In our small, pilot trial, administration of cyclosporine at the time of reperfusion was associated with a smaller infarct by some measures than that seen with placebo. These data are preliminary and require confirmation in a larger clinical trial.

Background-We previously demonstrated that ischemic postconditioning decreases creatine kinase release, a surrogate marker for infarct size, in patients with acute myocardial infarction. Our objective was to determine whether ischemic postconditioning could afford (1) a persistent infarct size limitation and (2) an improved recovery of myocardial contractile function several months after infarction. Methods and Results-Patients presenting within 6 hours of the onset of chest pain, with suspicion for a first ST-segment-elevation myocardial infarction, and for whom the clinical decision was made to treat with percutaneous coronary intervention, were eligible for enrollment. After reperfusion by direct stenting, 38 patients were randomly assigned to a control (no intervention; nϭ21) or postconditioned group (repeated inflation and deflation of the angioplasty balloon; nϭ17). Infarct size was assessed both by cardiac enzyme release during early reperfusion and by 201 thallium single photon emission computed tomography at 6 months after acute myocardial infarction. At 1 year, global and regional contractile function was evaluated by echocardiography. At 6 months after acute myocardial infarction, single photon emission computed tomography rest-redistribution index (a surrogate for infarct size) averaged 11.8Ϯ10.3% versus 19.5Ϯ13.3% in the postconditioned versus control group (Pϭ0.04), in agreement with the significant reduction in creatine kinase and troponin I release observed in the postconditioned versus control group (Ϫ40% and Ϫ47%, respectively). At 1 year, the postconditioned group exhibited a 7% increase in left ventricular ejection fraction compared with control (Pϭ0.04). Conclusions-Postconditioning affords persistent infarct size reduction and improves long-term functional recovery in patients with acute myocardial infarction.

Background-Opening of the mitochondrial permeability transition pore (mPTP) is a crucial event in lethal reperfusion injury. Phosphorylation (inhibition) of glycogen synthase kinase-3␤ (GSK3␤) has been involved in cardioprotection.We investigated whether phosphorylated GSK3␤ may protect the heart via the inhibition of mPTP opening during postconditioning. Methods and Results-Wild-type and transgenic GSK3␤-S9A mice (the cardiac GSK3␤ activity of which cannot be inactivated) underwent 60 minutes of ischemia and 24 hours of reperfusion. At reperfusion, wild-type and GSK3␤-S9A mice received no intervention (control), postconditioning (3 cycles of 1 minute ischemia and 1 minute of reperfusion), the mPTP inhibitor cyclosporine A (CsA; 10 mg/kg IV), or the GSK3␤ inhibitor SB216763 (SB21; 70 g/kg IV). Infarct size was assessed by triphenyltetrazolium chloride staining. The resistance of the mPTP to opening after Ca 2ϩ loading was assessed by spectrofluorometry on mitochondria isolated from the area at risk. In wild-type mice, infarct size was significantly reduced by postconditioning, CsA, and SB21, averaging 39Ϯ2%, 35Ϯ5%, and 37Ϯ4%, respectively, versus 58Ϯ5% of the area at risk in control mice (PϽ0.05). In GSK3␤-S9A mice, only CsA, but not postconditioning or SB21, reduced infarct size. Postconditioning, CsA, and SB21 all improved the resistance of the mPTP in wild-type mice, but only CsA did so in GSK3␤-S9A mice. Conclusion-These

This randomized study demonstrated that post-conditioning reduced infarct size and edema in patients with reperfused STEMI.

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A fermented formula may reduce the severity of acute diarrhea among healthy young infants. This outcome may be linked to the bifidogenic effects of fermentation products and their interactions with the intestinal immune system.

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Background-Genetically modified mice offer the unique opportunity to gain insight into the pathophysiology of pulmonary arterial hypertension. In mice, right heart catheterization is the only available technique to measure right ventricular systolic pressure (RVSP). However, it is a terminal procedure and does not allow for serial measurements.Our objective was to validate a noninvasive technique to assess RVSP in mice. Methods and Results-Right ventricle catheterization and echocardiography (30-MHz transducer) were simultaneously performed in mice with pulmonary hypertension induced acutely by infusion of a thromboxane analogue, U-46619, or chronically by lung-specific overexpression of interleukin-6. Pulmonary acceleration time (PAT) and ejection time (ET) were measured in the parasternal short-axis view by pulsed-wave Doppler of pulmonary artery flow. Infusion of U-46619 acutely increased RVSP, shortened PAT, and decreased PAT/ET. The pulmonary flow pattern changed from symmetrical at baseline to asymmetrical at higher RVSPs. In wild-type and interleukin-6 -overexpressing mice, the PAT correlated linearly with RVSP (r