Among patients with diabetes and stable ischemic heart disease, higher SYNTAX scores predict higher rates of major cardiovascular events and were associated with more favorable outcomes of revascularization compared with medical therapy among patients suitable for CABG. (Bypass Angioplasty Revascularization Investigation in Type 2 Diabetes; NCT00006305).

No abstract

The notorious predilection for rupture of splenic artery aneurysms in women of childbearing age is once more stressed by this case report. Although such ruptures usually result in a catastrophic interabdominal bleeding, in rare instances they lead to the formation of an arteriovenous fistula and consequent portal hypertension. Arterialization of the portal vein results in a progressive development of intrinsic hepatic morphologic changes and hepatoportal sclerosis, which further elevate the pressure in the portal system. This combination of pathophysiologic hemodynamic features closely resembles the original concept of Banti. He postulated that portal hypertension began with pathologic changes within the spleen which were associated with an increased blood flow through this organ. This led to increased flow and pressure in the portal venous system and ultimately cumulated in cirrhosis of the liver. This concept of the pathophysiology of portal hypertension has been universally abandoned, but it could serve as a model of the sequelae of an arteriovenous communication within the portal system.

After coronary artery bypass grafting (CABG) surgery, patients may remain at risk for myocardial ischemia and infarction and ventricular dysrhythmias. The hemodynamic responses to endotracheal extubation and the efficacy of intravenous lidocaine pretreatment were studied after CABG surgery and overnight mechanical ventilation. Twenty-five patients were divided into two groups: group 1 (n = 13) patients who had tracheal extubation after pretreatment with a placebo; group 2 patients who received lidocaine (1 mg/kg IV) before tracheal extubation. Hemodynamic data, electrocardiographic tracings, and arterial blood gases were obtained before tracheal extubation, during suctioning, and 1, 5, and 20 min after tracheal extubation. Group 1 patients displayed significant increases in heart rate, arterial blood pressure, rate-pressure product, right atrial pressure, and cardiac index during suctioning and within 1 min of tracheal extubation, returning to preextubation level by 5 min. There were no significant changes in pulmonary and systemic resistance indices. Hemodynamic changes in group 2 patients were similar to those in group 1. Both in the absence and presence of lidocaine, tracheal extubation caused hemodynamic responses that were small in magnitude and brief in duration. These responses were not associated with electrocardiographic or enzymatic evidence of myocardial ischemia or infarction, or with ventricular dysrhythmias. Compared with the well-documented hemodynamic responses to tracheal intubation, we found that extubation of the trachea after CABG surgery was associated with less pronounced responses. This may be related to avoidance of laryngoscopy and possibly accommodation to the endo-tracheal tube. These modest hemodynamic responses of extubation of the trachea after CABG surgery were not modified by intravenous lidocaine.

No abstract