Diastolic function and heart failure: an overview.
Diastolic dysfunction is being recognized increasingly as a primary cause of congestive heart failure. It may result from physiological abnormalities of myocardial relaxation, or anatomical abnormalities which increase resistance to ventricular inflow. With regard to physiological abnormalities, there is substantial evidence to indicate that myocardial ischaemia and hypertrophy are two conditions characterized by impaired inactivation and relaxation of myocardial cells. These conditions often co-exist in patients with idiopathic hypertrophic subaortic stenosis or calcific valvular aortic stenosis. Recent evidence also suggests a role for calcium overload in the diastolic dysfunction seen in some patients with advanced congestive heart failure. Diastolic dysfunction may be of fundamental importance in the pathophysiology of flash pulmonary oedema in patients with advanced ischaemic heart disease, since myocardial ischaemia in such patients may lead to a decline in relaxation rate, increased resistance to early diastolic filling and further impairment in diastolic coronary blood flow due to intramyocardial compression of capillaries and venules. During the transient ischaemia of angina pectoris, patients with multivessel coronary artery disease often show a striking upward shift in the left ventricular diastolic pressure-volume relationship, signifying a marked decrease in distensibility of the left ventricular chamber. With regard to anatomical abnormalities, diastolic dysfunction in heart failure may result from structural changes within the ventricular wall. Diastolic dysfunction of the left ventricle may result from extrinsic compression by pericardial effusion (tamponade), pericardial constriction, and right ventricular overload. Thus, a variety of physiological and anatomical abnormalities may lead to increased resistance to diastolic filling of one or both ventricles, resulting in diastolic heart failure.
Charles A. Dana Research Institute, Beth Israel Hospital, Boston, Massachusetts 02215.
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D003971:Diastole / Q000502:physiology*; D006333:Heart Failure / Q000503:physiopathology*; D006801:Humans; D009200:Myocardial Contraction / Q000502:physiology*