Fernando Friões

N-Terminal–Pro-Brain Natriuretic Peptide Predicts Outcome After Hospital Discharge in Heart Failure Patients

Background—Heart failure (HF) is responsible for a huge burden in hospital care. Our goal was to evaluate the value of N-terminal–pro-brain natriuretic peptide (NT-proBNP) in predicting death or hospital readmission after discharge of HF patients. Methods and Results—We included 182 patients consecutively admitted to hospital because of decompensated HF. Patients were followed up for 6 months. The primary end point was death or readmission. Twenty-six patients died in hospital. The median admission NT-proBNP level was 6778.5 pg/mL, and the median level at discharge was 4137.0 pg/mL (P<0.001). Patients were classified into 3 groups: (1) decreasing NT-proBNP levels by at least 30% (n=82), (2) no significant modifications on NT-proBNP levels (n=49), and (3) increasing NT-proBNP levels by at least 30% (n=25). The primary end point was observed in 42.9% patients. Variables associated with an increased hazard of death and/or hospital readmission in univariate analysis were length of hospitalization, heart rate, signs of volume overload, no use of ACE inhibitors, higher NYHA class at discharge, admission and discharge NT-proBNP, and the change in NT-proBNP levels. The variation in NT-proBNP was the strongest predictor of an adverse outcome. Independent variables associated with an increased risk of readmission or death were signs of volume overload and the change in NT-proBNP levels. Conclusions—Variations in NT-proBNP levels are related to hospital readmission and death within 6 months. NT-proBNP levels are potentially useful in the evaluation of treatment efficacy and might help clinicians in planning discharge of HF patients. Whether therapeutic strategies aimed to lower NT-proBNP levels modify prognosis warrants future investigation.

Prognostic Value of High-Sensitivity C-Reactive Protein in Heart Failure: A Systematic Review

BACKGROUND Several studies have suggested that high-sensitivity C-reactive protein (hsCRP) is a strong independent predictor of acute myocardial infarction and cardiovascular death. In the specific heart failure (HF) context, a low-grade inflammatory state can contribute to HF progression. AIMS To perform a systematic review on the current knowledge about low-grade inflammation, as assessed by hsCRP, in the prediction of HF in general and in high-risk populations as well as its prognostic value in established HF. METHODS We used a computerized literature search in the Medline database using the following key words: C-Reactive Protein, Heart Failure, Cardiomyopathy, Cardiac Failure, Prognosis, and Death. Articles were selected if they had measurements of hsCRP in different patient samples and reference to outcomes in terms of morbidity and mortality. RESULTS hsCRP is associated with incident HF in general and high-risk populations and provides prognostic information in HF patients. In almost all studies, the association of hsCRP with clinical events was independent of other baseline variables known to influence morbidity and mortality. Very different cutoffs have been proposed in each context across studies. CONCLUSIONS The prognostic power of hsCRP, whether we consider incident HF or adverse outcomes in established HF, is consistent in different patient populations.

Prognostic information provided by serial measurements of brain natriuretic peptide in heart failure

BACKGROUND Brain natriuretic peptide (BNP) levels predict prognosis in heart failure patients. We aimed to evaluate if serial measurements of BNP can give additional prognostic information. METHODS Eighty-four patients with systolic dysfunction had two measurements of BNP with an interval of 8 to 12 months and were followed in order to register the occurrence of death. The study was observational and prospectively designed. During follow-up, patients were treated according to state of the art. Physicians were kept blind to BNP levels. RESULTS The median follow-up was 1190 days. The median initial BNP level was 260.4 pg/ml and decreased to 123 pg/ml in the second measurement (P=0.001). The decrease in BNP was significantly associated with ACE-i dosage and with the use of a beta-blocker. All-cause mortality was 20.2%. Patients whose initial BNP level was above the median had a significantly higher hazard of dying (HR 2.96, 95% CI 1.06-8.26). The same was observed for those whose BNP increased between the first and the second measurement (HR 2.64, 95% CI 1.00-7.00). In multivariable analysis, baseline BNP above the median and increasing BNP were associated with shorter survival. CONCLUSIONS Higher baseline BNP and the increasing levels during follow-up were independently associated with mortality. The decrease in BNP levels was proportional to ACE-i dosage and larger among patients on beta-blockers. These results confirm the prognostic information provided by BNP determination and suggest that serial measurements give additional prognostic information.

B-Type Natriuretic Peptide Is Related to Left Ventricular Mass in Hypertensive Patients but Not in Athletes

A positive correlation has been previously documented between B-type natriuretic peptide (BNP) levels and left ventricular mass index (LVMI) in hypertensive patients. We evaluated 8 cycling athletes, 8 healthy age-matched controls; 17 hypertensive patients and 7 age-matched controls. LVMI was significantly higher in athletes and hypertensive patients than in their controls. Plasma levels of BNP in hypertensive patients were significantly higher than in athletes and their age-matched controls. No significant difference was found between athletes and their controls. Cycling athletes had significantly larger LVMI than hypertensive patients and controls, without elevated BNP levels. These results suggest that BNP levels are elevated in patients with increased LVM due to hypertension but not in physiologically increased LVM. Whether elevated BNP levels in athletes is a sign of structural heart disease merits further investigation.

Clinical syndrome suggestive of heart failure is frequently attributable to non-cardiac disorders : population-based study

To assess how often the clinical syndrome (CS) of heart failure is attributable to alternative, including non‐cardiac, explanations.

Low prealbumin is strongly associated with adverse outcome in heart failure

Objective Prealbumin is one of the best indicators of nutritional status. We previously showed that prealbumin predicted in-hospital mortality in heart failure (HF) patients. We evaluated if a low discharge prealbumin after admission with acute HF would predict morbidity and mortality. Methods We conducted a prospective observational study. Patients admitted with a primary diagnosis of HF were studied. Follow-up was up to 6 months. Endpoints analysed were: all-cause and HF-death; all-cause and worsening HF hospitalisation. Patients with discharge prealbumin ≤15.0 mg/dL and those with prealbumin >15 mg/dL were compared. A Cox-regression analysis was used to evaluate the prognostic impact of low prealbumin. Results We studied 514 patients. Mean age was 78 years and 45.7% were male. During follow-up, 101 patients died (78 for HF) and 209 patients were hospital readmitted (140 for worsening HF). Median prealbumin was 20.1 (15.3–25.3) mg/dL. Patients with lower prealbumin were more often women, older aged and with non-ischaemic HF; they had lower albumin, haemoglobin and total cholesterol; and higher glomerular filtration rate, C-reactive protein, B-type natriuretic peptide and length of hospital stay. Lower prealbumin associated with less β-blocker and statin use. Patients with discharge prealbumin ≤15 mg/dL had a multivariate adjusted HR of 6-month all-cause and HF death of 1.67 (1.00 to 2.80) and 2.12 (1.19 to 3.79) respectively and of all-cause and HF readmission of 1.47 (1.01 to 2.14) and 1.58 (1.01 to 2.47). Conclusions Patients with discharge prealbumin ≤15 mg/dL have an higher risk of 6 months morbidity and mortality. The unbalance between protein–energy demands and its availability predicts ominous HF outcome.

Higher C-Reactive Protein Predicts Worse Prognosis in Acute Heart Failure Only in Noninfected Patients

The prognostic role of C‐reactive protein (CRP) in acute heart failure (HF) is not fully understood, and the impact of an infectious process in its risk‐stratification power was not previously evaluated.

Depressive Symptoms and Heart Failure Stages

The authors measured depressive symptoms cross-sectionally, across evolving stages of heart failure as defined by the American College of Cardiology, from low risk, through high risk for heart failure (Stage A), asymptomatic cardiac dysfunction (Stage B), up to symptomatic heart failure (Stage C), in a community sample of 338 noninstitutionalized adults age >or=45 years. Depressive symptoms were measured with the Beck Depression Inventory (BDI). Women scored significantly higher on the BDI. Adjusted BDI scores increased linearly with heart failure stages in women, whereas, in men, only Stage C was associated with a significantly higher score.

Dipeptidyl peptidase IV and mortality after an acute heart failure episode.

Background: Dipeptidyl peptidase IV (DPP IV) is a key enzyme in B-type natriuretic peptide processing. DPP IV was never studied in human heart failure (HF). We aimed to measure DPP IV concentration in acute HF and determine its association with mortality. Methods and Results: Patients hospitalized with acute HF were eligible. We excluded patients with acute coronary syndromes. A discharge blood sample was collected from all patients and they were followed for a 6-month period. Outcome was HF death. Patients were compared across DPP IV quartiles. A Cox regression analysis was used to assess the prognostic power of DPP IV. We studied 164 patients. Median age was 78 years, 48.8% were men, and 63 had type 2 diabetes and 59.1% had left ventricular systolic dysfunction. Quartiles of DPP IV were <215.2; ≥215.2 and <269.3; ≥269.3 and <348.6; and ≥348.6 ng/mL; groups were homogenous between them. Seventeen patients died. Patients with DPP IV in the last quartile had a hazard ratio of HF death up to 6 months of 2.89, 95% confidence interval, 1.11–7.46. Association was B-type natriuretic peptide independent. Conclusions: Discharge DPP IV ≥348.6 ng/mL conferred an approximately 3-fold higher risk of 6-month HF death. Further studies would be important to understand the role of DPP IV in HF.

Prognostic value of worsening renal function in outpatients with chronic heart failure

INTRODUCTION AND OBJECTIVES Renal function impairment predicts poor survival in heart failure. Attention has recently shifted to worsening renal function, based mostly on serum creatinine and estimated glomerular filtration rate. We assessed the prognostic effect of worsening renal function in ambulatory heart failure patients. METHODS Data from 306 ambulatory patients were abstracted from medical files. Worsening renal function was based on the change in estimated glomerular filtration rate, serum creatinine and urea within 6 months of referral. Prognosis was assessed by the composite endpoint all-cause death or heart failure hospitalization, censored at 2 years. Hazard ratios were estimated for worsening renal function, adjusted for sex, age, diabetes, New York Heart Association class, left ventricular systolic dysfunction, medications and baseline renal function. RESULTS The agreement among definitions was fair, with kappa coefficients generally not surpassing 0.5. Worsening renal function was associated with poor outcome with adjusted hazard ratios (95% confidence interval) of 3.2 (1.8-5.9) for an increase of serum creatinine >0.3mg/dl; 2.2 (1.3-3.7) for an increase in serum urea >20mg/dl and 1.9 (1.1-3.3) for a decrease in estimated glomerular filtration rate >20%, independent of baseline renal function. The 2-year risk of death/heart failure hospitalization was approximately 50% in patients with an increase in serum creatinine or in serum urea; this positive predictive value was higher than for decreasing estimated glomerular filtration rate. CONCLUSIONS In conclusion, worsening renal function was significantly associated with a worse outcome. Different definitions identified different patients at risk and increasing creatinine/urea performed better than decreasing estimated glomerular filtration rate.