Key result
Unprovoked PE and greater thrombotic burden linked to ~125% higher risk of residual perfusion defects.
Why the study?
Residual perfusion defects are common after pulmonary embolism, but their prevalence and associated demographic, clinical, and echocardiographic factors needed evaluation.
Cohort (n=286)
Residual perfusion defects are common (25.2%) 6-72 months after pulmonary embolism and are associated with greater initial thrombotic burden, unprovoked PE, and specific echocardiographic findings.
Answers are grounded in this paper and cite their sources.
May prompt closer monitoring after unprovoked PE; leaves open prognostic impact and need for prospective trials.
BACKGROUND: Residual perfusion defects (RPD) after pulmonary embolism (PE) are common. PRIMARY AIM: This study aimed to determine the prevalence of RPD in a cohort diagnosed with PE 6-72 months earlier, and to determine demographic, clinical, and echocardiographic variables associated with RPD. METHODS: Patients aged 18-75 years with prior PE, confirmed by computed tomography pulmonary angiography 6-72 months earlier, were included. Participants (N = 286) completed a diagnostic work-up consisting of transthoracic echocardiography and ventilation/perfusion scintigraphy. Demographic, clinical, and echocardiographic characteristics between participants with RPD and those without RPD were explored in univariate analyses using t-test or Mann-Whitney U test. Multiple logistic regression analysis was used to assess the association between selected variables and RPD. RESULTS: RPD were detected in 72/286 patients (25.2 %, 95 % CI:20.5 %-30.5 %). Greater tricuspid annular plane systolic excursion (TAPSE) (adjusted odds ratio (aOR) 1.10, 95 % CI:1.00-1.21, p = 0.048) at echocardiographic follow-up, greater thrombotic burden at diagnosis, as assessed by mean bilateral proximal extension of the clot (MBPEC) score 3-4 (aOR 2.08, 95 % CI:1.06-4.06, p = 0.032), and unprovoked PE (aOR 2.25, 95 % CI:1.13-4.48, p = 0.021) were independently associated with increased risk of RPD, whereas increased pulmonary artery acceleration time was associated with a lower risk of RPD (aOR 0.72, 95 % CI:0.62-0.83, p < 0.001, per 10 ms). Dyspnoea was not associated with RPD. CONCLUSION: RPD were common after PE. Reduced pulmonary artery acceleration time and greater TAPSE on echocardiography at follow-up, greater thrombotic burden at diagnosis, and unprovoked PE were associated with RPD.
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Jervan et al. (2023) conducted a cohort in Pulmonary embolism (n=286). Unprovoked PE (aOR 2.25; 95% CI 1.13-4.48) and greater thrombotic burden independently increased the risk of residual perfusion defects, which were detected in 25.2% of patients.
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