Systemic sclerosisNatriuretic Peptides in Systemic Sclerosis-related Pulmonary Arterial Hypertension
Section snippets
Methods
To outline the role of NP in patients with SSc PAH, we performed an extensive internet search (PubMed) using the following keywords: natriuretic peptides, systemic sclerosis or scleroderma, and pulmonary arterial hypertension. The present study searched Medline for articles published between January 1998 and December 2008 related to this topic. Articles were selected if they had been published as full journal articles in English (abstracts, poster presentations, conference proceedings, or
Results
The literature search as described in Methods highlighted a number of published studies. These are presented later in this review, focusing on the value of the NP in the detection and risk stratification of SSc PAH. First, biology and assays of NP are briefly described.
Pathogenetic Mechanisms and NP Release in SSc PAH
Activation of neurohormonal systems with vasoconstrictor, antidiuretic, proinflammatory, hypertrophic, and cytoproliferative effects have been detected in SSc patients (40). While the activation of vasoconstrictor hormones (plasma catecholamine, renin-angiotensin-aldosterone system) represents a compensatory mechanism at least in the early phase of the disease, RV involvement determined by various degrees of pulmonary hypertension is a powerful stimulus for eliciting secretion of cardiac NP.
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Cited by (25)
B-type natriuretic peptide in rheumatic diseases: A cardiac biomarker or a sophisticated acute phase reactant?
2012, Autoimmunity ReviewsCitation Excerpt :Allanore et al. reported that NT-proBNP levels at a threshold of more than 97% manufacturer-provided normal levels, predict with 75% sensitivity and 83% specificity the future development of SScPAH in a prospective cohort of 101 patients during a median follow-up period of 29 months [52]. Derangement in the cardiac neuroendocrine axis is associated with parameters of right ventricular overload and may contribute to clinical evolution and ominous outcome in SScPAH [53,54]. Circulating levels of NP are elevated in patients with SScPAH and are linked with echocardiographic [55] and hemodynamic parameters such as mean pulmonary artery pressure, pulmonary vascular resistance and cardiac index, which are closely tied to the causal pathway of disease progression [56].
Pulmonary Hypertension in Systemic Sclerosis
2011, Seminars in Arthritis and RheumatismCitation Excerpt :It has been suggested that desaturation during a 6MWT may provide additional information regarding severity of scleroderma lung disease (70). The other surrogate measure of severity and response to therapy in pulmonary hypertension is brain natriuretic peptide (BNP) or N-terminal pro-brain natriuretic peptide (NT-proBNP) (71). The initial precursor of BNP is preproBNP, which is first cleaved to proBNP and then to BNP and NT-proBNP (72).
When the heart is burning: Amino-terminal pro-brain natriuretic peptide as an early marker of cardiac involvement in active autoimmune rheumatic disease
2011, International Journal of CardiologyCitation Excerpt :As a consequence, mainly in the late stage of the disease course, it is possible that inflammation does not represent a central feature in these patients [31]. For instance in our population, the mechanism most likely to be involved in natriuretic peptide elevation seems related to pulmonary arterial hypertension, as in other series previously published [34]. Focusing on the diseases in which we actually found an association between inflammation and natriuretic peptide elevation, it is of interest to highlight that in systemic vasculitides NT-proBNP has a strong correlation with left ventricular hypertrophy (as expressed by LVMI).
Diagnostic and prognostic markers and treatment of connective tissue disease-associated pulmonary arterial hypertension: current recommendations and recent advances
2020, Expert Review of Clinical ImmunologyBiomarkers for pulmonary vascular remodeling in systemic sclerosis: A pathophysiological approach
2018, Frontiers in Physiology
The first 2 authors contributed equally to this work.
The authors have no conflicts of interest to disclose.
Dr Giannakoulas has received training and research grants from the Hellenic Cardiological Society, the Hellenic Heart Foundation, and the DG Education & Culture–LLP Programme–Leonardo Da Vinci Mobility. Professor Gatzoulis and the Royal Brompton Adult Congenital Heart Centre and Centre for Pulmonary Hypertension have received support from the British Heart Foundation.