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Dr. van Beek is a Senior Clinical Lecturer in the Section of Academic Radiology, Royal Hallamshire Hospital.
Correspondence to: Edwin J.R. van Beek, Section of Academic Radiology, Royal Hallamshire Hospital, Glossop Rd, Sheffield S10 2JF; e-mail: e.vanbeek{at}sheffield.ac.uk
Despite the widespread use of thromboprophylaxis in high-risk situations, pulmonary embolism (PE) remains one of the most common life-threatening disorders. In fact, the prevalence of detected postmortem PE has not diminished during the last 3 decades.1 It has been estimated that, despite adequate therapy with heparin and oral anticoagulants, between 0.5% and 1.0% of patients (or up to 100,000 individuals per year in the United States) will develop chronic thromboembolic pulmonary hypertension (CTEPH) following a (first) pulmonary embolic event.2 3 The exact cause for this is unknown, although factors such as adequacy of clot resolution, the influence of inherited thrombophilia, or disorders in the fibrinolytic system all may play roles. Only a small minority of these patients may be identified at the onset of the condition, and adaptation of the therapeutic approach may help avoid the development of CTEPH in these patients.
Generally, the prognosis of patients with pulmonary hypertension is inversely related to the degree of pulmonary hypertension. Fewer than 10% of patients with pulmonary artery pressures > 50 mm Hg will survive 5 years.4 Currently, treatment for CTEPH may consist of (long-term) anticoagulant therapy and symptomatic relief of pulmonary hypertension using diuretics and vasodilators. Newer drug therapies, such as nitric oxide inhalation therapy and continuous infusion with prostaglandins, have shown promising results, and many patients will improve or remain stable for a prolonged period of time while receiving therapy.5 Nevertheless, for those patients who show progression of symptoms, pulmonary thromboendarterectomy, which was developed by a group at the University of California at San Diego, is regarded as the definitive therapeutic option.6 The technique is now used in many centers throughout the world. It was shown that the procedure led to an immediate and sustained reduction in pulmonary pressures and pulmonary vascular resistance values to normal levels.7
In this issue of CHEST, Menzel et al (see page 897) present the results of measurements using right heart catheterization and echocardiography in 39 patients before and after undergoing thromboendarterectomy. They demonstrate that the pulmonary vascular obstruction has a direct impact on both right and left ventricular function. This effect is a combination of flow-related, geometry-related, and complex humoral factors. Following pulmonary thromboendarterectomy, the flow through the pulmonary arterial bed increases and right and left ventricular functions return to normal values. The effects on patients were obvious within 2 weeks of surgery and further prove the beneficial immediate effect of thromboendarterectomy. Interestingly, most patients could have their parameters assessed by transthoracic, rather than transesophageal, echocardiography. This technique is almost universally available as a bedside method, albeit that it is operator-dependent. Nevertheless, this technique allows us to study the direct therapeutic effects on cardiac function in patients with CTEPH more closely than before. Furthermore, its noninvasive nature makes it a very useful tool for repeated studies in patients with CTEPH (and probably any other type of pulmonary hypertension), for whom the current standard is often invasive pressure assessment using right heart catheterization. This would also be beneficial for the monitoring of treatment effects in the evaluation of new therapies.
Although the study shows the direct pathophysiologic benefit of thromboendarterectomy for patients with CTEPH, one could take this one step further and extrapolate to patients with acute PE. In a massive PE, similar changes in right ventricular dilatation, abnormal cardiac geometry, and diminished cardiac index have been demonstrated.8 In patients with massive PEs (ie, those with hypotension and circulatory collapse), there is a general consensus that thrombolysis is the therapy of choice and that echocardiography may be used to monitor the improvement of cardiac function.8 However, there is a subgroup of patients with acute PEs who have normal hemodynamic parameters but exhibit echocardiographic evidence of right ventricular dysfunction. These patients seem to have a worse prognosis than patients without echocardiographic abnormalities.9 Furthermore, patients who present with acute PEs and pulmonary artery pressures > 50 mm Hg are more likely to suffer from persistent pulmonary hypertension at 1 year of follow-up.10 Hence, it seems likely that echocardiography may have a significant impact on the therapeutic management of subgroups of patients with acute PEs. There is limited evidence in the literature that echocardiography may have a role to play in the management of PE.8 9 10 However, there is an urgent need for prospective studies that assess the role of echocardiography in the identification of patients with PE who may benefit from thrombolytic therapy rather than heparin therapy, despite the absence of systemic hypotension or shock.
In order to allow the assessment of pathophysiology and the effects of treatment regime in patients with both chronic and acute PE, studies of similar design to that presented by Menzel et al are required. Furthermore, the standardization of measurement performed by echocardiography is also needed to reduce the observer variability. This structured approach would also allow a decision to be made on whether all patients with suspected acute PEs should undergo echocardiography in the diagnostic workup to identify those individuals who may benefit from more aggressive therapeutic regimens than heparin alone.
References
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