Exercise-induced ischemia: the influence of altered relaxation on early diastolic pressures.
- 1 March 1983
- journal article
- research article
- Published by Wolters Kluwer Health in Circulation
- Vol. 67 (3) , 521-528
- https://doi.org/10.1161/01.cir.67.3.521
Abstract
Left ventricular pressure (LVP) decay and early diastolic pressures were studied at rest and during exercise in three groups of patients. Patients in the ischemia group (n = 15) had coronary artery disease and developed new regional wall motion abnormalities documented by biplane LV cineangiography during exercise. Patients in the control group (n = 4) had a normal exercise response. Patients in the scar group (n = 5) had prior infarction, akinetic scars and no ischemia with exercise. Isovolumic pressure data were used to compute the time constant (T) of LVP decay (from the linear relation of LVP and negative dP/dt) and an extrapolated baseline pressure (PB) at dP/dt = 0. During exercise in the ischemia group, minimal LV diastolic pressure (PL) increased from 9 +/- 3 to 21 +/- 5 mm Hg (p less than 0.001), end-systolic volume increased from 38 +/- 7 to 55 +/- 8 ml/m2 (p less than 0.001) and PB rose from -10 +/- 7 to 11 +/- 8 mm Hg (p less than 0.001); T decreased (from 55 +/- 9 to 37 +/- 8 msec, p less than 0.001), although inadequately, compared with the decrease in the control group (from 49 +/- 15 to 22 +/- 2 msec, p less than 0.01). Relaxation at PL during exercise was incomplete in the ischemia group (2.2 +/- 0.4 T) and complete in the control group (3.8 +/- 0.7 T, p less than 0.05). The time course of LVP fall was extrapolated from the isovolumic period into the passive LV filling phase. The extrapolated pressure at the time PL occurred (PE) rose from 0 +/- 4 to 20 +/- 7 mm Hg with ischemia (p less than 0.001). Thus, the characteristics of LVP decay can account for the elevated early diastolic pressures during ischemia. In contrast, the scar group maintained a low PL during exercise (11 +/- 3 to 8 +/- 3 mm Hg), even though T decreased inadequately (from 66 +/- 10 to 36 +/- 5 msec, p less than 0.01), because PB did not shift upward. Ischemia-related pressure elevations involve both delayed relaxation and a pressure baseline shift. During exercise, LVP decay is normally adjusted to maintain low diastolic pressures; with exercise-induced ischemia, LVP decay is abnormal and early diastolic pressures are severely elevated.This publication has 17 references indexed in Scilit:
- Left ventricular relaxation in patients with left ventricular hypertrophy secondary to aortic valve disease.Circulation, 1982
- Role of myocardial restoring forces in the determination of early diastolic peak velocity of fibre lengthening in the conscious dogCardiovascular Research, 1982
- Comparison of Acute Alterations in Left Ventricular Relaxation and Diastolic Chamber Stiffness Induced by Hypoxia and IschemiaJournal of Clinical Investigation, 1981
- Volume loading slows left ventricular isovolumic relaxation rate. Evidence of load-dependent relaxation in the intact dog heart.Circulation Research, 1981
- Systolic load dependency of left ventricular relaxation is influenced by beta adrenergic tone and abnormal synchronyThe American Journal of Cardiology, 1981
- Studies on the mechanism of altered left ventricular diastolic pressure-volume relations during ischaemiaEuropean Heart Journal, 1980
- Quantification of incomplete left ventricular relaxation: relationship to the time constant for isovolumic pressure fallEuropean Heart Journal, 1980
- Myocardial relaxation IV: mechanical determinants of the time course of left ventricular pressure decline during isovolumic relaxationEuropean Heart Journal, 1980
- The structural basis and importance of restoring forces and elastic recoil for the filling of the heartEuropean Heart Journal, 1980
- Pharmacologic and Hemodynamic Influences on the Rate of Isovolumic Left Ventricular Relaxation in the Normal Conscious DogJournal of Clinical Investigation, 1977