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INTRODUCTION: Platelet/lymphocyte ratio (PLR) has been shown to be an inflammatory and thrombotic biomarker for coronary heart disease, but its prognostic value in ST-segment elevation myocardial infarction (STEMI) has not been fully investigated. AIM: To investigate the relationship between PLR and no-reflow, along with the in-hospital and long-term outcomes in patients with STEMI. MATERIAL AND METHODS: In the present study, we included 304 consecutive patients suffering from STEMI who underwent primary percutaneous coronary intervention (p-PCI). Patients were stratified according to PLR tertiles based on the blood samples obtained in the emergency room upon admission. No-reflow after p-PCI was defined as a coronary thrombolysis in myocardial infarction (TIMI) flow grade ≤ 2 after vessel recanalization, or TIMI flow grade 3 together with a final myocardial blush grade (MBG) < 2. RESULTS: The mean follow-up period was 24 months (range: 22-26 months). The number of patients characterized with no-reflow was counted to depict increments throughout successive PLR tertiles (14% vs. 20% vs. 45%, p < 0.001). In-hospital major adverse cardiovascular events and death increased as the PLR increased (p < 0.001, p < 0.001). Long-term MACE and death also increased as the PLR increased (p < 0.001, p < 0.001). Multivariable logistic regression analysis revealed that PLR remained an independent predictor for both in-hospital (OR = 1.01, 95% CI: 1.00-1.01; p = 0.002) and major long-term (OR = 1.01, 95% CI: 1.00-1.01; p < 0.001) adverse cardiac events. CONCLUSIONS: Platelet/lymphocyte ratio on admission is a strong and independent predictor of both the no-reflow phenomenon and long-term prognosis following p-PCI in patients with STEMI.
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The exact pathophysiology of slow coronary flow (SCF) phenomenon, characterized by delayed opacification of coronary arteries during coronary angiography, is still unknown, although endothelial dysfunction, inflammation, vasomotor disorders and atherosclerosis are shown. The present study was conducted to investigate whether there is a coagulation pathway abnormality in patients with SCF measuring plasma factor XI and XII activity. The study included 55 patients with angiographically proven SCF (group I) and 40 individuals with normal coronary flow (NCF, group II). Baseline demographic properties were similar in both groups. Echocardiographic parameters were also similar in patients with SCF and NCF. Factor XI activity was significantly higher in group I when compared with group II. Factor XII activity was also significantly higher in group I when compared with group II (108.9â±â19 vs. 98.8â±â20, Pâ=â0.018 and 131.2â±â17 vs. 119.1â±â16, Pâ=â0.001, respectively). We conclude that SCF phenomenon appears to be associated with enhanced procoagulant state, which may support the role of inflammation and atherosclerosis in the pathogenesis of this phenomenon.
