This study was designed to assess the parameters of myocardial oxidative stress and related cardiac morphological changes following intraperitoneal cocaine exposure in rats. The cardiac levels of reduced glutathione(GSH), oxidised glutathione(GSSG), ascorbic acid (AA), and the production of malondialdehyde (MDA) were measured, as well as the variations of activity in the enzyme systems involved in cell antioxidant defence, glutathione peroxidase (GSH-Px), glutathione reductase (GR) and superoxide dismutase (SOD). After chronic cocaine administration for 30 days GSH was significantly depleted in the heart from 30 min (P < 0.001) to 24 h (P < 0.001) after exposure, and GSSG was increased for a similar time (P < 0.05 at 30 min and P < 0.01 at 24 h). SOD increased during the first hour (P < 0.001), GR and GSH-Px both increased from 30 min to 24 h, and these increases were statistically significant (P < 0.01 and P < 0.001 at 30 min and P < 0.01 and P < 0.001 at 24 h, respectively). The AA levels increased after 1 h (P < 0.01), remaining significantly so for 24 h (P < 0.001) and MDA increased from 30 min to 24 h, all values being highly significant (P < 0.001). The body weight was significantly (P < 0.001) reduced in both cocaine groups (40 mg/kg x 30 days and 40 mg/kg x 10 days + 60 mg/kg x 20 days). The heart weight (P < 0.01) and its percentage of the body weight (P < 0.001) were significantly higher in these two groups than in the controls. Similarly, in the noradrenaline 4 mg/ kg x 30 days group, the body weight was significantly (P < 0.001) reduced and the heart weight (P < 0.01) and its percentage of body weight (P < 0.001) were significantly higher than in the controls. In comparing the cocaine and noradrenaline experiments, the frequency and extent of cardiac lesions obtained with 40 mg/kg x 10 days + 60 mg/kg x 20 days of cocaine were similar to those with 8 mg/kg of noradrenaline at 24 h. In this experimental model, cocaine administration compromised the antioxidant defence system of the heart associated with a significant increase of heart weight and the percentage of body weight.
Normal resting wall motion at echocardiography coupled to normal stress myocardial perfusion, rules out the presence of significant coronary allograft vasculopathy in many heart transplant recipients. Conversely, resting wall motion abnormalities and perfusion defects strongly predict cardiac events. Therefore, a strategy which reserves angiography for patients with resting wall motion abnormalities and/or perfusion defects may be safe and cost-effective.
Objectives: To assess the value of the European system for cardiac operative risk evaluation (EuroSCORE), a validated model for prediction of in-hospital mortality after cardiac surgery, in predicting long term event-free survival. Design and setting: Single institution observational cohort study. Patients: Adult patients (n = 1230) who underwent cardiac surgery between January 2000 and August 2002. Results: Mean age was 65 (11) years and 32% were women. Type of surgery was isolated coronary artery bypass grafting in 62%, valve surgery in 23%, surgery on the thoracic aorta in 4%, and combined or other procedures in 11%. Mean EuroSCORE was 4.53 (3.16) (range 0-21); 366 were in the low (0-2), 442 in the medium (3-5), 288 in the high (6-8), and 134 in the very high risk group (> 9). Information on deaths or events leading to hospital admission after the index discharge was obtained from the Regional Health Database. Out of hospital deaths were identified through the National Death Index. In-hospital 30 day mortality was 2.8% (n = 34). During 2024 person-years of follow up, 44 of 1196 patients discharged alive (3.7%) died. By Cox multivariate analysis, EuroSCORE was the single best independent predictor of long term all cause mortality (hazard ratio (HR) 1.55, 95% confidence interval (CI) 1.03 to 2.34, p , 0.0001). In the time to first event analysis, 227 either died without previous events (n = 20, 9%) or were admitted to hospital for an event (n = 207, 91%). EuroSCORE (HR 1.60, 95% CI 1.36 to 1.89, p , 0.0001), the presence of > 2 co-morbidities versus one (HR 1.49, 95% CI 1.09 to 2.02, p , 0.0001), and . 96 hours' stay in the intensive care unit after surgery (HR 2.04, 95% CI 1.42 to 2.95, p = 0.0001) were independently associated with the combined end point of death or hospital admission after the index discharge. Conclusions: EuroSCORE and a prolonged intensive care stay after surgery are associated with long term event-free survival and can be used to tailor long term postoperative follow up and plan resource allocation for the cardiac surgical patient. The European system for cardiac operative risk evaluation (EuroSCORE) was developed between 1995 and 1999 to provide a simple, additive risk model of perioperative mortality 1 2 in over 19 000 consecutive adult patients undergoing open heart surgery in 128 centres in eight European countries. EuroSCORE has been further evaluated in two cohorts (1995 and 1998-1999) from the Society of Thoracic Surgeons' North American database in over 500 000 patients.3 EuroSCORE predicted with good accuracy inhospital or 30 day mortality in both the European and US cohorts, regardless of baseline between-country differences. Furthermore, despite relevant differences in patient demographics and type of surgery within the European Union, EuroSCORE performance in the single participating countries varied from good to excellent. 4 The assessment of long term outcome after cardiac surgery according to preprocedural risk may also be important to enhance continuity of care and to pla...
To assess whether the combined evaluation of total Sequential Organ Failure Assessment (t-SOFA) score and pro- and anti-inflammatory cytokine profiles early after left ventricular assist device (LVAD) implant discriminates patients at high risk for multiple organ failure syndrome (MOFS) in the first month post-LVAD, we analyzed plasma interleukin (IL)-6, IL-8, IL-10, IL-1ra, IL-1beta, tumor necrosis factor-alpha (TNF-alpha), and urine neopterin levels before (day 0) and at 4 hours, 1, 3, 7, 14, and 30 days after LVAD implant in 23 recipients. Eight patients died of MOFS between days 7 and 30 (nonsurvivors). At preimplant, only blood urea nitrogen and age were higher in nonsurvivors than survivors. At 4 hours, IL-8, IL-10, and IL1-ra levels were higher in nonsurvivors than in survivors; t-SOFA was also higher and peaked on day 3 in nonsurvivors. Only IL-8 levels on day 1 were significantly associated with a t-SOFA > or =10 on day 3 (odds ratio 1.10, 95% confidence interval 1.01-1.21, p = 0.04). Neopterin, marker of monocyte activation, increased significantly only in nonsurvivors (p < 0.001). These findings suggest that an activated inflammatory system soon after LVAD implant is implicated in MOFS development. Early monitoring of inflammatory mediators and t-SOFA score may be a valuable tool for outcome prediction in LVAD recipients.
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