RESUMEN
Background: No reflow phenomenon is associated with major adverse cardiac events, prediction of no reflow using laboratory and noninvasive imaging techniques can help in early prevention and management of this phenomenon
Objectives: To investigate the predictive value of serum sP-selectin and endothelial dysfunction assessed by using brachial artery flow mediated dilation [FMD] in patients with STEMI undergoing primary PCI to address patients with high incidence of no reflow
Methods: The prognostic performance, clinical and angiographic correlates of sP-selectin and FMD was assessed in 96 patients admitted in National Heart Institute and Ain Shams University Hospitals by STEMI and underwent primary PCI as a reperfusion strategy. Each patient was subjected to [history taking, clinical examination, laboratory investigations including withdrawal of serum samples for detection of sP-selectin levels, echocardio-graphy, assessment of endothelial dysfunction by measuring the FMD, assessment of the angiographic results using TIMI flow grade and myocardial blush grade. Follow up of the patients during hospital stay and after one month for the incidence of MACE
Results: A significant correlation between patients with high serum sP-selectin and TIMI flow = II was found [P=0.038] and between the serum levels of the sP-selectin and the MBG score [P=0.009], also a significant correlation between the FMD and the MBG score among the study cases [P=0.029] as well as a significant correlation between the FMD and the serum P-selectin level among study cases [P=0.016]. There were no statistical significance between TIMI flow grade and brachial artery FMD [P=0.075]. Also no significant correlation was found between the patients' serum levels of sP-selectin, brachial artery FMD and the incidence of MACE during the hospital stay or during one month of follow up after discharge [P=0.127 and P=0.693, respectively]
Conclusions: Serum sP-selectin level in patients with STEMI treated by primary PCI can predict the patients who will develop no reflow phenomenon after PCI, FMD could not predict the incidence of no reflow among those patients
RESUMEN
The significance of low-molecular-weight heparins [LMWHs] in the management of acute stroke remains controversial. One hundred patients with acute ischemic stroke in evolution were enrolled [with symptoms of stroke within eight hours of randomization]. Patients were randomized to receive Unfractionated Heparin [UFH] at a dose 5000 IU by IV bolus, followed by a continuous IV infusion; or to Enoxaparin [ENOX] at a dose of 0.5 mg per kilogram body weight. Therapy was continued for 10 days. National Institutes of Health Stroke Scale [NIHSS] and Computed Tomography [CT] scan were performed in all patients at the time of admission, and after 48 hours of randomization. It was found that, the mean baseline National Institutes of Health Stroke Score [NIHSS] was 9.14 +/- 0.62 among patients randomized to UFH, vs. 7.86 +/- 0.54 among patients randomized to ENOX [p = 0.2]. At discharge, the mean NIHSS showed a statistically significant difference in favor of the ENOX group [7.9 +/- 0.82 for the UFH arm versus 4.96 +/- 0.54 for the ENOX arm; p = 0.002]. The mean NIHSS after therapy in patients who demonstrated neurological improvement was 5.6 +/- 0.46 in the UFH arm, as opposed to 3.65 +/- 0.39 in the ENOX arm [p = 0.001]. A deterioration in the clinical neurological condition [progressive stroke symptoms] inspite of treatment with anticoagulant therapy was seen in 20% [n = 10] of the patients in the UFH treatment arm and no patients in the ENOX treatment arm showed this condition [p = 0.005]. No statistically significant differences were observed for pulmonary embolism, deep venous thrombosis, recurrent strokes, or death. It was concluded that, Enoxaparin [+ aspirin] was superior to UFH [+ aspirin] in reducing adverse neurological disability after acute ischemic stroke in evolution. This superiority was not associated with reductions in mortality, and could be explained by blunting of von Willebrand factor release by Enoxaparin