Emphasizing statin safety in the hospitalized patient: a review.

This review examines the safe use of statin therapy in the hospitalized patient. Available data support initiation of statin therapy during hospitalization in patients with acute coronary syndromes or established cardiovascular disease and in high-risk patients with diabetes mellitus and chronic kidney disease (except for those on maintenance hemodialysis). Because of the increased risk of cardiovascular disease, statins are given to solid-organ transplant survivors and those treated with protease inhibitors for human immunodeficiency virus.

Management of severe hypertriglyceridemia in the hospital: a review.

For hospitalists, hypertriglyceridemia (HTG) is more than cardiovascular risk. Severe HTG occurs when serum triglycerides rise above 1000 mg/dL, and it carries a risk of abdominal pain and pancreatitis. The etiology of severe HTG is usually a combination of genetic and secondary factors.

Interventions to reduce 30-day rehospitalization: a systematic review.

Background: About 1 in 5 Medicare fee-for-service patients discharged from the hospital is rehospitalized within 30 days. Beginning in 2013, hospitals with high risk-standardized readmission rates will be subject to a Medicare reimbursement penalty.

Purpose: To describe interventions evaluated in studies aimed at reducing rehospitalization within 30 days of discharge.

PGE2 stimulates human brain natriuretic peptide expression via EP4 and p42/44 MAPK.

Brain natriuretic peptide (BNP) produced by cardiac myocytes has antifibrotic and antigrowth properties and is a marker of cardiac hypertrophy. We previously showed that prostaglandin E2 (PGE2) is the main prostaglandin produced in myocytes treated with proinflammatory stimuli and stimulates protein synthesis by binding to its EP4 receptor. We hypothesized that PGE2, acting through EP4, also regulates BNP gene expression.

Inhibition of cyclooxygenase-2 improves cardiac function after myocardial infarction in the mouse.

Cyclooxygenase (COX)-2 is expressed in the heart in animal models of ischemic injury. Recent studies have suggested that COX-2 products are involved in inflammatory cell infiltration and fibroblast proliferation in the heart. Using a mouse model, we questioned whether 1).