A clinical approach to the assessment of left ventricular diastolic function by Doppler echocardiography: update 2003

Patients with heart disease frequently have abnormalities of systolic function. However, it is now well recognised that abnormalities of diastolic function play a major role in producing the signs and symptoms of heart failure.1,2 Thirty to fifty per cent of patients with heart failure have normal systolic function, implicating diastolic dysfunction as a major pathophysiologic abnormality. It is important to understand and recognise abnormalities of diastolic filling of the heart for proper diagnosis, prognosis, and institution of treatment.3 Doppler echocardiography has become the primary tool for the assessment of diastolic function and left ventricular filling pressures. The purpose of this review is to summarise the physiology of diastole and develop a practical clinical approach for the non-invasive assessment of diastolic filling of the heart. ### Cellular definition At the cellular level diastole can be considered as beginning when ATP hydrolyses and actin–myosin crossbridges become unlinked allowing for sarcomeric relaxation. This is integrally related to decreasing intracellular concentrations of calcium owing to enhanced sarcoplasmic reuptake of calcium. These cellular processes actually occur in some cells while other cells are still demonstrating active contraction. Thus cellular diastole may actually begin while left ventricular pressure is still rising. Dysfunction at the cellular level is mediated principally via decreased ATP hydrolysis and/or impaired uptake of the intracellular calcium. When the actin–myosin interaction is prolonged, there is a delay and prolongation of sarcomeric expansion. Additionally, in the case of regional ischaemia, there may be regional cellular impairment such that the heart ceases to function as a syncytium. ### Mechanical definition Mechanically, diastole is considered to begin when the pressure within the left ventricle begins to fall—that is, during the isovolumic relaxation phase. This would occur after a significant number of myocardial cells had entered cellular diastole and is a metabolically active phase. The left ventricular pressure will continue …