Anticoagulants for Aortic Debris

abstract & commentary

Synopsis: More severe aortic atheroma are associated with high mortality and embolic events, and anticoagulant therapy is associated with a better outcome than antiplatelet therapy in such patients.

Source: Ferrari E, et al. J Am Coll Cardiol 1999; 33:1317-1322.

Aortic atherosclerosis is known to be associated with higher incidences of systemic emboli, but the prognostic value of specific atheroma characteristics and appropriate treatment are not well defined. Thus, Ferrari and colleagues from Nice, France, performed a prospective observational study of patients referred for transesophageal echocardiography (TEE) in whom aortic atheroma were found. Follow-up averaged 22 months, during which time treatment was at the discretion of the patients’ physicians. Independent observers identified aortic atheroma in 139 of 1116 TEEs (12%), of which 10 were lost to follow-up, resulting in a study population of 129 patients. Among those referred for embolic events or stroke, atheroma were found in about 25% and if no other etiology for the embolic event was found, about 50% had atheroma. Atheroma were classified as: grade I—1.0-3.9 mm thick; grade II— more than 4.0 mm thick; and grade III—mobile plaque (aortic debris). Of note, all but one of the plaques with a mobile component were greater than 4 mm thick. About half the patients were treated with oral antiplatelet drugs and half with oral anticoagulants (none received both). The primary end-point of embolic event or death occurred in 23% of the patients and was directly related to the severity of atheroma. The highest mortality was observed in those with debris (24%). Patients with grade II-III atheromata had more events when treated with antiplatelets vs. anticoagulants (relative risk = 5.9). Treatment did not affect outcome in grade I patients. Ferrari et al conclude that more severe aortic atheroma are associated with high mortality and embolic events, and that anticoagulant therapy is associated with a better outcome than antiplatelet therapy in such patients.

Comment by Michael H. Crawford, MD

TEE is frequently ordered to "rule out embolic source" even though this is not a reimbursable indication by the Health Care Financing Administration (HCFA). However, many such patients studied have aortic atheroma. This study confirms that such atheroma, especially if more severe, are a likely cause of embolic events and suggests that anticoagulant therapy is superior to antiplatelet therapy. Even though this was not a randomized treatment trial, the data for oral anticoagulation therapy are persuasive. The patients on oral anticoagulants more frequently had atrial fibrillation and left ventricular dysfunction, which should have made their prognosis worse. However, we do not know how many very sick patients were not put on anticoagulants and contributed to the event rate of the antiplatelet group. On the other hand, most of the patients treated with antiplatelet agents had mild atheroma.

Another interesting aspect of this observational study was that the majority of events were death vs. emboli (17 vs 12). This suggests that aortic atheroma are a marker for severe vascular disease that frequently involves the coronary and cerebral vasculature. Other reports have suggested benefits for such patients of oral anticoagulation therapy. Thus, it may be that patients with advanced generalized atherosclerosis do better with anticoagulants vs. antiplatelet drugs.

The major limitation of this study is that the patients had some event that occasioned a TEE. Thus, the results are only applicable to such patients and do not suggest that more widespread use of TEE is justified. In fact, one could argue from these data that all patients with embolic events should be treated with anticoagulants, at least for three months. Perhaps HCFA is correct and endocardiography is not indicated for embolic events unless other clinical information supports a cardiac etiology. These data and others would suggest that if an echocardiogram is considered appropriate, it should be a TEE, since many of the potential cardiac etiologies for embolic events are best identified by TEE (e.g., atrial septal aneurysms, aortic atheroma, left atrial thrombi). On the other hand, most cardiac etiologies for systemic emboli would be treated with anticoagulants anyway, so the debate will go on.

I can’t help remembering a 40-year-old woman referred for an echocardiogram for a stroke. I scoffed to my fellow that this would be a normal (read, unnecessary) study. The patient had a left atrial myxoma, so I asked the internist why he ordered the echo. He said because the patient had no risk factors for stroke and he suspected something unusual. Again, there is no substitute for astute clinical judgment. It’s too bad the HCFA doesn’t think we have any of this.

Severe aortic atherosclerosis is best managed by:

a. watchful waiting.

b. risk factor control.

c. aspirin.

d. warfarin.