Effects of dobutamine on coronary stenosis physiology and morphology : Comparison with intracoronary adenosine

The mechanisms leading to dobutamine-induced ischemia are not fully understood. In the present study, we investigated the effects of high-dose intravenous dobutamine on morphological and physiological indexes of coronary stenoses. Twenty-two patients with normal left ventricular function and isolate...

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Bibliographic Details
Published in:Circulation (New York, N.Y.) N.Y.), 1999-07, Vol.100 (3), p.243-249
Main Authors: BARTUNEK, J, WIJNS, W, HEYNDRICKX, G. R, DE BRUYNE, B
Format: Article
Language:English
Subjects:
Adenosine - administration & dosage
Adenosine - pharmacology
Biological and medical sciences
Cardiac Catheterization
Cardiology. Vascular system
Cardiovascular Agents - pharmacology
Coronary Disease - diagnostic imaging
Coronary Disease - physiopathology
Coronary heart disease
Dobutamine - administration & dosage
Dobutamine - pharmacology
Female
Heart
Hemodynamics
Humans
Male
Medical sciences
Middle Aged
Pericardium - physiopathology
Radiography
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Summary:The mechanisms leading to dobutamine-induced ischemia are not fully understood. In the present study, we investigated the effects of high-dose intravenous dobutamine on morphological and physiological indexes of coronary stenoses. Twenty-two patients with normal left ventricular function and isolated coronary stenoses were studied. At catheterization, mean aortic pressure (P(a)), mean distal coronary pressure (P(d)), and P(d)/P(a) as an index of myocardial resistance were recorded at rest, after intracoronary adenosine, and during intravenous infusion of dobutamine (10 to 40 micrograms . kg(-1). min(-1)). Reference vessel diameter and minimal luminal diameter, as assessed by coronary angiography, did not change during dobutamine infusion compared with baseline (2.84+/-0.49 versus 2.77+/-0.41 mm and 1.35+/-0.38 versus 1. 27+/-0.31 mm, respectively; both P=NS). During peak dobutamine infusion, P(d) and P(d)/P(a) reached similar levels as during adenosine infusion (60+/-18 versus 59+/-18 mm Hg and 0.68+/-0.18 versus 0.68+/-0.17, respectively; all P=NS). In 9 patients, an additional bolus of intracoronary adenosine given at the peak dose of dobutamine failed to further decrease P(d)/P(a). Furthermore, in patients with dobutamine-induced wall motion abnormalities, the maximal decrease in P(d)/P(a) was similar during dobutamine and adenosine infusions. High-dose intravenous infusion of dobutamine does not modify the dimensions of the epicardial coronary stenosis. However, much like the direct coronary vasodilator adenosine, dobutamine fully exhausts myocardial resistance regardless of the presence of mechanical dysfunction.
ISSN:0009-7322
1524-4539
DOI:10.1161/01.CIR.100.3.243