Background/Purpose: Cerebral vasoconstriction is thought to be the underlying pathogenetic mechanism of Reversible Cerebral Vasoconstriction Syndromes (RCVS). However, mediators of the syndrome at molecular levels have not been elucidated. We aim in this proposal to assess the role of Endothelin-1 (E-1), a potent vasoconstrictor, in the pathogenesis of RCVS.
Methods: Seven patients with RCVS, recruited from the Cleveland Clinic prospective RCVS registry were included. Five peripheral blood samples were collected during the cerebral vasoconstrictive acute attack (group 1) and four samples after complete resolution of the vascular abnormalities and resolution of the symptoms (group 2). Further, E-1 levels were measured from 10 healthy controls of similar races and genders, who were then matched to group 1 using a one-to-one Greedy matching algorithm based on age . Plasma E-1 levels were measured using Quantikine Endothelin-1 enzyme-linked immunosorbent assay kit (from R& D Systems) according to the user manual . Average E-1 levels for patients was compared to the average E-1 levels for matched healthy patients using mixed effects modeling to account for matched group clustering.
Results: During the acute vasoconstrictive attack, average plasma E-1 level differs significantly between the patients and the healthy controls (p = 0.002). Mean plasma E-1 levels for RCVS patients (group 1) was estimated to be about 1.2 pg/ml (95% CI 0.6 pg/ml – 1.7 pg/ml) higher as compared to the healthy controls. Paired samples from the same patients (during the acute attack and after resolution) were available from two patients (4 samples). In these patients, there was a trend for plasma E-1 level to decline to the average level of healthy controls (2.7 to 1.6 and 2.8 to 1.2) when comparing acute attack to the resolution phase levels. Average plasma E-1 levels of all patients in group 2 (the resolution phase, n=4) was 1.41pg/ml similar to the average plasma healthy control group.
Conclusion: Plasma Endothelin-1 (E-1) levels are significantly elevated in RCVS patients during the vasoconstrictive acute attack as compared to healthy controls, with a trend to decline after resolution of the vasoconstriction. These results suggest a potential role of E-1 in the pathogenesis of RCVS.
Disclosure:
T. Hammad,
None;
L. H. Calabrese,
None;
K. Uchino,
None;
S. John,
None;
M. Stillman,
None;
S. Tepper,
None;
C. O’Rourke,
None;
A. Janocha,
None;
S. Erzurum,
None;
R. Hajj-Ali,
None.
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ACR Meeting Abstracts - https://acrabstracts.org/abstract/enothelin-1-plays-a-role-in-the-pathogenesis-of-reversible-cerebral-vasoconstriction-syndrome/