PATHOPHYSIOLOGY AND NATURAL HISTORY CORONARY ARTERY DISEASE Dynamics of left ventricular filling at rest and during exercise

Left ventricular filling dynamics were examined at rest and during supine bicycle exercise in 33 patients at cardiac catheterization; 23 had coronary artery disease (ischemia group), five with prior infarction had an akinetic area at rest (scar group), and five had minimal cardiovascular disease (control). Peak filling rate and mean filling rate during the first half and second half of diastole were assessed by biplane angiography. Simultaneous micromanometer pressures were used to compute the time constant of isovolumic pressure decay (T). Peak filling rate and mean filling rate during the first half of diastole increased with exercise in all groups (from 615 to 1050 and 358 to 681 ml/sec in controls and comparably in the scar group and from 697 to 1035 and 347 to 768 ml/sec in the ischemia group). However, T was greater (reduced rate of pressure decay) with exercise in the ischemia group (38 vs 26 msec in controls; p < .05). Changes in the atrial driving pressure for filling appeared to counterbalance the difference in T. Mean filling rate during the second half of diastole increased with exercise in controls and in the scar group but only modestly in the ischemia group (from 202 to 349 ml/ sec). The reduction in late diastolic filling during exercise-induced ischemia was associated with increased filling in early diastole, with a middiastolic volume increase from 160 to 186 ml and an upward shift in the diastolic pressure-volume relation. Thus left ventricular filling is not impaired at rest in patients with coronary artery disease who have normal ejection fractions. Furthermore, the augmentation of early filling induced by exercise is not blunted but is maintained during ischemia, apparently at the expense of elevated left atrial pressure. However, late filling is restricted with ischemia by an increase in impedance. Circulation 68, No. 1, 59-67, 1983. LEFT VENTRICULAR FILLING is a dynamic process involving the interaction of active and passive properties of the atria and ventricles. The rate of left ventricular pressure decay and the atrial-ventricular pressure gradient are major influences on ventricular filling in the early stages, ' and the operative stiffness of the left ventricle becomes increasingly important as filling progresses.2 Finally, the strength and timing of atrial contraction provide the end-diastolic "kick" to ventricular filling, which is frequently of importance in disease states.3-9 During exercise and ischemia, cardiovascular function alters substantially. Ventricular filling must occur in an abbreviated diastole. During exercise, the rate of pressure decay in the norrmal ventricle increases sigFrom the Department of Internal Medicine, Medical Policlinic, Division of Cardiology, University Hospital, Zurich, Switzerland. Supported by a grant from the Swiss National Science Foundation. Address for correspondence: H. P. Krayenbuehl, Medical Policlinic, University Hospital, 8091, Zurich, Switzerland. Received April 30, 1982; revision accepted March 10, 1983. *Current address: Department of Medicine, University of Chicago. Vol. 68, No. 1, July 1983 nificantly and filling pressures remain unaltered, 10.11 whereas pressure decay is abnormal and filling pressures are grossly elevated in the ischemic ventricle. I'l3 A major question must therefore be answered: What effects on ventricular filling are caused by relaxation abnormalities in patients with coronary artery disease? Some data have suggested that early filling rates are limited both at rest and during exercise in patients with coronary artery disease,'4, '5 yet simultaneous accurate measurements of ventricular volume and pressure have not been previously reported. We have recently presented data on the abnormalities of ventricular pressure decay and their influence on diastolic pressures during exercise-induced ischemia in man.'0 In this part of our study, we focus on the alterations in ventricular filling in three groups of patients: coronary patients with exercise-induced ischemia, patients with prior infarction but no ischemia with exercise, and control subjects. In addition, we provide data on the influence of left ventricular pressure decay, the driving pressure for filling, and the inflow impedance of the left ventricle on filling. 59 by gest on A ril 2, 2017 http://ciajournals.org/ D ow nladed from