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confers better protection than levels below 2 It should be pointed out, however, that patients below 65 years of age in these trials did not clearly bene t from long-term prophylactic anticoagulation unless there were additional risk factors such as diabetes, hypertension, congestive heart failure, or cardiac valvular disease This group, (called lone brillators) which embodies a low risk for stroke, constitutes about one-third of adults with atrial brillation Aspirin does not appear to afford the same degree of protective bene t in these circumstances, but some studies suggest a slightly better outcome than with no treatment; it has been used in younger patients and in those unable to take warfarin In patients with atrial brillation of recent onset, an attempt should be made to restore normal sinus rhythm by the use of electrical cardioversion or a trial of antiarrhythmic drugs If these fail, prophylactic anticoagulant therapy is recommended Before attempting cardioversion of more long-standing atrial brillation, anticoagulation for several days or longer is recommended With regard to aspirin treatment when the stroke is of unknown origin but presumed to be embolic, the data are uncertain Most large trials comparing aspirin to warfarin have studied patients in whom cardiogenic embolus is not implicated (such as in the earlier mentioned WARSS study), but there are probably many cases that have a cardiac source nonetheless (see earlier discussion of treatment for thrombotic stroke) There is no unanimity of opinion about the use and timing of anticoagulation with warfarin after an embolic stroke, in part because the risk of recurrent stroke in the rst days is low (see comments on pages 696) On the basis of the aforementioned large trials of acute anticoagulation that show a 2 percent frequency of early recurrent stroke, many clinicians prefer to start warfarin and await its effects rather than using heparin Nonetheless, once a rm diagnosis of embolic occlusion has been made, and particularly if there has been a recent myocardial infarction, a recent onset of atrial brillation, or a demonstrated cardiac thrombus on the echocardiogram, our customary practice has been to begin heparin on the same or the next day, generally without a loading dose, followed by the institution of warfarin on the same or the two following days However, many of our colleagues no longer use heparin in this setting, and others even forgo the use of warfarin unless a de nite source of embolism is detected by echocardiography The recent trend has been to avoid heparin and simply start warfarin if it is indicted Whether the newer low-molecular-weight heparins, mentioned earlier in the chapter, yield an advantage over conventional heparin treatment is not known In patients with very large cerebral infarcts that have a component of deep (basal ganglionic) tissue damage and especially patients who are also hypertensive, there is a distinct risk of anticoagulant-related hemorrhage into the acute infarct (Shields et al) In these patients, anticoagulation therapy should perhaps be avoided in the acute setting Also in our opinion, the use of anticoagulant therapy is desirable for at least several weeks or months in most patients with acute myocardial infarction, especially if the left side of the heart is involved In cerebral embolism associated with subacute bacterial endocarditis, anticoagulant therapy should be used cautiously because of the danger of intracranial bleeding, and one proceeds instead with antibiotics We have generally not anticoagulated these patients Valvuloplasty, removal of verrucous lesions in endocarditis, and amputation of the atrial appendage have substantially reduced the incidence of embolism in the now infrequent rheumatic heart disease The need for special care in preventing emboli that arise.

from the cardiac chambers or the aortic arch from entering the carotid arteries during the performance of valvuloplasty is appreciated by all cardiac surgeons

Generalized Brain Ischemia and Hypoxia (See Chap 40)

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This constitutes a special group of infarctions that follow cardiac arrest and other forms of prolonged hypotension or hypoxia In the case of reduced blood ow to the cerebral hemispheres, there is a tendency for focal infarctions to occur in the regions of lowest blood ow that lie between the major surface arteries, so-called watershed infarctions In the extreme case, there is global infarction of the brain accompanied by the clinical syndrome of brain death Pure hypoxia-anoxia produces another type of damage in areas susceptible to reduced oxygen delivery, mainly the hippocampi; here a Korsakoff syndrome results Most often, ischemic and hypoxic states coexist and may produce complex patterns of cerebral damage This topic is discussed fully in Chap 40, The Acquired Metabolic Diseases of the Nervous System The special problem of cerebral ischemia during cardiac surgery with the use of a bypass pump is discussed further on in the section on Stroke with Cardiac Surgery

Description These are options to display a title for the report If you choose Define Own Language Dependent Title, you are given options to assign a language to your title entry This option enables you to format the template with display options, RRI settings, and other formatting options We will review these in detail in the next chapter Use this option to identify the data provider for the query settings Click the icon at the end of the field to see the list of queries and InfoProviders that can be used

(See also pages 730 to 734)

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This is a segmental, nonatheromatous, nonin ammatory arterial disease of unknown etiology It is uncommon (05 percent of 61,000 arteriograms in the series of So et al), but it is being reported with increasing frequency because of improved arteriographic techniques In our experience, it has often been an incidental nding in asymptomatic individuals undergoing aortic angiography First described in the renal artery by Leadbetter and Burkland in 1938, bromuscular dysplasia is now known to affect other vessels, including cervicocerebral ones The internal carotid artery is involved most frequently, followed by the vertebral and cerebral arteries The radiologic picture consists of a series of transverse constrictions, giving the appearance of an irregular string of beads or a tubular narrowing; it is observed bilaterally in 75 percent of cases Usually only the extracranial part of the artery is involved In the series of Houser and colleagues, 42 of 44 patients were women, and 75 percent were over 50 years of age All of the patients reported by So and coworkers were women, ranging in age from 41 to 70 years Cerebral ischemia may be associated with the process but the rate of this complication has not been established Our impression is that it is low Among 79 untreated asymptomatic patients followed for an average of 5 years, 3 had a cerebral infarct 4 to 18 years after the initial diagnosis in the study by Corrin et al Also, between 7 and 20 percent of affected individuals are found to have intracranial saccular aneurysms (rarely a giant aneurysm), which may be a source of subarachnoid hemorrhage, and 12 percent develop arterial dissections, as described below The pathology of this disease has been summarized by Schievink and colleagues The narrowed arterial segments show degeneration of elastic tissue and irregular arrays of brous and smooth muscle tissue in a mucous ground substance Dilatations are due to atrophy of the coat of the vessel wall There is atherosclerosis.

in some and arterial dissection in others Usually vascular occlusion is not present, though there may be marked stenosis In some instances the mechanism of the cerebral ischemic lesion is unexplained Possibly thrombi form in the pouches or in relation to intraluminal septa So and colleagues have recommended excision of the affected segments of the carotid artery if the neurologic symptoms are related to them and conservative therapy if the bromuscular dysplasia is an incidental arteriographic nding in an asymptomatic patient It is now possible to dilate the affected vessel by means of endovascular techniques, and several case reports have suggested that bene t is achieved at lower risk in this way than with surgical excision Associated intracranial saccular aneurysms should be sought by arteriography or magnetic resonance angiography and surgically obliterated if their size warrants it (page 722) It is not known if anticoagulation or antiplatelet therapy confer protection from stroke

TABLE 2-1

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