1
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Peripheral endothelial dysfunction in myalgic encephalomyelitis/chronic fatigue syndrome

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Aims

          Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a complex multisystem disease. Evidence for disturbed vascular regulation comes from various studies showing cerebral hypoperfusion and orthostatic intolerance. The peripheral endothelial dysfunction (ED) has not been sufficiently investigated in patients with ME/CFS. The aim of the present study was to examine peripheral endothelial function in patients with ME/CFS.

          Methods and results

          Thirty‐five patients [median age 40 (range 18–70) years, mean body mass index 23.8 ± 4.2 kg/m 2, 31% male] with ME/CFS were studied for peripheral endothelial function assessed by peripheral arterial tonometry (EndoPAT2000). Clinical diagnosis of ME/CFS was based on Canadian Criteria. Nine of these patients with elevated antibodies against β2‐adrenergic receptor underwent immunoadsorption, and endothelial function was measured at baseline and 3, 6, and 12 months follow‐up. ED was defined by reactive hyperaemia index ≤1.81. Twenty healthy subjects of similar age and body mass index were used as a control group. Peripheral ED was found in 18 of 35 patients (51%) with ME/CFS and in 4 healthy subjects (20%, P < 0.05). Patients with ED, in contrast to patients with normal endothelial function, reported more severe disease according to Bell score (31 ± 12 vs. 40 ± 16, P = 0.04), as well as more severe fatigue‐related symptoms (8.62 ± 0.87 vs. 7.75 ± 1.40, P = 0.04) including a higher demand for breaks [9.0 (interquartile range 7.0–10.0) vs. 7.5 (interquartile range 6.0–9.25), P = 0.04]. Peripheral ED showed correlations with more severe immune‐associated symptoms ( r = −0.41, P = 0.026), such as sore throat ( r = −0.38, P = 0.038) and painful lymph nodes ( r = −0.37, P = 0.042), as well as more severe disease according to Bell score ( r = 0.41, P = 0.008) and symptom score ( r = −0.59, P = 0.005). There were no differences between the patient group with ED and the patient group with normal endothelial function regarding demographic, metabolic, and laboratory parameters. Further, there was no difference in soluble vascular cell adhesion molecule and soluble intercellular adhesion molecule levels. At baseline, peripheral ED was observed in six patients who underwent immunoadsorption. After 12 months, endothelial function had improved in five of these six patients (reactive hyperaemia index 1.58 ± 0.15 vs. 2.02 ± 0.46, P = 0.06).

          Conclusions

          Peripheral ED is frequent in patients with ME/CFS and associated with disease severity and severity of immune symptoms. As ED is a risk factor for cardiovascular disease, it is important to elucidate if peripheral ED is associated with increased cardiovascular morbidity and mortality in ME/CFS.

          Related collections

          Most cited references 44

          • Record: found
          • Abstract: found
          • Article: not found

          Endothelial Cell Dysfunction and the Pathobiology of Atherosclerosis.

          Dysfunction of the endothelial lining of lesion-prone areas of the arterial vasculature is an important contributor to the pathobiology of atherosclerotic cardiovascular disease. Endothelial cell dysfunction, in its broadest sense, encompasses a constellation of various nonadaptive alterations in functional phenotype, which have important implications for the regulation of hemostasis and thrombosis, local vascular tone and redox balance, and the orchestration of acute and chronic inflammatory reactions within the arterial wall. In this review, we trace the evolution of the concept of endothelial cell dysfunction, focusing on recent insights into the cellular and molecular mechanisms that underlie its pivotal roles in atherosclerotic lesion initiation and progression; explore its relationship to classic, as well as more recently defined, clinical risk factors for atherosclerotic cardiovascular disease; consider current approaches to the clinical assessment of endothelial cell dysfunction; and outline some promising new directions for its early detection and treatment.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            lncRNA-MIAT regulates microvascular dysfunction by functioning as a competing endogenous RNA.

            Pathological angiogenesis is a critical component of diseases, such as ocular disorders, cancers, and atherosclerosis. It is usually caused by the abnormal activity of biological processes, such as cell proliferation, cell motility, immune, or inflammation response. Long noncoding RNAs (lncRNAs) have emerged as critical regulators of these biological processes. However, the role of lncRNA in diabetes mellitus-induced microvascular dysfunction is largely unknown.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Cross-sectional relations of digital vascular function to cardiovascular risk factors in the Framingham Heart Study.

              Digital pulse amplitude augmentation in response to hyperemia is a novel measure of peripheral vasodilator function that depends partially on endothelium-derived nitric oxide. Baseline digital pulse amplitude reflects local peripheral arterial tone. The relation of digital pulse amplitude and digital hyperemic response to cardiovascular risk factors in the community is unknown. Using a fingertip peripheral arterial tonometry (PAT) device, we measured digital pulse amplitude in Framingham Third Generation Cohort participants (n=1957; mean age, 40+/-9 years; 49% women) at baseline and in 30-second intervals for 4 minutes during reactive hyperemia induced by 5-minute forearm cuff occlusion. To evaluate the vascular response in relation to baseline, adjusting for systemic effects and skewed data, we expressed the hyperemic response (called the PAT ratio) as the natural logarithm of the ratio of postdeflation to baseline pulse amplitude in the hyperemic finger divided by the same ratio in the contralateral finger that served as control. The relation of the PAT ratio to cardiovascular risk factors was strongest in the 90- to 120-second postdeflation interval (overall model R(2)=0.159). In stepwise multivariable linear regression models, male sex, body mass index, ratio of total to high-density lipoprotein cholesterol, diabetes mellitus, smoking, and lipid-lowering treatment were inversely related to PAT ratio, whereas increasing age was positively related to PAT ratio (all P<0.01). Reactive hyperemia produced a time-dependent increase in fingertip pulse amplitude. Digital vasodilator function is related to multiple traditional and metabolic cardiovascular risk factors. Our findings support further investigations to define the clinical utility and predictive value of digital pulse amplitude.
                Bookmark

                Author and article information

                Contributors
                nadja.scherbakov@charite.de
                Journal
                ESC Heart Fail
                ESC Heart Fail
                10.1002/(ISSN)2055-5822
                EHF2
                ESC Heart Failure
                John Wiley and Sons Inc. (Hoboken )
                2055-5822
                10 March 2020
                June 2020
                : 7
                : 3 ( doiID: 10.1002/ehf2.v7.3 )
                : 1064-1071
                Affiliations
                [ 1 ] Berlin‐Brandenburg Center for Regenerative Therapies (BCRT) Augustenburger Platz 1 13353 Berlin Germany
                [ 2 ] DZHK (German Centre for Cardiovascular Research), partner site Berlin Berlin Germany
                [ 3 ] Department of Cardiology Charité ‐ Universitätsmedizin Berlin Berlin Germany
                [ 4 ] Center for Stroke Research Berlin (CSB) Charité ‐ Universitätsmedizin Berlin Berlin Germany
                [ 5 ] Institute of Medical Immunology, Campus Virchow Charité ‐ Universitätsmedizin Berlin Berlin Germany
                Author notes
                [* ] Correspondence to: Nadja Scherbakov, Berlin‐Brandenburg Center for Regenerative Therapies (BCRT), Augustenburger Platz 1, 13353 Berlin, Germany, and Department of Cardiology, Charité ‐ Universitätsmedizin Berlin, Berlin, Germany. Email: nadja.scherbakov@ 123456charite.de

                [†]

                These authors contributed equally to the work.

                Article
                EHF212633 ESCHF-19-00319
                10.1002/ehf2.12633
                7261521
                © 2020 The Authors. ESC Heart Failure published by John Wiley & Sons Ltd on behalf of the European Society of Cardiology

                This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

                Page count
                Figures: 2, Tables: 2, Pages: 8, Words: 2799
                Product
                Funding
                Funded by: Weidenhammer‐Zöbele Foundation
                Categories
                Original Research Article
                Original Research Articles
                Custom metadata
                2.0
                June 2020
                Converter:WILEY_ML3GV2_TO_JATSPMC version:5.8.3 mode:remove_FC converted:31.05.2020

                Comments

                Comment on this article

                Similar content 117

                Cited by 15

                Most referenced authors 442