2015 Volume 61 Issue 1 Pages 72-78
Background: Carbon monoxide (CO) was previously only considered as a highly toxic pollutant since it binds to hemoglobin with high affinity. Recently, however, it has been recognized as a signaling molecule with regulatory roles in many physiological and pathophysiological processes within the cardiovascular system. The aim of this study was to clarify the behavior of CO in patients with acute coronary syndrome (ACS).
Methods: We assessed 235 patients with suspected ACS, 98 smokers (88 male, 62 ± 14 years) and 137 nonsmokers (77 male, 72 ± 13 years), who had undergone emergent cardiac catheterization and blood sampling for calculation of carboxyhemoglobin (COHb). Patients were categorized into 4 groups: smoking patients with ACS (n=77), smoking patients without ACS (n=21), non-smoking patients with ACS (n=97), and non-smoker patients without ACS (n=40). We investigated whether biomarkers were related to COHb levels.
Results: LogCOHb was significantly higher in the smoking patients compared to non-smoking patients (0.30 ± 0.12 vs. 0.45 ± 0.18, P < 0.01). Interestingly, among the non-smoking patients, COHb was increased in the ACS patients compared to the non ACS patients (0.31 ± 0.12 vs. 0.25 ± 0.12 P < 0.01). In contrast, among the smoking patients, there was no difference in COHb between the ACS and non-ACS patients (0.45 ± 0.18 vs. 0.44 ± 0.18, n.s.). There were no correlations between COHb and any of the biomarkers.
Conclusions: These results suggest that endogenous CO may be useful to assess the risk of cardiovascular stress.
