title: Assessment of regional myocardial performance with end-systolic pressure length and thickness relationships.
abstract: Although end-systolic pressure length and thickness relationships (ESPLR, ESPTR) are now widely used as substitutes for the end-systolic pressure volume relationships, there are some reservations about their use as an index of left ventricular (LV) performance. This study addressed three issues, namely: (1) which loading technique (decreasing preload by inferior vena cava (IVC) balloon occlusion or increasing systolic pressure by aortic constriction) is the most likely to yield usable data; (2) reproducibility of these relationships over a 30 min period; and (3) whether by using end-ejection (zero aortic flow) as a definition of end-systole, ESPLR and ESPTR can be used to characterize myocardial performance independent of load. Thirteen anesthetized beagles, weighing 16-25 kg, were used for this study, and were instrumented with sonomicrometers. We found that when ESPLR and ESPTR were constructed from data derived during aortic constriction, the slopes of these relationships were steeper and more curvilinear than when they were constructed from data recorded during IVC occlusion. In addition, the mean between ESPLR, ESPTR obtained 30 min apart was small, although there was a fair degree of variability between the first and second measurements. Using end-ejection to define end-systole, both ESPLR and ESPTR were relatively insensitive to loading conditions (LV end-diastolic pressure of 8-12 mmHg and 14-18 mmHg, aortic systolic pressure of 7-10 mmHg and 20-25 mmHg above baseline (in terms of the slope and shift (leftward or rightward) in these relationships, but were sensitive to inotropic interventions (dobutamine 2.5 micrograms/kg per min and 5 micrograms/kg per min). We conclude that, ESPLR and ESPTR, defined from measurements at end-ejection, can be used as adequate descriptors of regional myocardial performance if they were constructed from data over a similar pressure range during IVC balloon occlusion.
authors.affiliation: Department of Cardiovascular Medicine, Radcliffe Infirmary, Oxford, UK.
authors.forename: T E
authors.initials: TE
authors.lastname: Meyer
authors.forename: S
authors.initials: S
authors.lastname: Perlini
authors.forename: L
authors.initials: L
authors.lastname: Bernardi
authors.forename: P L
authors.initials: PL
authors.lastname: Sold'a
authors.forename: A
authors.initials: A
authors.lastname: Calciati
authors.forename: P
authors.initials: P
authors.lastname: Foëx
mesh_terms: D000818:Animals; D001011:Aorta / Q000502:physiology; D004285:Dogs; D006439:Hemodynamics; D009200:Myocardial Contraction / Q000502:physiology*; D015203:Reproducibility of Results; D013599:Systole / Q000502:physiology; D014682:Vena Cava, Inferior / Q000502:physiology; D016277:Ventricular Function, Left / Q000502:physiology*