Autoimmunity in Long Covid and POTS

Abstract

Orthostatic intolerance and other autonomic dysfunction syndromes are emerging as distinct symptom clusters in Long Covid. Often accompanying these are common, multi-system constitutional features such as fatigue, malaise and skin rashes which can signify generalized immune dysregulation. At the same time, multiple autoantibodies are identified in both Covid-related autonomic disorders and non-Covid autonomic disorders, implying a possible underlying autoimmune pathology. The lack of specificity of these findings precludes direct interpretations of cause and association, but their prevalence with its supporting evidence is compelling.

Keywords: Long Covid; POTS; autoantibody; autoimmune; autoimmunity.

Figure 1.

Possible mechanisms contributing to POTS. The underlying mechanisms are likely related to excessive venous pooling on orthostasis which is caused by excessive venous distension. In response to this reduction in cardiac venous return, increased SNS output occurs, increasing venoconstriction which may be impaired if small fibre neuropathy is present. Additionally, autoantibody-mediated impairment of peripheral vasoconstriction may occur. Tachycardia occurs in response to reduced venous return, in order to maintain cardiac output. Deconditioning can result in smaller left ventricular mass, requiring higher heart rate to maintain cardiac output. Possible reasons for the higher prevalence in women could be smaller heart mass, smaller muscle pump and an overlap with autoimmunity. Figure adapted with permission from www.stopfainting.com