The effects of endothelial dysfunction and inflammation on slow coronary flow.

Objectives: We evaluated the effects of endothelial dysfunction and inflammation on slow coronary flow (SCF).

Study Design: The study included 26 patients (group 1; 13 females, 13 males; mean age 58.8 years) who had normal coronary arteries but SCF in three coronary vessels and 25 subjects (group 2, 14 females, 11 males; mean age 62.7 years) with normal coronary arteries and normal flow. Coronary flow was quantified according to the TIMI (Thrombolysis In Myocardial Infarction) frame count method for the left anterior descending (LAD), circumflex (Cx), and right coronary (RCA) arteries. Endothelial function was assessed by plasma asymmetric dimethylarginine (ADMA) levels, brachial artery endothelium-dependent flow-mediated dilatation (FMD), and nitroglycerin-mediated dilatation (NMD). Inflammation was assessed by high-sensitivity C-reactive protein (hs-CRP) levels.

Results: TIMI frame count was significantly higher in group 1 compared to group 2 for each artery (p<0.001). In group 1, the mean FMD was significantly lower (6.6±1.6% vs. 11.2±1.6%, p<0.001) and the mean ADMA level was significantly higher (0.8±0.2 µmol/l vs. 0.5±0.1 µmol/l, p=0.002), whereas NMD and hs-CRP levels did not differ significantly between the two groups (p>0.05). There was a significant correlation between plasma ADMA level and TIMI frame count (RCA: r=0.50, p=0.001; cLAD: r=0.46, p=0.004; Cx: r=0.32, p=0.04) and a significant negative correlation between FMD and TIMI frame count (cLAD: r=-0.68, p=0.0003; Cx: r=-0.54, p=0.0004; RCA: r=-0.46, p=0.004), but hs-CRP level was not correlated with TIMI frame count. In multivariate analysis, only ADMA (p=0.009) and FMD (p=0.02) were significant parameters to predict SCF.

Conclusion: Our results suggest that endothelial dysfunction as determined by increased ADMA level and impaired FMD, rather than inflammation, plays a role in the etiopathogenesis of SCF.