970 resultados para Los Angeles star.
Resumo:
BACKGROUND: In humans, it is not known whether physical endurance exercise training promotes coronary collateral growth. The following hypotheses were tested: the expected collateral flow reduction after percutaneous coronary intervention of a stenotic lesion is prevented by endurance exercise training; collateral flow supplied to an angiographically normal coronary artery improves in response to exercise training; there is a direct relationship between the change of fitness after training and the coronary collateral flow change. METHODS AND RESULTS: Forty patients (age 61+/-8 years) underwent a 3-month endurance exercise training program with baseline and follow-up assessments of coronary collateral flow. Patients were divided into an exercise training group (n=24) and a sedentary group (n=16) according to the fact whether they adhered or not to the prescribed exercise program, and whether or not they showed increased endurance (VO2max in ml/min per kg) and performance (W/kg) during follow-up versus baseline bicycle spiroergometry. Collateral flow index (no unit) was obtained using pressure sensor guidewires positioned in the coronary artery undergoing percutaneous coronary intervention and in a normal vessel. In the vessel initially undergoing percutaneous coronary intervention, there was an increase in collateral flow index among exercising but not sedentary patients from 0.155+/-0.081 to 0.204+/-0.056 (P=0.03) and from 0.189+/-0.084 to 0.212+/-0.077 (NS), respectively. In the normal vessel, collateral flow index changes were from 0.176+/-0.075 to 0.227+/-0.070 in the exercise group (P=0.0002), and from 0.219+/-0.103 to 0.238+/-0.086 in the sedentary group (NS). A direct correlation existed between the change in collateral flow index from baseline to follow-up and the respective alteration of VO2max (P=0.007) and Watt (P=0.03). CONCLUSION: A 3-month endurance exercise training program augments coronary collateral supply to normal vessels, and even to previously stenotic arteries having undergone percutaneous coronary intervention before initiating the program. There appears to be a dose-response relation between coronary collateral flow augmentation and exercise capacity gained.
Resumo:
BACKGROUND: It has been suggested that changes in blood coagulation and fibrinolysis might explain the observed association between depression and coronary artery disease (CAD). So far, only a few coagulation factors have been investigated in this regard, and the results were not consistent. DESIGN: The aim of our study was to analyse a broad range of coagulation and fibrinolytic factors, with emphasis on factors directly involved in clot formation and degradation or reflecting coagulation activation, in patients with CAD and controls without CAD, as assessed by coronary angiography, who also underwent a diagnostic procedure for depression. METHODS: We screened 306 patients with CAD and controls without CAD for depression using the Hospital Anxiety and Depression Scale and Allgemeine Depressions Skala-L questionnaires. In participants with positive screening result, diagnosis of major depression was confirmed or excluded by a structured interview. We analysed the following coagulation and fibrinolytic factors: fibrinogen, prothrombin fragment F1+2, factor XIII A-subunit, factor XIII B-subunit, tissue plasminogen activator, plasminogen activator inhibitor-1, thrombin-activable fibrinolysis inhibitor, and D-dimer. RESULTS: We did not observe significant associations between depression and CAD, nor between depression and cardiovascular risk factors. Coagulation and fibrinolytic factors showed no differences between patients with CAD and controls, but they were associated with several cardiovascular risk factors. Depression was not associated with coagulation and fibrinolytic factors. No associations were found either when both CAD and depression were taken into account. CONCLUSION: Our study gives no evidence that there is a significant relation among depression, CAD, and blood coagulation and fibrinolysis.
Resumo:
We found a significant positive correlation between local summer air temperature (May-September) and the annual sediment mass accumulation rate (MAR) in Lake Silvaplana (46°N, 9°E, 1800 m a.s.l.) during the twentieth century (r = 0.69, p < 0.001 for decadal smoothed series). Sediment trap data (2001-2005) confirm this relation with exceptionally high particle yields during the hottest summer of the last 140 years in 2003. On this base we developed a decadal-scale summer temperature reconstruction back to AD 1580. Surprisingly, the comparison of our reconstruction with two other independent regional summer temperature reconstructions (based on tree-rings and documentary data) revealed a significant negative correlation for the pre-1900 data (ie, late ‘Little Ice Age’). This demonstrates that the correlation between MAR and summer temperature is not stable in time and the actualistic principle does not apply in this case. We suggest that different climatic regimes (modern/‘Little Ice Age’) lead to changing state conditions in the catchment and thus to considerably different sediment transport mechanisms. Therefore, we calibrated our MAR data with gridded early instrumental temperature series from AD 1760-1880 (r = -0.48, p < 0.01 for decadal smoothed series) to properly reconstruct the late LIA climatic conditions. We found exceptionally low temperatures between AD 1580 and 1610 (0.75°C below twentieth-century mean) and during the late Maunder Minimum from AD 1680 to 1710 (0.5°C below twentieth-century mean). In general, summer temperatures did not experience major negative departures from the twentieth-century mean during the late ‘Little Ice Age’. This compares well with the two existing independent regional reconstructions suggesting that the LIA in the Alps was mainly a phenomenon of the cold season.