Serum nitric oxide levels in patients with coronary artery ectasia

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Abstract

Objective:

Serum levels of nitric oxide (NO) are decreased in patients with atherosclerosis and also are a risk factor for the development of atherosclerosis. Endothelial dysfunction and diffuse atherosclerosis have been proposed for the etiology of coronary artery ectasia (CAE). The purpose of this clinical trial was to determine the relationship between CAE and serum NO levels.

Methods:

This prospective controlled study was conducted between January 2008 and March 2012. Serum levels of NO were compared in 40 patients with CAE (mean age 60.1±7.3 years) and 40 patients with normal coronary arteries (mean age 57.6±5 years) as a control group. CAE was diagnosed when a segment of coronary artery was more than 1.5 times the diameter of the adjacent healthy segment. Patients with stenotic atherosclerotic plaques, slow coronary flow, previous history of revascularization, acute coronary syndromes, left ventricular dysfunction, valvular heart disease, and systemic diseases were not included in the study. The effect of NO on the outcome was studied by constructing a receiver operating characteristic (ROC) curve with CAE as the primary variable. Effects of different variables on CAE were calculated using binary logistics regression analysis.

Results:

Serum NO concentrations were significantly lower in patients with CAE than in the control group (42.1±20.1 µmol/L vs. 77.3±15.7 µmol/L, p<0.001). According to the results of the multivariate regression analysis, LDL and NO levels were identified as independent factors associated with CAE (OR=1.02, 95% CI 1–1.04, p=0.02 and OR=0.88, 95% CI 0.83–0.93, p=0.001, respectively). ROC analysis revealed that using a cut-off point of 63.3, NO level predicts CAE with a sensitivity of 87.5% and specificity of 90%.

Conclusion:

Our study indicates that decreased levels of NO are present in patients with CAE compared to patients with normal coronary arteries, supporting the hypothesis that decreased levels of NO might be associated with CAE development. (Anatol J Cardiol 2016; 16: 947-52)

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Most cited references 32

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The obligatory role of endothelial cells in the relaxation of arterial smooth muscle by acetylcholine.

Robert F. Furchgott, John Zawadzki (1980)

Despite its very potent vasodilating action in vivo, acetylcholine (ACh) does not always produce relaxation of isolated preparations of blood vessels in vitro. For example, in the helical strip of the rabbit descending thoracic aorta, the only reported response to ACh has been graded contractions, occurring at concentrations above 0.1 muM and mediated by muscarinic receptors. Recently, we observed that in a ring preparation from the rabbit thoracic aorta, ACh produced marked relaxation at concentrations lower than those required to produce contraction (confirming an earlier report by Jelliffe). In investigating this apparent discrepancy, we discovered that the loss of relaxation of ACh in the case of the strip was the result of unintentional rubbing of its intimal surface against foreign surfaces during its preparation. If care was taken to avoid rubbing of the intimal surface during preparation, the tissue, whether ring, transverse strip or helical strip, always exhibited relaxation to ACh, and the possibility was considered that rubbing of the intimal surface had removed endothelial cells. We demonstrate here that relaxation of isolated preparations of rabbit thoracic aorta and other blood vessels by ACh requires the presence of endothelial cells, and that ACh, acting on muscarinic receptors of these cells, stimulates release of a substance(s) that causes relaxation of the vascular smooth muscle. We propose that this may be one of the principal mechanisms for ACh-induced vasodilation in vivo. Preliminary reports on some aspects of the work have been reported elsewhere.

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Hypertension in mice lacking the gene for endothelial nitric oxide synthase.

P L Huang, Z. Huang, H Mashimo … (1995)

Nitric oxide (NO), a potent vasodilator produced by endothelial cells, is thought to be the endothelium-dependent relaxing factor (EDRF) which mediates vascular relaxation in response to acetylcholine, bradykinin and substance P in many vascular beds. NO has been implicated in the regulation of blood pressure and regional blood flow, and also affects vascular smooth-muscle proliferation and inhibits platelet aggregation and leukocyte adhesion. Abnormalities in endothelial production of NO occur in atherosclerosis, diabetes and hypertension. Pharmacological blockade of NO production with arginine analogues such as L-nitroarginine (L-NA) or L-N-arginine methyl ester affects multiple isoforms of nitric oxide synthase (NOS), and so cannot distinguish their physiological roles. To study the role of endothelial NOS (eNOS) in vascular function, we disrupted the gene encoding eNOS in mice. Endothelium-derived relaxing factor activity, as assayed by acetylcholine-induced relaxation, is absent, and the eNOS mutant mice are hypertensive. Thus eNOS mediates basal vasodilation. Responses to NOS blockade in the mutant mice suggest that non-endothelial isoforms of NOS may be involved in maintaining blood pressure.

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Nitric oxide-generating vasodilators and 8-bromo-cyclic guanosine monophosphate inhibit mitogenesis and proliferation of cultured rat vascular smooth muscle cells.

A Hassid, Uttam C Garg (1989)

Endothelium-derived relaxing factor has been recently identified as nitric oxide. The purpose of this study was to determine if vasodilator drugs that generate nitric oxide inhibit vascular smooth muscle mitogenesis and proliferation in culture. Three chemically dissimilar vasodilators, sodium nitroprusside, S-nitroso-N-acetylpenicillamine and isosorbide dinitrate, dose-dependently inhibited serum-induced thymidine incorporation by rat aortic smooth muscle cells. Moreover, 8-bromo-cGMP mimicked the antimitogenic effect of the nitric oxide-generating drugs. The antimitogenic effect of S-nitroso-N-acetylpenicillamine was inhibited by hemoglobin and potentiated by superoxide dismutase, supporting the view that nitric oxide was the ultimate effector. Sodium nitroprusside and S-nitroso-N-acetylpenicillamine significantly decreased the proliferation of vascular smooth muscle cells. Moreover, the inhibition of mitogenesis and proliferation was shown to be independent of cell damage, as documented by several criteria of cell viability. These results suggest that endogenous nitric oxide may function as a modulator of vascular smooth muscle cell mitogenesis and proliferation, by a cGMP-mediated mechanism.

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Author and article information

Journal

Journal ID (nlm-ta): Anatol J Cardiol

Journal ID (iso-abbrev): Anatol J Cardiol

Title: Anatolian Journal of Cardiology

Publisher: Kare Publishing (Turkey )

ISSN (Print): 2149-2263

ISSN (Electronic): 2149-2271

Publication date (Print): December 2016

Publication date (Electronic): 25 April 2016

Volume: 16

Issue: 12

Pages: 947-952

Affiliations

[1]Department of Cardiology, Division of Pathophysiology, Faculty of Medicine, Ankara University; Ankara- Turkey

[* ]Department of Internal Medicine, Division of Pathophysiology, Faculty of Medicine, Ankara University; Ankara- Turkey

[1 ]Department of Cardiology, Türkiye Yüksek İhtisas Educational and Research Hospital; Ankara- Turkey

[2 ]Department of Cardiovascular Surgery, Türkiye Yüksek İhtisas Educational and Research Hospital; Ankara- Turkey

Author notes

Address for correspondence: Dr. Kerim Esenboğa, Türkiye Yüksek İhtisas Hastanesi, Kızılay Sok., No: 4 Sıhhiye, Ankara- Türkiye E-mail: kerimesenboga@ 123456yahoo.com

Article

Publisher ID: AJC-16-947

DOI: 10.14744/AnatolJCardiol.2016.6556

PMC ID: 5324915

PubMed ID: 27147403

SO-VID: 76f197ba-50d6-402b-8cd4-a12b74bbfab2

License:

This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License

Serum nitric oxide levels in patients with coronary artery ectasia

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Karger: Cardiovascular System

Most cited references 32

The obligatory role of endothelial cells in the relaxation of arterial smooth muscle by acetylcholine.

Hypertension in mice lacking the gene for endothelial nitric oxide synthase.

Nitric oxide-generating vasodilators and 8-bromo-cyclic guanosine monophosphate inhibit mitogenesis and proliferation of cultured rat vascular smooth muscle cells.

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