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NewsletterPatent Foramen Ovale And Off-Pump Coronary Artery Bypass Graft Surgery Mark A. Chaney, MD
The popularity of off-pump coronary artery bypass graft surgery (OPCAB) is increasing. Advantages of this technique include avoidance of detrimental physiologic effects (neurologic, pulmonary, renal, hematologic etc.) of cardiopulmonary bypass (CPB). However, if one detects a patent foramen ovale (PFO) via routine intraoperative transesophageal echocardiography (TEE) in a patient scheduled for OPCAB, what is the correct clinical management? Should the PFO be surgically repaired (adding increased risk associated with initiation of CPB) or should the PFO be left alone? There is no easy answer yet new data recently published may assist in the decision-making process.
Although most strokes are a consequence of cerebrovascular disease, about 20% of ischemic strokes have been attributed to cardiogenic embolism (1). Among the cardiac anomalies detected by TEE that have been implicated as risk factors for stroke are PFO and atrial septal aneurysm (ASA). The presence of a PFO is highly associated with ASA (2). Approximately 50% of patients with ASA (protruding >10 mm beyond the plane of the intraatrial septum) demonstrate interatrial shunting, in the majority of cases through a PFO (2). The foramen ovale remains patent through adulthood in approximately 25% of individuals, allowing right-to-left interatrial shunting whenever the pressure in the right atrium exceeds that in the left atrium. The prevalence of PFO is greater in patients with unexplained cerebral ischemic events than in the general population (1). Three factors are important in determining the likelihood that a PFO will be of clinical significance: its size, the pressure gradient between the right and left atrium, and the direction of inferior vena cava flow (2). However, a causal relationship between PFO and stroke is not clear. Potential mechanistic links are complex and include paradoxical embolism of thrombus from the peripheral venous system, direct arterial embolism of thrombus from the endocardial surface of the atrial septum, cerebral ischemia related to occult paroxysmal atrial fibrillation, and associated vascular pathology. Although paradoxical embolism is a favored hypothesis, the relatively low rate of detectable deep venous thrombosis in patients with PFO who suffer stroke argues that another mechanism is operant in many cases.
TEE is now considered the "gold standard" for PFO detection on the basis of comparison with postmortem studies and with other methods (2). Passage of contrast material or color flow through the defect should be demonstrated to establish the diagnosis. A provocative procedure (Valsalva maneuver) that temporarily reverses pressure between the atria needs to be applied to demonstrate the passage of the contrast (usually agitated saline) through the septum. Contrast-based methods may lead to false-negative results when left atrial pressure far exceeds right atrial pressure and a pressure gradient cannot be reversed with any provocative maneuver. Assessment of flow through the PFO with color Doppler imaging avoids this limitation, but it assumes continuous left-to-right flow (unless a provocative maneuver is used).
Once a PFO is detected via TEE in a patient scheduled for OPCAB, more information is required before deciding on the correct clinical and surgical management. Most agree that asymptomatic PFO (no history of stroke, hypoxemia, etc.) do not require intervention. However, if the patient has a history of previous cryptogenic stroke (no clearly identifiable pathogenesis), four major choices exist: surgical closure, percutaneous device closure, medical therapy with an anticoagulant (warfarin), or medical therapy with an antiplatelet agent (aspirin). At present, it remains unclear what therapy is best (3,4). Recent data from the Patent Foramen Ovale in Cryptogenic Stroke Study indicates that medical therapy (with either warfarin or aspirin) is protective against death and recurrent stroke in stroke patients with PFO independent of the size of the defect or the presence of ASA (4). Thus, closure of a PFO (surgical or percutaneous) is usually not indicated. Most authorities now recommend closure of PFO only in young stroke survivors with no other apparent source of embolism when either recurrent ischemia has occurred during anticoagulant therapy or a contraindication to anticoagulant therapy exists (1).
In summary, despite considerable progress, much uncertainty still exists regarding management of patients scheduled for OPCAB in whom a PFO is detected via routine intraoperative TEE. The benefits of closure (decreased stroke risk) must be weighed against risks of initiation of CPB (neurologic, pulmonary, renal, hematologic, etc.) in each individual patient. Recent data indicates that most should be left alone and medical therapy should be contemplated. Lastly, one should keep in mind that cardiac manipulation during OPCAB may increase right-to-left shunting through a PFO and cause clinically significant hypoxemia (2).
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