PO:33:197 | Systemic sclerosis and endothelial dysfunction: the passive leg movement technique in the assessment of no-mediated vascular impairment

Silvia Guella¹, Giovanni Baldassarre³, Alessandro Gratton^2|3, Lucrezia Zuccarelli³, Elena Treppo², Emma Di Poi², Bruno Grassi³, Luca Quartuccio^2|3 | ¹SS Reumatologia-CMID Ospedale San Giovanni Bosco, Torino; ²Clinica di Reumatologia Ospedale Santa Maria della Misericordia, ASUFC, Udine; ³Dipartimento di Medicina, Università di Udine, Italy

Objectives: To evaluate nitric oxide (NO)-mediated vascular dysfunction in patients with Systemic Sclerosis (SSc) compared to age- and sex-matched healthy controls through passive leg movement (PLM).

Materials and Methods: Twenty-one patients and twenty-one controls were enrolled. PLM was performed in a seated position, and blood flow (BF) was measured at the right common femoral artery (CFA), distal to the inguinal ligament and approximately 2 cm from the femoral bifurcation, by assessing flow velocity and vessel diameter. Baseline BF, peak flow (hyperaemia) during PLM, and the area under the curve (AUC) of BF over time were calculated. Patients were stratified according to phenotype (limited: lcSSc; diffuse: dcSSc), disease complications, and ongoing therapies.

Results: The mean disease duration was 16.2 years (SD ±9.78). Fifteen patients (71%) had lcSSc. The most frequent autoantibodies were anti-centromere (47%) and anti-Scl70 (43%). Nine patients (43%) had a history of digital ulcers (DU), eight (38%) had pulmonary arterial hypertension (PAH), and eleven (52%) had interstitial lung disease (ILD). Seventeen patients (81%) were on vasoactive therapy and eight were taking immunosuppressive treatment (Table 1). At rest, CFA diameter and baseline BF were not significantly different between groups (p=0.14 and p=0.56, respectively). Both groups exhibited a PLM-induced response. Peak BF was significantly reduced in SSc patients (467.7 vs 552.5; p=0.038), as well as change from baseline (p=0.005). The AUC was also significantly lower in patients (p=0.01) (Figure 1). No differences were observed between lcSSc and dcSSc in terms of peak flow (p=0.34) or AUC (p=0.3). A higher modified Rodnan skin score (mRSS) correlated with a smaller CFA diameter (p=0.001). The presence of DU history did not affect the hyperaemic response (p=0.65). Patients with PAH showed a slightly higher peak flow (p=0.05), likely related to vasoactive therapies. No correlation was found between PLM-induced hyperaemia and vasoactive treatments. Patients on statins had significantly lower baseline BF compared to those not receiving statins (p=0.03), possibly related to the role of statins on endothelial function.

Conclusions: PLM-induced hyperaemia is significantly reduced in SSc, highlighting the role of NO-mediated endothelial dysfunction in this disease, regardless of phenotype. PLM proves to be a valid technique for evaluating microvascular impairment in SSc. However, the absence of correlations between PLM response and drugs used, suggests the need for new endothelial-targeted drugs aimed at reversing vascular damage. Further studies are warranted to better define the role of PLM in SSc and its potential applications in clinical practice and therapeutic evaluation.