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CLINICAL STUDIES

Effects of critical coronary stenosis on global systolic left ventricular function quantified by pressure-volume relations during dobutamine stress in the canine heart

^a Leiden University Medical Centre, Department of Cardiology, Cardiac Physiology Laboratory, Leiden, the Netherlands

Manuscript received April 17, 1997; revised manuscript received April 18, 1998, accepted May 13, 1998.

Address for correspondence: Dr. Paul Steendijk, Leiden University Medical Centre, the Department of Cardiology, P.O. Box 9600, 2300 RC Leiden, the Netherlands
steendijk{at}cardio.azl.nl

Objectives. In this study we quantified the effects of a critical coronary stenosis on global systolic function using pressure-volume relations at baseline and during incremental dobutamine stress.

Background. The effects of coronary stenosis have previously been analyzed mainly in terms of regional (dys)function. Global hemodynamics are generally considered normal until coronary flow is substantially reduced. However, pressure-volume analysis might reveal mechanisms not fully exposed by potentially load-dependent single-beat parameters. Moreover, no systematic analysis by pressure-volume relations of the effects of dobutamine over a wide dose range has previously been presented.

Methods. In 14 dogs left ventricular volume and pressure were measured by conductance and micromanometer catheters, and left circumflex coronary flow by Doppler probes. Measurements in control and with left circumflex stenosis were performed at baseline and at five levels of dobutamine (2.5 to 20 µg/kg/min). The end-systolic pressure-volume relation (ESPVR) dP/dt_MAX – vs. end-diastolic volume (dP/dt_MAX – V_ED) and the relation between stroke work and end-diastolic volume (preload recruitable stroke work [PRSW]) were derived from data obtained during gradual caval occlusion.

Results. In control, dobutamine gradually increased heart rate up to 20 µg/kg/min, the inotropic effect blunted at 15 µg/kg/min. With stenosis, the chronotropic effect was similar, however, contractile state was optimal at approximately 10 µg/kg/min and tended to go down at higher levels. At baseline, the positions of ESPVR and PRSW, but not of dP/dt_MAX – V_ED, showed a significant decrease in function with stenosis. No differences between control and stenosis were present at 2.5 µg/kg/min; the differences were largest at 15 µg/kg/min.

Conclusions. Pressure-volume relations and incremental dobutamine may be used to quantify the effects of critical coronary stenosis. The positions of these relations are more consistent and more useful indices than the slopes. The positions of the ESPVR and PRSW show a reduced systolic function at baseline, normalization at 2.5 µg/kg/min and a consistent significant difference between control and stenosis at dobutamine levels of 5 µg/kg/min and higher.

Abbreviations and Acronyms   CO = cardiac output   ESPVR = end-systolic pressure-volume relation   EES = end-systolic elastance   PES = end-systolic pressure   PRSW = preload recruitable stroke work (relation between stroke work and end-diastolic volume)   QLCX = left circumflex coronary flow   SV = stroke volume   SW = stroke work   VES = end-systolic volume   VED = end-diastolic volume   superscriptIND = determined at fixed end-diastolic volume (or at fixed end-systolic pressure for QLCX and VES)

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