Osteopontin (OPN) is a secreted glycophosphoprotein that has a role in inflammation, immune response and calcification. We hypothesized that plasma OPN levels are associated with adverse cardiovascular outcomes in patients with stable coronary artery disease (CAD) and preserved ejection fraction (EF) enrolled in the PEACE trial. We measured plasma OPN levels at baseline in 3567 CAD patients (mean age 64.5 ± 8.1 years, 81% men) by a sandwich chemiluminescent assay (coefficient of variation = 4.1%). OPN levels were natural log (Ln) transformed prior to analyses. We assessed whether Ln OPN levels were associated with the composite primary endpoint of cardiovascular death, non-fatal myocardial infarction and hospitalization for heart failure using multiple event multivariable Cox proportional hazards regression. Adjustment was performed for: (a) age and sex; (b) additional potential confounders; and (c) a parsimonious set of statistically significant 10 variates. During a median follow-up of 4.8 years, 416 adverse cardiovascular outcomes occurred in 366 patients. Ln OPN was significantly associated with the primary endpoint; HR (95% CI) = 1.56 (1.27, 1.92); P <0.001, and remained significant after adjustment for age and sex [1.31 (1.06, 1.61); P = 0.01] and after adjustment for relevant covariates [1.24 (1.01, 1.52); P = 0.04]. In a secondary analysis of the individual event types, Ln OPN was significantly associated with incident hospitalization for heart failure: HR (95% CI) = 2.04 (1.44, 2.89); P <0.001, even after adjustment for age, sex and additional relevant covariates. In conclusion, in patients with stable CAD and preserved EF on optimal medical therapy, plasma OPN levels were independently associated with the composite incident endpoint of adverse cardiovascular outcomes as well as incident hospitalization for heart failure.

BACKGROUND Elevated cardiac troponin (cTn) is often observed in patients with acute decompensated heart failure (ADHF). We assessed the magnitude of association and quality of supporting evidence between cTn and clinically important outcomes in persons hospitalized for ADHF. METHODS We searched MEDLINE In‐Process & Other Non‐Indexed Citations, MEDLINE, Embase, Cochrane Central Register of Controlled Trials, Cochrane Database of Systematic Reviews, and Scopus from inception through February 28, 2015. The outcomes analyzed included hospital length of stay (LOS), readmissions, and mortality. Random effects meta‐analysis was used to combine outcomes across studies. RESULTS We included 26 clinical studies. A detectable or elevated cTn was associated with increased LOS (odds ratio [OR]: 1.05; 95% confidence interval [CI]: 1.01‐1.10), increased in‐hospital mortality (OR: 2.57; 95% CI: 2.27‐2.91), and a composite of mortality and major adverse events (OR: 1.33; 95% CI: 1.03‐1.71) during hospitalization. ADHF patients with a detectable or elevated cTn were at increased risk for mortality and composite of mortality and readmission over the short term (mortality OR: 2.11; 95% CI: 1.43‐3.12; composite OR: 2.81; 95% CI: 1.60‐4.92), intermediate term (mortality OR: 2.21; 95% CI: 1.46‐3.35; composite OR: 2.30; 95% CI: 1.78‐2.99), and long term (mortality OR: 3.69; 95% CI: 2.64‐5.18; composite OR: 3.49; 95% CI: 2.08‐5.84). The overall confidence in estimates was moderate. CONCLUSIONS Among ADHF patients, a detectable or elevated cTn identifies subjects at increased risk for adverse clinical outcomes during acute hospitalization and those at higher risk for postdischarge mortality and composite of readmission and mortality. Journal of Hospital Medicine 2016;11:446–454. 2016 Society of Hospital Medicine

ardiovascular disease (CVD) is the leading cause of death of both men and women, and worldwide there are clear disparities between men and women in presentation, symptoms, response to therapy and outcomes. [1][2][3][4][5][6][7] There is a significant gap in basic and clinical knowledge of specific cellular mechanisms related to CVD in women, thus the biological basis of sex differences in CVD remains a frontier for discovery. The scarcity of information related to sex-specific differences in CVD is partly because women were excluded from research studies and because most basic science inquiries into biological factors contributing to CVD were conducted in male animals.

ObjectiveTo describe an exploratory project to develop and pilot a novel patient educational tool that explains the concept of pharmacogenomics and its impact on warfarin dosing that can be utilized by health professionals providing patient counseling.MethodsA pharmacogenomics educational tool prototype was developed by an interdisciplinary team. During the pilot of the tool, focus group methodology was used to elicit input from patients based upon their perspectives and experiences with warfarin. Focus group sessions were audio-recorded and transcribed, and the data was analyzed through consensus coding in NVivo.ResultsThe focus group participants were generally unfamiliar with the concept of pharmacogenomics but were receptive to the information. They thought the patient education tool was informative and would provide the most benefit to patients newly initiated on warfarin therapy.ConclusionsPreliminary results from this exploratory project suggest that implementation and further feasibility testing of this pharmacogenomics patient education tool should be performed in a population of newly initiated patients taking warfarin.

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