-aldosterone system has been shown to increase extracellular matrix fibrillar collagen and to be associated

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