Enhanced secretion of insulin plays a role in the development of atherosclerosis and restenosis of coronary arteries: elective percutaneous transluminal coronary angioplasty in patients with effort angina

Nishimoto, Yasuhiro; Miyazaki, Yutaka; Toki, Yukio; Murakami, Ryuichiro; Shinoda, Masanori; Fukushima, Akihiko; Kanayama, Hitoshi

doi:10.1016/s0735-1097(98)00428-8

Cited by 32 publications

(20 citation statements)

References 35 publications

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“…Additionally, endothelial dysfunction as an effect of insulin therapy might be responsible for accelerated atherosclerosis in untreated lesions or enhanced restenosis in treated lesions. 10,11 Hyperinsulinemia, which also occurs in insulin-requiring diabetic patients treated with insulin, may contribute to the atherogenic process. Although we did not collect information on the etiology of diabetes in insulin-treated patients in the Dynamic Registry, it is likely that the vast majority of patients were likely to have type 2, insulinresistant, diabetes.…”

Section: Discussionmentioning

confidence: 99%

Temporal changes in the outcomes of patients with diabetes mellitus undergoing percutaneous coronary intervention in the National Heart, Lung, and Blood Institute dynamic registry

Holper

Abbott

Mulukutla

et al. 2011

American Heart Journal

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Section: Discussionmentioning

confidence: 99%

Temporal changes in the outcomes of patients with diabetes mellitus undergoing percutaneous coronary intervention in the National Heart, Lung, and Blood Institute dynamic registry

Holper

Abbott

Mulukutla

et al. 2011

American Heart Journal

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“…There is no clear evidence that increased insulin or other physiologicaal changes associated with insulin resistance are individually linked to these changes, although this has been suggested by some human studies (34,40), nor is the role of hyperglycemia fully understood. Whereas other investigators have suggested that diabetic patients have an impaired response to NO and that this impairment in NO production can increase inflammation following injury (18,54,56), our study does not suggest or prove that the primary insult in DM is decreased NO bioavailability.…”

Section: Discussionmentioning

confidence: 99%

Nitric oxide modulates vascular inflammation and intimal hyperplasia in insulin resistance and the metabolic syndrome

Barbato

Zuckerbraun

Overhaus

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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. Nitric oxide modulates vascular inflammation and intimal hyperplasia in insulin resistance and the metabolic syndrome. Am J Physiol Heart Circ Physiol 289: H228 -H236, 2005. First published February 25, 2005 doi:10.1152/ajpheart.00982.2004.-Type 2 diabetes mellitus (DM) and the metabolic syndrome, both characterized by insulin resistance, are associated with an accelerated form of atherosclerotic vascular disease and poor outcomes following vascular interventions. These vascular effects are thought to stem from a heightened inflammatory environment and reduced bioavailability of nitric oxide (NO). To better understand this process, we characterized the vascular injury response in the obese Zucker rat by examining the expression of adhesion molecules, the recruitment of inflammatory cells, and the development of intimal hyperplasia. We also evaluated the ability of exogenous NO to inhibit the sequela of vascular injury in the metabolic syndrome. Obese and lean Zucker rats underwent carotid artery balloon injury. ICAM-1 and P-selectin expression were increased following injury in the obese animals compared with the lean rats. The obese rats also responded with increased macrophage infiltration of the vascular wall as well as increased neointima formation compared with their lean counterparts (intima/media ϭ 0.91 vs. 0.52, P ϭ 0.001). After adenovirus-mediated inducible NO synthase (iNOS) gene transfer, ICAM-1, P-selectin, inflammatory cell influx, and oxidized low-density lipoprotein (LDL) receptor expression were all markedly reduced versus injury alone. iNOS gene transfer also significantly inhibited proliferative activity (54% and 73%; P Ͻ 0.05) and neointima formation (53% and 67%; P Ͻ 0.05) in lean and obese animals, respectively. The vascular injury response in the face of obesity and the metabolic syndrome is associated with increased adhesion molecule expression, inflammatory cell infiltration, oxidized LDL receptor expression, and proliferation. iNOS gene transfer is able to effectively inhibit this heightened injury response and reduce neointima formation in this proinflammatory environment. restenosis; obesity

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“…46 Long-term cardiovascular events are often caused by disease progression at sites not treated with stents. Progression of disease was highlighted in the experience of the group from Toulouse, France.…”

Section: Should Drug-eluting Stents Change the Selection For Revasculmentioning

confidence: 99%

Surgery Is Preferred for the Diabetic With Multivessel Disease

King

2005

Circulation

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Enhanced secretion of insulin plays a role in the development of atherosclerosis and restenosis of coronary arteries: elective percutaneous transluminal coronary angioplasty in patients with effort angina

Abstract: Enhanced secretion of insulin during the OGTT might be useful as a predictor of coronary atherosclerosis and of restenosis after elective PTCA in nondiabetic patients with effort angina.

Cited by 32 publications

References 35 publications

Temporal changes in the outcomes of patients with diabetes mellitus undergoing percutaneous coronary intervention in the National Heart, Lung, and Blood Institute dynamic registry

Temporal changes in the outcomes of patients with diabetes mellitus undergoing percutaneous coronary intervention in the National Heart, Lung, and Blood Institute dynamic registry

Nitric oxide modulates vascular inflammation and intimal hyperplasia in insulin resistance and the metabolic syndrome

Surgery Is Preferred for the Diabetic With Multivessel Disease

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