Previous studies have suggested that microvascular abnormalities cause slow coronary flow (SCF). The role of inflammation has not been investigated, to date. The purpose of this study was to determine the role of inflammation in pathogenesis of SCF. The study included 32 patients with angiographically proven SCF (mean age 49 9 years) (group I) and 30 subjects with normal coronary flow (mean age 48 8 years) (group II). Blood samples were collected for high sensitive CRP (hs-CRP) measurements. Thrombolysis in myocardial infarction frame count (TFC) was compared in both groups. Distribution of sex, age, body mass index (BMI), arterial blood pressure, and ejection fraction were similar in the 2 groups. TFC was significantly higher in group I than in group II for each artery including left anterior descending coronary artery (LAD), left circumflex artery (Cx), and right coronary artery (RCA) (38.9 +/- 6.6 vs 22.1 +/- 1.8 frames, p = 0.000 1; 39.6 +/- 4.9 vs 22.3 +/- 1.8 frames, p = 0.001; 39.0 +/- 3.8 vs 22.0 +/- 1.8 frames, p=0.001, respectively). In group 1, serum hs-CRP concentration was significantly higher than that of group II (0.6 +/- 058 vs 0.24 +/- 0.1 mg/dL p = 0.03). Correlation analysis showed a positive correlation between hs-CRP level and TFC for each artery (for CTFCLAD, r=0.36 p=0.004; for TFCCx, r=0.42 P=0.003; and for TFCRCA, r=0.42, p=0.0001 respectively). Increased hs-CRP level suggests that inflammation may be associated with pathogenesis of SCF or at least in part contributes to its pathogenesis. Increased hs-CRP level may also be an early marker of impaired coronary blood flow.