The justification for, and excess risk of hemorrhage, when combining an antiplatelet agent with warfarin, has not been quantified. There seems to be relatively small risk if low-dose (81 mg) aspirin is included in a regimen of warfarin for atrial fibrillation. Beyond this statement, little can be said with authority but our personal experience, certainly tainted by the weaknesses engendered by the availability heuristic, is that subdural hematomas abound in elderly patients, with or without falls, who are on one or more agents. Even the relatively rapid reversal of anticoagulation with vitamin K and one of the clotting factor preparations or fresh plasma do little more than allow for safer surgery to remove intracerebral clots. Certain conditions such as chronic renal failure may confer a greater risk of cerebral hemorrhage with either drug, but the stroke risk from atrial fibrillation is also increased in comparison to patients with normal renal function as described in the epidemiologic study by Olesen and colleagues.
Closure of Patent Foramen Ovale (PFO)
The role of the patent foramen ovale as a cause of stroke that is otherwise cryptogenic, has been a matter of contention for decades. Certainly, in some instances, such as a young individual who has demonstrable clots in the venous system of the legs or pelvis or who has had a recent pulmonary embolism, this mechanism becomes an appealing explanation. As mentioned earlier in the chapter, several epidemiologic and other studies have demonstrated a statistical association between strokes in the presence of a PFO. It had also been a matter of some contention whether the size of the cardiac defect or the presence of an associated atrial septal aneurysm raise the risk of stroke. Even in younger patients, simply the discovery of a PFO with the use of echocardiography and injection of agitated saline or similar method that highlights the potential for movement of material from the right into the left atrium is not nearly proof of a causative mechanism.
Moreover, the value of anticoagulation, either alone or in comparison to closure of the PFO, has been uncertain. Three trials prior to 2014 suggested little or no benefit from closure of a PFO after stroke but three subsequent trials published in 2017 demonstrated substantial reductions in recurrent ischemic stroke with closure compared to antiplatelet or anticoagulant treatment (see Ropper 2017 for summary of these trials). It should be pointed out that the populations in the last three positive trials were restricted to younger patients and those with moderate to large shunts across the defect or atrial septal aneurysms.
Comments have already been made concerning the opening of an occluded carotid artery soon after a stroke. Here we discuss secondary stroke prevention in the patient who has had TIAs or minor stroke and who has passed the acute period. The segment of the vessels that most often lends itself to endarterectomy or stenting is the carotid sinus (the bulbous expansion of the internal carotid artery just above its origin from the common carotid) because this is the site where atherosclerotic narrowing occurs. Other sites suitable for surgical or endovascular management include the common carotid, innominate, and proximal subclavian arteries. As mentioned earlier in the chapter, carotid artery disease most often causes strokes and single or repetitive TIAs but may also result in a hemispheral hypoperfusion syndrome as a result of low blood flow distal to a severe stenosis.
Surgery and stenting are as yet applicable mainly to the group of patients with symptomatic carotid artery stenosis (the asymptomatic ones are discussed below) who have substantial extracranial stenosis but not complete occlusion, and, in special instances, in those with nonstenotic ulcerated plaques. In formerly collected cohorts, carotid stenosis accounted for less than 20 percent of all TIAs (Marshall); but from the perspective of interventional therapy, the term symptomatic encompasses both TIAs and large or small strokes ipsilateral to the stenosis, some of which may be evident only with cerebral imaging.