Journal of the American Society of Echocardiography
Clinical InvestigationsRisk Assessment with Imaging in Acute Pulmonary EmbolismA Multimodality Imaging Approach to Defining Risk in Patients With Acute Pulmonary Embolism
Introduction
Acute pulmonary embolism (PE) is the third most common cause of cardiovascular death in the United States, following myocardial infarction and stroke.1,2 Mortality rates in patients treated for PE may be as high as 20%, although a significant proportion of deaths are related to associated conditions.3,4 Nearly half of surviving patients with a PE have functional and exercise limitations 1 year later.3 Despite the high burden of both short-term and long-term morbidity and mortality, acute PE is most often treated with a conservative watch-and-wait strategy in which unfractionated heparin is given first and escalation to more aggressive therapies is only done if there is clinical deterioration. Unfortunately, once clinical deterioration occurs, prognosis worsens. In addition to the acute risks from PE, the chances of having chronic dyspnea5 or developing chronic thromboembolic pulmonary hypertension (2%–4% risk)6 may increase if the initial thrombus is incompletely resolved.
Classification schemes for acute PE may be confusing. For example, acute PEs are often categorized as “massive” or “submassive” and this categorization is frequently used for decisions regarding therapies. This terminology is misleading as the terms “massive” and “submassive” refer to hemodynamic measures such as hypotension and tachycardia, rather than the actual size of the thrombus or the extent of hypoperfused lung segments.3 Importantly, a patient can have a very large thrombus burden with normal heart rate, oxygenation, and blood pressure, or conversely, they can have a relatively small thrombus burden with tachycardia and hypotension from other causes. Clearly, other indicators of severity and risk that are more directly related to the embolism are needed. In patients with PE, the term RV “strain” is commonly used in a nonprecise fashion, to connote RV enlargement or dysfunction. This has typically not been defined quantitatively, and hence is highly subjective. Quantitative measures of myocardial strain measured with speckle-tracking echocardiography are increasingly being applied in a variety of disease states, and these measures have in most cases proven to be superior to other methods of assessing chamber performance.7 Measurement of RV free wall strain (RVFWS) or RV global longitudinal strain (RVGLS) are beginning to take hold as a way to quantify RV systolic function.7, 8, 9
Several of the features in the widely used simplified Pulmonary Embolism Severity Index (PESI) are not modifiable with therapy (age, cancer, chronic cardiopulmonary disease).10 When considering interventional clot reduction strategies, a risk score that directly reflects the amount of clot and the hemodynamic consequences of the clot is likely to be more effective in determining the risk-to-benefit ratio. As the potential benefits from newer catheter-directed therapies continue to improve and the risks decline, the need for better risk scores should keep pace.11 These scores should ideally include (1) the amount of thrombus that is present and the degree of obstruction to blood flow through the lungs, (2) the direct effects of the PE on RV function and hemodynamics, and (3) biomarkers that reflect RV overload and/or injury. Our goal was to develop a more holistic, less subjective model for describing the severity of PE and the likelihood of adverse outcomes. Use of such a tool, or something similar, could allow early institution of advanced therapies such as catheter-directed thrombolytic therapy or catheter or surgical embolectomy or fragmentation.
Section snippets
Design
This is a retrospective study involving all patients diagnosed with acute PE who were evaluated by our PE response team (PERT) at the Medical University of South Carolina from March 2015 to January 2018. The study was approved by the institutional review board for human research. Consent was waived due to the retrospective nature of the study. Inclusion criteria were patients who were evaluated by the PERT, had an acute PE on computed tomography (CT) pulmonary angiography (CTPA), and had a
Results
Out of 151 PERT activations, 150 patients were included in the study (one was excluded due to lack of an echo within 48 hours). Among these, 79 (52.7%) were female and 93 (62%) were Caucasian; the average age of our population was 62 ± 16.9 years. The mean systolic blood pressure was 123 ± 24 mm Hg, heart rate was 98 ± 19 bpm, and oxygen saturation was 94.9% ± 5%. Fifty-six of the patients (37%) were referred from outside hospitals. The patient demographics are shown in Table 1.
Of the 150
Discussion
We propose that current classification schemes for determining risk and thus therapeutic approaches in PE are not optimal due to subjectivity and lack of specificity for the thrombus burden or the direct hemodynamic effects of the PE. In this retrospective study of 150 patients presenting with acute PE that were evaluated by a PERT, we assessed clinical, biochemical, and quantitative imaging parameters (TTE and CTPA) for association with outcomes including all-cause mortality, use of
Conclusion
A combination of serum TnI, BNP, RVFWS, RV S’, and TAPSE/RVSP from echocardiography and thrombus load and RV/LV ratio from CT appears to provide good early risk stratification of patients with acute PE. This combination may help to identify patients that could benefit from more aggressive treatment strategies since the parameters in the model directly reflect the effects of the thromboembolism and these parameters can be modified by treatment. The high mortality rate in our cohort (9%) shows
Review Statement
Given his role as JASE Associate Editor, Sheldon E. Litwin, MD, had no involvement in the peer review of this article and has no access to information regarding its peer review. Full responsibility for the editorial process for this article was delegated to David M. Dudzinski, MD.
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Cited by (0)
Conflicts of Interest: None.
David M. Dudzinski, MD, served as guest editor for this report.