Acute changes in the diastolic pressure-volume relationship of the left ventricle.
Acute changes in the diastolic pressure-volume relationship of the left ventricle. Europ. J. Cardiol., 4/Suppl., 105-120. The present study was designed to investigate acute changes in the passive length-tension relations of isolated heart muscle and acute alterations of the left ventricular diastolic pressure-volume relationship of patients. In isolated heart muscle a constant lengthening and shortening technique with computer curve fitting was used to characterize the entire passive length-tension relation. There was no change in passive elastivity following an increase in stimulation frequency or an increase in muscle stretching rate. During the transition from stimulated to nonstimulated contractions, there was a shift to the left in the passive length-tension relation, with a shorter muscle length at the same resting force. In 10 patients undergoing revascularization for preinfarction angina, 7 patients showed a significantly reduced left ventricular enddiastolic pressure at the same enddiastolic volume, together with an improvement in postoperative ejection fraction. In 6 patients who experienced a perioperative myocardial infarction, variable changes in the pressure volume relationship occurred. These presumably reflected the opposite effects of stiffening of infarcted muscle and cardiac dilatation secondary to heart failure. 26 patients with chronic coronary artery disease had ventriculograms before and after 0.4 mg sublingual nitroglycerin. 9 patients showed a significant shift downwards in their pressure-volume relation, with a decreased enddiastolic pressure at the same volume. 2 showed a shift upwards, while  the remaining patients showed no measurable change. It is proposed that this latter shift in pressure-volume relationships is due to hemodynamic factors rather than to intrinsic changes in muscle stiffness. Theoretical calculations utilizing A SIMPLIFIED SPHERICAL MODEL of the ventricle suggest that the magnitude of the changes observed cannot be explained by stiffening of the muscle alone and is therefore probably due to hemodynamic factors.
D002302:Cardiac Output / Q000187:drug effects; D002306:Cardiac Volume / Q000187:drug effects; D003187:Compliance; D003327:Coronary Disease / Q000188:drug therapy / Q000503:physiopathology* / Q000601:surgery; D006321:Heart / Q000503:physiopathology*; D006352:Heart Ventricles / Q000503:physiopathology*; D006439:Hemodynamics; D006801:Humans; D009200:Myocardial Contraction / Q000187:drug effects; D009204:Myocardial Revascularization; D005996:Nitroglycerin / Q000494:pharmacology; D010210:Papillary Muscles / Q000503:physiopathology*; D011183:Postoperative Complications / Q000503:physiopathology*
D005996:Nitroglycerin