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Boston, MA
Dr. Goldhaber is associated with Brigham and Women’s Hospital, Harvard Medical School.
Correspondence to: Samuel Z. Goldhaber, MD, FCCP, Cardiovascular Division, Brigham and Women’s Hospital, Harvard Medical School, 75 Francis St, Boston, MA 02115; e-mail: sgoldhaber{at}partners.org
Pulmonary embolism (PE) encompasses a wide spectrum of illnesses, with diverse prognoses and management strategies. Some PEs, detected serendipitously by chest CT scanning, cause no apparent adverse symptoms or signs. They are anatomically tiny and have minimal clinical impact, at least in patients without concomitant proximal leg deep vein thrombosis. The heparin treatment is required as a "bridge" to warfarin treatment. In this situation, the major debate is about whether to hospitalize the patients for the traditional 5 to 7 days, to abbreviate the hospital stay by using low-molecular-weight heparin in lieu of continuous IV infusion of unfractionated heparin, or even to consider complete outpatient therapy1 2 with subsequent office follow-up. At the other end of the spectrum are patients who are critically ill and in cardiogenic shock. Their survival will depend on the rapid detection of the PE followed by implementation of the following emergency treatment plan: successful debulking of the clot, either with thrombolysis3 4 or embolectomy.5 6
These two divergent scenarios represent the extremes, not the every day "usual" PEs that confront those of us who commonly treat patients with this disease. Most patients with PE have mild symptoms and signs of cardiopulmonary distress but do not, at least initially, appear to have a life-threatening illness. They are often triaged to a stepdown unit rather than to an ICU. They usually maintain a normal systemic arterial pressure, although they often present for initial evaluation with tachycardia and anxiety. Most patients survive and improve clinically within a day or two. However, recurrent PE will unexpectedly strike some patients who appear to be on the path to recovery. Those who relapse will require an escalation of therapy, with emergently administered thrombolysis, catecholamine agents, cardiopulmonary resuscitation, or mechanical ventilation.
The group of patients presenting with PE of intermediate severity poses a challenge. How can we risk stratifying them appropriately at the time the PE is initially diagnosed? What predictive tools are available to assist us in our clinical assessment?
The medical history and physical examination are excellent starting points. Transient syncope or cyanosis portend a major PE with a complicated hospital course. Finding a left parasternal heave, an accentuated P2, a tricuspid regurgitation murmur, or distended neck veins in patients with newly diagnosed PE indicates the presence of right ventricular dysfunction. Simple bedside scoring systems of PE severity can help to predict which patients will develop major adverse events such as recurrent thromboembolism, hemorrhage, or death. In the Geneva Prognostic Index,7 the maximum number of points, based on clinical parameters, is 8. Those patient with ≥ 5 points had a > 50% likelihood of a major adverse clinical event. The index assigns cancer and hypotension 2 points each, with 1 point each assigned for heart failure, prior deep vein thrombosis, hypoxemia, or ultrasound-proven deep vein thrombosis. The Geneva Prognostic Index7 was used to identify low-risk patients with a score of 0 or 1 for participation in a trial of outpatient treatment of PE.2
The ECG may assist in risk stratification by revealing signs of right heart strain due to pulmonary hypertension from underlying PE.8 Traditional worrisome features are right bundle branch block, right axis deviation, and T-wave inversion in leads V1 to V4. A Qr pattern in lead V1 also has been described recently.9
Cardiac biomarkers, especially troponin levels, have emerged as the most promising tool for the risk stratification of patients with PE.10 The circulating troponin level indicates irreversible myocardial cell damage and is much more sensitive than creatine kinase (CK) or CK-MB levels. The release of cardiac troponin is predicated on acute right ventricular shear stress, with ensuing right ventricular microinjury11 and microinfarction. A dilated, overloaded right ventricle will increase right ventricular oxygen demand and diminish perfusion of the right coronary artery, even in the absence of atherosclerosis of the right coronary artery. The troponin release is often quantitatively small, far less than typically observed in an ST-segment elevation myocardial infarction. Nevertheless, a "troponin leak" correlates well with the presence of right ventricular dysfunction.12 13
Similar prognostic information can be obtained from echocardiography14 for both short-term outcomes15 and long-term outcomes.16 However, round-the-clock echocardiography is rarely available and may be plagued by technical difficulties in imaging the free wall of the right ventricle, particularly when attempted by less experienced operators in the middle of the night. In contrast, troponin assays are inexpensive, have a quick turnaround time, are well-standardized, and are immediately available at virtually all acute care hospitals.
In the current issue of CHEST (see page 1947), Pruszczyk et al, investigators from Warsaw, Poland, who have established a center for excellence in PE and are well-known for their expertise with echocardiographic assessment of PE patients, have focused their attention on cardiac troponin levels. They selected for their study PE patients in the middle of the clinical spectrum. All 64 patients presented with normal systemic arterial pressure. Their average heart rate was 100 beats/min. The right ventricle was dilated in most patients and, on average, was as large as the left ventricle. Half of the 64 patients in the cohort had elevations in troponin levels. Only about half of the patients with troponin elevations had an abnormally high CK–MB level, indicating how much more sensitive troponin assays are compared with CK–MB assays for detecting myocardial injury.
Of the eight patients (12.5%) who died during the index hospitalization, all had elevated troponin levels. Seven additional patients who survived nevertheless required an escalation of therapy with thrombolysis, including one patient who required therapy with vasopressor agents and cardiopulmonary resuscitation. Six of these seven patients also had elevated troponin levels. In contrast, all PE patients with normal troponin levels survived without complications from PE. A multivariate analysis showed that only elevated troponin levels predicted an adverse hospital course. Somewhat surprisingly, neither age nor the degree of right ventricular dilatation emerged as independent risk factors for a complicated hospital course. Patients with an elevated troponin level were 20 times more likely to die or to require an escalation of therapy due to a complicated hospitalization compared with patients with normal troponin levels.
Based on this study and the totality of evidence, we can now declare with confidence that cardiac troponin levels should be obtained in normotensive patients with acute PE to assist clinicians in risk stratification. Those patients with normal troponin levels can almost certainly be treated with anticoagulation therapy alone. If concern persists about the prognosis in individual patients, the prediction of a benign clinical course can be confirmed with echocardiography, showing normal or near-normal right ventricular function. Some patients with normal troponin levels may be appropriate for triage to a treatment strategy that reduces their length of hospital stay.
PE patients with elevated troponin levels should undergo further testing of right ventricular function with echocardiography. If the echocardiogram shows moderate or severe right ventricular dysfunction in the presence of an elevated troponin level, this may portend a lethal combination.17 These patients should be assessed to determine whether thrombolysis or embolectomy is a clinically appropriate strategy.
Finally, the article by Pruszczyk et al raises several important questions. First, what is the optimal role and timing of the serial measurement of troponin levels in patients with PE? Second, is an elevated troponin level actually more important prognostically than right ventricular dysfunction on an echocardiogram, or is it just equivalent? Third, will other biomarkers, such as brain natriuretic peptide, be more useful, equivalent, or complementary to cardiac troponin levels?
References
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