Poor Outcomes In Heart Failure Research Articles

Relation of Level of B-Type Natriuretic Peptide With Outcomes in Patients With Infective Endocarditis

Elevated B-type natriuretic peptide (BNP) is a marker of poor outcomes in heart failure, acute coronary syndromes, and sepsis. Elevated cardiac troponin I (cTnI) is associated with adverse outcomes in infective endocarditis. It was hypothesized that elevated BNP would be associated with increased rates of morbidity and mortality in patients with infective endocarditis, particularly when combined with elevated cTnI. Consecutively enrolled patients in the International Collaboration on Endocarditis Prospective Cohort Study (ICE-PCS) were evaluated at a single center. The association between elevated BNP and a composite outcome of death, intracardiac abscess, and central nervous system event and the individual components of the composite was determined. Similar analyses were performed in patients who had BNP and cTnI measured. Of 103 patients, 45 had BNP measured for clinical indications. The median BNP level was higher in patients with the composite outcome (1,498 vs 433 pg/ml, p = 0.03) and in those who died (2,150 vs 628 pg/ml, p = 0.04). Elevated BNP was significantly associated with the composite outcome (p <0.01) and intracardiac abscess (p = 0.02). Patients with elevation of BNP and cTnI had a significantly higher probability of the composite outcome (69%) than patients with either BNP or cTnI elevated (29%) or neither BNP nor troponin elevated (0%) (p for trend <0.01). In conclusion, these data demonstrate a significant association between elevated BNP alone and in combination with cTnI for serious outcomes in infective endocarditis and warrant prospective evaluation.

Red cell distribution width in chronic heart failure: a new independent marker for prognosis?

Red cell distribution width in chronic heart failure: a new independent marker for prognosis?

Proteinuria, Chronic Kidney Disease, and the Effect of an Angiotensin Receptor Blocker in Addition to an Angiotensin-Converting Enzyme Inhibitor in Patients With Moderate to Severe Heart Failure

Chronic kidney disease (CKD) is an established risk factor for poor outcomes in heart failure (HF). Whether proteinuria provides additional prognostic information is not known. Renin-angiotensin blockade medications improve outcomes in HF but are underutilized in HF patients with renal dysfunction because of safety concerns and a lack of evidence of their effectiveness. In the Valsartan in Heart Failure Trial (Val-HeFT), 5010 patients with class II, III, or IV heart failure were randomly assigned to receive valsartan or placebo. The 2 primary outcomes were death and first morbid event, defined as death, sudden death with resuscitation, hospitalization for HF, or administration of intravenous inotropic or vasodilator drugs for 4 hours or more without hospitalization. The study cohort was divided into subgroups according to the presence of CKD (estimated glomerular filtration rate <60 mL x min(-1) x 1.73 m(-2)) and proteinuria (positive dipstick). Multivariable Cox proportional hazards regression models were used to examine the relationships between study outcomes and proteinuria, including its interaction with CKD. The interaction between valsartan and CKD was also tested. The effect of valsartan on estimated glomerular filtration rate was estimated by generalized linear models, including tests of interactions between treatment and CKD. At baseline, CKD was found in 58% and dipstick-positive proteinuria in 8% of patients. Dipstick-positive proteinuria was independently associated with mortality (hazard ratio [HR] 1.28, 95% confidence interval [CI] 1.01 to 1.62, P=0.05) and first morbid event (HR 1.28, 95% CI 1.06 to 1.55, P=0.01). The increased risk of death associated with dipstick-positive proteinuria was similar for those with and without CKD (HR 1.26, 95% CI 0.96 to 1.66 versus HR 1.37, 95% CI 0.83 to 2.26; P=0.94), as was the hazard for first morbid event (HR 1.26, 95% CI 1.01 to 1.57 versus HR 1.42, 95% CI 0.98 to 2.07; P=0.71). Valsartan reduced estimated glomerular filtration rate compared with placebo to a similar extent (P=0.52) in the subgroups with CKD (mean reduction -3.6 mL x min(-1) x 1.73 m(-2)) and without CKD (mean reduction -4.0 mL x min(-1) x 1.73 m(-2)) and by -3.8 mL x min(-1) x 1.73 m(-2) in both groups combined. The beneficial effect of valsartan on first morbid events was similar in those with and without CKD (HR 0.86, 95% CI 0.74 to 0.99 versus HR 0.91, 95% CI 0.73 to 1.12; P=0.23) and was significant in the subgroup with CKD. The effect of valsartan on mortality did not differ in patients with and without CKD (HR 1.01, 95% CI 0.85 to 1.20 versus HR 0.91, 95% CI 0.69 to 1.25; P=0.08). CKD was common and dipstick-positive proteinuria was infrequent in this sample of patients with HF. After controlling for other risk factors, including CKD, the relatively small subgroup with dipstick-positive proteinuria did have worse outcomes. Valsartan reduced the estimated glomerular filtration rate by the same amount in patients with and without CKD and reduced the risk of the first morbid event in patients with CKD, which suggests its beneficial effects in patients with HF and CKD.

A history of atrial fibrillation and outcomes in chronic advanced systolic heart failure: a propensity-matched study

Atrial fibrillation (AF)-associated poor outcomes in heart failure (HF) are often attributed to older age, advanced disease, and comorbidity burden of HF patients with AF. Therefore, we examined the effect of AF on outcomes in a propensity-matched study in which patients with and without AF were well balanced on all measured baseline characteristics. Of the 2708 advanced chronic systolic HF patients in the Beta-Blocker Evaluation of Survival Trial, 653 had a history of AF. Propensity scores for AF were calculated for each patient and were used to assemble a cohort of 487 pairs of patients with and without AF who were balanced on 74 baseline characteristics. Matched Cox regression analyses were used to estimate associations of AF with outcomes during 23 months of mean follow-up. All-cause mortality occurred in 187 (rate, 2046/10,000 person-years of follow-up) and 181 (rate, 1885/10,000 person-years) matched patients with and without AF, respectively [matched hazard ratio (HR) when AF was compared with no-AF 1.03, 95% confidence interval (CI) 0.79-1.33; P = 0.84]. Heart failure hospitalization occurred in 215 (rate, 3171/10,000 person-years) and 184 (rate, 2405/10,000 person-years) matched patients with and without AF, respectively (matched HR when AF was compared with no-AF 1.28, 95% CI 1.00-1.63; P = 0.049). Hazard ratios and 95% CIs for AF-associated HF hospitalization for bucindolol and placebo groups were, respectively, 1.08 (0.81-1.43) and 1.54 (1.17-2.03; P for interaction = 0.09). A history of AF had no intrinsic association with mortality but was associated with HF hospitalization in chronic systolic HF.

Microvolt T-Wave Alternans, Peak Oxygen Consumption, and Outcome in Patients with Severely Impaired Left Ventricular Systolic Function

Abnormal microvolt T-wave alternans (MTWA) and low peak oxygen consumption (VO2) both predict poor outcome in heart failure. However, their independent predictive properties have not been assessed in large-scale cohorts. This was an observational prospective cohort study of 303 consecutive patients referred for metabolic stress testing. All had an ejection fraction < or = 40% and were considered candidates for transplantation. The exercise laboratory did not collect MTWA data from patients with implanted pacemakers or defibrillators. The primary end point was a composite of all-cause death or United Network for Organ Sharing status 1 transplantation. During a 2.8-year period, there were 34 deaths and 17 transplantations. Patients with abnormal MTWA had a higher event rate of 23% (31 of 136) vs 12% (20 of 167), with an unadjusted hazard ratio (HR) of 1.90 (95% confidence interval [CI], 1.90-3.33; p = 0.03). The association remained significant after adjustment for 3 clinical variables (HR, 1.89; 95% CI, 1.05-3.39; p = 0.03). After adding peak VO2 to the model, the association was no longer significant (adjusted HR, 1.18; 95% CI, 0.64-2.17, p = 0.60). After accounting for peak VO2 and 28 other confounders in a matched propensity analysis, MTWA was not predictive (propensity-matched HR, 0.79; 95% CI, 0.37-1.66; p = 0.53). These results confirm the association of abnormal MTWA with poor outcome amongst patients with impaired left ventricular systolic function. However, this association is markedly attenuated after accounting for peak VO2.

Abstract 4778: Postoperative ST2 Blood Concentrations Predict One Year Mortality in Coronary Artery Bypass Patients

Soluble ST2 (sST2) is released from myocytes in response to mechanical overload and predicts poor outcome in heart failure and myocardial infarction. We evaluated the capability of early sST2 release after coronary artery bypass surgery (CABG) to predict mortality during the first postoperative year. We prospectively evaluated sST2 baseline prior to CABG (BL), immediately after CABG (post), and 24h and 72h. The primary endpoint of the study was all-cause mortality at 1 year. Of the 210 patients enrolled, death occurred in 3 (1.5%) within 30 days and 20 (9.5%) by 1 year. sST2 levels did not change immediately post-CABG (BL: 0.32±0.42, post: 0.42±0.46) but became significantly elevated at 24h and 72h (3.39±3.08, 0.95±1.04 ng/ml; P&lt;0.001). Compared to survivors, sST2 was significantly elevated in decedents at 24h (7.68±3.15 vs. 2.78±2.56, P&lt;0.001) and 72h (1.56±1.62 vs. 0.88±0.44, P&lt;0.03). On ROC analysis, sST2 at 24h strongly predicted death at 1 yr (AUC 0.868, 95% CI=0.77– 0.96). In multivariate analysis, sST2 level was a more powerful predictor of death (OR 17.0, P&lt;0.0001) than traditional predictors (STS risk score, age, left ventricular ejection fraction) or other biomarkers (OR 1.59, P&lt;0.0001) including troponin I, CPK-MB, and NT-pBNP. Although operative mortality was better than predicted by STS score, the 9.5% risk of death over 1yr highlights the need to better stratify mortality risk in order to guide appropriate follow-up after hospital discharge. As a strong predictor of 1yr mortality, independent of traditional laboratory or clinical variables, the sST2 level at 24 hrs may help advance this goal.

Increased Cardiothoracic Ratio and Adverse Outcomes in Chronic Heart Failure: A Propensity-Matched Study

Background: A cardiothoracic ratio (CTR) > 0.5 is considered abnormal, and has been associated with poor outcomes in heart failure (HF). An increased CTR may be a marker of other measures of ventricular remodeling and thus confound studies of association of CTR and HF outcomes. The objective of this study was to examine the association of CTR with outcomes in a propensity-matched cohort of HF patients. Methods: In the Digitalis Investigation Group (DIG) trial, 4690 of the 7788 patients with HF had a CTR > 0.5 at baseline.

A Propensity Matched Study of New York Heart Association Class and Natural History End Points in Heart Failure

The association between higher New York Heart Association (NYHA) functional class and poor outcome in heart failure (HF) is well known. However, to what extent these associations are confounded by covariates such as age, the severity of disease, and co-morbidity burden is unknown. In the Digitalis Investigation Group (DIG) trial, 2,441 of the 7,788 patients with chronic HF had NYHA class III or IV symptoms. Propensity scores for NYHA classes III and IV were calculated for each patient and were then used to match 1,863 patients in NYHA classes III and IV with 1,863 patients in NYHA classes I and II. Kaplan-Meier and matched Cox regression analyses were used to estimate associations of NYHA class III or IV with mortality and hospitalizations during a median of 37 months of follow-up. Compared with 34% (641 of 1,863) patients in NYHA classes I and II (mortality rate 1,175 in 10,000 person-years of follow-up), 42% (777 of 1,863) patients in NYHA classes III and IV (mortality rate 1,505 in 10,000 person-years) died from all causes (hazard ratio 1.29, 95% confidence interval [CI] 1.14 to 1.45, p <0.0001). Hospitalizations due to all causes occurred in 66% (1,232 of 1,863) patients in NYHA classes I and II (hospitalization rate 3,898 in 10,000 person-years) and 71% (1,322 of 1,863) patients in NYHA classes III and IV (hospitalization rate 4,793 in 10,000 person-years) (hazard ratio 1.16, 95% CI 1.05 to 1.28, p = 0.003). The hazard ratios for patients in NYHA classes III and IV, compared with those for those in NYHA classes I and II, for other outcomes were 1.29 for cardiovascular mortality (95% CI 1.12 to 1.48, p <0.0001), 1.49 for HF mortality (95% CI 1.20 to 1.84, p <0.0001), 1.18 for cardiovascular hospitalization (95% CI 1.06 to 1.32, p = 0.002), and 1.17 for HF hospitalization (95% CI 1.03 to 1.34, p = 0.017). In conclusion, baseline NYHA class is a marker of hospitalization, disease progression, and mortality in a wide spectrum of ambulatory patients with chronic HF.