Endothelial dysfunction and vascular homestasis in ME/CFS
A sub-study of the RituxME trial by Norwegian researchers found a problem in the blood vessels on the heart in a group of people with ME/CFS. Treatment with Rituximab caused a slight but significant improvement in symptoms within 18 months. They conclude that the vascular or circulatory system could play a role in ME/CFS.
Endothelial dysfunction is a type of non-obstructive coronary artery disease (CAD) in which there are no heart artery blockages, but the large blood vessels on the heart’s surface constrict (narrow) instead of dilating (opening). This condition tends to affect more women than men and causes chronic chest pain. (Stanford)
Endothelial dysfunction in ME/CFS patients, by Miriam Kristine Sandvik, Kari Sørland, Elisabeth Leirgul, Ingrid Gurvin Rekeland, Christina Særsten Stavland, Olav Mella, Øystein Fluge in PLoS One, 2023 Feb 2;18(2):e0280942 [doi: 10.1371/journal.pone.0280942]
Research abstract
Objective:
A few earlier studies have found impaired endothelial function in patients with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS). The present study investigated large-vessel and small-vessel endothelial function in patients with ME/CFS.
Study design:
The study was a substudy of the RituxME trial, a national, multicenter, randomized, double-blind, placebo-controlled phase III study on the effect of rituximab vs. placebo in ME/CFS patients in Norway.
Flow-mediated dilation (FMD) and post-occlusive reactive hyperemia (PORH) was measured at baseline and after 18 months of treatment in 39 patients and compared with healthy controls. Other outcome measures were symptom severity and various physical function measures.
Results:
ME/CFS patients had markedly reduced FMD compared to healthy controls at baseline (5.1% vs. 8.2%, p< 0.0001, adjusted for arterial diameter and sex), and significantly lower microvascular regulation measured by PORH than healthy controls (1354 PU vs. 2208 PU, p = 0.002).
There were no differences between the treatment and placebo groups in symptom changes or vascular measures. As a group, the ME/CFS patients experienced a slight, but significant improvement in clinical symptoms after 18 months. PORH, but not FMD, was similarly improved (1360 to 1834 PU, p = 0.028). There was no significant correlation between FMD and PORH.
There were non-significant tendencies towards associations between symptom severity/physical function measures and lower FMD and PORH, and a significant correlation between PORH and steps per 24 hours at baseline.
Conclusions:
ME/CFS patients had reduced macro- and microvascular endothelial function, indicating that vascular homeostasis may play a role in the clinical presentation of this disease.
