Hemodynamic and Clinical Predictors of Thrombolysis in Post-COVID Venous Thromboembolism: A Retrospective Cohort Study

Abstract

Objectives: Post-acute venous thromboembolism (VTE) is a well-recognized complication of COVID-19, driven by persistent endothelial dysfunction and thromboinflammation. Identifying simple clinical predictors of VTE may optimize therapy and limit adverse outcomes. We propose a pragmatic risk-stratification approach, based on clinical and echocardiographic parameters. Methods: We conducted a retrospective cohort study in a Romanian tertiary hospital (March 2020-April 2022) in 54 adults with laboratory-confirmed COVID-19 and imaging-confirmed VTE. Demographics, comorbidities, laboratory markers, and echocardiographic variables-particularly tricuspid annular plane systolic excursion (TAPSE), peripheral oxygen saturation (SpO₂), and left-ventricular end-diastolic diameter (LVEDD)-were collected. The primary outcome was the percentage of patients receiving systemic thrombolysis. Statistical analyses included Mann-Whitney U tests, chi-square, Spearman correlations, and multivariable logistic regression. Results: The mean age was 61.2 ± 14.7 years, and 63% were men. Eleven patients (20.4%) underwent thrombolysis. Compared with conservatively managed patients, those receiving thrombolysis had lower TAPSE (13.0 vs. 20.8 mm), lower SpO₂ (90.1 vs. 97.0%), and smaller LVEDD (24.4 vs. 46.1 mm); all differences were statistically significant. Each 1 mm decrease in TAPSE and 1% decrease in SpO₂ increased the likelihood of thrombolysis (adjusted odds ratios 1.58 and 1.34, respectively). Inflammatory markers and right-ventricular diameter were not associated with treatment. Conclusions: Reduced TAPSE, lower SpO₂, and decreased LVEDD identify post-COVID VTE patients at elevated risk of hemodynamic compromise requiring thrombolysis. A point-of-care assessment incorporating these variables may improve early risk stratification and guide therapeutic decisions.

Keywords: COVID-19; SpO2; TAPSE; VTE; echocardiography; post-COVID syndrome; pulmonary embolism; thrombolysis.

Figure 1

Pathophysiologic mechanisms contributing to post-COVID venous thromboembolism. Legend: IL-6—interleukin-6; TNF-α—tumor necrosis factor-alpha; NETs—neutrophil extracellular trap; “↑”—increase; “→”—result.

Figure 2

TAPSE by thrombolysis group. Legend: TAPSE—tricuspid annular plane systolic excursion.

Figure 3

Oxygen saturation by thrombolysis group. Legend: SpO₂—peripheral oxygen saturation.

Figure 4

LV size by thrombolysis group. Legend: LVEDD—left ventricular end-diastolic diameter; diamonds represent outliers, defined as values outside 1.5 times the interquartile range (IQR).

Figure 5

Integrated molecular and hemodynamic cascade in post-COVID venous thromboembolism leading to thrombolytic therapy. Legend: SARS-CoV-2—severe acute respiratory syndrome coronavirus 2; IL-6—interleukin-6; TNF-α—tumor necrosis factor-alpha; NETs—neutrophil extracellular traps; PAI-1—plasminogen activator inhibitor-1; PE—pulmonary embolism; PVR—pulmonary vascular resistance; RV—right ventricle; TAPSE—tricuspid annular plane systolic excursion; LV—left ventricle; LVEDD—left ventricle end-diastolic diameter; SV—stroke volume; SpO₂—peripheral oxygen saturation; “→”—result; “↑”—increase; “↓”—decrease; color code: immune system—red, vascular system—blue, cardiac system—green.