Should this patient have an echocardiogram?
This woman has had a cortical infarction, which is usually due to thromboembolism. The most likely sources of emboli are cardiac diseases or proximal arterial lesions such as atherosclerotic disease or an arterial dissection. Because her vascular evaluation does not show any severe disease of major intracranial or extracranial arteries, the likelihood of a cardiac source for stroke increases.
Despite the absence of an abnormality on the electrocardiogram and the absence of cardiac symptoms, an echocardiogram remains an important component of her evaluation. Transesophageal echocardiography is the preferred test because it is more likely to detect a cardiac source of emboli than a transthoracic study. While the transesophageal echocardiogram is a minimally invasive procedure, it has a superior sensitivity to detect thrombi or other pathology in the left atrium or left atrial appendage. With contrast enhancement, it can be used to help detect an intracardiac right-to-left shunt, a finding that is most commonly found among persons with a patent foramen ovale (PFO).
A PFO is the only abnormality found on the transesophageal echocardiogram, and the remainder of the patient's evaluation, including tests for a hypercoagulable state, is normal.
Should the stroke be attributed to the PFO? What is the risk of another stroke that may be attributed to the PFO?
The patient has a cryptogenic stroke (a stroke without an obvious explanation), and the only potential explanation for neurological symptoms is a PFO. Approximately 20% of healthy patients have a PFO, and the frequency of the cardiac change may be as high as 40% among persons with cryptogenic stroke (a stroke without an obvious cause). This congenital cardiac abnormality usually produces no symptoms but could be the conduit for an embolus to arise in the venous system and then travel to the cerebral vasculature (paradoxical embolism).
The potential relationship of PFO and stroke is of special concern among young adults. Still, a direct cause-and-effect association between PFO and stroke is hard to establish, according to the American Academy of Neurology. Recent epidemiological studies, one published in the Aug. 16, 2005 Circulation and one published in the Feb. 20, 2007 Journal of the American College of Cardiology, have not been able to confirm a strong interaction with the cardiac change and stroke. While some cases of stroke likely are due to paradoxical embolism secondary to PFO, there probably is not an interaction in many cases. The risk of recurrent stroke among patients with ischemic stroke related to PFO also is not well established, according to the American Academy of Neurology, and may not be as high as originally assumed. However, there may be some factors, such as the concomitant presence of an atrial septal aneurysm, which may predict a greater risk of recurrent embolism.
What is the best treatment of a patient with a stroke and a PFO?
Because of the considerable uncertainty about the natural history of persons with PFO and stroke, the best management of affected patients also is in doubt. Choices for treatment include antiplatelet agents (most commonly aspirin), oral anticoagulants, endovascular placement of an occlusive device and direct surgical closure, according to an article in the November 2005 Current Treatment Options in Neurology. Most of the evidence about specific therapies comes from case reports and clinical series, and as a result the comparisons are best considered to be indirect. Data from clinical trials are limited.
Since the risk of recurrent stroke appears to be low, antiplatelet agents often are prescribed. A French study published in the Dec. 13, 2001 New England Journal of Medicine looked at the utility of aspirin among young adults with cryptogenic stroke and found that the rates of new ischemic events were similar among those persons who did and did not have PFO. Recent guidelines from the American Heart Association/American Stroke Association Council on Stroke state that antiplatelet agents are a reasonable choice for treatment of patients with PFO and recent stroke. Oral anticoagulants have been recommended because the thrombi presumably are of venous origin. However, a clinical trial published in the June 4, 2002 Circulation found that oral anticoagulation was not superior to aspirin. Guidelines from the American Heart Association/American Stroke Association Council on Stroke concluded that oral anticoagulants are a reasonable choice for treatment of patients who have PFO and a hypercoagulable disorder.
At least two studies, one in the July/August 2005 Journal of Cardiac Surgery and one in the December 2004 Scandinavian Cardiovascular Journal, have reported direct surgical closure of the PFO. However, this operation may not be necessary and the risk of a major cardiac procedure, including the likelihood of stroke, may outweigh the benefit in lowering the risk of recurrent embolism. Endovascular placement of a device to occlude the PFO has been used, and several devices are available. Small series (two published in the January 2004 and May 2006 Mayo Clinic Proceedings and one published in the Oct. 9, 2007 Circulation) show that these devices can be placed with reasonable safety, although their utility is unknown. Clinical trials are testing these devices, and pending their completion, the American Academy of Neurology has noted that data are not available to make a recommendation about placement of a PFO occlusive device.
A sensible approach would be to refer the above patient to a center that is participating in one of the trials testing the utility of PFO closure devices. Otherwise, medical treatment with an antiplatelet agent seems to be the most reasonable response for prevention of recurrent stroke.