Quality of medical therapy in heart failure patients undergoing elective revascularisation: A protective effect of disease modifying therapy at discharge.

The STICH(-ES) trial showed that coronary artery bypass grafting was superior to medical therapy alone in treating ischemic heart failure. However, dosages of disease modifying drugs were not reported. We included 128 (84% male, mean age 66 ± 11 years) consecutive patients with ischemic heart failure and an ejection fraction ≤35% undergoing isolated elective coronary artery bypass grafting. We defined optimal medical therapy (OMT) as prescription of ≥50% dosages of guideline recommended medications (i.e. beta-blocker (BB) and renin angiotensin system (RAS) antagonist) plus prescription of a mineralocorticoid receptor antagonist (MRA). The mean logistic EuroSCORE was 12.3 ± 13.8%. The five year survival was 74%. At discharge, 111 patients (87%) were on a BB and 106 (83%) were on a RAS antagonist. Forty-nine patients (38%) received an MRA. Only 8 patients (6%) received OMT. A Cox regression analysis revealed EuroSCORE (p < 0.001) and the use of MRA (p = 0.003) and BB (p = 0.037) at discharge as significant predictors of 5 year survival. Prescription rates of heart failure medication are comparable to those reported in the STICH trial, but rates of OMT are very low at admission and discharge. Prescription of BB and MRA was associated with improved survival, highlighting the need for disease management programs and rigorous discharge management.

NT-proBNP has a high negative predictive value to rule-out short-term cardiovascular events in patients with diabetes mellitus.

AIMS: This study evaluated the predictive value of NT-proBNP for patients with diabetes mellitus and compared the prognostic aptitude of this neurohumoral marker to traditional markers of cardiovascular events. METHODS AND RESULTS: A prospective observational study was conducted in 631 diabetic patients. The composite endpoint consisted of unplanned hospitalization for cardiovascular events or death within the observation period of 12 months. Of all variables analysed (age, gender, history of hypertension, ischaemic heart disease/any cardiac disease, smoking, duration of diabetes, body mass index, blood pressure, New York Heart Association-class, Dyspnoea score, Minnesota Living with Heart Failure Questionnaire, LDL-cholesterol, HbA(1c), creatinine, glomerular filtration rate), the logarithm of NT-proBNP gave the most potent information in a stepwise Cox regression analysis (P < 0.0001). Bootstrapping with 500 samples supports this result in 95% samples. The negative predictive value of a normal value (<125 pg/mL) of NT-proBNP for short-term cardiovascular events in diabetic patients is 98%. CONCLUSION: We have demonstrated a strong and independent correlation between NT-proBNP and short-term prognosis of cardiovascular events for patients with diabetes mellitus. With a high negative predictive value it can identify individuals who are not at intermediate risk for cardiovascular events. NT-proBNP proved to be of higher predictive value than traditional cardiovascular markers, in this unselected cohort.

Oncostatin-M in myocardial ischemia/reperfusion injury may regulate tissue repair.

AIM: Oncostatin-M, a member of the gp 130 family of cytokines, has been associated with inflammation, connective tissue production, and extracellular matrix turnover. Since the reperfused heart is associated with an intense inflammatory reaction followed by scar formation, we tested the hypothesis that oncostatin-M is upregulated in response to cardiac injury and may play a part in cardiac repair. METHODS: Using a canine model of myocardial ischemia/reperfusion injury, we examined the expression of oncostatin-M at various time points of reperfusion, ranging from 1 h to 7 days. In situ hybridization was used to determine oncostatin-M mRNA expression. Immunohistochemistry was performed to detect oncostatin-M protein. Stimulatory effects of oncostatin-M on isolated endothelial cells and fibroblasts were investigated. RESULTS: Oncostatin-M mRNA expression was detected in ischemic segments within the first 3 h of reperfusion and was persistent over the whole observation period. At the early time points, infiltrating and endothelial cells were the primary source of oncostatin-M mRNA expression. At later time points, macrophages and myofibroblasts were the main contributors. We previously demonstrated in vivo that monocyte-chemoattractant-protein (MCP-1) mRNA is induced early after reperfusion. We stimulated isolated endothelial cells with oncostatin-M and postischemic lymph, which have both upregulated MCP-1 expression in endothelial cells. In addition, isolated fibroblasts stimulated with oncostatin-M demonstrated a dose-dependent proliferative response. CONCLUSION: Oncostatin-M may contribute to the process of healing after myocardial infarction.