CMAJ • June 19, 2007; 176 (13). doi:10.1503/cmaj.1060177.
© 2007 Canadian Medical Association or its licensors
All editorial matter in CMAJ represents the opinions of the authors and not necessarily those of the Canadian Medical Association.
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Letters

Vascular inflammation

Craig S. McLachlan

Department of Physiology, National University of Singapore, Singapore

I read with interest the recent article by Ramón Arroyo-Espliguero and Juan Kaski on the role of vascular inflammation as a possible mechanism underlying cardiac syndrome X.1 The hypothesis that systemic or vascular inflammation is involved in endothelial dysfunction is attractive. If it is correct, a reduction in systemic plasma inflammatory markers should improve endothelial function and thereby normalize coronary flow in patients with cardiac syndrome X.2

Some cardiac drugs, such as statins, have a therapeutic anti-inflammatory effect. Statins have been shown to have a beneficial clinical effect in patients with cardiac syndrome X, which appears to have led some people to support the idea that inflammation is a likely cause for this condition.2 On the other hand, statins can also increase the expression of endothelial nitric oxide synthase,3 which produces endothelial nitric oxide. Nitric oxide has been recognized as an endothelial mediator that directly regulates vascular smooth-muscle tone. For example, it has been shown that intracoronary administration of the nitric oxide synthase inhibitor NG-monomethyl-L-arginine reduces epicardial coronary artery diameter and blood flow.4 Other drugs of clinical benefit in cardiac syndrome X, such as angiotensin- converting- enzyme inhibitors and estrogens, also reduce inflammation and increase the expression of endothelial nitric oxide synthase.5 Therefore, before we assume that cardiac syndrome X results primarily from vascular inflammation, we should first consider further the role played by endothelial nitric oxide synthase.

REFERENCES

  1. Arroyo-Espliguero R, Kaski JC. Microvascular dysfunction in cardiac syndrome X: the role of inflammation. CMAJ 2006;174:1833-4.[Free Full Text]
  2. Li JJ, Li YS, Zhang Y, et al. Inflammation: a possible pathogenic link to cardiac syndrome X. Med Hypotheses 2006;66:87-91.[CrossRef][Medline]
  3. Landmesser U, Engberding N, Bahlmann FH, et al. Statin-induced improvement of endothelial progenitor cell mobilization, myocardial neovascularization, left ventricular function, and survival after experimental myocardial infarction requires endothelial nitric oxide synthase. Circulation 2004;110:1933-9.[Abstract/Free Full Text]
  4. Kaufmann PA, Rimoldi O, Gnecchi-Ruscone T, et al. Systemic inhibition of nitric oxide synthase unmasks neural constraint of maximal myocardial blood flow in humans. Circulation 2004;110:1431-6.[Abstract/Free Full Text]
  5. Wang J, Tokoro T, Matsui K, et al. Pitavastatin at low dose activates endothelial nitric oxide synthase through PI3K-AKT pathway in endothelial cells. Life Sci 2005;76:2257-68.[CrossRef][Medline]




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