Therapeutic considerations for prevention and treatment of thrombotic events in COVID-19

Thrombosis is a known complication of SARS-CoV-2 infection, particularly within a severely symptomatic subset of patients with COVID-19 disease, in whom an aggressive host immune response leads to cytokine storm syndrome (CSS). The incidence of thrombotic events coinciding with CSS may contribute to the severe morbidity and mortality observed in association with COVID-19. This review provides an overview of pharmacologic approaches based upon an emerging understanding of the mechanisms responsible for thrombosis across a spectrum of COVID-19 disease involving an interplay between immunologic and pro-thrombotic events, including endothelial injury, platelet activation, altered coagulation pathways, and impaired fibrinolysis.

The mechanistic basis linking cytokine storm to thrombosis in COVID-19

It is now well established that infection with SARS-CoV-2 resulting in COVID-19 disease includes a severely symptomatic subset of patients in whom an aggressive and/or dysregulated host immune response leads to cytokine storm syndrome (CSS) that may be further complicated by thrombotic events, contributing to the severe morbidity and mortality observed in COVID-19. This review provides a brief overview of cytokine storm in COVID-19, and then presents a mechanistic discussion of how cytokine storm affects integrated pathways in thrombosis involving the endothelium, platelets, the coagulation cascade, eicosanoids, auto-antibody mediated thrombosis, and the fibrinolytic system.

Enhanced external counterpulsation for management of symptoms associated with long COVID

Study objective Enhanced external counterpulsation (EECP) as a possible therapy for Long COVID. Design Retrospective analysis of a contemporary, consecutive patient cohort. Setting 7 outpatient treatment centers. Participants Long COVID patients. Intervention 15–35 EECP treatments. Main outcome measures The change from baseline in 1) Patient Reported Outcome Measurement Information System (PROMIS) Fatigue;2) Seattle Angina Questionnaire (SAQ-7);3) Duke Activity Status Index (DASI);4) 6-Minute Walk Test (6MWT);5) Canadian Cardiovascular Society (CCS) Angina Grade;6) Rose Dyspnea Scale (RDS);and 7) Patient Health Questionnaire (PHQ-9). Results Compared to baseline, the PROMIS Fatigue, SAQ7, DASI, and 6MWT improved by 4.63 ± 3.42 (p < 0.001), 21.44 ± 16.54 (p < 0.001), 18.08 ± 13.82 (p < 0.001), and 200.00 ± 180.14 (p = 0.002), respectively. CCS and RDS improved in 63% and 44% of patients, respectively. All patients unable to work prior to EECP were able to return post-therapy. Conclusions and relevance EECP significantly improved validated fatigue and cardiovascular-related markers in patients with Long COVID.