Epidemiology and Prevention of Stroke WILLIAM



Data regarding the epidemiological characteristics of cerebrovascular disease are extremely difficult to obtain and more difficult to validate. Studies which present incidence rates by age, sex, and race differ widely with respect to the methods used to ascertain the information, the definition of the clinical disease, and the size of the population base under consideration (7). In many reports there has been no attempt made to distinguish between different etiological categories such as subarachnoid hemorrhage, intracerebral hemorrhage, and cerebral infarction. Ideally one should be able to consider, in addition, the severity of disease among the cases recorded, but unfortunately one is unable to achieve this goal by examining available data. The various manifestations of stroke are known largely from series of clinical cases, and data obtained from these sources cannot be appropriately extrapolated to a general population (8). Even fewer data are available with respect to prevalence of stroke. The prevalence of any disease is the joint function of incidence, rate of recovery, and duration of survival. Information regarding prevalence would be invaluable in the planning of any health care delivery system for stroke patients and, therefore, knowledge of the extent of residual disability becomes a very critical consideration. Although very little definitive information is currently available, a recent survey suggests that of every 100 persons who survive the acute illness, 10 will be able to return to work virtually without impairment, 40 will have mild residual disability, 40 will be so disabled that they require special services, and 10 will need institutional care (11). Mortality figures for a variety of specific populations can be found in published reports but there is little or no precise information with respect to the relative distribution of fatal stroke among the generally accepted clinical categories. Most epidemiological studies have been based on hospital cases or on postmortem examination and, therefore, it is likely that those individuals with less severe cerebrovascular disorders are 178

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seriously under reported. Unfortunately, these are the cases about which we need to know the most if we are to understand the role played by various risk factors, particularly those that influence the development of atherosclerosis and the mechanisms of coagulation. Because of limitations of time, attention will be directed only to risk factors and prevention as they relate to ischemic cerebrovascular disease and not to hemorrhage. Since stroke, particularly ischemic stroke, is considered generally to be a clinical consequence of atherosclerosis, investigators have been led to look for causative factors similar to those associated with ischemic cardiac disease. Regrettably, all that can be said with any degree of accuracy is that the risk of stroke increases sharply with increasing age, and that in most white populations, it occurs about 10 years later than myocardial infarction (6). It is almost impossible, however, recognizing the competing risks for the two diseases, namely myocardial and cerebral infarction, to be certain how many persons who died of the former might have suffered the latter had they survived for the additional 10 years. The harvesting effect of the first illness influences one's ability to obtain information about a concomitant serious vascular disorder which characteristically manifests itself clinically later in life. Numerous factors have been considered as possibly being related to the occurrence of stroke. The evidence for some is minimal so that it is difficult to put a specific degree of priority on each in the present state of our knowledge. The problem in discussing risk factors and stroke prevention becomes even more difficult when one takes into consideration the fact that cerebral infarction due to intravascular occlusion has quite a different pathogenesis from that of intracranial hemorrhage of either the intracerebral or subarachnoid type. Furthermore, cerebral infarction may be due to either atherosclerotic occlusion in situ of an extracranial or intracranial artery, to an embolus originating from an ulcerated atheromatous plaque in an internal carotid artery, or an embolus from a cardiac source. It is evident, however, that the most important concerns with regard to stroke prevention are the identification and treatment of individuals with: (1) hypertension, (2) transient cerebral ischemic attacks, and (3) cardiac disorders that are frequently associated with cerebrovascular complications (14). Consequently, in this presentation no attempt will be made to discuss all risk factors which might conceivably be involved but to devote attention to those which are most frequently implicated and most readily identifiable and treatable. Hypertension appears to be the most important alterable factor that is associated with nonembolic cerebral infarction, but the information is far


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from complete at present. From the best available data, it appears that strokes are from 2 to 4 times as frequent in hypertensive as in comparable normotensive individuals (11). Actuarial data indicate that mortality from cerebrovascular disease increases as blood pressure elevates, starting with the lowest levels at which hypertension may be suspected. Diastolic pressures appear to be no more reliable than systolic pressures as indicators of risk for stroke, and no reliable information concerning individuals with systolic hypertension in the absence of diastolic elevation is available at the present time. It is reasonable to ask whether control of existing hypertension lowers subsequent stroke incidence. Information regarding this question is known only from studies of individuals who have already had an identifiable cerebral infarction and then allocated in a random fashion to antihypertensive therapy or placebo (1, 5, 12). It is generally accepted that sufficient evidence has accumulated to indicate that hypertension is not only a significant cause of stroke but also the most readily treatable risk factor for this condition. It would appear justified, therefore, to undertake extensive drug trials in hypertensive populations with the view to preventing cerebral infarction and hemorrhage. Induced hypotension of an excessive or prolonged degree from any cause, including shock, severe hemorrhage, surgery, dehydration, various medications, and diagnostic procedures may lead to diffuse cerebral ischemia. In the presence of atherosclerotic arterial disease, the reduction of blood flow may become critical in a region supplied by a vessel, the lumen of which has been severely compromised. Whenever procedures which may cause such hypotension are undertaken, careful monitoring of blood pressure is of critical importance. Transient cerebral ischemic attacks and amaurosis {ugax are recognized generally as precursors of ischemic stroke since the best available evidence suggests that approximately one-third of affected individuals are likely to have a cerebral infarct within 5 years of the onset of such episodes (13). This is more than 10 times the rate of expected stroke incidence for persons of the same age and sex in the general population. Conversely, approximately three of every four persons with cerebral infarction and four of every five with documented internal carotid artery occlusion will give a history of one or more transient ischemic attacks (9). Some physicians hold to the belief that long term anticoagulant therapy with coumarin type drugs in patients with transient ischemic attacks prevent stroke in a high percentage of cases (10). However, many others consider that the possibility of serious hemorrhagic complications from the protracted use of such agents outweighs any potential advantage, or that the anticoagulant drugs are ineffective. Numerous other


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medical treatments including agents presumed to be cerebral vascular dilators (so-called vasoactive drugs) have been recommended for patients with transient ischemic attacks, but there is absolutely no substantiating data, although these agents are widely employed both in Europe and North America. Transient ischemic attacks are associated in a high percentage of cases with angiographic evidence of severe stenosis of the extracranial portion of the appropriate internal carotid artery or with ulcerated plaque in a similar location. Arterial reconstructive surgery with removal of the offending lesion has been shown to be beneficial in preventing subsequent cerebral infarction in the territory supplied by that vessel (2). Usually a person with transient ischemic attacks who is a candidate for carotid endarterectomy will have either a well localized bruit over the carotid bifurcation in the midcervical region or decreased ipsilateral retinal artery pressure as measured by ophthalmodynamometry or some similar noninvasive procedure. Individuals with this combination of symptoms and signs should be studied carefully by arteriography and, if an appropriate lesion is demonstrated, a carotid endarterectomy would be considered to be an appropriate method of treatment. However, since symptomatic patients seldom have a solitary lesion it would seem reasonable to recommend medical therapy postoperatively. Platelet-fibrin emboli in retinal arterioles either with or without associated cholesterol emboli may also arise from an ulcerated plaque. In all probability they occur more commonly than cholesterol emboli but are not observed as often. They are the type of emboli usually seen when the fundus of the eye is examined during the transient episodes of monocular blindness. Presumably if these emboli originate from a lesion proximal to the ophthalmic artery, it is likely that others from the same source may pass further downstream and obstruct cerebral vessels as well. Observation of either cholesterol em boli or platelet-fibrin em boli in the retinal arteries associated with symptoms of monocular blindness or cerebral ischemia is considered presumptive evidence of a lesion correctable by surgery; therefore, arteriography should be done in all such patients. Many authorities recommend no further studies or treatment for an asymptomatic patient with normal or even decreased ipsilateral retinal artery pressure who has a localized systolic bruit over the carotid bifurcation. However, others advise angiography and surgery in selected persons with asymptomatic carotid bruit, especially those in whom major surgical procedures are contemplated either in the thorax or abdomen. Recognizing, however, that there is surgical risk involved,


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carotid procedures should be carried out only in the facility where the operative team is experienced in arterial surgery and capable of managing any ensuing complications (4). In the past several years, evidence has been accumulating that transient ischemic attacks may be eliminated or reduced in frequency by administration of nonsteroidal anti-inflammatory drugs which modify platelet function in intra-arterial coagulation (3). This is based upon the assumption that most transient ischemic attacks are due to downstream embolization of fibrinoplatelet emboli formed on irregular, roughened, or ulcerated atherosclerotic plaques. Prevention by suppressing platelet aggregation seems promising in transient ischemic attacks, but there is no certainty that the pathogenesis of such attacks is the same as that for cerebral infarction. One could conceivably eliminate the former without reducing the risk of the latter. Several studies are currently underway, one in Canada and the other in the United States, to study this problem. Thus far, no definitive report has been released. Embolic infarction characteristically presents as a single, abrupt event which reaches its peak very quickly. Recent advances in the prevention and treatment of many cardiovascular diseases have changed the incidence of stroke associated with these disorders. For example, the use of prophylactic antibiotics has reduced the incidence of rheumatic heart disease and subacute bacterial endocarditis and consequently has reduced the incidence of cerebral embolism. Cerebral infarction following the insertion of a prosthetic heart valve is now one of the common neurological problems encountered by cardiovascular specialists. Most authorities agree, however, that the frequency of stroke from this cause can be reduced by employing judicious postoperative anticoagulant or platelet suppressive therapy. The highest correlation between embolic cerebral infarction and prior cardiac rhythm disorder occurs with atrial fibrillation. Patients with either chronic or intermittent fibrillation should be considered as stroke prone. Anticoagulant therapy should be considered for all patients with long standing atrial fibrillation, especially when there is evidence of valvular heart disease. When an acute myocardial infarction occurs, there are usually no detectable physical findings suggestive of endomural thrombi unless the patient already demonstrates evidence of an embolus to the brain or elsewhere. On the other hand, myocardial infarction is occasionally recognized only after the occurrence of a stroke and, therefore, it is advisable in all acute stroke patients to obtain an electrocardiogram as soon as possible after the onset of the neurological disorder. Public education should be provided in terms of the known risk factors



REFERENCES 1. Carter, A. B., and Barham, A. Hypotensive therapy in stroke survivors. Lancet. 1: 485-497, 1970. 2. Fields, W. S. Selection of stroke patients for arterial reconstructive surgery. Am. J. Surg., 125: 527-529 1973. 3. Fields, W. S., and Hass, W. K. (eds): Aspirin, Platelets and Stroke. 163 pp. Warren H. Green, Inc., St. Louis, 1971. 4. Fields, W. S., Maslenikov, V., Meyer, J. S., Hass, W. K., Remington, R. D. and MacDonald, M. Joint study of extracranial arterial occlusion: V. Progress report of prognosis following surgery or nonsurgical treatment for transient cerebral ischemic attacks and cervical carotid artery lesions. J.A.M.A. 211: 1993-2003, 1970. 5. Hypertensive Stroke Cooperative Study group. Effect of antihypertensive treatment on stroke recurrence. J.A.M.A. 229: 409-418, 1974. 6. Kannel, W. B., Dawber, T. R., Cohen, M. E. and McNamara, P. M. Vascular disease of the brain: epidemiologic aspects: The Framingham Study. Am. J. Public Health, 55: 1355-1366, 1965. 7. Kuller, L., Cook, L. P. and Friedman, G. D. Survey of stroke epidemiology studies. Draft report by the Committee of Criteria and Methods, Council on Epidemiology, American Heart Association, 1971. 8. Kurtzke, J. F., Epidemiology of Cerebrovascular Disease, 197 pp. Springer-Verlag, Berlin, 1969.

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for cerebrovascular disease in order to facilitate early institution of medical or surgical care in the potential stroke victim. Furthermore, those persons who are considered stroke prone should be urged to have proper evaluation and treatment. It has been adequately demonstrated beyond any doubt that people vary in their patterns of response to dangerous situations. The person who does not seek attention when threatened with any illness may be weighing different competing risks. The average individual assumes that most preventive health measures are excessively expensive, and if there is a low risk of acquiring a certain disease, he may not wish to pay the cost involved in avoiding the potential disorder. He seldom considers, however, that its treatment may be far more expensive than the preventive care he could have obtained initially. Usually it is only after the patient has become ill that he and his family are susceptible to health education. At that time he may be willing to examine all aspects of the predisposing causes and learn how to avoid another incident or be more amenable to following suggestions which may lead to a satisfactory recovery. In spite of the fact that there are limitations in our knowledge with regard to stroke prevention, the public should know this also and be made aware of the available diagnostic measures and treatment. A continuing campaign' should be conducted which will focus on the responsibility of the individual for changing his own health habits, particularly in relation to the prevention of serious illness.



Effects of treatment on morbidity in hypertension: results in patients with diastolic blood pressures averaging 115-129 mm. Hg. J.A.M.A., 202: 1028-1034, 1967. 13. Whisnant, J. P., Anderson, E. M., Aronson, S. M., Harrison, C. E., Haynes, M. A., Kurtzke, J. F., Lindsay, W. H., Ostfeld, A. M., Rentz, L. E., and Sundt, T. M. Jr. Report of the Joint Committee for Stroke Facilities V. Clinical Prevention of Stroke. Stroke, 3: 803-825, 1972. 14. Whisnant, J. P. Matsumoto, N., and Kurland, L. T. Transient cerebral ischemic attacks in a community: Rochester, Minn., 1955-1969. Circulation, 44(Suppl. 2): 94, 1971.

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9. In Cerebral Vascular Diseases; Transaction of the Fourth Conference, edited by C. H. Millikan, R. G. Siekert, and J. P. Whisnant, pp. 221-235, Grune & Stratton, New York, 1965. 10. Millikan, C. H. Reassessment of anticoagulant therapy in various types of occlusive cerebrovascular disease. Stroke, 2: 201-208, 1971. 11. Stallones, R. A., Dyken, M. L., Fang, H. C. H., Heyman, A., Seltser, R., and Stamler, J. Report of the Joint Committee for Stroke Facilities I. Epidemiology for Stroke Facilities Planning. Stroke, 3: 359-371, 1972. 12. Veterans Administration Cooperative Study Group on Antihypertensive Agents.

Epidemiology and prevention of stroke.

CHAPTER Epidemiology and Prevention of Stroke WILLIAM s. FIELDS, M.D. Data regarding the epidemiological characteristics of cerebrovascular diseas...
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