SSRIs: A Premature Burial

Anaesthesiology and Intensive Care, Copenhagen University Hospital: Bispebjerg, Copenhagen, Denmark.
Clinical Pharmacology &#38 Therapeutics (Impact Factor: 7.39). 12/2012; 93(3). DOI: 10.1038/clpt.2012.190
Source: PubMed
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    ABSTRACT: Several studies have found that depression is an independent predictor of poor outcome after the onset of clinical coronary artery disease. There are few data concerning depression as a risk factor for the development of coronary artery disease. To determine if clinical depression is an independent risk factor for incident coronary artery disease. The Johns Hopkins Precursors Study is a prospective, observational study of 1190 male medical students who were enrolled between 1948 and 1964 and who continued to be followed up. In medical school and through the follow-up period, information was collected on family history, health behaviors, and clinical depression. Cardiovascular disease end points have been assessed with reviews of annual questionnaires, National Death Index searches, medical records, death certificates, and autopsy reports. The cumulative incidence of clinical depression in the medical students at 40 years of follow-up was 12%. Men who developed clinical depression drank more coffee than those who did not but did not differ in terms of baseline blood pressure, serum cholesterol levels, smoking status, physical activity, obesity, or family history of coronary artery disease. In multivariate analysis, the men who reported clinical depression were at significantly greater risk for subsequent coronary heart disease (relative risk [RR], 2.12; 95% confidence interval [CI], 1.24-3.63) and myocardial infarction (RR, 2.12; 95% CI, 1.11-4.06). The increased risk associated with clinical depression was present even for myocardial infarctions occurring 10 years after the onset of the first depressive episode (RR, 2.1; 95% CI, 1.1-4.0). Clinical depression appears to be an independent risk factor for incident coronary artery disease for several decades after the onset of the clinical depression.
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    ABSTRACT: To compare precision and apparent bias between cohort, nested case-control, self-controlled case series, case-crossover, and case-time-control study designs. Study designs were implemented to evaluate the association between thiazolidinediones (TZDs) and heart failure, TZDs and fracture, and liver enzyme-inducing anticonvulsants and fracture. Effect estimates were similar for the cohort and case-control study; for the association between TZDs and fracture in women, the hazard ratio was 1.36 (1.18, 1.56) and odds ratio (OR) was 1.44 (1.21, 1.70). For this clinical example, the self-controlled case series gave upward bias when follow-up was censored at the outcome (incidence rate ratio [IRR], 7.08; 4.96, 10.09) but was otherwise unbiased (IRR, 1.41; 1.14, 1.75). The retrospective case-crossover OR was 3.24 (2.18, 4.80), which was reduced by either bidirectional sampling (OR, 1.20; 0.98, 1.46) or with the case-time-control design (OR, 1.40; 1.09, 1.81). Findings on apparent bias were similar for the other two clinical examples. In each clinical example, within-person designs had considerably lower precision than the cohort or case-control study designs. When long-term exposures are analyzed, within-person study designs may have lower precision and greater susceptibility to bias. Bias may be reduced by sampling follow-up both before and after the outcome or with the case-time-control study design.
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