Clinical utility of biomarkers in heart failure

Müeller, Christian

doi:10.1002/ejhf.893

Cited by 4 publications

(5 citation statements)

References 19 publications

(54 reference statements)

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“…The plasma concentration of natriuretic peptides can be used as an initial diagnostic test in patients with dyspnoea to rule out the possibility of heart failure [1]. The upper limit of normal in the non-acute setting for NT-proBNP is 125 ng/L; in our cohort, we found NT-proBNP to be below this level in nearly 20% of patients with known HF, which is probably a sign of a very well compensated heart failure [15,16].…”

Section: Discussionmentioning

confidence: 85%

Prognostic value of NT-proBNP added to clinical parameters to predict two-year prognosis of chronic heart failure patients with mid-range and reduced ejection fraction – A report from FAR NHL prospective registry

et al. 2019

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BackgroundAccording to guidelines, the prognosis of patients with chronic heart failure can be predicted by determining the levels of natriuretic peptides, the NYHA classification and comorbidities. The aim our work was to develop a prognostic score in chronic heart failure patients that would take account of patients’ comorbidities, NYHA and NT-proBNP levels.Methods and resultsA total of 1,088 patients with chronic heart failure with reduced ejection fraction (HFrEF) (LVEF<40%) and mid-range EF (HFmrEF) (LVEF 40–49%) were enrolled consecutively. Two-year all-cause mortality, heart transplantation and/or LVAD implantation were defined as the primary endpoint (EP). The occurrence of EP was 14.9% and grew with higher NYHA, namely 4.9% (NYHA I), 11.4% (NYHA II) and 27.8% (NYHA III–IV) (p<0.001). The occurrence of EP was 3%, 10% and 15–37% in patients with NT-proBNP levels ≤125 ng/L, 126–1000 ng/L and >1000 ng/L respectively. Discrimination abilities of NYHA and NT-proBNP were AUC 0.670 (p<0.001) and AUC 0.722 (p<0.001) respectively. The predictive value of the developed clinical model, which took account of older age, advanced heart failure (NYHA III+IV), anaemia, hyponatraemia, hyperuricaemia and being on a higher dose of furosemide (>40 mg daily) (AUC 0.773; p<0.001) was increased by adding the NT-proBNP level (AUC 0.790).ConclusionThe use of prediction models in patients with chronic heart failure, namely those taking account of natriuretic peptides, should become a standard in routine clinical practice. It might contribute to a better identification of a high-risk group of patients in which more intense treatment needs to be considered, such as heart transplantation or LVAD implantation.

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Section: Discussionmentioning

confidence: 85%

Prognostic value of NT-proBNP added to clinical parameters to predict two-year prognosis of chronic heart failure patients with mid-range and reduced ejection fraction – A report from FAR NHL prospective registry

et al. 2019

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“…3 Atrophy affects multiple organs including the heart. 9,10 Although the field of HF biomarkers is rich and reflects different mechanisms of HF development and progression, 11 none of the available biomarkers are used to assess cardiac impairment in CC. [4][5][6][7] Although several inflammatory, hormonal, and oxidative stress molecules have been suggested as markers of prognosis in cachexia, 8 there are no universally accepted specific biomarkers for this condition.…”

Section: Introductionmentioning

confidence: 99%

“…This scenario becomes even more intriguing and complex considering that CC may lead to the development of HF, which appears as an additional contributing factor that exacerbates wasting in the cancer patients. 9,10 Although the field of HF biomarkers is rich and reflects different mechanisms of HF development and progression, 11 none of the available biomarkers are used to assess cardiac impairment in CC. 12 Neutrophil gelatinase-associated lipocalin (NGAL) is a 25 kDa secretory protein belonging to the lipocalins superfamily, which was initially identified as a component of neutrophil granules, associated with matrix metalloproteinase-9 13 and later found to be expressed at low levels in several tissues.…”

Section: Introductionmentioning

confidence: 99%

Cardiac expression of neutrophil gelatinase‐associated lipocalin in a model of cancer cachexia‐induced cardiomyopathy

et al. 2018

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AimsCachexia is a severe consequence of cancer. Although cancer‐induced heart atrophy leads to cardiac dysfunction and heart failure (HF), biomarkers for their diagnosis have not been identified. Neutrophil gelatinase‐associated lipocalin (NGAL) is an aldosterone‐responsive gene increased in HF. We studied NGAL and its association with aldosterone levels in a model of cancer cachexia‐induced cardiomyopathy.Methods and resultsRats were injected with Yoshida 108 AH‐130 hepatoma cells to induce tumour. Cachectic rats were treated daily, for 16 days, with placebo or with 5 or 50 mg/kg/day of spironolactone. Cardiac function was analysed by echocardiography at baseline and at Day 11. Weight loss and atrophy of lean body and fat mass of cachectic rats were significantly attenuated by spironolactone. Cardiac dysfunction of tumour‐bearing rats was improved by spironolactone. Plasma aldosterone was up‐regulated from 337 ± 7 pg/mL in sham animals to 591 ± 31 pg/mL in the cachectic rats (P < 0.001 vs. sham). Treatment with 50 or 5 mg/kg/day of spironolactone reduced plasma aldosterone to 396 ± 22 and 391 ± 25 pg/mL (P < 0.01 vs. placebo). Plasma levels of NGAL were also increased in cachectic rats (1.462 ± 0.3603 μg/mL) than in controls (0.0936 ± 6 μg/mL, P < 0.001). Spironolactone treatment (50 mg/kg/day) significantly reduced cardiac mRNA and protein NGAL levels (P < 0.05 and P < 0.001 vs. placebo, respectively). NGAL mRNA and protein levels were overexpressed in cachectic animal hearts treated with placebo, compared with control (P < 0.05 and P < 0.01 vs. sham). Spironolactone treatment at 50 mg/kg/day reduced significantly cardiac NGAL (P < 0.05 and P < 0.001 vs. placebo).ConclusionsCancer cachexia induced increased levels of aldosterone and NGAL, contributing to worsening cardiac damage in cancer cachexia‐induced cardiomyopathy. Spironolactone treatment may greatly attenuate cardiac dysfunction and lean mass atrophy associated with cancer cachexia.

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“…On the second point, we understand the authors' impression about the lack of high‐sensitivity cardiac troponin T (hs‐TnT) and N‐terminal pro‐B‐type natriuretic peptide (NT‐proBNP) in our study. These are, of course, among the most extensively studied and better established biomarkers in heart failure . Unfortunately, these two biomarkers were not serially evaluated in the PROTECT trial and, subsequently, we were not able to analyse them in the study.…”

Section: Performance Of Biomarkers In the Rule‐out Region Of The Recementioning

confidence: 99%

Risk stratification in acute heart failure: reply

Demissei

Voors

2018

European J of Heart Fail

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We would like to thank Schneider et al. for raising important and thoughtful questions related to our work. 1 We have addressed the specific questions raised as follows.Regarding the first point, we acknowledge the relevance of systolic blood pressure at AUC, area under the curve; BNP, B-type natriuretic peptide; BUN, blood urea nitrogen; CI, confidence interval; CRP, C-reactive protein; cTnI, cardiac troponin I; GDF-15, growth differentiation factor 15; IL-6, interleukin-6; proADM, pro-adrenomedullin; WAP-4c, whey acidic protein four-disulphide core domain protein HE4.

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Clinical utility of biomarkers in heart failure

Cited by 4 publications

References 19 publications

Prognostic value of NT-proBNP added to clinical parameters to predict two-year prognosis of chronic heart failure patients with mid-range and reduced ejection fraction – A report from FAR NHL prospective registry

Prognostic value of NT-proBNP added to clinical parameters to predict two-year prognosis of chronic heart failure patients with mid-range and reduced ejection fraction – A report from FAR NHL prospective registry

Cardiac expression of neutrophil gelatinase‐associated lipocalin in a model of cancer cachexia‐induced cardiomyopathy

Risk stratification in acute heart failure: reply

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