On the basis of the findings of our literature search, we suggest that SSRI-induced increase in gastric acid secretion may explain the GI bleeding risk and that SSRI-related effects on platelet reactivity, endothelial reactivity, and inflammatory markers may explain the ischemic heart disease protective effect. Because the absolute risk of GI bleeds with SSRIs is low, precautions are probably necessary only in high-risk patients, such as those with acid-peptic disease and those with a history of bleeds. We discuss management issues and areas for future research.

Depression and heart disease are commonly comorbid. Selective serotonin reuptake inhibitors (SSRIs) are commonly used to treat depression. In March 2011, we carried out a 15-year search of PubMed for preclinical and clinical publications related to SSRIs and ischemic heart disease (IHD) or congestive heart failure (CHF). We identify and discuss a number of mechanisms by which SSRIs may influence cardiovascular functioning and health outcomes in patients with heart disease; many of the mechanisms that we present have received little attention in previous reviews. We examine studies with positive, neutral, and negative outcomes in IHD and CHF patients treated with SSRIs. SSRIs influence cardiovascular functioning and health through several different mechanisms; for example, they inhibit serotonin-mediated and collagen-mediated platelet aggregation, reduce inflammatory mediator levels, and improve endothelial function. SSRIs improve indices of ventricular functioning in IHD and heart failure without adversely affecting electrocardiographic parameters. SSRIs may also be involved in favorable or unfavorable drug interactions with medications that influence cardiovascular functions. The clinical evidence suggests that, in general, SSRIs are safe in patients with IHD and may, in fact, exert a cardioprotective effect. The clinical data are less clear in patients with heart failure, and the evidence for benefits with SSRIs is weak.

Myocarditis" implies damage to heart muscle, often accompanied by impairments in heart function, as a result of inflammation caused by infection, a toxin, or immune hypersensitivity. [1][2][3] Clinical signs and symptoms (eg, fever, tachycardia, shortness of breath, myalgia, malaise), laboratory measures of damage to heart muscle (eg, creatine kinase [CK], troponin I [TROP]) and inflammation (eg, eosinophils [EOS], C-reactive protein [CRP]), and measures of heart function (eg, echocardiogram) can support the clinical diagnosis of "Presumptive Myocarditis" (PrMy) in patients. 4 Active monitoring of TROP and CRP

Considering the high prevalence of mental illness in prisons, one might expect a high prevalence of ECT responsive mental illness and, hence, provision of ECT to some prisoners with mental illness. However, our survey suggests that the use of ECT in prisons in the United States is low. Stigma, ethical concerns, and logistical concerns were the main hindrances for providing ECT to prisoners with mental illness. Given that ECT is the standard of care in certain clinical scenarios, physicians are obligated to offer such treatment to inmates when necessary. It can be argued that failure of the prison to offer the standard of care is unethical and unconstitutional.