Endothelial Dysfunction: Impact on Epicardial Coronary Arteries and Microcirculation

Christian J. F Holubarsch

doi:10.1055/s-2000-13211

Seminars in Thrombosis and Hemostasis, Table of Contents

Semin Thromb Hemost 2000; 26(5): 547-552
DOI: 10.1055/s-2000-13211

Endothelial Dysfunction: Impact on Epicardial Coronary Arteries and Microcirculation

Christian J. F. Holubarsch

Department of Cardiology and Angiology, University of Freiburg, Freiburg, Germany

Abstract

ABSTRACT

This article examines the relationship between endothelial dysfunction and ``small vessel disease.'' Newer technologies have facilitated the study of this issue. Using a Doppler wire and the intracoronary administration of acetylcholine and papaverine, a difference can be made between functional and chronic-trophic disturbances of the coronary reserve. Papaverine induces smooth muscle cell-mediated vasodilation, acetylcholine induces nitric oxide (NO)-mediated vasodilation. The data revealed that endothelial dysfunction may be related to disturbances in the microcirculation. In addition to those vasomotor-related properties, other factors such as antithrombotic, antiadhesive disturbances contribute to the disturbed microcirculation. Newer techniques, such as serial positron emission tomography, may yield an even better understanding of these processes.

KEYWORD

Endothelium - endothelial dysfunction - NO - small vessel disease - Doppler technology

Full Text

References

REFERENCES

1 Opherk D, Zebe H, Weihe E. Reduced coronary dilatory capacity and ultrastructural changes of the myocardium in patients with angina pectoris but normal coronary arteries. Circulation . 1981; 63 817-825
2 Strauer B E. Ventricular function and coronary hemodynamics in hypertensive heart disease. Am J Cardiol . 1979; 44 999-1009
3 Marcus M L. The Coronary Circulation in Health and Disease. New York: McGraw-Hill 1983: 285-306
4 Furchgott R F, Zawadski J V. The obligatory role of endothelial cells in the relaxation of arterial smooth muscle by acetylcholine. Nature . 1980; 288 373-376
5 Ignarro L J, Harbison R G, Wood K S, Kadowitz P J. Activation of purified guanylate cyclase by endothelium-derived relaxing factor from pulmonary artery and vein: stimulation by acetylcholine, bradykinin, and arachidonic acid. J Pharmacol Exp Ther . 1986; 237 893-900
6 Ignarro L J, Buga G M, Wood K S, Burns R E, Chandhuri G. Endothelium-derived relaxing factor produced and released from artery and vein is nitric oxide. Proc Natl Acad Sci USA . 1987; 84 9265-9269
7 Zeiher A M, Drexler H, Wollschläger H, Just H. Endothelial dysfunction of the coronary microvasculature is associated with impaired coronary flow regulation in patients with early atherosclerosis. Circulation . 1991; 84 1984-1992
8 Rajagopalan S, Kurz S, Münzel T. Angiotensin II-mediated hypertension in the rat increases vascular superoxide production via membrane NADH/NADPH oxide activation. J Clin Invest . 1996; 97 1916-1923
9 Münzel T, Kurz S, Rajagopalan S. Hydralazine prevents nitroglycerine tolerance by inhibiting activation of a membrane-bound NADH oxidase: A new action for an old drug. J Clin Invest . 1996; 98 1465-1470
10 Mancini G BJ, Henry G C, Macaya C. Angiotensin-converting enzyme inhibition with quinapril improves endothelial vasomotor dysfunction in patients with coronary artery disease. Circulation . 1996; 94 258-265
11 Solzbach U, Hornig B, Jeserich M, Just H. Vitamin C improves endothelial dysfunction of epicardial coronary arteries in hypertensive patients. Circulation . 1997; 96 1513-1519
12 Celermajer D S, Sorensen K E, Georgakopoulos D. Cigarette smoking is associated with dose-related and potentially reversible impairment of endothelium-dependent dilation in healthy young adults. Circulation . 1993; 88 2149-2155
13 Celermajer D S, Adams M R, Clarkson P. Passive smoking and impaired endothelium-dependent arterial dilation in healthy young adults. N Engl J Med . 1996; 334 150-154
14 Vogel R A, Corretti M C, Plotnick C D. Effect of a single high-fat meal on endothelial function in healthy subjects. Am J Cardiol . 1997; 79 350-354
15 Egashira K, Hirooka Y, Kai H. Reduction in serum cholesterol with pravastatin improves endothelium-dependent coronary vasomotion in patients with hypercholesterolemia. Circulation . 1994; 89 2519-2524
16 Huggins G S, Pasternak R C, Alpert N M, Fischman A J, Gewirtz H. Effects of short-term treatment of hyperlipidemia on coronary vasodilator function and myocardial perfusion in regions having substantial impairment of baseline dilator reserve. Circulation . 1998; 98 1291-1296
17 John S, Schleich M, Langenfeld M. Increased bioavailability of nitric oxide after lipid-lowering therapy in hypercholesterolemic patients. A randomized, placebo-controlled, double-blind study. Circulation . 1998; 98 211-216
18 Treasure C B, Klein J L, Weintraub W S. Beneficial effect of cholesterol-lowering therapy on the coronary endothelium in patients with coronary artery disease. N Engl J Med . 1995; 332 481-487
19 Laufs U, La Fata V, Plutzky J, Liao I K. Upregulation of endothelial nitric oxide synthase by HMG-CoA reductase inhibitors. Circulation . 1998; 97 1129-1135
20 Nitzsche E V, Coi Y, Czermin J. Noninvasive quantification of myocardial blood flow in humans. A direct comparison of the (13N) ammonia and the (15O) water techniques. Circulation . 1996; 93 2000-2006
21 Kelm M, Preik-Steinhoff H, Preik M, Strauer B E. Serum nitrite sensitively reflects endothelial NO formation in human forearm vasculature: Evidence for biochemical assessment of endothelial L-arginine-NO pathway. Cardiovasc Res . 1999; 41 765-772