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We investigated 2 hypotheses: (1) a relationship between platelet indices and stable coronary artery disease (CAD) and acute ST-segment elevation myocardial infarction (STEMI) and (2) a relationship between platelet indices on admission and thrombolysis outcomes in patients with STEMI. A total of 260 patients were enrolled. The white blood cell (WBC) and platelet distribution width (PDW) were found to be increased in patients with STEMI (P for both < .001). White blood cell and PDW were independent predictors of acute STEMI. Mean platelet volume (MPV) and PDW were significantly higher in the thrombolysis failure group than in the thrombolysis success group (9.9 ± 1.8 vs 9.2 ± 1.5 fL, P = .021 and 17.7 ± 1.0 vs 16.4 ± 2.1 fL, P < .001, respectively). Mean platelet volume and PDW were independent predictors of thrombolysis failure. Patients with acute STEMI had higher PDW than did patients with stable CAD. In addition, higher PDW and MPV seem to correlate with thrombolysis failure in patients with STEMI.

Background: To date, no validated biomarkers with high sensitivity and specificity have been established for diagnosis of pulmonary embolism (PE) in patients with deep venous thrombosis (DVT). There is a need to develop simple and reliable noninvasive tests that can accurately identify patients with PE, even in small hospitals or clinics. The aim of this study was to investigate the value of mean platelet volume (MPV) and platelet distribution width (PDW) for predicting occurrence of PE in patients with DVT. Methods: Records of acute DVT patients were reviewed retrospectively. Group 1 consisted of 50 patients with acute DVT and group 2 consisted of 50 patients with acute DVT who developed PE during follow-up. The control group consisted of patients with uncomplicated primary varicose veins of the lower limbs. Venous peripheral blood samples for measurement of MPV, PDW, and platelet count were drawn on admission, before the treatment, and at the time of PE diagnosis. Results: MPV and PDW levels at the time of PE diagnosis were higher in group 2 than group 1 (P,0.001 and P=0.026, respectively). Receiver operating characteristics analysis revealed that a 5.2% increase in admission PDW during follow-up provided 70% sensitivity and 82% specificity (area under the curve, 0.80), and a 6.6% increase in admission MPV during follow-up provided 74% sensitivity and 83% specificity (area under the curve, 0.84) for prediction of PE occurrence in patients with DVT. PDW and MPV levels at the time of PE diagnosis were found to be independent risk factors for the occurrence of PE in patients with DVT. Conclusion: Serial measurements of MPV and PDW, and percent change in MPV and PDW appears to be a useful marker for predicting occurrence of acute PE in patients with a first episode of acute proximal DVT.

BackgroundDespite the advances in medical and interventional treatment modalities, some patients develop epicardial coronary artery reperfusion but not myocardial reperfusion after primary percutaneous coronary intervention (PCI), known as no-reflow. The goal of this study was to evaluate the safety and efficacy of intracoronary epinephrine in reversing refractory no-reflow during primary PCI.MethodsA total of 248 consecutive STEMI patients who had undergone primary PCI were retrospectively evaluated. Among those, 12 patients which received intracoronary epinephrine to treat a refractory no-reflow phenomenon were evaluated. Refractory no-reflow was defined as persistent TIMI flow grade (TFG) ≤2 despite intracoronary administration of at least one other pharmacologic intervention. TFG, TIMI frame count (TFC), and TIMI myocardial perfusion grade (TMPG) were recorded before and after intracoronary epinephrine administration.ResultsA mean of 333 ± 123 mcg of intracoronary epinephrine was administered. No-reflow was successfully reversed with complete restoration of TIMI 3 flow in 9 of 12 patients (75%). TFG improved from 1.33 ± 0.49 prior to epinephrine to 2.66 ± 0.65 after the treatment (p < 0.001). There was an improvement in coronary flow of at least one TFG in 11 (93%) patients, two TFG in 5 (42%) cases. TFC decreased from 56 ± 10 at the time of no-reflow to 19 ± 11 (p < 0.001). A reduction of TMPG from 0.83 ± 0.71 to 2.58 ± 0.66 was detected after epinephrine bolus (p < 0.001). Epinephrine administration was well tolerated without serious adverse hemodynamic or chronotropic effects. Intracoronary epinephrine resulted in significant but tolerable increase in heart rate (68 ± 13 to 95 ± 16 beats/min; p < 0.001) and systolic blood pressure (94 ± 18 to 140 ± 20; p < 0.001). Hypotension associated with no-reflow developed in 5 (42%) patients. During the procedure, intra-aortic balloon pump counterpulsation was required in two (17%) patients, transvenous pacing in 2 (17%) cases, and both intra-aortic balloon counterpulsation and transvenous pacing in one (8%) patients. One patient (8%) died despite all therapeutic measures.ConclusionIntracoronary epinephrine may become an effective alternative in patients suffering refractory no-reflow following primary PCI.

Our findings provide evidence to support the hypothesis that endothelial dysfunction may be an important factor in the pathogenesis of SCF.