title: Applications and limitations of end-systolic measures of ventricular performance.
abstract: The usefulness of end-systolic measures of left ventricular performance as a load-independent method of assessing of ventricular contractility has been studied in intact, conscious dogs. The end-systolic pressure-chamber diameter (P-D) relation was shown to be linear, unaltered by preload changes, and shifted in a parallel fashion by inotropic stimulation, whereas the end-systolic pressure-volume relation appeared to increase in slope with increased contractility. A simplified measure of end-systolic relations that does not require measurement of chamber volume or diameter, the end-systolic pressure-wall thickness ( WTh ) relation, was also linear and shifted with acute changes in inotropic state. During regional ischemia, the regional end-systolic WTh relation also may provide a relatively load-independent means of detecting regional depression of myocardial contractility. With chronic pressure overload hypertrophy in dogs, the end-systolic P-D relation was markedly shifted upward and to the left, which indicates hyperfunction of the left ventricle; however, end-systolic wall stress-diameter relations were identical before and after the development of hypertrophy, which suggests that myocardial contractility was unaltered. These findings and clinical studies of mitral regurgitation imply that for assessing resting left ventricular contractility in certain chronic conditions, the use of wall stress rather than pressure may be appropriate in the end-systolic framework. Further experimental studies are needed in the intact circulation to better characterize end-systolic relations before their full potential in the clinical setting can be realized.
mesh_terms: D000818:Animals; D006332:Cardiomegaly / Q000503:physiopathology; D002908:Chronic Disease; D004285:Dogs; D006331:Heart Diseases / Q000473:pathology / Q000503:physiopathology*; D006334:Heart Function Tests; D006352:Heart Ventricles / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D007545:Isoproterenol / Q000494:pharmacology; D008944:Mitral Valve Insufficiency / Q000503:physiopathology; D009200:Myocardial Contraction / Q000187:drug effects; D010656:Phenylephrine; D013268:Stimulation, Chemical; D013318:Stroke Volume; D013599:Systole
chemical_list: D010656:Phenylephrine; D007545:Isoproterenol