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Korean Circ J. 1995 Oct;25(5):960-966. Korean. Original Article. https://doi.org/10.4070/kcj.1995.25.5.960
Lee KS , Kwon HM , Lee BK , Cha DH , Yoon YW , Kim HS .
Abstract

BACKGROUND: Angina with normal coronary angiogram has been called syndrome X or microvasclar angina. Pathophysiologic mechanisms for chest pain in this group of patients are not known exactly. This study was performed to compare the insulin level of the patients with syndrome X with that of the healthy asymptomatic volunteers. METHODS: The syndrome X group was consisted of 18 patients(11 men and 7 women). All patients had typical chest pain and positive exercise test with a completely normal coronary andgiogram. Patients with hypertension, diabetes mellitus, and there taking any drug known to affect the insulin secretion were excluded. The control group was consisted of 38 healthy subjects(25 men and 11 women) who were not taking any medications. We measured the plasma glucose insulin and C-peptide concentration during oral glucose tolerance test in both groups. RESULTS: Fasting plasma glucose was normal in all patients in both groups. There were no significant differences in plasma glucose level, during the oral grucose tolerance test. There were no significant differences between control and wyndrome X group in the fasting plasma insulin concentration(5.1+/-2.4 vs 5.9+/-2.7 microg/ml, p>0.05). However, the insulin levels at 60min(47.6+/-20.0 vs 84.0+/-68.0 microg/ml) and 120 min(31.4+/-18.2 vs 92.9+/-83.8 microg/ml)were significantly higher in the syndrome X group(p<0.05). THere were no significant differences in the C-peptide concentrations at fasting, 60 min and 120 min after oral glucose tolerance test between control and syndrome X group(p>0.05). CONCLUSION: As shown in above results, there were significant differences in insulin concentrations, but nor in C-peptide concentrations between control and syndrome X group. Thus it can be suggested that the increased dinsulin level in these patients is resulted from the altered insulin action to the target tissues, not from the pancreatic overproduction of insulin. We suggest that this hyperinsulinemia resulted from the insulin resistance play a possible role in the abnormality of microvascular circulation as a mechanism of Syndrome X.

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