The hemodynamic compromise seen in association with acute RV dilatation within an intact pericardium is partly attributable to impaired LV systolic performance and cannot be wholly ascribed to changes in LV preload or compliance.

Myocardial contractility is constantly changing from beat to beat in atrial fibrillation because of the influence of the force-interval relationships.

The conductance technique can be used to study perioperative changes in right ventricular performance. Insertion of the conductance catheter through the outflow tract provides stable and reproducible data. There is significant impairment of right ventricular contractility in the early postoperative period.

Abstract-Experimental studies have demonstrated that intravenous magnesium (Mg) can protect the ischemic myocardium and has an antithrombotic effect. In patients with myocardial infarction, the reperfusion injury is complicated by the presence of a thrombogenic area in the affected coronary artery that may cause repetitive thrombus formation and embolization. We investigated the effect of Mg on infarct size in a randomized study in pigs. Myocardial infarction was induced by a 50-minute mechanical occlusion of the left anterior descending artery combined with an arterial injury, which stimulated a dynamic thrombus formation with emboli shedding on reperfusion. Magnesium sulfate (6 mmol/20 min plus 3 mmol/h) or saline was started at 30 minutes after coronary occlusion. Real-time ventricular pressure-volume loops were generated from the left ventricle by using a microtip pressure manometer and a conductance catheter. Platelet accumulation in the myocardium was evaluated by using 111 In-labeled platelets. After 4 hours of reperfusion, the infarct size/area at risk ratio in the placebo group was 46Ϯ0.06% (nϭ8) compared with 22Ϯ0.07% (nϭ6) in the Mg-treated animals (Pϭ0.03). Ejection fraction decreased significantly in the control group but not in the Mg-treated animals (Pϭ0.03). Platelet accumulation in the myocardium did not change significantly between the Mg-and placebo-treated animals (placebo group, 191Ϯ19%; Mg group, 177Ϯ29%; NS). The present study demonstrates that intravenous Mg infusion is able to reduce infarct size by Ͼ50% and preserve the ejection fraction in this model where ischemia/reperfusion injury was evaluated in the presence of a thrombogenic area in the nutrient artery. Key Words: magnesium Ⅲ animals Ⅲ reperfusion injury Ⅲ thrombosis Ⅲ platelets E xperimental data indicate that intravenous magnesium (Mg) may be a promising agent in the treatment of acute infarction not only during reperfusion of the ischemic myocardium, 1,2 but also as an antithrombotic drug. 3,4 Acute myocardial infarction (MI) is caused, in most cases, by the formation of an occlusive thrombus in the coronary artery. 5 The therapeutic aim in MI patients is to obtain recanalization of the artery, to salvage the ischemic myocardium. However, after thrombolysis or angioplasty, intermittent occlusion of the artery often occurs because of recurrent thrombus formation at the thrombogenic plaque. Thrombus formation and embolization is likely to occur repetitively, until the disrupted plaque is sealed off as part of a healing process. This may lead to recurrent episodes of ischemia/ reperfusion as well as accumulation of microaggregates from the thrombus in the myocardium downstream to the lesion.In animal models of reperfusion injury, a mechanical and standardized occlusion of the nutrient artery has generally been used. However, the clinical setting differs with respect to the experimental setup, because reestablishment of coronary blood flow is not always well defined in patients. In the present model, reperfusion injury was combine...