Search

Diabetic nephropathy is a common complication in patients with either type I or type II diabetes. The pathogenesis of diabetic nephropathy is thought to involve both metabolic and vascular factors [...]

Duteplase, 98% double-chain recombinant tissue-type plasminogen activator, was administered intravenously in 488 patients with acute myocardial infarction in a multicenter, open, safety and patency study. Duteplase dosing was based on body weight. Duteplase was administered as a bolus of 0.04 MIU/kg of thrombolytic activity followed by 0.36 MIU/kg over 1 hour and 0.067 MIU/kg/hour for 3 additional hours. The patency rate of the infarct-related artery at 90 minutes was 69% (330 of 478). The reocclusion rate at 3 to 48 hours was 6% (18 of 301). Reinfarction occurred in 7.6% of patients (37 of 488), but 12 reinfarctions occurred after coronary angioplasty. Serious bleeding occurred in 7.6% of patients (37 of 488), predeminantly at the catheterization entry site. Them were 3 instances of central nervous system bleeding, 1 fatal. Fibrinogen levels declined to 83% of baseline at 24 hours. Weight-based dosing may explain the low incidence of serious bleeding in this study. The in-hospital mortality was 6.6% (32 of 488). This study documents that the dose of duteplase used in the international Study of Infarct Survival-3 results in a 90-minute coronary artery patency rate and safety profile comparable to those reported in published studies on the approved dose of alteplase. (Am J Cardiol 1993;71:386-392)

The clinical, angiographic and demographic characteristics of 42 patients with low-grade (0.10) but were significantly older (52 [+ or -] 12 vs 56 [+ or -] 10 years, p = 0.02). Prior acute MI or angina was unusual in group I. Sixty percent had no significant (>50%) residual coronary artery disease while 25% had residual single artery disease. Average significant (>50% diameter stenosis) residual vessel disease was 0.6 [+ or -] 1.0 for group I and 1.9 [+ or -] 0.9 for group II (p (Am J Cardiol 1990;66:773-778), Most heart attacks are caused by a clot blocking a coronary artery narrowed by atherosclerotic (fatty) plaques. It is not known how well patients recover after acute myocardial infarction (AMI) when they have arterial narrowing of less than 50 percent and receive thrombolytic (clot-dissolving) therapy. Although occlusion does not usually occur until the inner diameter of the artery is narrowed by 70 percent or more, 10 to 20 percent of patients requiring thrombolytic therapy after AMI have noncritical stenosis (narrowing) of 50 percent or less. This is an indication of the limitations of coronary angiography (an invasive technique for X-ray visualization of the heart and blood vessels) for predicting the potential for AMI. To measure the effects of low-grade versus critical residual stenosis after AMI, 198 patients with AMI who received thrombolytic therapy were divided into two groups, based on degree of stenosis. The 42 patients with low-grade (less than 50 percent) stenosis were predominantly male smokers; these patients are discussed. Follow-up was terminated in the event of subsequent coronary bypass, angioplasty (mechanical dilatation of the affected artery), total blockage of the infarct site, or death. Patients were monitored for a minimum of 6 months, and an average of 18 months. Data was gathered on symptoms, including typical and atypical angina (chest pain due to inadequate oxygen supply to the heart), dyspnea (difficulty breathing), medical regimen, other risk factors for heart disease, subsequent hospitalizations, and repeat coronary angiography or exercise testing. Although only 1 of the 42 patients died during follow-up, the data suggest a strong likelihood of further heart problems for these patients. Compared with greater atherosclerosis, recurrent clotting at the site of the infarction is more likely to explain total blockages or rapid narrowing of the affected artery. Because this is a small retrospective study, and variables such as type, dosage, and route of thrombolysis, duration and intensity of heparinization (anti-clotting medication), and time to angiography were not measured, it is difficult to draw firm conclusions. The authors report that they found no clear advantage with any given combination of treatments. (Consumer Summary produced by Reliance Medical Information, Inc.)

Reperfusion early during myocardial infarction improves ejection fraction and this improvement may represent myocardial salvage in the injured segment. Alternatively, reperfusion of injured myocardium may cause intramyocardial hemorrhage with resultant increased stiffness causing a dyskinetic segment to become akinetic, thus improving ejection fraction without concomitant myocardial salvage. To evaluate this possibility, diastolic stiffness was assessed in a closed chest, anesthetized, normothermic dog model immediately after a 1 or 3 h occlusion of the left anterior descending coronary artery and during the 4 weeks after occlusion.

Effects of moderate spontaneous hypothermia on left ventricular systolic and diastolic function during acute myocardial infarction were documented in 17 anesthetized dogs with micromanometric pressure and ventriculographic dimension recordings acquired at baseline and at 1 and 3 h after coronary occlusion. In Group 1 (n = 5), core temperature was allowed to decline spontaneously. In Groups 2 (n = 6) and 3 (n = 6), core temperature was maintained at normothermic levels. Hypothermia impaired isovolumic relaxation markedly despite its lack of effect on ventricular volumes or ejection fraction. At 32.3 °C, τ1/2, defined as the time needed for the left ventricular pressure at the time of peak negative rate of change of left ventricular pressure (dPdt) to fall by 50%, was increased by 129% 3 h after occlusion. In addition, at this temperature significant changes were found in heart rate, cardiac output, minute work, peak positive and peak negative dPdt, systolic ejection time, mean velocity of circumferential fiber shortening, mean aortic pressure and end-diastolic pressure.