Serum biomarkers in valvular heart disease

Gardezi, Syed K M; Coffey, Sean; Prendergast, Bernard; Myerson, Saul G.

doi:10.1136/heartjnl-2016-310482

Cited by 13 publications

(7 citation statements)

References 101 publications

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“…In accordance with previous studies, we found a strong association between BNP and mortality after AVR. However, if invasive haemodynamic parameters were entered into the multivariate model, BNP was not an independent predictor of death anymore.…”

Section: Discussionsupporting

confidence: 93%

“…In patients with aortic stenosis (AS), B‐type natriuretic peptide (BNP) and the N‐terminal part of its precursor peptide, N terminal proBNP (NT‐proBNP) are markers of prognosis . This applies for both asymptomatic patients managed conservatively in whom BNP predicts the occurrence of symptoms and the need for aortic valve replacement (AVR) and patients undergoing AVR in whom BNP and NT‐proBNP predict clinical outcomes after surgical AVR (SAVR) and transcatheter AVR (TAVR), respectively .…”

Section: Introductionmentioning

confidence: 99%

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Relationship between B‐type natriuretic peptide and invasive haemodynamics in patients with severe aortic valve stenosis

et al. 2020

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AimsIn patients with aortic stenosis (AS), B-type natriuretic peptide (BNP) is a prognostic marker. However, there is little information on the association between BNP and invasive haemodynamics in AS. The aim of the present study was to assess the hitherto not well-defined relationship between BNP and invasive haemodynamics in patients with severe AS undergoing aortic valve replacement (AVR) with a view to understand the link between high BNP and poor prognosis in these patients. In particular, we were interested in the association between BNP and combined pre-capillary and post-capillary pulmonary hypertension (CpcPH). Methods and results BNP was measured in 252 patients (age 74 ± 10 years, 58% male patients) with severe AS [indexed aortic valve area 0.4 ± 0.1 cm 2 /m 2 and left ventricular ejection fraction (LVEF) 57 ± 12%] the day before cardiac catheterization. Patients were followed for a median (interquartile range) period of 3.1 (2.3-4.3) years after surgical (n = 157) or transcatheter (n = 95) AVR. The prevalence of CpcPH (mean pulmonary artery pressure ≥ 25 mmHg, mean pulmonary artery wedge pressure-15 mmHg, and pulmonary vascular resistance > 3 Wood units) was 13%. The median BNP plasma concentration was 188 (78-452) ng/L. The indexed aortic valve area was similar across BNP quartiles (P = 0.21). Independent predictors of higher BNP (ln transformed) included lower haemoglobin (beta = À0.18; P < 0.001), lower LVEF (beta = À0.20; P < 0.001), more severe mitral regurgitation (beta = 0.20; P < 0.001), higher mean pulmonary artery wedge pressure (beta = À0.37; P < 0.001), and higher pulmonary vascular resistance (beta = 0.21; P < 0.001). In a multivariate model with CpcPH rather than its haemodynamic components, CpcPH was independently associated with higher BNP (0.21; P < 0.001). Higher ln BNP was associated with higher mortality [hazard ratio 1.90 (95% confidence interval 1.33-2.71); P < 0.001] in the univariate analysis. Patients in the third and fourth BNP quartiles had a more than six-fold risk of death compared with patients in the first and second quartiles [hazard ratio 6.29 (95% confidence interval 1.86-21.27); P = 0.003]. In the multivariate analysis, lower LVEF [hazard ratio 0.96 (95% confidence interval 0.94-0.99) per 1% increase; P = 0.01] and CpcPH [hazard ratio 4.58 (95% confidence interval 1.89-11.09); P = 0.001] but not BNP were independently associated with mortality. The areas under the receiver operator characteristics curve for BNP for the prediction of CpcPH and mortality were 0.88 and 0.74, respectively. Conclusions In patients with severe AS, higher BNP is a marker of the presence of CpcPH and its contributors. The association between BNP and such an adverse haemodynamic profile at least in part explains the ability of BNP to predict long-term post-AVR mortality.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Relationship between B‐type natriuretic peptide and invasive haemodynamics in patients with severe aortic valve stenosis

et al. 2020

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“…For example, while NT-proBNP may be elevated in those with AS, LV hypertrophy due to AS may normalise wall stress and therefore attenuate the anticipated rise in the biomarker. Because there is also considerable overlap in natriuretic peptide concentrations across elderly patients with and without AS,24 a strategy of integrating NT-proBNP with orthogonal biomarkers may inform clinical practice better than NT-proBNP alone.…”

Section: Discussionmentioning

confidence: 99%

Multiple biomarker panel to screen for severe aortic stenosis: results from the CASABLANCA study

et al. 2018

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ObjectiveSevere aortic valve stenosis (AS) develops via insidious processes and can be challenging to correctly diagnose. We sought to develop a circulating biomarker panel to identify patients with severe AS.MethodsWe enrolled study participants undergoing coronary or peripheral angiography for a variety of cardiovascular diseases at a single academic medical centre. A panel of 109 proteins were measured in blood obtained at the time of the procedure. Statistical learning methods were used to identify biomarkers and clinical parameters that associate with severe AS. A diagnostic model incorporating clinical and biomarker results was developed and evaluated using Monte Carlo cross-validation.ResultsOf 1244 subjects (age 66.4±11.5 years, 28.7% female), 80 (6.4%) had severe AS (defined as aortic valve area (AVA) <1.0 cm2). A final model included age, N-terminal pro-B-type natriuretic peptide, von Willebrand factor and fetuin-A. The model had good discrimination for severe AS (OR=5.9, 95% CI 3.5 to 10.1, p<0.001) with an area under the curve of 0.76 insample and 0.74 with cross-validation. A diagnostic score was generated. Higher prevalence of severe AS was noted in those with higher scores, such that 1.6% of those with a score of 1 had severe AS compared with 15.3% with a score of 5 (p<0.001), and score values were inversely correlated with AVA (r=−0.35; p<0.001). At optimal model cut-off, we found 76% sensitivity, 65% specificity, 13% positive predictive value and 98% negative predictive value.ConclusionsWe describe a novel, multiple biomarker approach for diagnostic evaluation of severe AS.Trial registration number NCT00842868.

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“…Many studies have investigated potential biomarkers to evaluate fibrosis and chronic inflammation processes in patients with RHD and ST2 is a sensitive marker for detecting cardiac fibrosis, including fibrosis progression in RHD. [4][5][6] Strengths and limitations of this study ► A novel study that analysed the ST2 expression in mitral valves in patients with rheumatic heart. ► This study proposed novel and affordable treatment targeting the rheumatic heart valve fibrosis reduction.…”

Section: Introductionmentioning

confidence: 99%

Randomised controlled trial into the role of ramipril in fibrosis reduction in rheumatic heart disease: the RamiRHeD trial protocol

et al. 2021

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IntroductionRheumatic heart disease (RHD) is a major burden in developing countries and accounts for 80% of all people living with the disease, where it causes most cardiovascular morbidity and mortality in children and young adults. Chronic inflammation and fibrosis of heart valve tissue due to chronic inflammation in RHD will cause calcification and thickening of the impacted heart valves, especially the mitral valve. This fibrogenesis is enhanced by the production of angiotensin II by increased transforming growth factor β expression and later by the binding of interleukin-33, which is known to have antihypertrophic and antifibrotic effects, to soluble sST2. sST2 binding to this non-natural ligand worsens fibrosis. Therefore, we hypothesise that ACE inhibitors (ACEIs) would improve rheumatic mitral valve stenosis.Methods and analysisThis is a single-centre, double-blind, placebo-controlled, randomised clinical trial with a pre–post test design. Patients with rheumatic mitral stenosis and valve dysfunction will be planned for cardiac valve replacement operation and will be given ramipril 5 mg or placebo for a minimum of 12 weeks before the surgery. The expression of ST2 in the mitral valve is considered to be representative of cardiac fibrosis. Mitral valve tissue will be stained by immunohistochemistry to ST2. Plasma ST2 will be measured by ELISA. This study is conducted in the Department of Cardiology and Vascular Medicine, Universitas Indonesia, National Cardiac Center Harapan Kita Hospital, Jakarta, Indonesia, starting on 27 June 2019.Ethics and disseminationThe performance and dissemination of this study were approved by the ethics committee of National Cardiovascular Center Harapan Kita with ethical code LB.02.01/VII/286/KEP.009/2018.Trial registration numberNCT03991910.

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Serum biomarkers in valvular heart disease

Cited by 13 publications

References 101 publications

Relationship between B‐type natriuretic peptide and invasive haemodynamics in patients with severe aortic valve stenosis

Relationship between B‐type natriuretic peptide and invasive haemodynamics in patients with severe aortic valve stenosis

Multiple biomarker panel to screen for severe aortic stenosis: results from the CASABLANCA study

Randomised controlled trial into the role of ramipril in fibrosis reduction in rheumatic heart disease: the RamiRHeD trial protocol

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