BACKGROUND: Patients with coronary artery disease (CAD) are often insulin resistant, a state that predisposes to increased atherosclerosis. Recently, it was suggested that a "vascular insulin resistance" could explain this association, causing endothelial dysfunction and hence atherosclerosis. We therefore studied the vascular insulin response in patients with CAD. MATERIALS AND METHODS: Nine non-diabetic patients with documented CAD and 31 lean healthy controls were examined. Forearm blood flow was measured by venous occlusion plethysmography. Dose-response studies of acetylcholine (ACh) and sodium nitroprusside (SNP) elicited endothelium-dependent and -independent vasodilation and were repeated during intra-arterial insulin infusion. RESULTS: Patients were insulin resistant as determined by HOMA index. Insulin infusion resulted in high physiological levels of insulin in the forearm without systemic effects. Patients had a reduced ACh response but insulin infusion increased the ACh response equally in patients and controls (a mean increase of 74+/-37 vs 57+/-24%, patients vs controls, p=0.12). A minor increase of the SNP response was also noted during insulin infusion. CONCLUSION: Vascular insulin response is intact in non-diabetic CAD patients in spite of insulin resistance and endothelial dysfunction.
BACKGROUND:Patients with coronary artery disease (CAD) are often insulin resistant, a state that predisposes to increased atherosclerosis. Recently, it was suggested that a "vascular insulin resistance" could explain this association, causing endothelial dysfunction and hence atherosclerosis. We therefore studied the vascular insulin response in patients with CAD. MATERIALS AND METHODS: Nine non-diabeticpatients with documented CAD and 31 lean healthy controls were examined. Forearm blood flow was measured by venous occlusion plethysmography. Dose-response studies of acetylcholine (ACh) and sodium nitroprusside (SNP) elicited endothelium-dependent and -independent vasodilation and were repeated during intra-arterial insulin infusion. RESULTS:Patients were insulin resistant as determined by HOMA index. Insulin infusion resulted in high physiological levels of insulin in the forearm without systemic effects. Patients had a reduced ACh response but insulin infusion increased the ACh response equally in patients and controls (a mean increase of 74+/-37 vs 57+/-24%, patients vs controls, p=0.12). A minor increase of the SNP response was also noted during insulin infusion. CONCLUSION: Vascular insulin response is intact in non-diabetic CADpatients in spite of insulin resistance and endothelial dysfunction.