Effect of Hyperinsulinemia on Coronary Collateral Circulation

The effects of endogen hormons autocoids on coronary collateral (CC) development are not wellknown. Our study sought to investigate the effects of endogen insulin (EI) and C peptid (Cp) on CC development in cases with and wihtout NIDDM. As a study group (SG), we have taken 75 cases (23 with DM, 52 without DM), had >%90 coronary stenosis at only one coronary artery and without critical coronary stenosis (>%50) at others with retrograd CC, and as a control group(CG) we have taken 17 nondiabethic cases, had >%90 coronary stenosis at only one coronary artery and without critical coronary stenosis (>%50) at others, but no CC. EI and CP levels (after 8 hours fasting) were examined for all patients following coronary angiograms. In both groups age, sex, blood pressure, degree of coronary stenosis were similar. In SG mean CC was found less in cases with diabetes than without diabetes (1,35±0,65 and 1,73±0, 74 respectively; p=0,0 18). Although no significant difference was found between SG and CG for insulin levels (11,8±7,9 and 12,5±7,7 Ulu respectively; p>0,05), Cp level was higher in SG (4,3±2,8 and 2,4± 1,2 ng/ml respectively; p=0,004). In SG, no significant difference was found between the cases with and without diabetes for EI levels ( 14,1±8,6 and 10,8±7,5 Ulu respectively; p>0,05), while Cp level was higher in diabetic group (5,4±3,2 and 3,8±2,5 respectively; p=0,021). Cases without diabetes in SG and CG when compared , no significant difference was found for EI levels ( 10,8±7,5 and 12,5±7,7 Ulu respectively; p<0,05), while Cp level was higher in cases without diabetic in SG (3,8±2,5 and 2,4±1,2 respectively; p=0,014). Inside SG, no direct correlation was found between EI and Cp levels with CC (r=0,08 and r=0, 11 respectively).
CONCLUSION
CC development seems to be more related to Cp level than EI level. The degree of CC has found higher in cases with elevated Cp level. But inverse relationship has seen with diabethics and this is thought to be related to peripheral insulin resistance.