Obesity is associated with impaired coronary collateral vessel development

Abstract

BACKGROUND: Chronic myocardial ischaemia due to coronary artery stenosis or occlusion has been shown to increase the growth of coronary collateral circulation. Collateralization leads to increased oxygen delivery to the area at risk and hence may reduce ischaemia, prevent infarction and preserve contractile function. However, there is considerable variation among patient subsets in terms of the presence or degree of collateralization. We aimed to evaluate the relationship between obesity and coronary collateral development in patients with ischaemic heart disease. METHODS AND RESULTS:In all, 215 patients (mean age, 57.878.9 y) with body mass index (BMI)Z30 kg/m 2 were enrolled into our study. A total of 90 age-and sex-matched patients (mean age, 58.7710 y) with BMIo25 kg/m 2 and significant coronary artery disease were selected as a control group. The mean age and distribution of risk factors for coronary heart disease were not significantly different between two groups other than poorer HDL cholesterol and triglyceride profile in obese patients. The mean BMI was significantly higher in the patient group (33.372.4 vs 22.871.7, Po0.001). The mean number of diseased vessels and maximum lesion severity were not significantly different between the two groups. The mean Rentrop collateral score of the patient group was significantly worse than the control group (1.0870.68 vs 2.1070.72, Po0.001). CONCLUSIONS: Our findings suggest that collateral vessel development is poorer in obese patients (defined as BMIZ30 kg/m 2 ) with ischemic heart disease compared to normal range BMI, and the risk of having poor collateral vessel development is significantly increased. However, this might be reflecting the cluster of risk factors, associated with metabolic syndrome, in which insulin resistance plays a major role.

Insulin activates hypoxia-inducible factor-1α in human and rat vascular smooth muscle cells via phosphatidylinositol-3 kinase and mitogen-activated protein kinase pathways: impairment in insulin resistance owing to defects in insulin signalling

“…Furthermore, the deep reduction of the insulin effects on the HIF-1/VEGF pathway we observed in VSMC taken from a well-known animal model of insulin resistance supports the hypothesis that this phenomenon can play a role in the already observed reduction of vascularisation in the insulin-resistant states [1,2].…”

“…The reduction of the effects of insulin on the HIF-1/ VEGF pathway in VSMC from an animal model of insulinresistance and obesity could be an aspect of this 'growth factor dysfunction', providing a possible molecular basis for the reduced formation of new vessels in the insulinresistant states [1,2] that probably contributes to the increased prevalence of cardiovascular events observed in obesity [50].…”

“…doi.org/10.1007/s00125-006-0156-0 symptoms [1]. Also, body mass index independently influences the degree of collateral development in patients with coronary artery disease [1].…”

“…doi.org/10.1007/s00125-006-0156-0 symptoms [1]. Also, body mass index independently influences the degree of collateral development in patients with coronary artery disease [1]. Impairment of vascular endothelial growth factor (VEGF) synthesis/action could play a role in this phenomenon, as observed in insulinresistant rats [2].…”

Cardioprotection by Adiponectin

“…Finally, adiponectin has antiapoptotic actions in human endothelial cells that are dependent on the induction of AMPK signaling ). Collectively, these findings suggest that down-regulation of the adiponectin-AMPK regulatory pathway may participate in endothelial cell dysfunction and vessel rarefaction that are observed in obese states (Al Suwaidi et al 2001, Lind and Lithell 1993, Steinberg et al 1996, Yilmaz et al 2003.…”