Tag: hypercoagulability

Impaired exercise capacity in post-COVID syndrome: the role of VWF-ADAMTS13 axis

Abstract:

Post-COVID syndrome (PCS) or Long-COVID is an increasingly recognised complication of acute SARS-CoV-2 infection, characterised by persistent fatigue, reduced exercise tolerance chest pain, shortness of breath and cognitive slowing. Acute COVID-19 is strongly linked with increased risk of thrombosis; a prothrombotic state, quantified by elevated Von Willebrand Factor (VWF) Antigen (Ag):ADAMTS13 ratio, and is associated with severity of acute COVID-19 infection. We investigated if patients with PCS also had evidence of a pro-thrombotic state associating with symptom severity.

In a large cohort of patients referred to a dedicated post-COVID-19 clinic, thrombotic risk including VWF(Ag):ADAMTS13 ratio, was investigated. An elevated VWF(Ag):ADAMTS13 ratio (≥1.5) was raised in nearly one-third of the cohort and four times more likely in patients with impaired exercise capacity as evidenced by desaturation ≥3% and/or rise in lactate level more than 1 from baseline on 1-minute sit to stand test and/or 6-minute walk test (p<0.0001). 20% (56/276) had impaired exercise capacity, of which 55% (31/56) had a raised VWF(Ag):ADAMTS13 ratio ≥1.5 (p<0.0001). FVIII and VWF(Ag) were elevated in 26% and 18% respectively and support a hypercoagulable state in some patients with PCS.

These findings suggest possible ongoing microvascular/endothelial dysfunction in the pathogenesis of PCS and highlight a potential role for antithrombotic therapy in the management of these patients.

Source: Prasannan N, Heightman M, Hillman T, Wall E, Bell R, Kessler A, Neave L, Doyle AJ, Devaraj A, Singh D, Dehbi HM, Scully M. Impaired exercise capacity in post-COVID syndrome: the role of VWF-ADAMTS13 axis. Blood Adv. 2022 May 11:bloodadvances.2021006944. doi: 10.1182/bloodadvances.2021006944. Epub ahead of print. PMID: 35543533; PMCID: PMC9098525. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9098525/ (Full text)

Sulodexide: A Benefit for Cardiovascular Sequelae of Long COVID Patients?

Dear Editor,

The elaborate and precise review of Harry N. Magnani didactically demonstrates the complex pathophysiological aspects of coronavirus disease 2019 (COVID-19) emphasizing the roles of vascular endothelial dysfunction and coagulation cascade as key features of disease progression.  Moreover, this article brings up that glycosaminoglycane (GAG) antithrombotics likely interfere with inflammatory and coagulation activity in an effective fashion.  Thereafter this postulate has become advocated as the application of sulodexide (Vessel Due F; ALFASIGMA, Italy) (SDX), an unexpensive and orally administrable GAG antithrombotic drug reduced the necessity for both hospital admission and oxygen supplementation in the early phase of SARS-Cov-2 infection under a randomized placebo-controlled out-patient trial.  Interestingly, these patients also showed lower serum levels of C-reactive protein (CRP) and D-dimer as markers of inflammation and prothrombotic state. Of note, instead of regularly recommended and prescribed 250 RLU twice-daily dose, the clinical trial applied the higher, 500 RLU twice-daily dosing regimen in which an antithrombotic effect was safely achieved in a clinical setting.

Read the rest of this article HERE.

Source: Szolnoky G, González-Ochoa AJ. Sulodexide: A Benefit for Cardiovascular Sequelae of Long COVID Patients? Clin Appl Thromb Hemost. 2022 Jan-Dec;28:10760296221084300. doi: 10.1177/10760296221084300. PMID: 35333125; PMCID: PMC8961374. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8961374/ (Full text)

Is chronic fatigue syndrome associated with platelet activation?

Abstract:

Chronic fatigue syndrome (CFS) is a debilitating condition that has no known aetiology or pathophysiology. Recent investigations by other workers have suggested that individuals with CFS may have a hypercoagulable state. This study investigated various aspects of platelet activation and function in 17 patients with CFS and in 16 age-matched and sex-matched healthy controls. Platelet aggregation, platelet volume and coagulation tests were performed.

Platelet aggregation was investigated by means of the photometric changes using citrated platelet-rich plasma, whole blood aggregation was calculated as the percentage fall in single platelet counts and the coagulation tests were performed on an automatic microcentrifugal analyser.A trend was observed for the patients to have lower aggregation results and a reduced mean platelet volume. However, this only reached statistical significance for one result; the rate of the aggregation slope by 1.0 microg/ml collagen [CFS patients, 18 (9-28) versus controls, 32.5 (19-36); Mann-Whitney U test, P = 0.029].

No significant differences were found for any of the measurements of coagulation. These results are in contrast to previously reported findings. However, due to the heterogeneous nature of the disease, and the resulting lifestyles of the patients, caution should be taken when comparing one group of patients with another. Nevertheless, we certainly found no evidence of increased platelet activation or of a hypercoagulable state in patients with CFS and, on the basis of these results, anti-platelet or anti-coagulant therapy is not warranted.

 

Source: Kennedy G, Norris G, Spence V, McLaren M, Belch JJ. Is chronic fatigue syndrome associated with platelet activation? Blood Coagul Fibrinolysis. 2006 Mar;17(2):89-92. https://www.ncbi.nlm.nih.gov/pubmed/16479189