Epidemiology and pathophysiology of vascular thrombosis in acclimatized lowlanders at high altitude: A prospective longitudinal study

Nair, Velu; Singh, Sharanjit; Ashraf, Mohammad Zahid; Yanamandra, Uday; Sharma, Vivek; Prabhakar, Amit; Ahmad, Rabiah; Chatterjee, Tathagata; Behera, Vineet; Guleria, Vivek Singh; Patrikar, Seema; Gupta, Shivi; Vishnoi, Madan Gopal; Rigvardhan,; Kalshetty, Kiran; Sharma, Prafull; Bajaj, Nitin; Khaling, Thyelnai D.; Wankhede, Tanaji Sitaram; Bhattachar, Srinivasa; Datta, R. Κ.; Ganguli, Late Prosenjit

doi:10.1016/j.lansea.2022.05.005

Cited by 11 publications

(6 citation statements)

References 37 publications

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“…44 Other studies suggest that subjects living in areas of higher altitude have higher rates of thrombosis due to decreased levels of anticoagulants such as tissue factor pathway inhibitor (p<0.001), thrombomodulin (p=0.016), enhanced coagulation (FXa: p<0.001) (PVIIa: p<0.001), and dampened fibrinolysis. 58 The enhancement of coagulation and dampening of anticoagulant factors could promote thrombus formation and subsequent VTE development in high altitude patients. In addition, other studies postulate that high altitude induced VTEs are caused by increased expression of platelet activation genes and elevated mean platelet count (p=0.005).…”

Section: Smoking Secondary Polycythemia and Vtementioning

confidence: 99%

Secondary polycythemia and venous thromboembolism: a systematic review

et al. 2023

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Background Secondary polycythemia is an acquired condition characterized by an elevation in red blood cell (RBC) mass either in response to tissue hypoxia or inappropriate erythropoietin (EPO) secretion. It is proposed that the elevation of RBC mass in secondary polycythemia can lead to hyperviscosity and VTE. This systematic review aims to assess the relationship between secondary polycythemia and venous thromboembolism and discuss diagnostic strategies and management of secondary polycythemia and VTE. Methods This systematic review was conducted on September 2, 2022, and followed PRISMA guidelines to select and analyze relevant articles using the following databases: PubMed, ScienceDirect, and CINAHL. The queries used were “secondary polycythemia AND venous thromboembolism,” “secondary polycythemia AND deep vein thrombosis,” “secondary polycythemia AND pulmonary embolism,” “chronic obstructive pulmonary disease AND venous thromboembolism,” “chronic obstructive pulmonary disease AND deep vein thrombosis,” “chronic obstructive pulmonary disease AND pulmonary embolism,” “high altitude AND venous thromboembolism,” “high altitude AND deep vein thrombosis,” “high altitude AND pulmonary embolism,” “smoking AND venous thromboembolism,” “smoking AND deep vein thrombosis”, “smoking AND pulmonary embolism”, “hypoventilation AND venous thromboembolism”, “hypoventilation AND deep vein thrombosis”, “hypoventilation AND pulmonary embolism”, “testosterone AND venous thromboembolism”, “testosterone AND deep vein thrombosis”, and “testosterone AND pulmonary embolism.” The search duration was set from 2012–2022. Relevant publications were selected based on the inclusion and exclusion criteria. Results The initial search generated 5,946 articles. After narrowing the search based on inclusion and exclusion criteria, 30 articles were selected for this systematic review. Conclusion We found evidence to support the relationship between secondary polycythemia and VTE. Therapies targeting the factors that lead to secondary polycythemia can correct it and prevent VTE progression. If VTE occurs as a result of secondary polycythemia, anticoagulation therapy is recommended or inferior vena cava filters if contraindicated.

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Section: Smoking Secondary Polycythemia and Vtementioning

confidence: 99%

Secondary polycythemia and venous thromboembolism: a systematic review

et al. 2023

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confidence: 99%

“…In this issue of The Lancet Regional Health – Southeast Asia, Velu Nair and colleagues 8 report the results of a challenging, large prospective longitudinal study that investigated thrombotic events in a cohort of 960 acclimatized lowlanders at high altitude. 8 Of these 960 male soldiers, 750 ascended to altitudes above 15.000ft (4472 m). Clinical screening and determination of markers of coagulation and fibrinolysis were performed in blood samples obtained from these individuals once at sea level and twice at high altitude (at 12–15,000ft and at >15,0000ft, respectively).…”

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confidence: 99%

“…Also, the fibrinolytic capacity in these individuals was affected by a moderate, albeit not significant, reduction in tissue-type plasminogen activator (tPA), a profibrinolytic serine protease. In addition, Velu Nair and colleagues 8 provide strong evidence that not only coagulation and fibrinolysis are affected by staying at high altitude but that such environment might also impact on activation of the endothelium as indicated by the increased levels of adhesion molecules such as vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM), and CD40 ligand in the individuals who experienced a thrombotic event. Such activation of the endothelium most likely can be linked to a generalized inflammatory state as evidenced by increased C-reactive protein (CRP) and myeloperoxidase (MPO) levels.…”

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confidence: 99%

“… 5 , 6 , 7 In conclusion , this challenging study improves our understanding on the mechanisms that might underly high altitude induced thrombosis. 8 …”

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confidence: 99%

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