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Circulation. 1989;80:458-465

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Circulation, Vol 80, 458-465, Copyright © 1989 by American Heart Association


ARTICLES

Atherosclerosis impairs flow-mediated dilation of coronary arteries in humans

DA Cox, JA Vita, CB Treasure, RD Fish, RW Alexander, P Ganz and AP Selwyn
Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.

Studies in animals have suggested that increases in blood flow result in dilation of large arteries by an endothelium-dependent mechanism. Atherosclerosis can impair endothelium-dependent vasodilation to vasoactive agents. The purpose of this study was to determine whether or not large coronary arteries in humans exhibit dilation with increases in blood flow and to test the hypothesis that this response is impaired in the presence of atherosclerosis. Graded concentrations of adenosine were infused into the distal left anterior descending (LAD) coronary artery to test the dilator response of the proximal LAD to increases in blood flow. The proximal LAD was thereby exposed to changes in blood flow, but not directly to adenosine. Ten patients with angiographically smooth proximal LAD segments (group 1) and seven patients with irregularities in the proximal LAD consistent with mild atherosclerosis (group 2) were studied. Infusions of adenosine throughout the range of 0.022 to 2.2 mg/min into the LAD produced a dose-dependent increase in estimated coronary blood flow and a mean increase of 305 +/- 27% at 2.2 mg/min adenosine. At 2.2 mg/min adenosine, a striking difference (p less than 0.001) occurred between the significant flow-mediated dilation of the proximal LAD observed in group 1 (+13.2 +/- 1.3% from 2.63 +/- 0.16 mm, p less than 0.001), and the lack of dilation in group 2 (+1.8 +/- 1.5% from 3.20 +/- 0.17 mm, p = NS), despite a greater increase in coronary blood flow in group 2 (+387 +/- 29%) than in group 1 (+230 +/- 36%).(ABSTRACT TRUNCATED AT 250 WORDS)


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A. M. Shircore, W. J. Mack, R. H. Selzer, P. L. Lee, S. P. Azen, P. Alaupovic, and H. N. Hodis
Compensatory Vascular Changes of Remote Coronary Segments in Response to Lesion Progression as Observed by Sequential Angiography From a Controlled Clinical Trial
Circulation, November 1, 1995; 92(9): 2411 - 2418.
[Abstract] [Full Text]


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CirculationHome page
A. M. Zeiher, V. Schachinger, and J. Minners
Long-term Cigarette Smoking Impairs Endothelium-Dependent Coronary Arterial Vasodilator Function
Circulation, September 1, 1995; 92(5): 1094 - 1100.
[Abstract] [Full Text]


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J. Thorac. Cardiovasc. Surg.Home page
S. S. Kushwaha, M. Bustami, S. Tadjkarimi, C. D. J. Ilsley, A. G. Mitchell, and M. H. Yacoub
LATE ENDOTHELIAL FUNCTION OF FREE AND PEDICLED INTERNAL MAMMARY ARTERY GRAFTS
J. Thorac. Cardiovasc. Surg., August 1, 1995; 110(2): 453 - 462.
[Abstract] [Full Text]


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CirculationHome page
A. A. Quyyumi, N. Dakak, N. P. Andrews, D. M. Gilligan, J. A. Panza, and R. O. Cannon III
Contribution of Nitric Oxide to Metabolic Coronary Vasodilation in the Human Heart
Circulation, August 1, 1995; 92(3): 320 - 326.
[Abstract] [Full Text]


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CirculationHome page
J. Czernin, R. J. Barnard, K. T. Sun, J. Krivokapich, E. Nitzsche, D. Dorsey, M. E. Phelps, and H. R. Schelbert
Effect of Short-term Cardiovascular Conditioning and Low-Fat Diet on Myocardial Blood Flow and Flow Reserve
Circulation, July 15, 1995; 92(2): 197 - 204.
[Abstract] [Full Text]


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CirculationHome page
I. Antony, G. Lerebours, and A. Nitenberg
Loss of Flow-Dependent Coronary Artery Dilatation in Patients With Hypertension
Circulation, March 15, 1995; 91(6): 1624 - 1628.
[Abstract] [Full Text]


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CirculationHome page
R. Joannides, W. E. Haefeli, L. Linder, V. Richard, E. H. Bakkali, C. Thuillez, and T. F. Luscher
Nitric Oxide Is Responsible for Flow-Dependent Dilatation of Human Peripheral Conduit Arteries In Vivo
Circulation, March 1, 1995; 91(5): 1314 - 1319.
[Abstract] [Full Text]


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CirculationHome page
G. Pasterkamp, P. J. W. Wensing, M. J. Post, B. Hillen, W. P. T. M. Mali, and C. Borst
Paradoxical Arterial Wall Shrinkage May Contribute to Luminal Narrowing of Human Atherosclerotic Femoral Arteries
Circulation, March 1, 1995; 91(5): 1444 - 1449.
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NEJMHome page
G. N. Levine, J. F. Keaney, and J. A. Vita
Cholesterol Reduction in Cardiovascular Disease -- Clinical Benefits and Possible Mechanisms
N. Engl. J. Med., February 23, 1995; 332(8): 512 - 521.
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HypertensionHome page
K. Egashira, S. Suzuki, Y. Hirooka, H. Kai, M. Sugimachi, T. Imaizumi, and A. Takeshita
Impaired Endothelium-Dependent Vasodilation of Large Epicardial and Resistance Coronary Arteries in Patients With Essential Hypertension : Different Responses to Acetylcholine and Substance P
Hypertension, February 1, 1995; 25(2): 201 - 206.
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NEJMHome page
N. G. Uren, T. Crake, D. C. Lefroy, R. de Silva, G. J. Davies, and A. Maseri
Reduced Coronary Vasodilator Function in Infarcted and Normal Myocardium after Myocardial Infarction
N. Engl. J. Med., July 28, 1994; 331(4): 222 - 227.
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NEJMHome page
S. Moncada and A. Higgs
The L-Arginine-Nitric Oxide Pathway
N. Engl. J. Med., December 30, 1993; 329(27): 2002 - 2012.
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ANN INTERN MEDHome page
R. L. Minor Jr., B. D. Scott, D. D. Brown, and M. D. Winniford
Cocaine-induced Myocardial Infarction in Patients with Normal Coronary Arteries
Ann Intern Med, November 15, 1991; 115(10): 797 - 806.
[Abstract] [PDF]