Background Diastolic dysfunction (DD) is the earliest hallmark of cardiac disease in systemic sclerosis (SSc) and is due to endothelial dysfunction and ischemia-reperfusion damage. NT-proBNP is released by endothelial cells and ischemic myocites enhancing the recruitment of endothelial progenitor cells (EPC) from bone marrow for vasculogenesis and cardiac regeneration. This mechanism has not been explored in SSc.
Objectives To investigate the relation among DD and its severity, NT-proBNP levels and EPC recruitment in patients with SSc compared to healthy controls.
Methods Cross sectional study was carried out; 100 SSc patients and 56 healthy controls were included. Systolic dysfunction, structural cardiopathy, neoplasms, overlap syndrome, diabetes and hypertension were excluded. DD was stratified in mild, moderate and severe according to 2009 EAE/ASE guidelines. NT-proBNP was measured by electroquimioluminiscence. EPC were characterized by flow cytometry into three subtypes according to the expression of CD309, CD34 and CD133.We performed univariate, multivariate and subanalysis among DD subtypes and organic damage in SSc. P value of 0.05 was considered significant.
Results Mean age was 48.28±3.88 for controls and 49.48±9.88 for patients (p=0.19); 53 controls (95%) and 97 patients (97%) were women (p=0.23). Diastolic dysfunction was present in 1 control (1.7%) and 61 SSc patients (61%) (p=0.0003). NT-proBNP levels were 22.24 pg/ml ±8.48 for controls, 50.51 pg/ml (12-253) for patients without DD and 336.15 pg/ml (17-2250) for patients with DD (p=0.0001). CD309/34+ EPC was 0.84 cels/ml (0.1-3.1) for controls, 1.71 cels/ml (0.1-5.5) for patients without DD and 0.86 cels/ml (0.01-5.5) for patients with DD (p=0.0001); same tendency was observed with other two subtypes of EPC. Subanalysis showed that EPC was different (p=0.0001) among mild, moderate and severe DD.
Conclusions NTproBNP is related to severity of asymptomatic DD and could be useful as a predictive biomarker of cardiac damage in SSc. We observed that EPC recruitment in the presence of DD is diminished compared to controls, nevertheless in absence of DD, EPC recruitment is higher than controls. This observation suggest that recruitment of EPC is substancial in the cardiac regeneration and the lost of this mechanism of regeneration could explain the progression of cardiac damage in SSc.
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Disclosure of Interest None declared
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