We investigated whether the additional determination of ceruloplasmin (Cp) levels could improve the prognostic value of N-terminal pro-B-type natriuretic peptide (NT-proBNP) in heart failure (HF) patients in a 1-year follow-up. Cp and NT-proBNP levels and clinical and laboratory parameters were assessed simultaneously at baseline in 741 HF patients considered as possible heart transplant recipients. The primary endpoint (EP) was a composite of all-cause death (non-transplant patients) or heart transplantation during one year of follow-up. Using a cut-off value of 35.9 mg/dL for Cp and 3155 pg/mL for NT-proBNP (top interquartile range), a univariate Cox regression analysis showed that Cp (hazard ratio (HR) = 2.086; 95% confidence interval (95% CI, 1.462–2.975)), NT-proBNP (HR = 3.221; 95% CI (2.277–4.556)), and the top quartile of both Cp and NT-proBNP (HR = 4.253; 95% CI (2.795–6.471)) were all risk factors of the primary EP. The prognostic value of these biomarkers was demonstrated in a multivariate Cox regression model using the top Cp and NT-proBNP concentration quartiles combined (HR = 2.120; 95% CI (1.233–3.646)). Lower left ventricular ejection fraction, VO2max, lack of angiotensin-converting enzyme inhibitor or angiotensin receptor blocker therapy, and nonimplantation of an implantable cardioverter-defibrillator were also independent risk factors of a poor outcome. The combined evaluation of Cp and NT-proBNP had advantages over separate NT-proBNP and Cp assessment in selecting a group with a high 1-year risk. Thus multi-biomarker assessment can improve risk stratification in HF patients.
Background
The catabolic predominance in acute heart failure (HF) leads to significant weight loss. The low body weight before HF (preHF) and the loss during its natural course, both are risk factors of sarcopenia and worse clinical outcome in HF. Modern therapy can inhibit or even reverse catabolism resulting in oedema-free weight gain. It is unknown if therapy-induced weight gain can protect against low appendicular skeletal muscle mass (ASM) – the key prerequisite of sarcopenia.
Aims
We intended to assess whether therapy-induced oedema-free weight gain protects against low ASM.
Material and methods
In 802 patients with HF (age: 52±10 years 13% women, LVEF: 24±7%, NYHA: 2.6±0.7), we analysed weight changes from preHF to minimal oedema-free weight during HF (minHF), and then weight occurring after removal of all reversible factors aggravating HF with optimisation of therapy (indexHF). At index date we performed dual X-ray densitometry (DXA) calculating ASM as the sum of lean mass within the legs and arms adjusted to body size. The low ASM was defined as ≤7 and 6 kg/m2 in men and women respectively. The catabolic (C) and anabolic (A) components of weight change ware calculated based of formulas: C=100*(minHF-preHF)/preHF, A=100*(indexHF-minHF)/minHF. Using logistic regression we estimated the risk of low ASM after adjustment for potential confounders.
Results
The median C and A were −11.7% and 3.3% respectively. The low ASM was found in 230 (28.7%) patients. In multivariable model comprising age, gender, weight preHF, C and A, the odds for low as compared to normal ASM are shown in table 1.
Odds ratio ± 95% CI Normal ASM Low ASM Gender (man v. women) 1.0 0.87 (0.81–0.94), p=0.0002 Weight preHF (per 1 kg/m2 increase) 1.0 0.85 (0.83–0.87), p<0.0001 Age (per 5 years increase) 1.0 1.05 (1.02–1.08), p=0.0003 C (per 1% increment) 1.0 1.05 (1.04–1.06), p<0.0001 A (per 1% increment) 1.0 0.98 (0.97–0.99), p<0.0001
Conclusions
In HF higher body weight preHF and oedema-free weight gain decreases the risk of low ASM independently of age, gender and weight loss.
of patients living with HF is likely to be around 2 million or even more. 2,3 According to the National Health Fund data posted on the Ministry of Health website, the number is likely to be around 1.2 million people. 4 INTROduCTION Heart failure (HF) has become an epidemic worldwide. The most recent estimation of the global prevalence shows an intimidating number of at least 64 million affected. 1
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