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 Presentation

"Insulin Resistance and Cardiovascular Disease - Role of the Endothelium"

Dr. Subodh Verma (biography)
English - 2002-11-23 - 47 minutes
(36 slides)
(27 slides)

Summary :
The link between diabetes and cardiovascular disease is of special interest to all cardiologists. An emerging concept is that endothelial dysfunction, high C-reactive protein and inflammation may actually be the mechanistic basis for the link between diabetes and cardiovascular disease. The American Heart Association is recognizing the growing problem of the metabolic syndrome and how it is a very important target for intervention. As it said in 2002: “Treating Insulin Resistance early should be part of a global cardiovascular and metabolic strategy”. Insulin resistance directly affects the endothelium, which leads to endothelial dysfunction, a precursor for adverse cardiovascular events. Our understanding of the genetics of insulin resistance has evolved from thinking that the insulin resistance “gene” manifests in type 2 diabetes when the individual is exposed to sufficient environmental insult, e.g., too much McDonald’s. We now know that not only type 2 diabetes manifests but a host of other conditions such as hypertension, dyslipidemia, atherosclerosis and PCOS. We therefore are really talking about insulin resistance in connection to Cardiovascular Dysmetabolic Syndrome. Identification of this syndrome is central to primary prevention of atherosclerosis and CVD, and we will see here how insulin resistance leads to endothelial dysfunction and then CVD.

More information is available about C-Reactive Protein.

Learning objectives :
The participant will learn how insulin resistance leads to endothelial dysfunction, a precursor for CVD; and also why C-reactive protein can be used to predict CVD:

- The endothelium releases various factors, one of which, NO, is implicated in heart disease. Others are angiotensin and endothelin-1, and insulin resistant patients produce less NO and more angiotensin and endothelin-1. They also overexpress the AII receptor, and ACE.

- Insulin plays a role in vasodilatation by stimulating NO release, which increases glucose uptake. Not only does an insulin resistant person have impaired glucose, fat and protein metabolism, but also resistance to the effects of insulin to stimulate release of NO.

- The vascular insulin resistance resulting in decreased production of NO decreases blood flow to skeletal muscle and accounts for about 25% of whole body insulin resistance. Treatment of vascular insulin resistance by ACE inhibitors may thus have a role in preventing new onset diabetes.

- New data suggest that insulin sensitizers improve endothelial function and are pleiotropic anti-atherosclerotic, anti-inflammatory drugs.

- Insulin resistance also promotes atherosclerosis and impaired vascular function through impaired fibrinolysis, due to excess PAI-1 levels. PAI-1 levels were shown to be lowered by Rosiglitazone (McGill JB et al. Diabetes. 1994; 43: 104-109).

- Insulin resistance may independently elevate BP, and hence insulin sensitizers may lower BP.

- Microalbuminuria is linked to IR, and albumin excretion is reduced by Rosiglitazone.

- Insulin resistance causes increased ACE and AII receptor expression, and Rosiglitazone reduces vascular ACE content.

- Insulin resistant patients have higher levels of CRP.

- Low levels of CRP quench NO in the endothelium, and stimulate endothelin-1 and IL-6 (Verma et al. Circulation. 2002). Rosiglitazone reduces CRP levels and CRP –induced endothelial dysfunction.

- Patients with metabolic syndrome have more vulnerable plaques, i.e., plaques more vulnerable to rupture.


Bibliographic references :
Verma S. 2002. Endothelin Antagonism and Insulin's Vascular Effects. Hypertension. Dec;40(6):e12-3
http://www.ncbi.nlm.nih.gov/entrez

Verma S, Arikawa E, Lee S, Dumont AS, Yao L, McNeill JH. 2002. Exaggerated coronary reactivity to endothelin-1 in diabetes: reversal with bosentan. Can J Physiol Pharmacol; Oct;80(10):980-6.
http://www.ncbi.nlm.nih.gov/entrez

   


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