Guillain-Barré syndrome after streptokinase therapy for acute myocardial infarction

Some drugs including streptokinase have been reported to precipitate Guillain-Barré syndrome. We report a 70-year-old man with acute anterior myocardial infarction who developed Guillain-Barré syndrome seven days after thrombolytic therapy with streptokinase.     

Tirofiban for catheter intervention in acute myocardial infarction?

This editorial refers to "Facilitation of primary coronary angioplastyby early start of a glycoprotein 2b/3a inhibitor: results ofthe ongoing tirofiban in myocardial infarction evaluation (On-TIME)trial"¹ by A.W.J. Van 't Hof et al. on page 837. The primary goal of treatment in acute myocardial infarctionis re-perfusion of ischaemic myocytes to salvage myocardiumand thus improve the long-term clinical outcome. An indispensablepre-requisite for this goal is full patency (TIMI grade 3 flow)of the infarct-related artery. In 1993, the Zwolle group wasamong the first who published compelling data that this purposeis best served by percutaneous catheter intervention (PCI).¹Even in patients who need to be transported to the PCI centerfrom another hospital, PCI is superior to fibrinolysis.² A criticaltime limit for     

Reply to “Acid suppressants during hospitalization and after discharge in patients after gastroduodenal ESD”

Journal of Gastroenterology -     

EflFect of hepatocyte growth factor on left ventricular remodeling after acute myocardial infarction in canine

Background and objectives To investigate the effect of hepatocyte growth factor (HGF) on left ventricular (LV) remodeling after acute myocardial infarction (AMI). Methods AMI was produced by ligation of proximal left anterior descending coronary artery (LAD) in 12 mongrel canines. These animals were randomized into 2 groups. In HGF group (n=6), canines were injected with pc-DNA3-HGF 1 ml (about 300ug) at the margin of infarcted myocardium; in control group (n=6) canines were injected with equal volume of normal saline. Cardiac function and left ventricular remodeling were evaluated with echocardiography at 1,4, 8 weeks after MI. LV myocardium specimens were obtained at 8 weeks and stained with hematoxylin and eosin for histological examination or with sirius red to assess the collagen content. Results Compared with control group, LVEF in HGF group was significantly higher at 4 weeks (49.61 6.66 vs 39.84 6.39; P<0.05) and at 8 weeks (51.57 8.53 vs 40.61 7.67; P<0.05) after AMI, while LVESV was significantly lower in HGF group than that in control group at 8 weeks after AMI (18.98 3.47 vs 25.66 5.86; P<0.05). Posterior left ventricular wall thickness decreased significantly from 1 wk to 8 wks after AMI in control group, while remained unchanged in HGF group.Compared with control group, histological examination showed more neovascularization and less scar, and sirius red staining indicated higher volume of typeⅢcollagen (7.10±4.06% vs 3.77±1.09%; P<0.05) and lower collagenⅠ/Ⅲratio value (1.11±0.52 vs 2.94±2.48; P<0.05) in HGF group. Conclusion HGF gene transfer might improve cardiac function and LV remodeling after acute myocardial infarction by stimulating angiogenesis, reducing fibrosis, and reducing myocardial scarring.     

Contemporary percutaneous reperfusion therapy for acute myocardial infarction in the elderly

Elderly patients with acute myocardial infarction have not been specifically studied in the context of a large randomized clinical trial. Estimates of the efficacy of available treatments are gleaned from subset analyses of clinical trials, retrospective analysis and single center experiences. In western countries the population is aging and a disproportionate number of myocardial infarctions occur in the elderly. Usage of appropriate therapy in this age group is becoming increasingly important given the potential for benefit but also the potential for harm. Recent publications have found steady improvement in outcomes in the elderly population utilizing contemporary interventions. (J Geriatr Cardiol 2005;2(1) :48-53).     

Postconditioning in acute myocardial infarction: Primary angioplasty revisited?

Early reperfusion of ischemic myocardium is the mean to improve prognosis of acute myocardial infarction. Nevertheless, reperfusion injury due to immediate acidosis correction and subsequent Ca²⁺ overload results in formation of the mitochondrial permeability transition pore. The consequence is the death of viable myocardium due to onconecrosis and apoptosis. Mechanical (Stuttering reperfusion) or pharmacological postconditioning (cyclosporine A, adenosine…) is able to prevent reperfusion injury resulting in more myocardial salvage.     

Update on mechanical revascularization in acute myocardial infarction: which role and when?

Mechanical revascularization in the acute myocardial infarction by primary angioplasty has several advantages over thrombolytic therapy. The short-term patency rates of the infarct-related artery range from 95 to 99% and a normal flow is achieved in more than 90% of the cases. This prompt and effective reperfusion is probably responsible for the improved prognosis with primary angioplasty. The better outcome after primary angioplasty is observed both in low- and in high-risk patients, in all ages and in patients presenting late (>6 h) after the chest pain. Pooled analysis of randomized studies, show that primary angioplasty as compared to thrombolysis, has a lower incidence of death, stroke and reinfarction. Additional advantages of primary PTCA include the possibility of reperfusion in patients in whom lysis is contraindicated or less effective (e.g. patients in cardiogenic shock, or with prior coronary artery bypass surgery) and the ability to provide prognostic information helpful in the patient triage. Thus, primary PTCA results in better outcome than thrombolysis when performed in centers with success rates comparable to those achieved in the randomized trials. Further studies are still needed to assess its long-term efficacy. Several randomized trials are underway to assess the role of stents and the use of more potent antiplatelet drugs, as the GPIIb/IIIa receptor blockers, in adjunct to balloon angioplasty in the treatment of acute myocardial infarction.     

Plasma oxidized LDL: a predictor for acute myocardial infarction?

OBJECTIVES: Oxidized LDL has been attributed a key role in the development of atherosclerosis. Previous studies have demonstrated increased plasma levels of oxidized LDL in patients with established coronary artery disease. The aim of the present study was to investigate if plasma oxidized LDL also predicts risk for development of coronary heart disease (CHD). DESIGN: We used a nested case-control design to study the association between plasma levels of oxidized LDL and risk for development of acute myocardial infarction (AMI) and/or death by CHD. SUBJECTS: Oxidized LDL was analysed by ELISA in cases (n = 26), controls (n = 26) and controls with LDL cholesterol >5.0 mmol L-1 (n = 26). RESULTS: Oxidized LDL correlated with total plasma and LDL cholesterol in both cases (r = 0.72, P < 0.01, r = 0.69, P < 0.01, respectively) and controls (r = 0.71, P < 0.01, r = 0.77, P < 0.01, respectively). The oxidized LDL/plasma cholesterol ratio was higher amongst cases (13.5, range 10.7-19.8) than in controls (12.6, range 9.5-15.8, P < 0.05) and hypercholesterolaemic controls (12.2, range 8.0-16.0, P < 0.01). CONCLUSIONS: These findings identify high plasma oxidized LDL/total cholesterol ratio as a possible indicator of increased risk for AMI.