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value of anticoagulants (atrial brillation is an exception see further on) The two situations in which the immediate administration of heparin has drawn the most support from our own clinical practice are in uctuating basilar artery thrombosis and in impending carotid artery occlusion from thrombosis or dissection (see further on) In these situations, the administration of heparin may be initiated while the nature of the illness is being clari ed; the drug is then discontinued if contraindicated by new ndings It must be acknowledged that satisfactory clinical studies in support of this approach of acute anticoagulation have not been carried out The issue of heparinization in cases of recent cardioembolic cerebral infarction is addressed further on in this chapter, under Embolic Infarction However, in anticipation of the later discussion it can again be stated that there is little evidence in support of heparin use in most strokes In the event heparin is given, if t-PA has not been used in the preceding 24 h, the heparin may be given intravenously, beginning with a bolus of 100 U/kg followed by a continuous drip (1000 U/ h) and adjusted according to the partial thromboplastin time (PTT) Bleeding into any organ may occur when the PTT is much greater than 3 times the pretreatment level When the PTT exceeds 100 s, it is preferable to discontinue the heparin, check the blood clotting values, and then reinstitute the infusion at a lower rate (rather than simply lower the infusion rate) In circumstances of uctuating basilar artery ischemia, it has been our practice to permit higher values of PTT The use of low-molecular-weight heparin (anti factor Xa enoxaparin or nadroperin) given subcutaneously within the rst 48 h of the onset of symptoms may improve outcome from stroke In a limited randomized trial, there was no increase in the frequency of hemorrhagic transformation of the ischemic region when compared to placebo treatment (Kay et al) Because the outcome measures in this study were coarse (death or dependence 6 months after stroke), further investigations of this approach need to be carried out We can only infer that the use of low-molecular-weight heparin (approximately 4000 U subcutaneously, twice daily) appears to be safe and is possibly bene cial Whether anticoagulant therapy is effective in preventing strokes in patients with TIAs or recent stroke is a question that has never been answered satisfactorily Swanson has reviewed several trials evaluating heparin (including the International Stroke Trial and the TOAST study) and suggested that there was no net bene t from heparin in acute stroke because of an excess of cerebral hemorrhages However, there was in these series a low incidence, estimated as 2 percent, of recurrent stroke in the rst weeks after a cerebral infarction in the untreated groups An early recurrent stroke rate this low almost precludes demonstrating a bene t from the use of heparin or heparinoid drugs The long-term use of warfarin following atherothrombotic stroke is also still under critical analysis To date it seems to be of some slight value in the prevention of further thrombosis and embolism There are data to suggest that the greatest usefulness of warfarin is in the rst 2 to 4 months following the onset of ischemic attack(s); after that time the risk of intracranial hemorrhage may exceed the bene ts of anticoagulant therapy (Sandok et al) However, in comparison to aspirin, discussed below, there is no reason to favor warfarin in cases of atherothrombotic stroke This was amply shown in the so-called WARSS study (not including cardioembolic stroke) published by Mohr and colleagues (2001); over 2 years the recurrent stroke rate was about 16 percent in both groups.

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and, surprisingly the rate of cerebral hemorrhage was similar (near 2 percent) In contrast to the situation with atherothrombotic disease, warfarin has been found to be superior for prevention of a second stroke in cardioembolic disease, as discussed further on Of course, the use of anticoagulant drugs makes an accurate diagnosis imperative Intracranial hemorrhage must be excluded by CT scan An estimation of prothrombin and partial thromboplastin activity is needed before therapy is started, but if this is not feasible, the initial doses of anticoagulant drugs can usually be given safely if there is no clinical evidence of bleeding anywhere in the body and there has been no recent surgery Warfarin therapy, beginning with a dose of 5 to 10 mg daily, is relatively safe provided that the international normalized ratio (INR) is brought to 2 to 3 (formerly measured as a prothrombin time between 16 and 19 s) and the level is determined regularly (once a day for the rst 5 days, then two or three times a week for a week or two, and nally once every several weeks) There is no reliable evidence that complications are more frequent in the presence of hypertension if the INR is not allowed to exceed two to three times normal; therefore the authors have not withheld anticoagulant therapy in these patients However, when the blood pressure is greater than 220/120 mmHg, an attempt is made to lower it gradually at the same time Numerous drugs may alter the anticoagulant effects of the coumarins or add to the risk of bleeding aspirin, cholestyramine, alcohol, barbiturates, carbamazepine, cephalosporin and quinolone antibiotics, sulfa drugs, and high-dosage penicillin being the most important ones The INR must be determined regularly if the administration of warfarin is necessary Hemorrhagic skin necrosis is a rare but dangerous complication It is due to a paradoxical microthrombosis of skin vessels and is liable to occur in patients with unsuspected de ciencies of endogenous clotting proteins (S and C) Although the disseminated form of skin necrosis occurs within days of initiating warfarin therapy, we have seen one patient with a form of this lesion following local skin injury after months on treatment Any type of serious bleeding from warfarin overdosage demands immediate administration of fresh plasma and large doses of vitamin K An INR above 5 in a patient who must remain anticoagulated for example, one with a prosthetic heart valve may be corrected with small doses of vitamin K (05 to 2 mg), preferably given intravenously The problem that continues to plague all attempts to use longterm anticoagulants, as already noted for heparin in the acute situation, is the risk of hemorrhage, which approaches 10 percent, with a mortality of 1 percent The risk of intracranial hemorrhage has been estimated by Whisnant and colleagues to be 5 percent overall and considerably higher in elderly patients who have been treated for more than 1 year Thus, it would appear that with longterm administration of anticoagulants, except in certain circumstances such as a severely stenotic cerebral vessel, atrial brillation, prosthetic heart valve, and certain blood disorders the risk of hemorrhage outweighs the bene t from prevention of stroke Antiplatelet Drugs Aspirin (325 mg daily) has proved to be perhaps the most consistently useful drug in the prevention of thrombotic and embolic strokes One currently favored approach, based in part on the above-mentioned WARSS trial, is to simply administer aspirin in all cases of acute stroke (except perhaps if t-PA has been used) The acetyl moiety of aspirin combines with the platelet membrane and inhibits platelet cyclo-oxygenase, thus preventing the production of thromboxane A2, a vasoconstricting prostaglan-.

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