Ventilation/Perfusion Scintigraphy for the Diagnosis of Pulmonary Embolism and Chronic Thromboembolic Pulmonary Hypertension

2021 ◽  
pp. 89-105
Author(s):  
Yodphat Krausz ◽  
Mahmood Zidan ◽  
Simona Ben-Haim
2010 ◽  
Vol 125 (5) ◽  
pp. e202-e205 ◽  
Author(s):  
Sulaiman Surie ◽  
Nadine S. Gibson ◽  
Victor E.A. Gerdes ◽  
Berto J. Bouma ◽  
Berthe L.F. van Eck – Smit ◽  
...  

2017 ◽  
Vol 49 (5) ◽  
pp. 1601980 ◽  
Author(s):  
Raffaele Pesavento ◽  
Lucia Filippi ◽  
Antonio Palla ◽  
Adriana Visonà ◽  
Carlo Bova ◽  
...  

The impact of residual pulmonary obstruction on the outcome of patients with pulmonary embolism is uncertain.We recruited 647 consecutive symptomatic patients with a first episode of pulmonary embolism, with or without concomitant deep venous thrombosis. They received conventional anticoagulation, were assessed for residual pulmonary obstruction through perfusion lung scanning after 6 months and then were followed up for up to 3 years. Recurrent venous thromboembolism and chronic thromboembolic pulmonary hypertension were assessed according to widely accepted criteria.Residual pulmonary obstruction was detected in 324 patients (50.1%, 95% CI 46.2–54.0%). Patients with residual pulmonary obstruction were more likely to be older and to have an unprovoked episode. After a 3-year follow-up, recurrent venous thromboembolism and/or chronic thromboembolic pulmonary hypertension developed in 34 out of the 324 patients (10.5%) with residual pulmonary obstruction and in 15 out of the 323 patients (4.6%) without residual pulmonary obstruction, leading to an adjusted hazard ratio of 2.26 (95% CI 1.23–4.16).Residual pulmonary obstruction, as detected with perfusion lung scanning at 6 months after a first episode of pulmonary embolism, is an independent predictor of recurrent venous thromboembolism and/or chronic thromboembolic pulmonary hypertension.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
E Klok ◽  
G.J.A.M Boon ◽  
Y.M Ende-Verhaar ◽  
R Bavalia ◽  
M Delcroix ◽  
...  

Abstract Background The current diagnostic delay of chronic thromboembolic pulmonary hypertension (CTEPH) after acute pulmonary embolism (PE) is unacceptably long exceeding 1 year, causing loss of quality-adjusted life years and excess mortality. Validated screening strategies to diagnose CTEPH earlier are lacking. Importantly, performing echocardiography in all PE patients for this purpose has a low diagnostic yield, is associated with overdiagnosis and is not cost-effective. Moreover, expertise in performing high-quality PH-dedicated echocardiograms may not be available outside expert centers. Aim To validate a simple screening strategy aimed at identifying CTEPH early in the course after acute PE, avoiding echocardiography if possible (Figure 1). Methods In this prospective, international, multicenter management study, consecutive PE survivors were managed according to the predefined algorithm starting three months after acute PE. All were followed for a total period of two years. The study protocol was approved by all local IRBs and all patients provided informed consent. Results 424 patients were included across three European countries (Table 1). Following the algorithm, CTEPH was considered excluded in 343 (81%) patients based on clinical pre-test probability assessment by the “CTEPH prediction score”, evaluation of symptoms and application of the “CTEPH rule-out criteria” (Figure 1); only 19% was subjected to echocardiography. Only 1 of 343 patients managed without echocardiography was diagnosed with CTEPH, 10 months after initial PE, for a failure rate of 0.29% (95% CI 0–1.6%). Overall, 13 patients were diagnosed with CTEPH (incidence 3.1%), of whom 10 within 4 months after PE diagnosis. Conclusions The algorithm accurately ruled out CTEPH and avoided echocardiography in 81% of patients. The vast majority of CTEPH cases were identified early in the course of acute PE which is a considerable improvement compared to current clinical practice with an economic use of healthcare resources. Figure 1. Study flowchart Funding Acknowledgement Type of funding source: Foundation. Main funding source(s): This study was supported by unrestricted grants from Bayer/Merck Sharp & Dohme (MSD) and Actelion Pharmaceuticals Ltd. F.A. Klok and G.J.A.M. Boon were supported by the Dutch Heart Foundation (2017T064).


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