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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This review presents current epidemiological evidence indicating that a cold environment contributes to increased cardiovascular, especially coronary heart disease, morbidity and mortality, and examines the factors which might explain these findings. Most epidemiological studies have revealed a peak in the coronary morbidity and mortality during the cold season, and a strong negative correlation between the air temperature or its drop and the occurrence of coronary heart disease. These associations could be apparent, indirect or causative. A small part of the increased coronary morbidity and mortality could be due to, for example erroneous recording of cause of death (eg. death due to respiratory diseases). Part of the increased coronary manifestations of cold seem to be due to changes in living circumstances and habits associated with cold. The gradual development of hypothermia among people living in poor socio-economic conditions may lead to a disastrous chain of events. Snowfalls and storms associated with cold weather may increase the incidence of cardiac complications by exposing people to exceptional physical efforts and circumstances. Some of the effects of cold are direct: cold increases the myocardial oxygen demand by increasing sympathetic stimulation, systolic blood pressure and cardiac diastolic pressure and volume. At the same time the myocardial oxygen supply may be impeded by coronary vasoconstriction especially in vessels damaged by atherosclerosis. In addition to these short term effects cold may augment atherosclerosis for example by increasing blood pressure and the blood concentration of cholesterol, catecholamines, corticoids and thrombocytes during the cold season.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The heart and the cold. 331 46

The time course of changes in rSO2 were studied in 58 patients during the uncomplicated course of cardiac operations under extracorporeal circulation (EC) and moderate hypothermia. rSO2 was also compared with central hemodynamic parameters, bioelectrical cerebral activity, and hemoglobin oxygen saturation of the bulb of the internal jugular vein (jbSO2). In the pre- and postperfusion period there was a significant correlation of rSO2 and jbSO2 (p = 0.01), yet with a low correlation coefficient (r = 0.348). During EC, no correlation was found between rSO2 and jbSO2 (p = 0.09, r = 0.386). Changes in rSO2, blood pressure, EEC, body temperature were analyzed in 2 groups of patients at the stages of an operation under EC. Group 1 comprised patients with cardiac valvular apparatus lesions and Group 2 included those with coronary heart disease who differed not only in age, but also in the history of mainly cerebrovascular atherosclerotic lesions, hypertensive disease, myocardial infarction, etc. In patients from both groups, a reduction in rSO2 occurred at the beginning of EC and at the maximum of cooling. But if in Group 1 patients, the significant reductions in rSO2 at the beginning of EC coincided both with that in mean blood pressure (BPmean), as compared to the baseline values (from 75.55 +/- 10.68 to 66.5 +/- 11.73 mm Hg, p = 0.01), and with the change in the frequency spectrum of EEC (a decrease in the frequency of the right edge, as compared to the baseline values, from 20.77 +/- 1.44 to 19.58 +/- 1.14 Hz, p = 0.01), in Group 2 patients, all significant decreases in rSO2 were accompanied only by a significant reduction in BPmean, but without changes in the frequency spectrum of EEG. It should be noted that over the uncomplicated course of an operation all changes in rSO2 were in the normal range of age-related values.
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PMID:[Cerebral oximetry during cardiac surgery under extracorporeal circulation]. 1261 Dec 95

Prediction model for lethal outcome after operation for thoracoabdominal aortic aneurysm (TAAA) has been constructed based on assessment of preoperative risk factors. The main risk factors of lethal outcome at TAAA repair are: Crawford's operation (OR 12.25), deep hypothermia and circulatory arrest (OR 10.86), renal failure (OR 6.8), coronary heart disease (OR 2.49), chronic non-specific lung diseases (OR 2.29), age >50 years (OR 2.18), TAAA of II type by Crawford (OR 2.12). The prognostic system permits to access individual risk with high accuracy including at the patients with combination of different risk factors.
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PMID:[Prediction of surgical outcome for thoracoabdominal aortic aneurysm]. 1816 17

Coronary heart disease (CHD) is the leading cause of death and disability in Europe. For patients presenting with an acute ST-segment elevation myocardial infarction (STEMI), timely myocardial reperfusion using either thrombolytic therapy or primary percutaneous coronary intervention (PPCI) is the most effective therapy for limiting myocardial infarct (MI) size, preserving left-ventricular systolic function and reducing the onset of heart failure. Despite this, the morbidity and mortality of STEMI patients remain significant, and novel therapeutic interventions are required to improve clinical outcomes in this patient group. Paradoxically, the process of myocardial reperfusion can itself induce cardiomyocyte death-a phenomenon which has been termed 'myocardial reperfusion injury' (RI), the irreversible consequences of which include microvascular obstruction and myocardial infarction. Unfortunately, there is currently no effective therapy for preventing myocardial RI in STEMI patients making it an important residual target for cardioprotection. Previous attempts to translate cardioprotective therapies (antioxidants, calcium-channel blockers, and anti-inflammatory agents) for reducing RI into the clinic, have been unsuccessful. An improved understanding of the pathophysiological mechanisms underlying RI has resulted in the identification of several promising mechanical (ischaemic post-conditioning, remote ischaemic pre-conditioning, therapeutic hypothermia, and hyperoxaemia), and pharmacological (atrial natriuretic peptide, cyclosporin-A, and exenatide) therapeutic strategies, for preventing myocardial RI, many of which have shown promise in initial proof-of-principle clinical studies. In this article, we review the pathophysiology underlying myocardial RI, and highlight the potential therapeutic interventions which may be used in the future to prevent RI and improve clinical outcomes in patients with CHD.
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PMID:Myocardial reperfusion injury: looking beyond primary PCI. 2353 10