This refers to the opening of an occluded carotid artery immediately after a stroke with the intention of improving the clinical outcome; the issue of endarterectomy for the prevention of future strokes is another matter and is taken up in a later section. In past decades, there had been limited experience with immediate surgical removal of a clot from the carotid artery or the performance of a bypass to restore function. Ojemann and colleagues (1995) operated on 55 such patients as an emergency procedure; 26 of these had stenotic vessels and 29 acutely thrombosed vessels. Of the latter, circulation was restored in 21, with an excellent or good clinical result in 16. In 26 patients with stenotic carotid arteries, an excellent or good result was obtained in 19. Usually several hours will have elapsed before the diagnosis is established. If the interval is longer than 12 h, opening the occluded vessel is usually of little value and may present additional dangers. In any case, this approach has been largely supplanted by the above-described endovascular techniques, for which the results have been generally poor. Reoperation because the vessel has closed or caused an embolus immediately after carotid endarterectomy is a special circumstance in which rapid removal of a clot or repair of an intimal tear is performed more or less routinely and is also mentioned in a later section. This subject is reviewed again further on.
The separate issue of the endovascular treatment of intracranial atherosclerosis is considered here for convenience. The risks of manipulating intracranial vessels are obvious, particularly those of the circle of Willis with no surrounding tissue because they are located within the subarachnoid space. In an attempt to determine if a stent and angioplasty would improve outcome in patients who had TIAs or minor strokes as a result of an intracranial stenosis, Chimowitz and colleagues (2011) reported that their trial was stopped early because of poor outcomes of the group who were treated by stent in comparison to medical management. The treatment of symptomatic intracranial atherosclerosis therefore remains problematic and is delegated to the antiplatelet drugs and lipid-lowering agents discussed further on.
Several considerations weigh in any discussion of the institution and choice of antiplatelet or anticoagulant treatment (meant here to denote the agents that alter the clotting cascade) for stroke. First is the distinction between anticoagulation to prevent the progression of an acute stroke and the prophylactic use of anticoagulation for the prevention of future strokes. Second, the pivotal issue in prevention of further strokes is whether the stroke or TIA is atherothrombotic or cardioembolic. As discussed further on, several studies point conclusively to a role for anticoagulation in stroke due to certain cardioembolic sources, particularly atrial fibrillation, while the indications in acute stroke are less certain.
Heparin treatment during an acute evolving stroke The two situations in which the immediate administration of heparin or an equivalent agent such as enoxaparin have drawn the most support from clinical practice are in basilar artery thrombosis with fluctuating deficits and in impending carotid artery occlusion from thrombosis or dissection. In these situations, the administration of heparin may be initiated while the nature of the illness is being clarified; the drug is then discontinued if contraindicated by new findings. Satisfactory clinical studies in support of this approach of acute anticoagulation have not been carried out and most authoritative writers find no evidence for the use of heparin in these situations (e.g., see Report of the Joint Stroke Guideline Development Committee authored by Coull et al). One fact seems fairly clear—that the administration of anticoagulants is not of great value for acute amelioration once the stroke is fully developed. Most clinical trials have too few such cases to evaluate the results of treatment.