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Lipoprotein(a) selectively impairs receptor-mediated endothelial vasodilator function of the human coronary circulation.

Abstract：

OBJECTIVES:We investigated the influence of lipoprotein(a) [Lp(a)] serum levels on different endothelium-dependent vasodilator stimuli representing different mechanisms of endothelium-dependent vasodilation. BACKGROUND:Lp(a) is an independent predictor for the development and progression of coronary artery disease. Impairment of endothelium-dependent vasodilation of epicardial arteries has been shown in patients with high levels of Lp(a). METHODS:In 108 patients with angiographically normal or minimally diseased coronary vessels, vasomotor responses to acetylcholine, cold pressor testing, increased blood flow and nitroglycerin were assessed. RESULTS:Lp(a) levels > or = 30 mg/dl were associated with significant dose-dependent enhancement of the vasoconstrictor response to acetylcholine [receptor-mediated vasodilation, p = 0.002; acetylcholine 10(-6) mol/liter, -29 +/- 21% vasoconstriction with Lp(a) levels > or = 30 mg/dl vs, -5.6 +/- 25% with Lp(a) levels < 30 mg/dl]. In addition, vasoconstrictor response to cold pressor test (receptor- and flow-mediated vasodilation) was significantly enhanced in patients with Lp(a) levels > or = 30 mg/dl (-13 +/- 12% vs. 1.2 +/- 16%, p = 0.005). In contrast, strictly endothelium-dependent, but non-receptor-mediated, flow-dependent dilation and endothelium-independent dilation with nitroglycerin were not compromised. Linear regression analysis revealed an inverse relation between Lp(a) and both acetylcholine-induced (r = -0.34, p = 0.0007) and cold pressor test-induced (r = -0.44, p = 0.0001) vasodilation. By multivariate analysis, Lp(a) was a strong and independent predictor of paradoxic vasoconstriction only in response to acetylcholine and cold pressor testing. Impairment of coronary blood flow increase in patients with Lp(a) levels > or = 30 mg/dl did not reach statistical significance. CONCLUSIONS:High Lp(a) levels are associated with a selective impairment of vasodilator capacity of receptor-mediated endothelial stimuli. Impaired dilator capacity of the coronary circulation associated with elevated Lp(a) levels may contribute to the pathogenesis of myocardial ischemia in response to trigger mechanisms involving receptor-mediated stimulation such as sympathetic activation.

journal_name

J Am Coll Cardiol

journal_title

Journal of the American College of Cardiology

authors

Schachinger V,Halle M,Minners J,Berg A,Zeiher AM

doi

10.1016/s0735-1097(97)00237-4

subject

Has Abstract

pub_date

1997-10-01 00:00:00

pages

927-34

issue

eissn

0735-1097

issn

1558-3597

pii

S0735-1097(97)00237-4

journal_volume

pub_type

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Lipoprotein(a) selectively impairs receptor-mediated endothelial vasodilator function of the human coronary circulation.