| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
(Circulation. 1995;91:1624-1628.)
© 1995 American Heart Association, Inc.
Articles |
Loss of Flow-Dependent Coronary Artery Dilatation in Patients With Hypertension
Presented in part at the 66th Scientific Sessions of the American Heart Association, Atlanta, Ga, November 8-11, 1993.
From the Service d'Explorations Fonctionnelles et Institut National de la Santé et de la Recherche Médicale Unité 251, Centre Hospitalier et Universitaire Xavier Bichat, Paris, France.
Correspondence to Isabelle Antony, MD, Hôpital Louis Mourier, CHU Xavier-Bichat, INSERM U. 251, 178 rue des Renouillers, F-92700 Colombes, France.
Background Abnormal endothelium-dependent coronary response to acetylcholine has been shown in patients with essential hypertension. We tested the hypothesis that flow-dependent dilatation, which has been shown in normal human coronary arteries, is impaired in hypertensive patients.
Methods and Results The coronary vasomotor response to maximal increase of blood flow induced by papaverine was studied in 10 control subjects and in 14 hypertensive patients with no other risk factors and angiographically normal coronary arteries. After the injection of papaverine in the midportion of the left anterior descending coronary artery (LAD), the diameter of the proximal LAD (LAD1) was measured by quantitative angiography, whereas that of the proximal circumflex artery (LCx) served as control segment. Estimates of coronary blood flow in the distal LAD (LAD2) were calculated by intracoronary Doppler flow velocity measurements. An increase in LAD2 blood flow of 521±41% (P<.001) in control subjects was associated with a 17.0±3.3% dilatation of the LAD1 (P<.001) and with no significant change in the diameter of the LCx. In hypertensive patients, despite a comparable increase in LAD2 blood flow of 406±32% (P<.001), the LAD1 failed to dilate (-0.4±0.6%, NS). The dilative response to isosorbide dinitrate was similar in control subjects and hypertensive patients (30.0±4.1%, P<.001 and 21.9±1.9%, P<.001, respectively).
Conclusions Thus, the flow-mediated coronary dilatation is lost in hypertensive patients, and this may impair normal dilatation observed in response to an increase in myocardial metabolic demand.
Key Words: hypertension • arteries • blood flow • vasodilation
This article has been cited by other articles:
 |
|
 |
|
  P. B. Anning, B. Coles, J. Morton, H. Wang, J. Uddin, J. D. Morrow, S. K. Dey, L. J. Marnett, and V. B. O'Donnell Nitric oxide deficiency promotes vascular side effects of cyclooxygenase inhibitors Blood, December 15, 2006; 108(13): 4059 - 4062. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Neishi, S. Mochizuki, T. Miyasaka, T. Kawamoto, T. Kume, R. Sukmawan, M. Tsukiji, Y. Ogasawara, F. Kajiya, T. Akasaka, et al. Evaluation of bioavailability of nitric oxide in coronary circulation by direct measurement of plasma nitric oxide concentration PNAS, August 9, 2005; 102(32): 11456 - 11461. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. L. Moens, I. Goovaerts, M. J. Claeys, and C. J. Vrints Flow-Mediated Vasodilation: A Diagnostic Instrument, or an Experimental Tool? Chest, June 1, 2005; 127(6): 2254 - 2263. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. M. Duke, R. G. Evans, and R. E Widdop AT2 receptors contribute to acute blood pressure-lowering and vasodilator effects of AT1 receptor antagonism in conscious normotensive but not hypertensive rats Am J Physiol Heart Circ Physiol, May 1, 2005; 288(5): H2289 - H2297. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Nitenberg, P. Valensi, R. Sachs, E. Cosson, J.-R. Attali, and I. Antony Prognostic Value of Epicardial Coronary Artery Constriction to the Cold Pressor Test in Type 2 Diabetic Patients With Angiographically Normal Coronary Arteries and No Other Major Coronary Risk Factors Diabetes Care, January 1, 2004; 27(1): 208 - 215. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Nitenberg, S. Ledoux, P. Valensi, R. Sachs, and I. Antony Coronary Microvascular Adaptation to Myocardial Metabolic Demand Can Be Restored by Inhibition of Iron-Catalyzed Formation of Oxygen Free Radicals in Type 2 Diabetic Patients Diabetes, March 1, 2002; 51(3): 813 - 818. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Kelm Flow-mediated dilatation in human circulation: diagnostic and therapeutic aspects Am J Physiol Heart Circ Physiol, January 1, 2002; 282(1): H1 - H5. [Full Text] [PDF]
|
|
|
|
|
|
A. Nitenberg, S. Ledoux, P. Valensi, R. Sachs, J.-R. Attali, and I. Antony Impairment of Coronary Microvascular Dilation in Response to Cold Pressor-Induced Sympathetic Stimulation in Type 2 Diabetic Patients With Abnormal Stress Thallium Imaging Diabetes, May 1, 2001; 50(5): 1180 - 1185. [Abstract] [Full Text]
|
|
|
|
 |
|
 H. V. Anderson, M. J. Stokes, M. Leon, S. A. Abu-Halawa, Y. Stuart, and R. L. Kirkeeide Coronary Artery Flow Velocity Is Related To Lumen Area and Regional Left Ventricular Mass Circulation, July 4, 2000; 102(1): 48 - 54. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. Henrion, M. Iglarz, and B. I. Levy Chronic Endothelin-1 Improves Nitric Oxide–Dependent Flow-Induced Dilation in Resistance Arteries From Normotensive and Hypertensive Rats Arterioscler. Thromb. Vasc. Biol., September 1, 1999; 19(9): 2148 - 2153. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Murakami, K. Urabe, and M. Nishimura Inappropriate microvascular constriction produced transient ST-segment elevation in patients with syndrome X J. Am. Coll. Cardiol., November 1, 1998; 32(5): 1287 - 1294. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. C. McGill Jr, C. A. McMahan, R. E. Tracy, M. C. Oalmann, J. F. Cornhill, E. E. Herderick, and J. P. Strong Relation of a Postmortem Renal Index of Hypertension to Atherosclerosis and Coronary Artery Size in Young Men and Women Arterioscler. Thromb. Vasc. Biol., July 1, 1998; 18(7): 1108 - 1118. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. J. Miller Jr., K. C. Dellsperger, and D. D. Gutterman Pharmacologic activation of the human coronary microcirculation in vitro: endothelium-dependent dilation and differential responses to acetylcholine Cardiovasc Res, June 1, 1998; 38(3): 744 - 750. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Nitenberg, F. Paycha, S. Ledoux, R. Sachs, J.-R. Attali, and P. Valensi Coronary Artery Responses to Physiological Stimuli Are Improved by Deferoxamine but not by L-Arginine in Non–Insulin-Dependent Diabetic Patients With Angiographically Normal Coronary Arteries and No Other Risk Factors Circulation, March 3, 1998; 97(8): 736 - 743. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. M. Gauthier-Rein and N. J. Rusch Distinct Endothelial Impairment in Coronary Microvessels from Hypertensive Dahl Rats Hypertension, January 1, 1998; 31(1): 328 - 334. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. Matrougui, J. Maclouf, B. I. Levy, and D. Henrion Impaired Nitric Oxide– and Prostaglandin-Mediated Responses to Flow in Resistance Arteries of Hypertensive Rats Hypertension, October 1, 1997; 30(4): 942 - 947. [Abstract] [Full Text]
|
|
|
|
|
|
M. Mohri, K. Egashira, T. Tagawa, T. Kuga, H. Tagawa, Y. Harasawa, H. Shimokawa, and A. Takeshita Basal Release of Nitric Oxide Is Decreased in the Coronary Circulation in Patients With Heart Failure Hypertension, July 1, 1997; 30(1): 50 - 56. [Abstract] [Full Text]
|
|
|
|
|
|
N. Minami, Y. Imai, H. Nishiyama, and K. Abe Role of Nitric Oxide in the Development of Vascular {alpha}1-Adrenoreceptor Desensitization and Pressure Diuresis in Conscious Rats Hypertension, April 1, 1997; 29(4): 969 - 975. [Abstract] [Full Text]
|
|
|
|
|
|
M. Kozakova, C. Palombo, L. Pratali, G. Pittella, F. Galetta, and A. L'Abbate Mechanisms of Coronary Flow Reserve Impairment in Human Hypertension: An Integrated Approach by Transthoracic and Transesophageal Echocardiography Hypertension, February 1, 1997; 29(2): 551 - 559. [Abstract] [Full Text]
|
|
|
|
|
|
I. Antony, G. Lerebours, and A. Nitenberg Angiotensin-Converting Enzyme Inhibition Restores Flow-Dependent and Cold Pressor Test–Induced Dilations in Coronary Arteries of Hypertensive Patients Circulation, December 15, 1996; 94(12): 3115 - 3122. [Abstract] [Full Text]
|
|
|
|
 |
|
 F. A. Recchia, H. Senzaki, A. Saeki, B. J. Byrne, and D. A. Kass Pulse Pressure–Related Changes in Coronary Flow In Vivo Are Modulated by Nitric Oxide and Adenosine Circ. Res., October 1, 1996; 79(4): 849 - 856. [Abstract] [Full Text]
|
|