Effect of ischemic preconditioning on cardiovascular outcomes in patients with symptomatic coronary artery disease: a cohort study.

BACKGROUND: Despite the powerful myocardial protection of ischemic preconditioning (IP) observed in experimental studies, it remains a challenge to observe such protection in humans. Thus, the aim of this study was to evaluate the possible effects of IP on clinical outcomes in patients with coronary artery disease (CAD). PATIENTS AND METHODS: In this cohort study, patients with multivessel CAD, preserved systolic ventricular function, and stable angina were prospectively selected. They underwent two sequential exercise stress tests (EST) to evaluate IP presence. IP was considered present if patients had an improvement in the time to the onset of 1.0-mm STsegment deviation in the second EST. The primary end point was the composite rate of cardiac death, nonfatal myocardial infarction, or revascularization during 1-year follow-up. Patients with (IP+) and without (IP-) the cardioprotective mechanism were compared regarding clinical end points. RESULTS: A total of 229 patients completed EST and had IP evaluated: 165 (72%) were IP+ and 64 (28%) were IP - patients. Of these, 218 patients had complete follow-up. At 1-year, event-free survival regarding the primary end point was 95.5 versus 83.6% (P = 0.0024) and event-free survival regarding cardiac death or myocardial infarction was 99.4 versus 91.7% (P=0.0020), respectively, in IP + and IP - groups. The unadjusted hazard ratio (IP + /IP-) for the primary end point was 4.63 (1.52-14.08). After multivariate analysis, IP was still significantly associated with better clinical outcomes (P = 0.0025). CONCLUSION: This data suggest that IP may contribute to better clinical outcomes in patients with ischemic heart disease.

Cancer-related deaths among different treatment options in chronic coronary artery disease: results of a 6-year follow-up of the MASS II study.

INTRODUCTION: The primary end points of randomized clinical trials evaluating the outcome of therapeutic strategies for coronary artery disease (CAD) have included nonfatal acute myocardial infarction, the need for further revascularization, and overall mortality. Noncardiac causes of death may distort the interpretation of the long-term effects of coronary revascularization. MATERIALS AND METHODS: This post-hoc analysis of the second Medicine, Angioplasty, or Surgery Study evaluates the cause of mortality of patients with multivessel CAD undergoing medical treatment, percutaneous coronary intervention, or surgical myocardial revascularization [coronary artery bypass graft surgery (CABG)] after a 6-year follow-up. Mortality was classified as cardiac and noncardiac death, and the causes of noncardiac death were reported. RESULTS: Patients were randomized into CABG and non-CABG groups (percutaneous coronary intervention plus medical treatment). No statistical differences were observed in overall mortality (P=0.824). A significant difference in the distribution of causes of mortality was observed among the CABG and non-CABG groups (P=0.003). In the CABG group, of the 203 randomized patients, the overall number of deaths was 34. Sixteen patients (47.1%) died of cardiac causes and 18 patients (52.9%) died of noncardiac causes. Of these, seven deaths (20.6%) were due to neoplasia. In the non-CABG group, comprising 408 patients, the overall number of deaths was 69. Fifty-three patients (77%) died of cardiac causes and 16 patients (23%) died of noncardiac causes. Only five deaths (7.2%) were due to neoplasia. CONCLUSION: Different treatment options for multivessel coronary artery disease have similar overall mortality: CABG patients had the lowest incidence of cardiac death, but the highest incidence of noncardiac causes of death, and specifically a higher tendency toward cancer-related deaths.

Impact of metabolic syndrome on the outcome of patients with stable coronary artery disease: 2-year follow-up of the MASS II study.

OBJECTIVE: We characterized the impact of the metabolic syndrome (MetS) and its components on cardiovascular adverse events in patients with symptomatic chronic multivessel coronary artery disease, which have been followed prospectively for 2 years. METHODS: Patients enrolled in the MASS II study were evaluated for each component of the MetS, as well as the full syndrome. RESULTS: The criteria for MetS were fulfilled in 52% of patients. The presence of MetS (P<0.05), glucose intolerance (P=0.007), and diabetes (P=0.04) was associated with an increased mortality in our studied population. Moreover, despite a clear tendency for each of its components to increase the mortality risk, only the presence of the MetS significantly increased the risk of mortality among nondiabetic study participants in a multivariate model (P=0.03, relative risk 3.5, 95% confidence interval 1.1-6). Finally, MetS was still associated with increased mortality even after adjustment for diabetes status. These results indicate a strong and consistent relationship of the MetS with mortality in patients with stable coronary artery disease. CONCLUSION: Although glucose homeostasis seems to be the major force driving the increased risk of MetS, the operational diagnosis of MetS still has information for stratifying patients when diabetes information is taken into account.

Characterization of reactive astrocytes in the chronic phase of the pilocarpine model of epilepsy.

PURPOSE: Astrogliosis is a prominent finding in human temporal lobe epilepsy. Work in animal models of temporal lobe epilepsy, however, have mostly concentrated on the acute phases of the studied models or have failed to demonstrate reactive gliosis during the chronic phases of such models. METHODS: Here we used the pilocarpine model of chronic seizures and Cajal's gold sublimate technique for the staining reactive astrocytes to study this issue. RESULTS: For half of the animals (nine of 17) subject to pilocarpine-induced status epilepticus (SE), when assessed 60 days later, variable levels of reactive astrocytes were seen in many thalamic, hippocampal, amygdalar, and neocortical areas. For the remaining half of the animals, however (eight of 17), despite a similar SE induction, as well as for controls, we could not detect stained reactive astrocytes. CONCLUSIONS: We hypothesize that these results might underlie possible differences in the frequency of recurrent spontaneous seizures.