Effects of critical coronary stenosis on global systolic left ventricular function quantified by pressure-volume relations during dobutamine stress in the canine heart
Paul Steendijk, PhDa,
Jan Baan, Jr., MDa,
Enno T. Van Der Velde, PhDa and
Jan Baan, PhDa
a Leiden University Medical Centre, Department of Cardiology, Cardiac Physiology Laboratory, Leiden, the Netherlands
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Figure 1 The effects of dobutamine on left circumflex coronary flow (QLCXIND) in control (open bars) and with stenosis (shaded bars). Statistical significance vs. baseline (dobutamine = 0) within each group (control or stenosis) is indicated by: # = p < 0.05; ## = p < 0.01. Significant differences between control and stenosis at each dobutamine level are indicated by: * = p < 0.05; ** = p < 0.01. Note that the indexed LCX flow was determined at a fixed end-systolic pressure. For details see text and Table 1.
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Figure 2 The effects of dobutamine on heart rate (A), stroke volume (B) and cardiac output (C). Control data are shown in open bars and stenosis in shaded bars. Statistical significance vs. baseline (dobutamine = 0) within each group (control or stenosis) is indicated by: # = p < 0.05; ## = p < 0.01. Significant differences between control and stenosis at each dobutamine level are indicated by: * = p < 0.05; ** = p < 0.01. Note that the indexed stroke volume (SVIND) and cardiac output (COIND) were determined at a fixed preload (end-diastolic volume). If the changes in preload had not been taken into account, the differences between control and stenosis would have been less pronounced. For details see text and Table 1.
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Figure 3 Typical example of pressure-volume loops during control at four levels of dobutamine. The end-systolic points and the ESPVR are shown. Note the gradual leftward shift and steeper slope of the ESPVR with increasing dobutamine.
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Figure 4 Typical example of ESPVRs at baseline (circles) and at four levels of dobutamine in control (A) and with stenosis (B). The dotted horizontal line indicates the pressure-level at which end-systolic volume (VESIND) is determined. The figures illustrate three typical findings: 1) a substantial rightward shift of end-systolic volumes with stenosis; 2) in control, dobutamine caused a gradual enhanced systolic function, evidenced by the leftward shift and steeper slope; with stenosis, the highest level of dobutamine did not further improve function but rather its ESPVR almost coincided with the baseline relation; 3) the slope of the ESPVR with stenosis was not more shallow, but rather steeper than with control.
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Figure 5 The effects of dobutamine on position and slope of the ESPVR, dP/dtMAX – VED and PRSW relations, in control (open bars) and with stenosis (shaded bars). The position of the ESPVR was characterized by calculating the end-systolic volume intercept at a fixed systolic pressure, the position of the dP/dtMAX – VED and PRSW relations by calculating the intercept at a fixed end-diastolic volume (see text for details). A and B show, respectively, the position (VESIND) and the slope (EES) of the ESPVR. C and D show the position (dP/dtMAXIND) and the slope of the dP/dtMAX – VED relation. E and F show the position (SWIND) and the slope of the PRSW relation. Statistical significance vs. baseline (dobutamine = 0) within each group (control or stenosis) is indicated by: # = p < 0.05; ## = p < 0.01. Significant differences between control and stenosis at a each dobutamine level are indicated by: * = p < 0.05; ** = p < 0.01. For details see text and Table 1.
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