Early experience with arterial thromboembolic complications in patients with COVID-19

J Vasc Surg. 2021 Feb;73(2):381-389.e1. doi: 10.1016/j.jvs.2020.07.089. Epub 2020 Aug 28.


Background: Little is known about the arterial complications and hypercoagulability associated with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. We sought to characterize our experience with arterial thromboembolic complications in patients with hospitalized for coronavirus disease 2019 (COVID-19).

Methods: All patients admitted from March 1 to April 20, 2020, and who underwent carotid, upper, lower and aortoiliac arterial duplex, computed tomography angiogram or magnetic resonance angiography for suspected arterial thrombosis were included. A retrospective case control study design was used to identify, characterize and evaluate potential risk factors for arterial thromboembolic disease in SARS-CoV-2 positive patients. Demographics, characteristics, and laboratory values were abstracted and analyzed.

Results: During the study period, 424 patients underwent 499 arterial duplex, computed tomography angiogram, or magnetic resonance angiography imaging studies with an overall 9.4% positive rate for arterial thromboembolism. Of the 40 patients with arterial thromboembolism, 25 (62.5%) were SARS-CoV-2 negative or admitted for unrelated reasons and 15 (37.5%) were SARS-CoV-2 positive. The odds ratio for arterial thrombosis in COVID-19 was 3.37 (95% confidence interval, 1.68-6.78; P = .001). Although not statistically significant, in patients with arterial thromboembolism, patients who were SARS-CoV-2 positive compared with those testing negative or not tested tended to be male (66.7% vs 40.0%; P = .191), have a less frequent history of former or active smoking (42.9% vs 68.0%; P = .233) and have a higher white blood cell count (14.5 vs 9.9; P = .208). Although the SARS-CoV-2 positive patients trended toward a higher the neutrophil-to-lymphocyte ratio (8.9 vs 4.1; P = .134), creatinine phosphokinase level (359.0 vs 144.5; P = .667), C-reactive protein level (24.2 vs 13.8; P = .627), lactate dehydrogenase level (576.5 vs 338.0; P = .313), and ferritin level (974.0 vs 412.0; P = .47), these differences did not reach statistical significance. Patients with arterial thromboembolic complications and SARS-CoV-2 positive when compared with SARS-CoV-2 negative or admitted for unrelated reasons were younger (64 vs 70 years; P = .027), had a significantly higher body mass index (32.6 vs 25.5; P = .012), a higher d-dimer at the time of imaging (17.3 vs 1.8; P = .038), a higher average in hospital d-dimer (8.5 vs 2.0; P = .038), a greater distribution of patients with clot in the aortoiliac location (5 vs 1; P = .040), less prior use of any antiplatelet medication (21.4% vs 62.5%; P = .035), and a higher mortality rate (40.0% vs 8.0%; P = .041). Treatment of arterial thromboembolic disease in COVID-19 positive patients included open thromboembolectomy in six patients (40%), anticoagulation alone in four (26.7%), and five (33.3%) did not require or their overall illness severity precluded additional treatment.

Conclusions: Patients with SARS-CoV-2 are at risk for acute arterial thromboembolic complications despite a lack of conventional risk factors. A hyperinflammatory state may be responsible for this phenomenon with a preponderance for aortoiliac involvement. These findings provide an early characterization of arterial thromboembolic disease in SARS-CoV-2 patients.

Keywords: Hyperinflammatory; SARS-CoV-2; Thromboembolism.

MeSH terms

  • Acute Disease
  • Aged
  • Aged, 80 and over
  • Arterial Occlusive Diseases* / diagnosis
  • Arterial Occlusive Diseases* / etiology
  • Arterial Occlusive Diseases* / therapy
  • COVID-19 / complications*
  • Female
  • Hospitalization
  • Humans
  • Inflammation* / etiology
  • Male
  • Middle Aged
  • Retrospective Studies
  • Risk Factors
  • SARS-CoV-2*
  • Severity of Illness Index
  • Thromboembolism* / diagnosis
  • Thromboembolism* / etiology
  • Thromboembolism* / therapy
  • Thrombosis* / diagnosis
  • Thrombosis* / etiology
  • Thrombosis* / therapy