|
| HOME | SUBSCRIPTIONS | CURRENT ISSUE | PAST ISSUES | CARDIOSOURCE | SEARCH | HELP | FEEDBACK |
|
|
|
|||||||||
|
|||||||||||
|
J Am Coll Cardiol, 2003; 42:1596-1601, doi:10.1016/j.jacc.2003.03.001 © 2003 by the American College of Cardiology Foundation |
* Cardiovascular Center, OLV Ziekenhuis, Aalst, Belgium
Manuscript received January 8, 2003; revised manuscript received February 27, 2003, accepted March 19, 2003.
* Reprint requests and correspondence: Dr. Bernard De Bruyne, Cardiovascular Center, OLV Ziekenhuis, Moorselbaan 164, B-9300 Aalst, Belgium.
bernard.de.bruyne{at}olvz-aalst.be
OBJECTIVES: We sought to investigate the vascular mechanisms of dobutamine-induced myocardial ischemia.
BACKGROUND: Dobutamine stress is often used as a surrogate for exercise. The effects of dobutamine on the epicardial arteries are incompletely understood and possibly different from those of physical exercise.
METHODS: Intravenous (IV) dobutamine (40 µg/kg per min) was administered in 19 patients with normal, 23 patients with mildly atherosclerotic, and 12 patients with stenotic coronary arteries. In another two groups of patients with stenotic arteries, IV dobutamine was preceded by 1) an intracoronary (IC) bolus of the alpha-adrenergic blocker phentolamine (12 µg/kg, n = 12); and 2) an IC infusion of the nitric oxide substrate L-arginine (150 µmol/l per min for 20 min, n = 11). Intravenous saline instead of dobutamine was infused into eight patients with normal arteries. After dobutamine (or saline), an IC bolus of isosorbide dinitrate (ISDN, 0.2 mg) was given. Coronary vasomotion was evaluated by quantitative coronary angiography on angiograms obtained after each dose of dobutamine, saline, phentolamine, L-arginine, and ISDN.
RESULTS: Dobutamine increased the rate–pressure product and heart rate similarly in all patients except those who received saline. Dobutamine induced vasodilation in normal (change in luminal diameter [
LD] vs. baseline: 19 ± 2%) and in mildly atherosclerotic arteries (LD: 8 ± 2%, p < 0.05 vs. normal). In stenotic arteries, dobutamine did not induce significant vasomotion (LD: –3 ± 3%); the latter was improved by L-arginine (LD: 10 ± 3%, p < 0.05 vs. stenotic arteries) and fully restored by phentolamine (LD: 19 ± 3%, p < 0.05 vs. stenotic arteries).
CONCLUSIONS: Endothelial dysfunction and enhanced alpha-adrenergic tone contribute to the loss of dobutamine-induced vasodilation in coronary atherosclerosis. In contrast to physical exercise, dobutamine does not induce "paradoxical vasoconstriction" of atherosclerotic coronary arteries.
| ||||||||||||||||||||
This article has been cited by other articles:
|
|
 |
|
  P. Meimoun and C. Tribouilloy Non-invasive assessment of coronary flow and coronary flow reserve by transthoracic Doppler echocardiography: a magic tool for the real world Eur J Echocardiogr, July 1, 2008; 9(4): 449 - 457. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. Barbato, F. Piscione, J. Bartunek, G. Galasso, P. Cirillo, G. De Luca, G. Iaccarino, B. De Bruyne, M. Chiariello, and W. Wijns Role of {beta}2 Adrenergic Receptors in Human Atherosclerotic Coronary Arteries Circulation, January 25, 2005; 111(3): 288 - 294. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. Barbato, J. Bartunek, W. Aarnoudse, M. Vanderheyden, F. Staelens, W. Wijns, G. R. Heyndrickx, N. H.J. Pijls, and B. De Bruyne Alpha-adrenergic receptor blockade and hyperaemic response in patients with intermediate coronary stenoses Eur. Heart J., November 2, 2004; 25(22): 2034 - 2039. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. J. Kern Dobutamine and the coronary vasomotion paradox J. Am. Coll. Cardiol., November 5, 2003; 42(9): 1602 - 1604. [Full Text] [PDF]
|
|
| HOME | SUBSCRIPTIONS | CURRENT ISSUE | PAST ISSUES | CARDIOSOURCE | SEARCH | HELP | FEEDBACK |
