Use of brain natriuretic peptide (BNP) and N-terminal pro-BNP (NT-proBNP) for cardiovascular (CV) risk assessment in patients with end-stage kidney disease (ESKD) remains unclear. We examined the associations between different threshold elevations of these peptide levels and clinical outcomes in patients with ESKD.

Systematic review and meta-analysis.

We searched MEDLINE and EMBASE (through September 2019) for observational studies of adults with ESKD (estimated glomerular filtration rate≤15mL/min/1.73m² or receiving maintenance dialysis).

Studies that reported NT-proBNP or BNP levels and future CV events, CV mortality, or all-cause mortality.

Cohort characteristics and measures of risk associated with study-specified peptide thresholds.

Hazard ratios (HRs) for clinical outcomes associated with different NT-proBNP and BNP ranges were categorized into common thresholds and pooled using random-effects meta-analysis.

We identified 61 studies for inclusion in our review (19,688 people). 49 provided sufficient detail for inclusion in meta-analysis. Pooled unadjusted HRs for CV mortality were progressively greater for greater thresholds of NT-proBNP, from 1.45 (95% CI, 0.91-2.32) for levels>2,000pg/mL to 5.95 (95% CI, 4.23-8.37) for levels>15,000pg/mL. Risk for all-cause mortality was significantly higher at all NT-proBNP thresholds ranging from> 1,000 to> 20,000pg/mL (HR range, 1.53-4.00). BNP levels>550pg/mL were associated with increased risk for CV mortality (HR, 2.54; 95% CI, 1.49-4.33), while the risks for all-cause mortality were 2.04 (95% CI, 0.82-5.12) at BNP levels>100pg/mL and 2.97 (95% CI, 2.21-3.98) at BNP levels>550pg/mL. Adjusted analyses demonstrated similarly greater risks for CV and all-cause mortality with greater NT-proBNP concentrations.

Incomplete outcome reporting and risk for outcome reporting bias. Estimation of risk for CV events for specific thresholds of both peptides were limited by poor precision.

ESKD-specific NT-proBNP and BNP level thresholds of elevation are associated with increased risk for CV and all-cause mortality. This information may help guide interpretation of NT-proBNP and BNP levels in patients with ESKD.

Several previous studies have shown obesity to be counterintuitively associated with more favorable mortality in patients with acute myocardial infarction (AMI); however, the association of obesity with in-hospital mortality of cardiogenic shock complicating AMI has not been previously examined. We queried the 2004 to 2013 National Inpatient Sample databases to identify all patients ≥18 years hospitalized with the principal diagnosis of AMI. Multivariable regression models adjusting for demographics, hospital characteristics, and co-morbidities were used to examine differences in incidence and in-hospital mortality of cardiogenic shock complicating AMI between obese and nonobese patients. Of 6,097,817 patients with AMI, 290,894 (4.8%) had cardiogenic shock. There was no difference in risk-adjusted incidence of cardiogenic shock between obese and nonobese patients (adjusted odds ratio 1.00, 95% CI 0.98 to 1.01; p = 0.46). Of the patients with cardiogenic shock complicating AMI, 8.9% had a documented diagnosis of obesity. Obese patients were on average 6 years younger and had higher prevalence of most cardiovascular co-morbidities. Obese patients were more likely to receive revascularization (73.0% vs 63.4%, p <0.001) and had lower risk-adjusted in-hospital mortality compared with nonobese patients (28.2% vs 36.5%; adjusted odds ratio 0.89, 95% CI 0.86 to 0.92; p <0.001). Similar findings were seen in subgroups of patients with cardiogenic shock complicating ST elevation or non-ST elevation MI. In conclusion, this large retrospective analysis of a nationwide cohort of patients with cardiogenic shock complicating AMI demonstrated that obese patients were younger, more likely to receive revascularization, and had modestly lower risk-adjusted in-hospital mortality compared with nonobese patients.

Many acute cardiovascular disease states are associated with neutrophil infiltration of myocardium and subsequent release of superoxide (O2 (-) ) and myeloperoxidase (MPO), which contribute to inflammatory reactions. B-Type natriuretic peptide (BNP) is known to exert anti-inflammatory and antifibrotic effects, but it is not known whether these may include interactions with neutrophils. In neutrophils isolated from 20 healthy subjects, we assessed the effect of BNP on the 'neutrophil burst' (O2 (-) production and MPO release) stimulated by phorbol myristate acetate (PMA) and N-formyl-methionyl-leucyl-phenylalanine (fMLP), respectively. Effects of BNP on cGMP accumulation, and the effects of the cell-permeable cGMP analogue 8-(4-chlorophenylthio) guanosine-cGMP (8-p-CPT-cGMP) and protein kinase G (PKG) inhibition with KT5823 on the neutrophil-BNP interaction were also evaluated. B-Type natriuretic peptide suppressed O2 (-) release from neutrophils by 23 ± 6% (P < 0.001) and 24 ± 8% (P < 0.05) following PMA and fMLP stimulation, respectively. Although BNP did not significantly increase cGMP formation, 8-p-CPT-cGMP suppressed both PMA- and fMLP-induced neutrophil O2 (-) release by 16% and 28%, respectively (P < 0.05). The PKG inhibitor KT5823 attenuated the effects of BNP on both fMLP- and PMA-associated O2 (-) production. Neither BNP nor 8-p-CPT-cGMP significantly affected MPO release from neutrophils. Suppression of O2 (-) release from neutrophils by BNP may contribute to its anti-inflammatory and antifibrotic actions.

Higher blood pressure in acute heart failure has been associated with improved survival; however, the relationship between blood pressure and survival in stabilized patients at hospital discharge has not been established.

In 7448 patients with heart failure (75.2+/-11.5 years; 49.9% men) discharged from the hospital in Ontario, Canada, we examined the association of systolic blood pressure (SBP) and diastolic blood pressure with long-term survival. Parametric survival analysis was performed, and survival time ratios were determined according to discharge blood pressure group. A total of 25 427 person-years of follow-up were examined. In those with left ventricular ejection fraction < or =40%, median survival was decreased by 17% (survival time ratio, 0.83; 95% CI, 0.71 to 0.98; P=0.029) when discharge SBP was 100 to 119 mm Hg and decreased by 23% (survival time ratio, 0.77; 95% CI, 0.62 to 0.97; P=0.024) when discharge SBP was <100 mm Hg, compared with those in the reference range of 120 to 139 mm Hg. Survival time ratios were 0.75 (95% CI, 0.60 to 0.92; P=0.007) and 0.75 (95% CI, 0.53 to 1.07; P=0.12) when discharge SBPs were 140 to 159 and > or =160 mm Hg, respectively. In those with left ventricular ejection fraction >40%, survival time ratios were 0.69 (95% CI, 0.51 to 0.93), 0.83 (95% CI, 0.71 to 0.99), 0.95 (95% CI, 0.80 to 1.14), and 0.76 (95% CI, 0.61 to 0.95) for discharge SBPs <100, 100 to 119, 140 to 159, and > or =160 mm Hg, respectively.

In this long-term population-based study of patients with heart failure, the association of discharge SBP with mortality followed a U-shaped distribution. Survival was shortened in those with reduced or increased values of discharge SBP.

The mortality impact of recurrent cardiac hospitalizations has not been delineated in community-based heart failure patients. We determined if a "dose-dependent" relationship exists between heart failure events and death, accounting for temporal changes in age, comorbidities, and disease severity.

Among heart failure patients in the Enhanced Feedback For Effective Cardiac Treatment Study with onset between April 1999 and March 2001, we compared long-term survival (until March 2006) in those with recurrent heart failure or cardiovascular events, relative to those free of such events.

In 9138 patients, 28,442 person-years of follow-up were examined (mean age: 75.3 years, 49.6% male). Recurrent heart failure events occurred 1, 2, 3, and >or=4 times in 2352 (25.7%), 1020 (11.2%), 505 (5.5%), and 596 (6.5%) patients, respectively. Cardiovascular readmissions occurred 1, 2, 3, and >or=4 times in 2522 (27.6%), 1509 (16.5%), 975 (10.7%), and 1672 (18.3%) patients, respectively. Compared with those without recurrent heart failure events, the adjusted relative mortality rates for 1, 2, 3, and >or=4 heart failure events were 2.41 (95% confidence interval [CI], 2.24-2.60), 3.00 (95% CI 2.72-3.32), 4.00 (95% CI, 3.51-4.56), and 5.16 (95% CI, 4.55-5.85), respectively. Compared with those without cardiovascular events, the adjusted relative mortality rates for 1, 2, 3, and >or=4 cardiovascular events were 3.33 (95% CI, 3.05-3.63), 4.61 (95% CI, 4.16-5.10), 6.29 (95% CI, 5.59-7.07), and 8.95 (95% CI, 8.05-9.95), respectively.

The risk of death increases progressively and independently with each heart failure or cardiovascular event. The number of prior events predicts mortality and should be ascertained in patients with heart failure.

Making a prognosis is one of the primary functions of the medical profession. At the end of the nineteenth century prognostication took up approximately ten percent of medical textbooks, by 1970 this had fallen to nearly zero. Given medical technology's awesome ability to prolong the process and suffering of dying today's patients need to know their prognosis in order to make choices about their treatment options. Whilst precise predictions of the future are obviously not possible, relatively simple mathematical modelling techniques can make reasonable estimates of likely outcomes for individual patients. The life expectancy of a patient of any age with any illness can be estimated provided the disease-specific mortality of the illness is known. Decision analysis or logistic regression models can then be used to determine the risks and benefits of various treatment options. A patient's prognosis does not just depend on their age and primary diagnosis, but also on the severity of their illness, their functional capacity both prior to and during the illness and the number of co-morbidities also suffered from. Several predictive instruments have been developed to help simplify the prediction of the outcome of individual patients. There are conflicting reports on how these models compare with doctors' intuition--whatever their strengths and weaknesses it is unlikely that they worsen clinical judgement. Therefore, all doctors should become familiar with them and use them appropriately.

An understanding of the life expectancy of patients with heart failure (HF) may assist in difficult treatment decisions such as placement of an implantable cardioverter-defibrillator or initiation of end-of-life care. However, previous studies have focused on predicting shorter-term mortality and limited data currently exist to predict expected survival among hospitalized patients with HF.

We studied 9943 patients who were newly hospitalized with HF between 1999 and 2001 in Ontario, Canada. Median survival was calculated using survival analysis and stratified by baseline characteristics and the EFFECT HF risk score. These analyses were repeated for the 1467 patients who had left ventricular ejection fraction of < or = 30%.

The average age of our HF cohort was 75.8 years and 50.4% of the patients were female. After a median follow-up of 6 years, hospitalized patients with HF had a 5-year mortality rate of 68.7% and a median survival of 2.4 years. Mortality varied substantially across risk groups such that median survival was only 8 months for patients in the high-risk group and only 3 months in the very high risk group. Similarly, among patients with depressed left ventricular ejection fraction, median survival was only 6 and 3 months in the high- and very high risk groups, respectively.

Prognostic estimations using median survival may improve the ability of physicians to identify subgroups of patients with HF who have limited life expectancy. This information may assist in communicating prognostic information and guiding difficult treatment decisions among hospitalized patients with HF.