Recognition and treatment of left ventricular diastolic dysfunction

Abstract

B ASED ON EXTENSIVE research, it has become possible to focus on individual factors that cause or contribute to the clinical syndrome of congestive heart failure. These factors include the effects of ischemia and hypertrophy, changes in the peripheral circulation, alterations in reflex and neurohumoral function, the interdependent function of the right and left ventricles, and of signal importance to the clinician, the difference between systolic and diastolic dysfunction of the left ventricle.‘-” This article will discuss the distinction between systolic and diastolic dysfunction (Fig 1) and will answer three clinically relevant questions. What is diastolic dysfunction? How is it diagnosed? How is it treated? Diastolic dysfunction of the left ventricle (LV) is defined as an impaired capacity to accept blood or fill without a compensatory increase in left atria1 pressure. In its mildest form, diastolic dysfunction may appear as a slow or delayed pattern of relaxation and filling, with little or no elevation of LV diastolic pressure (there is generally little or no systolic dysfunction); thus, in patients with LV hypertrophy or coronary disease, an alteration in diastolic filling can serve as a sensitive and early indicator of disease.‘re2’ Diastolic dysfunction may also appear as overt congestive heart failure, even in the presence of normal or near-normal systolic function.22*23 In some ways diastolic dysfunction is similar to mitral stenosis; in this case, however, impaired filling is due to a reduced effective mitral orifice area. Thus, the concept of diastolic dysfunction as a mechanism underlying heart failure is similar to the description of “backward failure” as originally proposed by Hope.24 In recent years, clinicians and physiologists alike have reexamined their concepts about the pathophysiology of heart failure. The major focus has been to clarify the distinction between diastolic dysfunction (or failure) and systolic dysfunction. Simply stated, systolic dysfunction is the inability of the myofibrils to shorten against a load; thus, the left ventricle loses its ability to eject blood into a high-pressure aorta. Diastolic dysfunction implies that the ventricle can not accept blood at low pressures; ventricular filling is slow, delayed, or incomplete unless atria1 pressure increases. Consequently, pulmonary and/or systemic venous congestion develops. Thus, the signs and symptoms of pulmonary and/or systemic venous congestion are not necessarily the result of systolic dysfunction, instead they are related to alterations in diastolic properties of the LV chamber. These properties may consist of changes in the passive (or “static”) diastolic properties of the LV and/or changes in the “active” processes of relaxation and filling.