INTRODUCTION: In this study, we aimed to investigate the relationship between glycated haemoglobin (HbA1c) levels and the severity of coronary artery disease (CAD) in < 40 years old patients. MATERIAL AND METHODS: The study population consisted of 211 premature coronary atherosclerotic patients (pCAP) (aged 36.4 ± 2.5 years) and 160 control subjects (36.4 ± 2.4 years). The severity of CAD was evaluated by the Gensini scoring system. HbA1c levels and the other basic biochemical parameters were analysed, and relations with severity of CAD were evaluated. RESULTS: There were statistically significant differences in serum HbA1c levels between the two groups (pCAP = 6.1 ± 1.8%, control = 4.7 ± 1.2%, p < 0.001). HbA1c levels significantly positively correlated with the Gensini score in pCAP (r = 0.662, p < 0.001). In linear multivariate regression analysis (including age, sex, HbA1c, smoking, diabetes mellitus and hypertension as dependent parameters), only HbA1c was found to be an independent risk factor for the presence of severe CAD (Beta = 0.374, p < 0.001). In ROC curve analysis, the optimal cut-off value of HbA1c to predict severe CAD was 6.52%, with 74.4% sensitivity and 75.1% specificity (area under the curve 0.781, 95% confidence interval 0.661 to 0.901, p < 0.001). CONCLUSIONS: HbA1c levels were found to be correlated with the Gensini score in pCAP with and without diabetes. In this respect, glucose metabolism abnormalities, indicated by HbA1c, may play an important role in premature CAD.
INTRODUCTION: In this study, we aimed to investigate the relationship between glycated haemoglobin (HbA1c) levels and the severity of coronary artery disease (CAD) in < 40 years old patients. MATERIAL AND METHODS: The study population consisted of 211 premature coronary atheroscleroticpatients (pCAP) (aged 36.4 ± 2.5 years) and 160 control subjects (36.4 ± 2.4 years). The severity of CAD was evaluated by the Gensini scoring system. HbA1c levels and the other basic biochemical parameters were analysed, and relations with severity of CAD were evaluated. RESULTS: There were statistically significant differences in serum HbA1c levels between the two groups (pCAP = 6.1 ± 1.8%, control = 4.7 ± 1.2%, p < 0.001). HbA1c levels significantly positively correlated with the Gensini score in pCAP (r = 0.662, p < 0.001). In linear multivariate regression analysis (including age, sex, HbA1c, smoking, diabetes mellitus and hypertension as dependent parameters), only HbA1c was found to be an independent risk factor for the presence of severe CAD (Beta = 0.374, p < 0.001). In ROC curve analysis, the optimal cut-off value of HbA1c to predict severe CAD was 6.52%, with 74.4% sensitivity and 75.1% specificity (area under the curve 0.781, 95% confidence interval 0.661 to 0.901, p < 0.001). CONCLUSIONS: HbA1c levels were found to be correlated with the Gensini score in pCAP with and without diabetes. In this respect, glucose metabolism abnormalities, indicated by HbA1c, may play an important role in premature CAD.