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EDUCATION EXHIBIT |
1 Department of Pulmonary Medicine
2 Department of Radiology, University of Texas M. D. Anderson Cancer Center, Houston, Texas
Acute PE is a common cardiopulmonary condition with a prevalence that exceeds 1 per 1000 and a mortality rate of 58% for hemodynamically unstable patients and 15% for those who are hemodynamically stable (1). Death is believed to be secondary to a recurrent PE, and thus both hemodynamically stable and unstable patients are treated. Currently, we treat hemodynamically stable patients with a course of low-molecular-weight heparin followed by oral vitamin K antagonist as secondary prophylaxis, decreasing PE-related mortality rates to 1.5%–7% (2). Although we lack adequate controlled studies, the prevalent general consensus is that treatment of acute PE associated with hemodynamic shock (defined as a systolic blood pressure < 90 mm Hg and signs of end-organ hypoperfusion) should include thrombolytic therapy or mechanical modalities such as catheter-based or surgical embolectomy, with the goal of emergently reducing RV afterload. Thrombolysis has been shown to acutely decrease pulmonary vascular resistance and thereby improve RV function and restore hemodynamic parameters (3,4).
The excellent review by Ghaye et al (5) describes the ability of CT angiography to help assess RV dysfunction. The authors summarize the capability of CT angiography for determining cardiac measurements, morphology, and pulmonary clot load and vessel diameter. The authors establish the utility of CT angiography and compare it to established echocardiographic techniques for describing RV dysfunction in acute PE. To establish the impact of the use of echocardiography and/or CT angiography for evaluating RV dysfunction in acute PE, one has to answer two questions. First, can we use the assessment of RV dysfunction by imaging modalities for risk stratification of patients with acute PE? Second, will the use of thrombolysis guided by the presence of RV dysfunction have an impact on clinical outcome?
A recent review analyzed the findings of seven studies that assessed the prognostic value of echocardiography in acute PE. The conclusion was that there is at least a twofold increased risk of PE-related mortality in patients with RV dysfunction, with a prevalence of 40%–70% (2). In a subsequent study, 1,035 patients underwent echocardiographic evaluation within 1 hour of a diagnosis of PE. The 30-day survival rate in patients with RV hypokinesis was 83.7% compared with 90.6% in patients with normal RV function (P < .001) (6). The current review of Ghaye et al (5) describes several studies on the prognostic value of RV dysfunction as determined with CT angiography in acute PE. A very practical measurement is the ratio between RV diameter and LV diameter (RVd/LVd) on a four-chamber view. An RVd/LVd greater than 0.9 was predictive of PE-related adverse events and mortality (7,8). Thus, assessment of RV dysfunction with CT angiography or with echocardiography can permit risk stratification of patients with acute PE.
Given that RV dysfunction is predictive of increased mortality and that thrombolytic therapy decreases pulmonary vascular resistance and improves RV function, it would be logical to think that thrombolytic therapy should be used in patients with acute PE and documented RV dysfunction regardless of the presence of shock; however, no prospective randomized case-control study has addressed this hypothesis yet, to our knowledge, and the subject remains controversial in the literature. Clinical trials and case series have analyzed the use of thrombolytics in sub-massive PE. Konstantinides et al (9) randomized 256 patients to receive unfractionated heparin plus placebo or heparin plus alteplase, a form of thrombolytic therapy. The prevalence of the primary end point (a combination of in-hospital death and clinical deterioration requiring escalation of treatment) was significantly lower in the heparin plus alteplase group (P = .006). On the other hand, a recent meta-analysis found no evidence of a benefit from thrombolytic therapy compared with heparin for the initial treatment of unselected patients with acute PE (10).
A final point is choosing between echocardiography and CT. RV dysfunction detected with both modalities has proved to be predictive of higher morbidity and mortality; however, as no study has compared both techniques using this outcome as an end point, to our knowledge, other factors should dictate our choice. The most important is that only CT angiography is diagnostic and predictive, as it can demonstrate the presence of clot, the degree of clot burden in the PAs, and the relative size of the RV in one study. Many clinicians may be uncomfortable prescribing thrombolysis or anticoagulation to patients without confirming the actual presence of venous thrombi in the peripheral or central circulation. Also, CT angiography allows us to detect other lesions in the thorax that may explain the patient’s presenting symptoms. Echocardiography has the advantages that it does not need contrast agents, can be performed at the bedside, allows a better estimate of PA pressures, and may point to other cardiac structural or functional abnormalities to explain the patient’s symptoms. A final consideration is accessibility, as echocardiography is operator dependent and a qualified practitioner may not be available, whereas CT is available around the clock in many hospitals.
In conclusion, CT assessment of RV dysfunction is valid as a predictive tool and perhaps will be useful in the future to stratify high-risk patients, but the clinical utility of this selection will depend on the development of proved therapeutic strategies with an impact on morbidity and mortality.
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