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Impaired coronary collateral vessel development in patients with metabolic syndrome

Turhan, Hasana; Yasar, Ayse S.b; Erbay, Ali R.b; Yetkin, Ertana; Sasmaz, Haticeb; Sabah, Irfanb

Pathophysiology and Natural History
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Background The development of coronary collateral vessels is the physiological response of myocardial tissue to hypoxia or ischemia, which results in an increase in blood supply to the tissue. However, a lack of collateral vessels or the presence of poor collateralization in some patients despite the presence of significant coronary stenosis or obstruction and evidence of myocardial ischemia suggest that some other factors may affect the development of collateral circulation. In the present study we aimed to evaluate coronary collateral circulation in patients with metabolic syndrome with advanced coronary artery disease and compare the results with those of patients without metabolic syndrome.

Method The study population comprised 102 patients with metabolic syndrome and advanced coronary artery disease (≥90% diameter stenosis in at least one major epicardial coronary artery) and 102 control participants without metabolic syndrome who also had ≥90% diameter stenosis in at least one major epicardial coronary artery. The diagnosis of metabolic syndrome was based on the National Cholesterol Education Program Adult Treatment Panel III clinical definition. Coronary collateral vessels were analysed according to the Cohen and Rentrop grading system. Both groups were also divided into two additional groups according to the Rentrop collateral score as patients with poor collateral circulation (Rentrop score 0–1) and good collateral circulation (Rentrop score 2–3).

Results The mean Rentrop collateral score for patients with metabolic syndrome was significantly lower than for those without metabolic syndrome (1.38±0.79 compared with 1.99±1.08, respectively, P<0.001). When two groups were compared with respect to poor and good collateral circulation, poor collateral circulation was found to be significantly higher in the metabolic syndrome group (70% compared with 32%, respectively, P<0.001). Moreover, multivariate logistic regression analysis revealed a significant relationship between poor collateral circulation and metabolic syndrome (odds ratio=4.29, 95% confidence interval=1.73–10.69, P=0.002).

Conclusion We have shown for the first time that the development of coronary collateral vessels is poorer in patients with metabolic syndrome with advanced ischemic heart disease than in control participants without metabolic syndrome. Thus, it can be suggested that metabolic syndrome is one of the significant factors affecting the development of coronary collateral vessels adversely.

The current study was designed to evaluate coronary collateral circulation in patients with metabolic syndrome with advanced coronary artery disease and compare the results with those of patients without metabolic syndrome. Study population included 102 patients with metabolic syndrome and advanced coronary artery disease (≥ 90% diameter stenosis in at least one major epicardial coronary artery) and 102 control subjects without metabolic syndrome who also had ≥90% diameter stenosis in at least one major epicardial coronary artery. Coronary collateral vessels were analysed according to Cohen and Rentrop grading system. Both groups were divided into two additional groups according to the Rentrop collateral score as patients with poor collateral circulation (Rentrop score 0–1) and good collateral circulation (Rentrop score 2–3). The prevalence of poor collateral circulation was found to be significantly higher in patients with metabolic syndrome compared with subjects without metabolic syndrome (70% vs 32% respectively, P < 0.001). Moreover, multivariate logistic regression analysis revealed a significant association between poor collateral circulation and metabolic syndrome (OR=4.29, 95% CI=1.73–10.69, P=0.002). These findings have suggested that metabolic syndrome might be one of the significant factors affecting the development of coronary collateral vessels adversely.

aDepartment of Cardiology, Inonu University, Malatya

bDepartment of Cardiology, Turkiye Yuksek Ihtisas Hospital, Ankara, Turkey

Correspondence and requests for reprints to Hasan Turhan MD, Turkocagi Caddesi, 20 Sokak, Number 2/2, Balgat 06520, Ankara, Turkey

Tel: +902867658; e-mail: drhturhan@yahoo.com

Received 22 February 2005 Accepted 14 April 2005

© 2005 Lippincott Williams & Wilkins, Inc.