Michaels’s TIA Not Necessarily due to PFO
In the spirit of diagnostic parsimony, I would not attribute Bret Michaels’s recent “warning stroke” or transient ischemic attack (TIA) to a patent foramen ovale (PFO)*—which is a common, and often incidental, finding in the work-up of stroke. It should be noted that my opinion is contrary to that of Michaels’s treating MD in Arizona, at least as it is reported by the media. It should also be stressed that Michaels’s treating physician knows a helluva lot more about Michaels’s condition(s) than I do.
Nevertheless my educated, but armchair, inclination is to ascribe Michaels’s TIA to delayed vasospasm due to his subarachnoid hemorrhage (SAH), the cause of which was reportedly never identified. While vasospasm typically occurs 3-5 days after the initial SAH bleed, the risk can continue for several weeks thereafter. The herald symptom of Michaels’s SAH, an explosive headache, began on April 22nd. Vasospasm 1 month later is not outside the realm of possibility and more likely, in my mind, than a completely separate process of an embolic TIA due to a PFO.
According to CNN, the presumed embolic TIA of the “Celebrity Apprentice” winner is now being treated with a daily injection of Lovenox (enoxaparin; sanofi-aventis US), an anticoagulant. This is tricky business given that such treatment increases Michaels’s risk of bleeding generally, including bleeding into the brain.
Data regarding the follow-up risk of stroke or TIA with PFO and the potential benefit of surgical closure in asymptomatic PFO were discussed here last summer.
* The vestige congenital hole between the left and right atria.
Image from Wikipedia: Horizontal CT cut showing hyperdense subarachnoid blood in the basal cistern.