Regular ArticleEchocardiographic assessment of pulmonary arterial pressure in the follow-up of patients with pulmonary embolism
Introduction
Doppler echocardiography remains the most commonly used and easily accessible tool for population-based screening of pulmonary hypertension. Chronic thromboembolic pulmonary hypertension (CTEPH) is one of the leading causes of severe pulmonary hypertension and can be devastating for those individuals who are affected [1]. The disorder is the consequence of the incomplete resolution of the pulmonary vascular obstruction associated with acute pulmonary embolism (PE). Pulmonary thromboembolism or in situ thrombosis in CTEPH may be triggered or aggravated by abnormalities in either the clotting cascade, endothelial cells, or platelets, all of which interact in the coagulation process [2]. Indeed, growing evidence suggests that the pathophysiology of this condition is complex and only partly elucidated. Platelet abnormalities and biochemical features of a procoagulant environment within the pulmonary vessels suggest a role for local thrombosis in initiating the disease. In most cases, it remains unclear whether thrombosis and platelet dysfunction are a cause or consequence of the disease. In addition, inflammatory infiltrates can be usually detected in pulmonary endarterectomy specimens. There is also evidence suggesting The obstructive lesions observed in the distal pulmonary arteries of non-obstructed areas (virtually identical to those observed in PAH) have been suggested to be related to a variety of factors, such as shear stress, pressure, inflammation, and the release of cytokines and vasculotrophic mediators [2]. Despite this pathophysiological complexity, it is noteworthy that CTEPH remains the only cause of severe pulmonary hypertension which is potentially surgically curable without the need to resort to lung transplantation [3]. Although a timely and accurate diagnosis of CTEPH is a fundamental prerequisite for targeted, effective treatment [4], the condition still remains difficult to predict.
CTEPH is believed to complicate 3.8% of acute pulmonary embolic events [5], but incidence figures might be underestimated because some cases are not apparent clinically. Substantial limitations of current screening strategies are confirmed by a recent study showing that 91% of patients submitted for screening have a negative test result [6]. To devise an effective screening strategy for avoiding underdiagnosis [7], the definition of a high-risk group and the development of simple and reliable diagnostic screening test are necessary.
The aim of this study was to identify a group of subjects at high-risk of having PAP > 50 mm Hg on echocardiography and to select cases with PE in need of a strict follow-up protocol.
Section snippets
Study Design
We examined a total of 744 consecutive patients with acute symptomatic pulmonary embolism who were enrolled in a Spanish multicenter study designed to compare the efficacy and safety of early discharge versus standard hospitalization [8], [9]. The recruitment phase took place in seven hospitals between January 2003 and December 2004. The study complied with the tenets of the Declaration of Helsinki and was approved by ethics committees at all sites. All participants gave written informed
Results
A total of 759 patients with symptomatic PE, newly diagnosed between January 2003 and December 2004, were eligible for the study. Of them, 15 (2%) were excluded because of missing follow-up data. The median period of follow-up was 14 months (range, 6–83 months). Patients who were lost to follow-up did not differ from those who remained in the study. The final cohort consisted of 744 patients (395 females, mean age: 69.0 ± 16.0 years; 349 males, mean age: 65.5 ± 15.0 years).
During follow-up, there were
Discussion
In this multicenter study of patients with PE, the incidence of an estimated pulmonary artery systolic pressure > 50 mm Hg at 36 months was 8.3% and showed a significant association with a severe index thromboembolic episode. Unfortunately, a major caveat of this study is the lack of data on the final diagnosis of CTEPH, as well as on the persistence of multiple segmental or lobar perfusion defects in sequential lung scans or angiographic evidence of vascular narrowing or occlusion at follow-up.
Conflict of interest
There are not any conflict of interest.
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Prevalence and predictors of chronic thromboembolic pulmonary hypertension following severe forms of acute pulmonary embolism
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2018, Heart Failure ClinicsThe economic burden of incident venous thromboembolism in the United States: A review of estimated attributable healthcare costs
2016, Thrombosis ResearchCitation Excerpt :After subtracting pre-index treatment costs, the incremental cost of treating PTS was roughly $7800. CTEPH, a condition requiring lifelong anticoagulation [44–46], develops in roughly 1% [47–51], or 4% [52,53] of survivors of PE. Patients who develop CTEPH are much more expensive to treat than other PE patients, with average monthly expenditures of $5500 and $600, respectively [54].
External validation of a simple non-invasive algorithm to rule out chronic thromboembolic pulmonary hypertension after acute pulmonary embolism
2015, Thrombosis ResearchCitation Excerpt :The resulting increased pulmonary vascular resistance ultimately leads, if left untreated, to progressive pulmonary hypertension and death [2,3]. The exact prevalence of CTEPH in patients who have suffered acute PE is debated: most studies report cumulative rates of 0.57% to 4.0% within the first 2 years after PE diagnosis, depending on patient selection and diagnostic criteria [4–8]. Screening programs for CTEPH after an episode of acute PE are still at a preliminary stage, and their cost effectiveness remains a subject of debate.
Echocardiographic evolution of pulmonary artery pressure after acute pulmonary embolism. Results from IPER registry
2014, Thrombosis ResearchCitation Excerpt :In spite of the low accuracy of echo-Doppler to correctly measure the degree of PH [4,5], echocardiography remains to date the most utilized and often the only method to investigate, both in the acute phase and over time, the course of pulmonary artery systolic pressure (PAsP). Several studies considered the echocardiographic follow-up at least 6 months after an episode of acute PE [6–14]. Some of them [13,14] correlated the value of echocardiographycally derived PAsP in the acute phase with the persistence of PH 12 or 16 months later.