Elsevier

Thrombosis Research

Volume 127, Issue 4, April 2011, Pages 303-308
Thrombosis Research

Regular Article
Echocardiographic assessment of pulmonary arterial pressure in the follow-up of patients with pulmonary embolism

https://doi.org/10.1016/j.thromres.2010.12.010Get rights and content

Abstract

Background

Echocardiography remains a clinically useful screening test for chronic thromboembolic pulmonary hypertension (CTEPH) in patients with a history of pulmonary embolism (PE). To devise an effective screening strategy, the definition of a high-risk group is necessary.

Methods

We examined a total of 744 patients with acute symptomatic pulmonary embolism (PE) who were enrolled in a Spanish multicenter study. Patients were monitored every 6 months during the first two years, and then once a year thereafter. Transthoracic echocardiography was used to screen patients with a clinical suspicion of CTEPH during follow-up. Pulmonary arterial hypertension was defined as an estimated pulmonary artery systolic pressure (PAP) > 50 mm Hg. The index thromboembolic episode was considered severe if: (a) the patient was immobilized for medical reasons; or (b) systolic blood pressure was less than 90 mm Hg; or (c) troponin T values were above the reference range.

Results

The incidence of PAP > 50 mm Hg at 36 months was 8.3% (95% confidence interval = 4.6%–14.5%). Statistical analysis showed a highly significant association between a severe index thromboembolic episode and the subsequent detection of PAP > 50 mm Hg on echocardiography, with high positive likelihood ratio (2.40) and negative predictive value (> 0.97).

Conclusions

Patients with a severe index thromboembolic episode would constitute a high-risk group for the development of CTEPH. This group of patients should be subjected to a strict follow-up protocol.

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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