Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2013 Nov;34(41):3175-81.
doi: 10.1093/eurheartj/eht351. Epub 2013 Sep 7.

Endothelial dysfunction over the course of coronary artery disease

Enrique Gutiérrez  1 , Andreas J Flammer, Lilach O Lerman, Jaime Elízaga, Amir Lerman, Francisco Fernández-Avilés
Affiliations
Review

Endothelial dysfunction over the course of coronary artery disease

Enrique Gutiérrez et al. Eur Heart J. 2013 Nov.

Abstract

The vascular endothelium regulates blood flow in response to physiological needs. Endothelial dysfunction is closely related to atherosclerosis and its risk factors, and it constitutes an intermediate step on the progression to adverse events throughout the natural history of coronary artery disease (CAD), often affecting clinical outcomes. Understanding the relation of endothelial function with CAD provides an important pathophysiological insight, which can be useful both in clinical and research management. In this review, we summarize the current knowledge on endothelial dysfunction and its prognostic influence throughout the natural history of CAD, from early atherosclerosis to post-transplant management.

Keywords: Acetylcholine; Coronary heart disease; Endothelial dysfunction; Heart failure; Heart transplant.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Endothelium-derived vasoactive substances. Shear stress and activation of a variety of receptors leads to a release of nitric oxide by inducing endothelial nitric oxide synthase. It exerts relaxation of vascular smooth muscle cells and exerts antiproliferative effects as well as inhibits thrombocyte aggregation and leucocyte adhesion. Other endothelium-derived relaxing factors, including endothelium-derived hyperpolarizing factor and prostacyclin, are also shown. ACE, angiotensin-converting enzyme; Ach, acetylcholine; AI, angiotensin I; AII, angiotensin II; AT1, angiotensin 1 receptor; Bk, bradykinin; COX, cyclooxygenase; ECE, ET-converting enzyme; EDHF, endothelium-derived hyperpolarizing factor; ETA and ETB, endothelin A and B receptors; ET-1, endothelin-1; l-Arg, l-arginine; M, muscarinic acetylcholine receptor; PGH2, prostaglandin H2; ROS, reactive oxygen species; S1, serotoninergic receptor; TX, thromboxane receptor; TXA2, thromboxane; 5-HT, serotonin. Reproduced with kind permission from Springer Science and Business Media. Source: Springer. Pflügers Arch- Eur J Physiol (2010) 459:1005–1013. Human endothelial dysfunction: EDRFs. Flammer and Lüscher.
Figure 2
Figure 2
Illustration of the reciprocal interaction between endothelial dysfunction, inflammation and the natural history of coronary artery disease. Blue arrows marked with the box ‘ED’ represent processes in which endothelial dysfunction modifies the evolution or prognosis of coronary artery disease. Red arrows represent ways in which coronary artery disease contributes to a worse endothelial function.
Figure 3
Figure 3
Illustration of the post-stent epicardial reactivity to acetylcholine in the various studies referenced in the text–. The values express the change in coronary artery lumen diameter (%) to acetylcholine or exercise, measured by angiography; horizontal short lines represent average, and vertical bars standard deviation. The red vertical line separates drug-eluting stents from bare metal stents. As can be appreciated, patients with drug-eluting stents exhibit a vasoconstrictive response, while patients with bare metal stents have a roughly neutral vascular response. AEES, absorbable everolimus eluting scaffold; BMS, bare metal stent; PES, paclitaxel eluting stent; DES, drug eluting stent; SES, sirolimus eluting stent; ZES, zotarolimus eluting stent.
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. de Agostini AI, Watkins SC, Slayter HS, Youssoufian H, Rosenberg RD. Localization of anticoagulantly active heparan sulfate proteoglycans in vascular endothelium: antithrombin binding on cultured endothelial cells and perfused rat aorta. J Cell Biol. 1990;111:1293–1304. - PMC - PubMed
    1. van Hinsbergh WM. Endothelial permeability for macromolecules. Mechanistic aspects of pathophysiological modulation. Arterioscler Thromb Vasc Biol. 1997;17:1018–1023. - PubMed
    1. Urbich C, Dimmeler S. Endothelial progenitor cells: characterization and role in vascular biology. Circ Res. 2004;95:343–353. - PubMed
    1. Furchgott RF, Zawadzki JV. The obligatory role of endothelial cells in the relaxation of arterial smooth muscle by acetylcholine. Nature. 1980;288:373–376. - PubMed
    1. Griendling KK, Harrison DG, Alexander RW. Biology of the vessel wall. In: Fuster V, Walsh R, Harrington R, editors. Hurst's The Heart. 13th ed. Mcgraw-hill; 2010.

Publication types

MeSH terms

-