Demographic, clinical, and echocardiographic factors associated with residual perfusion defects beyond six months after pulmonary embolism.

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.

Informations de copyright

Copyright © 2023 The Authors. Published by Elsevier Ltd.. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: F. Klok has received research support from Bayer, Bristol-Myers Squibb, Actelion, Boston Scientific, Leo Pharma, FarmX, The Netherlands Organisation for Health Research and Development, The Dutch Thrombosis Association, The Dutch Heart Foundation and the Horizon Europe program, all outside this work and paid to his institution. K.Stavem reports consulting fees from MSD and UCB unrelated to this study. W.Ghanima reports fees for participation in Advisory board from Amgen, Novartis, Pfizer, Principia Biopharma Inc- a Sanofi Company, Sanofi, SOBI, Grifols, UCB, Argenx, Cellphire, and lecture honoraria from Amgen, Novartis, Pfizer, Bristol Myers Squibb, SOBI, Grifols, Sanofi and Bayer. W.Ghanima reports research grants from Bayer, BMS/Pfizer and UCB. A.Dhayyat, D.Rashid, J.Gleditsch, K.Steine M.Tavoly, S.Haukeland-Parker, and Ø.Jervan declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.