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Angina pectoris is chest pain that results from myocardial ischemia, or the temporary reduction in cardiac blood flow. Unstable angina is a rapidly deteriorating type of angina, caused in part by the formation of intracoronary thrombi (blood clots in the coronary arteries), that often presages the onset of more a more severe cardiovascular emergency such as heart attack. The long-term (for periods greater than six days) use of anticlotting drugs, such as heparin, is well established as a therapeutic strategy for the treatment of unstable angina. With current economic pressures to reduce the duration of hospital stays, it is of interest to know whether there is any therapeutic advantage to be gained by short-term intravenous administration of heparin. (The intravenous route of administration requires hospital care.) To determine the effect of short-term heparin administration on the frequency of ischemic events, a study was carried out involving 47 patients being treated for unstable angina. Twenty patients received intravenous heparin in addition to their other medications for the first 36 hours of evaluation; the remainder received an inactive saline (salt) solution in addition to the medications they had been taking. In both groups these medications included calcium channel blockers, beta adrenergic blocking agents, nitrates, and aspirin. Myocardial ischemia was monitored by electrophysiological monitoring of cardiac function. There was no difference in the frequency of ischemic events between the groups receiving heparin and saline. About 40 percent of both groups suffered ischemic episodes, the majority of which (85 percent) were asymptomatic. The failure of heparin to reduce the incidence of ischemia may be attributable to a masking effect of aspirin (which has much the same effect), the length of treatment, or the possibility that heparin might not exert its effects on angina solely by reducing myocardial ischemia. (Consumer Summary produced by Reliance Medical Information, Inc.)

Objective. The aim of this study was to determine the effect of vitamin D supplementation on improving mood (depression and anxiety) and health status (mental and physical) in women with type 2 diabetes mellitus (T2DM). Methods. Fifty women with T2DM and significant depressive symptomology were enrolled into the “Sunshine Study,” where weekly vitamin D supplementation (ergocalciferol, 50,000 IU) was given to all participants for six months. The main outcomes included (1) depression (Center for Epidemiologic Studies Depression, CES-D, and Patient Health Questionnaire, PHQ-9), (2) anxiety (State-Trait Anxiety), and (3) health status (Short Form, SF-12). Results. Forty-six women (92%) completed all visits. There was a significant decrease in depression (CES-D and PHQ-9, p<0.001) and anxiety (state and trait, p<0.001). An improvement in mental health status (SF-12, p<0.001) was also found. After controlling for covariates (race, season of enrollment, baseline vitamin D, baseline depression (PHQ-9), and body mass index), the decline in depression remained significant (CES-D, p<0.001). There was a trend for a better response to supplementation for women who were not taking medications for mood (antidepressants or anxiolytics) (p=0.07). Conclusions. Randomized trials to confirm that vitamin D supplementation can improve mood and health status in T2DM women are needed. [ABSTRACT FROM AUTHOR]

Discusses heparin-induced thrombocytopenia (HIT) and HIT with thrombosis syndrome. Pathophysiology and clinical expression; Diagnosis; Treatment.

Heparin-induced thrombocytopenia is one of the most difficult problems facing clinicians today. Despite recent understanding of the pathophysiology of this disorder, there are many unresolved issues about diagnosis, prevention, and treat ment. In this article, difficulties physicians encounter when faced with a suspected heparin-induced thrombocytopenia pa tient will be reviewed as well as our experience in 113 patients with heparin-induced thrombocytopenia which highlights the failure of current preventive strategies for heparin-induced thrombocytopenia. The experience of using warfarin in 51 pa tients with heparin-induced thrombocytopenia will also be re viewed. Key Words: Heparin-induced thrombosis—Heparin- induced thrombocytopenia— Prevention of heparin-induced thrombocytopenia. [ABSTRACT FROM PUBLISHER]