UNLABELLED: Left ventricular diastolic pressure-volume relations (PVR) were analysed from biplane ventriculograms and simultaneous pressure measurements in 33 patients at rest (R) and during ergometer exercise (E) (8 normals [N], 8 patients with coronary artery disease [CAD], 8 patients with congestive cardiomyopathy [COCM], 5 patients with aortic insufficiency [AI] and 5 patients with pressure overload (4 with aortic stenosis [A-St.] and 1 coarctation of the aorta). In N and AI diastolic PVR was essentially unchanged with E, the time constant of isovolumic relaxation (T) decreased significantly (N: delta T = -24.4 +/- 11.6%, p less than 0.001; AI: delta T = -27.3 +/- 6.8%, p less than 0.005). In CAD diastolic PVR was shifted upwards in all cases with angina pectoris during E (7/8), minimal rate of left ventricular pressure change (dp/dtmin) and T did not change significantly. In COCM diastolic PVR was shifted upwards in 4 cases, while dp/dtmin increased significantly (R = -1107 +/- 327, E = -1508 +/- 626 mm Hg-s-1, p less than 0.05), T on the average was unchanged (R = 53 +/- 10.5, E = 51 +/- 14.2 msec). In A-St. in 3 of 4 cases diastolic PVR was significantly shifted upwards with E, dp/dtmin increased (R = -1633 +/- 93, E = -2093 +/- 170 mm Hg-s-1, p less than 0.001), T in contrast to N and AI was prolonged (R = 33.8 +/- 4, E = 39.9 +/- 1.9 msec). CONCLUSION: In N and AI diastolic ventricular function is not altered with exercise. In COCM and especially in A-St., however, there are similar alterations like in CAD with angina pectoris. Changes in T indicate that shifts of the PVR with exercise in non-ischemic heart disease are related to a disturbed ventricular relaxation.
UNLABELLED: Left ventricular diastolic pressure-volume relations (PVR) were analysed from biplane ventriculograms and simultaneous pressure measurements in 33 patients at rest (R) and during ergometer exercise (E) (8 normals [N], 8 patients with coronary artery disease [CAD], 8 patients with congestive cardiomyopathy [COCM], 5 patients with aortic insufficiency [AI] and 5 patients with pressure overload (4 with aortic stenosis [A-St.] and 1 coarctation of the aorta). In N and AI diastolic PVR was essentially unchanged with E, the time constant of isovolumic relaxation (T) decreased significantly (N: delta T = -24.4 +/- 11.6%, p less than 0.001; AI: delta T = -27.3 +/- 6.8%, p less than 0.005). In CAD diastolic PVR was shifted upwards in all cases with angina pectoris during E (7/8), minimal rate of left ventricular pressure change (dp/dtmin) and T did not change significantly. In COCM diastolic PVR was shifted upwards in 4 cases, while dp/dtmin increased significantly (R = -1107 +/- 327, E = -1508 +/- 626 mm Hg-s-1, p less than 0.05), T on the average was unchanged (R = 53 +/- 10.5, E = 51 +/- 14.2 msec). In A-St. in 3 of 4 cases diastolic PVR was significantly shifted upwards with E, dp/dtmin increased (R = -1633 +/- 93, E = -2093 +/- 170 mm Hg-s-1, p less than 0.001), T in contrast to N and AI was prolonged (R = 33.8 +/- 4, E = 39.9 +/- 1.9 msec). CONCLUSION: In N and AI diastolic ventricular function is not altered with exercise. In COCM and especially in A-St., however, there are similar alterations like in CAD with angina pectoris. Changes in T indicate that shifts of the PVR with exercise in non-ischemic heart disease are related to a disturbed ventricular relaxation.
Authors: D Baller; H G Wolpers; A Hoeft; H Korb; A Rösick; G Hellige; H J Bretschneider Journal: Basic Res Cardiol Date: 1984 Mar-Apr Impact factor: 17.165