Two hour bivalirudin infusion after PCI for ST elevation myocardial infarction.

The standard of care for STEMI PCI for the past decade has been aspirin, clopidogrel, heparin, and a glycoprotein IIbIIIa receptor inhibitor (GPI). A bivalirudin strategy was shown to be superior to a GPI strategy in the HORIZONS AMI trial for net adverse clinical events (combined MACE and bleeding). An increased risk of acute stent thrombosis in the bivalirudin arm may have prevented broader adoption of bivalirudin for this indication. We hypothesized that acute stent thrombosis risk could be ameliorated by a 2 h infusion of bivalirudin following STEMI PCI. We implemented a multicenter, prospective registry for all STEMI patients in Vermont treated at a single PCI center. Each patient was routinely pre-loaded with dual antiplatelet therapy and 75% received an unfractionated heparin bolus prior to PCI. The utilization of bivalirudin bolus and continued 2 h infusion after PCI was routine with GPI bailout optional. 128 consecutive STEMI patients underwent primary PCI from October 1, 2008 to September 30, 2009. 92% of primary PCI patients received bivalrudin during and after the procedure with a 9% rate of bail out GPI. There was one case of probable or definite acute stent thrombosis (0.7%), and this single case occurred despite use of bailout GPI. Despite the prolonged infusion of bivalirudin, major bleeding occurred in only 1.7% of STEMI patients. In conclusion, prolonging bivalirudin for 2 h after STEMI PCI may be a promising method to alleviate acute stent thrombosis risk without losing the bleeding complication benefit of the bivalirudin strategy.

Biomarker profiles as descriptors of left ventricular remodeling after acute myocardial infarction.

BACKGROUND: Biomarker expression can predict subsequent cardiovascular events. The goal of this study was to determine the pattern of expression in blood of a broad array of cytokines and growth factors taken 24-72 h after an ST elevation myocardial infarction (STEMI) involving the left anterior descending (LAD) coronary artery. METHODS: Blood was taken from 16 patients with LAD STEMI. Cytokine and growth factor expressions were quantified with the use of a Milliplex cytokine/chemokine array analysis that tested 42 analytes. Results from patients were compared with those in blood from 20 healthy volunteers. RESULTS: Most (15/16) participants had positive remodeling without reduction in left ventricular function during follow-up. Analytes were grouped based on their function into those that activate class 1 T-helper cells (Th1 activates cell-mediated immunity), those that activated a Th2 response (activates humoral immunity and attenuates cell-mediated immunity), chemokines (attract leukocytes), and growth factors (promote a healing response). Elevation of cytokines involved in the Th2 response predominated over the Th1 response demonstrating a balance favoring tolerance and limiting activation of cell-mediated immunity. The concentration of selected chemokines favoring cell-mediated immunity was not elevated. The concentration of selected growth factors was increased. CONCLUSION: The cytokine expression, 24-72 h after an LAD STEMI, suggests that positive ventricular remodeling is associated with growth factor expression and limitation of cell-mediated immunity. Subsequent studies are warranted to determine whether deviation from this pattern identifies patients at an increased risk of adverse remodeling after myocardial infarction.