Introduction: Carbon monoxide (CO), produced within the blood vessel wall, has been known for the regulation of vascular smooth muscle tone. CO is synthesized endogenously by heme oxygenase type 1 in response to ischemic stress. CO acts as a vasodilator and inhibits platelet aggregation. The relation between venous carboxyhemoglobin (COHb) and coronary artery diseases has not been investigated.
Methods: Total of 105 patients (47 women and 58 men) with suspected coronary artery diseases were divided into four groups: acute myocardial infarction (AMI) (n=19), unstable angina pectoris (UAP) (n=34), stable angina pectoris (SAP) (n=28), and control (n=24). All patients underwent coronary angiography (CAG) in evaluation of rest or effort angina, and venous COHb was measured after the CAG.
Results: COHb in UAP was significantly higher than those of SAP (1.08 ± 0.99 % vs. 0.46 ± 0.46 %, p=0.002) and control (1.08 ± 0.99 % vs. 0.26 ± 0.29 %, p<0.001). COHb showed no significant difference between UAP and AMI (1.08 ± 0.99 % vs. 0.64 ± 0.51 %, p=0.104). Total cholesterol in UAP was significantly higher than that of control (176.8 ± 39.7 mg/dL vs. 143.6 ± 29.1 mg/dL, p=0.033). Patients in UAP showed significantly higher triglyceride (148.2 ± 87.3 mg/dL vs. 78.5 ± 41.0 mg/dL, p=0.001) and uric acid (6.1 ± 1.5 mg/dL vs. 4.5 ± 1.9 mg/dL, p=0.012) than those of SAP. C-reactive protein (CRP) progressively increased from control to AMI; however, only CRP in AMI was significantly higher than that of control (6.2 ± 5.7 mg/L vs. 0.8 ± 0.9 mg/L, p=0.003). There were no significant differences in age, body mass index, fasting blood sugar, HDL-cholesterol, LDL-cholesterol, and lipoprotein(a) among four groups.
Conclusion: Our results suggest that acute coronary syndrome is associated with higher COHb, and increase in COHb might be due to the acute compensatory mechanism in response to ischemic stress.
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