RESUMO
BACKGROUND: Increased microvascular resistance due to chronic inflammation is assumed to be one of the mechanisms associated with coronary slow flow (CSF). Previous studies have shown that the platelet-to-lymphocyte ratio (PLR) and the neutrophil-lymphocyte ratio (NLR) are markers of inflammation for various diseases. In this study we aimed to evaluate the relationship between CSF and PLR-NLR. METHODS: Seventy-eight patients with CSF and 50 patients with normal coronary flow were enrolled into this study. The study subjects underwent medical examination and testing, after which their platelet-to-lymphocyte ratios and NLR values were calculated. An independent observer measured the coronary flow rate by Thrombolysis in Myocardial Infarction Frame Count (TFC) method. The platelet-to-lymphocyte ratio and NLR values were compared between the groups and correlation analysis was performed to explore the relationship between mean TFC with PLR and NLR. RESULTS: Platelet-to-lymphocyte ratio and NLR values were significantly higher in patients with CSF (p < 0.001). There was a positive significant correlation between TFC with NLR and PLR (Spearman's Rho: 0.59, p < 0.001 and Spearman's Rho: 0.30, p = 0.001, respectively). Multivariate logistic regression analysis revealed that NLR is the one independent predictor for CSF. CONCLUSIONS: This study demonstrated an association between CSF and PLR-NLR. Although the exact mechanism could not be explained, our findings support the possible role of inflammation in CSF physiopathology.
RESUMO
The coexistence of coronary artery disease (CAD) and chronic obstructive pulmonary disease (COPD) is frequent because of common etiological factors. Beta-blockers remain underutilized in patients with CAD who also have COPD. This study was performed to evaluate the safety of beta-1 selective blocker agents in CAD patients with COPD. Fifty patients (aged 57.3 +/- 10.1 years) were enrolled in this study; 27 patients received metoprolol CR (controlled release), and 23 received metoprolol (conventional). The patients were stratified according to the severity of COPD (21 severe, 21 moderate, and 8 mild), started on metoprolol CR or conventional metoprolol, and titrated up to the maximum tolerated dose. The clinical controls were done during the first week and then at the first and third month. Patients received a mean total daily dose of 92.5 +/- 18 mg of metoprolol CR or 189 +/- 36.7 mg of metoprolol. Seven patients could not receive the maximum dose. There was no significant decrease in forced expiratory volume in 1 s (FEV(1)) in either group (basal vs last FEV(1): 54.5% +/- 13.4% vs 54.3% +/- 13% in the metoprolol CR group and 49.6% +/- 14.5% vs 53.2% +/- 12.8% in the metoprolol group). No adverse event was experienced. Metoprolol, a beta-1 selective blocker, can be used safely at the maximum dose in CAD patients with COPD.