American Heart Journal January, 1966, Volume 71, Number 1

Editorial

The prevention of strokes

John Marshall, M.D.* London, England

T he occurrence of a completed stroke must always be regarded as a major

setback in the life of a patient. Inevitably there is some degree of brain damage and, although vigorous rehabilitation can do much to minimize the effects, the majority of patients are left with some disability, which may be of considerable degree. Therefore, the prevention of completed strokes must be given high priority in the practice of those concerned with cerebro- vascular disease.

Our knowledge of the basic causes of degenerative vascular disease is as yet fragmentary and much work remains to be done on the pathogenesis of athero- sclerosis before we can hope to prevent those vascular changes which are ulti- mately responsible for the completed stroke. Nevertheless, there are at the present time interventions open to the physician which will make a significant contribution to the prevention of com- pleted strokes. These can be classified under three broad headings: the eradica- tion of sources of emboli, the investigation and treatment of transient ischemic at- tacks, and the management of hyperten- sion. These three areas of endeavor will be discussed in turn.

The risks of embolization in certain

conditions, such as atria1 fibrillation, myo- cardial infarction, cardiomyopathy, and endomyocardial fibrosis, is well recognized, but the extent of the threat to the nervous system is not always fully appreciated. In unselected series of completed strokes, embolization is the cause in from 5 to 10 per cent ,of cases. r,2 Alternatively, when seen from the cardiac standpoint in cases of mitral stenosis giving rise to emboli, 75 per cent go to the cerebral circulation3 In many of the cases of cerebral embolism it is already known that the patient suffers from cardiac disease, but it should be remembered that in the case of mitral stenosis as many as 12 per cent of patients may first present because of cerebral embolism.3 The prevention of the first embolus in this latter group is clearly impossible, except perhaps by routine examination of people in positive health. Yet, even after the first embolus, there is scope for prophylaxis, for further emboli- zation is likely to occur in about 60 per cent of cases.3 Moreover, whereas the mortality from a first embolus is about 7 per cent, that from further emboli is about 27 per cent.4

Although the exact place of anticoagu- lant therapy in the management of cere- brovascular disease is still the subject of

From the Institute of Neurology, London, England. Received for publication April 30, 1965. *Reader in Clinical Neurology, University of London. Address: In&it Ite of Neurology, Queen Square, London, W.C.1.

England.

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2 Marshall

some disagreement, there is practically universal acquiesence in its value in cases of cerebral embolization. The evidence in support of this is considerable2s5 and there cannot be any real doubt upon this ques- tion. Ideally, treatment should begin before the first embolus occurs, hence the necessity for instituting anticoagulant ther- apy in all cases in which a potential source of emboli is known to be present until such time as that source can be eradicated, whenever this is practicable. The impor- tance of this was shown by a series of 105 patients with mitral stenosis in whom valvotomy was deferred because symptoms were trivial or absent. Over a period of 49; years, 15 patients experienced a cere- bral embolus, five of which proved to be fata1.6 If embolization has already oc- curred, treatment should be started im- mediately with heparin, to be followed by coumarin or inanedione derivatives; it must be continued until all danger of further embolization is past.

The importance of transient ischemic attacks (T.1.A.s) in the field of cerebro- vascular disease cannot be exaggerated. These short-lived disturbances of neuro- logical function frequently give warning that a completed stroke is impending. This danger is much greater when the T.1.A.s are occurring in the distribution of the carotid artery and its branches than when the vertebrobasilar territory is in- volved. In a series of patients with com- pleted strokes which had been preceded by transient ischemic attacks in the carotid territory, no less than 76 per cent had ex- perienced only one or t\l:o T.1.A.s before- hand, 47 per cent occurring in the month prior to the stroke.7 The appearance of T.1.A.s in the carotid territory is, there- fore, a signal for immediate action.

The first step must be to ascertain the immediate cause, for there are a variety of these. Anemia8 and polycythemiag have both been incriminated and can be eliminated at the first examination of the patient by appropriate hematologic exami- nation. Transient falls in blood pressure may also be responsible.‘O This cause can usually be detected from the history of the attacks; their occurrence against a back- ground of lowered cardiac output, as in myocardial infarction, or fall in blood vol-

ume, as in severe hemorrhage, is suggestive; alternatively, the patient may be receiving hypotensive therapy \\,hic-h is poorly con- trolled. Correction of these factors will stop the attacks. Transient hypertensive crises ma\- also occurll and give rise to focal neurological symptoms and signs instead of the more generalized disturbance of cerebral function usually associated with hypertensive encephalopathy. Such patients have malignant hypertension or show evidence of being on the verge of developing it. Jmmediate control of the blood pressure is essential.

These four conditions, although readily detected at the first examination, account for only a minority of cases of T.1.A.s. For the remainder, four-vessel angiography is essential for a proper assessment of the case. There may be clues in the history as to what is likely to be found. Thus, a past history of pain in a cervical root and a story that the T.T.,Ls tend to occur when- ever the patient turns his neck suggests intermittent compression of the vertebral artery by osteophytes clue to cervical spondylosis.‘2 The association of attacks in the vertebrobasilar territory with use of the upper limbs and the finding of a difference in the level of blood pressure in the two arms raises the question of the presence of a subclavian-steal.13 The pres- ence of a bruit over the bifurcation of the carotid artery in the neck indicates that a stenosis may be present. These and other stenotic and compressive lesions of the carotid or vertebrobnsilar arteries can only be diagnosed accurately by angiog- raphy, which must therefore be carried out as a necessary step toward rational treatment. This may be b>, nleans of sur- gery, as in endarterectomy or the removal of osteophytes, or by the restriction of neck movements through the use of a collar.

Alternatively, anticoagulant therapy may be instituted. The justification for this is the increasing evidence that athero- sclerotic plaques in the great vessels may provide a site for the formation of fibrin- platelet or cholesterol-debris emboli which subsequently impact in cerebral or retinal vesseIs.14-17 In addition, there is clinical evidence from controlled trials of the value of anticoagulant therapy in transient

Volww 7 1 Number 1

ischemic attacks.‘*Jg Therapy should be continued for at least a year after the last attack.20

The third way by which it may be pos- sible to forestall the development of a completed stroke is by the proper manage- ment of hypertension. Although hypoten- sive therapy rapidly found a place in the management of uncomplicated hyperten- sion and that giving rise to cardiac symp- toms, its use in patients with cerebrovascu- lar disease has been approached with con- siderable diffidence. This probably was due to the widespread belief that “cerebral thrombosis” is caused by low blood pres- sure. This, in turn, was due to a failure to distinguish between those cases in which cerebral infarction develops in association with a sudden and profound fall in blood pressures, as may occur in myocardial infarction and gastrointestinal hemorrhage, and those cases of uncomplicated cerebral infarction in which the blood pressure is, on the average, higher than that of the normal population.21

Cerebrovascular accidents are a common cause of death in patients with untreated hypertension, and the incidence of this cause may be considerably reduced by the use of hypotensive therapy.22J3 This bene- ficial effect on mortality has been shown to be present even when the patient has al- ready experienced a stroke24; furthermore, there is a significant reduction in the further incidence of nonfatal strokes. There can be no doubt, therefore, as to the value of lowering the blood pressure in the pre- vention of strokes. Certain points must be observed when giving hypotensive therapy to patients with cerebrovascular disease. So severe a reduction in blood pressure as is necessary for the young man with malignant hypertension should not be sought; a diastolic level of about 100 mm. Hg is satisfactory for the cerebrovascular patient. Drugs which have a marked postural hypotensive effect should be avoided. The patient must be carefully instructed about the advisability of taking some gentle exercise on the bed before first rising in the morning, and about the need to lower the head immediately if ever he should experience hypotensive symptoms.

Although our understanding of cerebro-

Prevention qf strokes 3

vascular disease is far from complete, we, nevertheless, already have some means by which we can reduce the incidence of its most devastating effects. Until such time as we can eliminate the basic causes of degenerative vascular disease, the care- ful application of these means will prove to be rewarding.

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REFERENCES

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McBrien. D. I.. Bradlev. R. D.. and Ashton. W. : The ‘natuie’of retinal emboli in stenosis of the internal carotid artery, Lancet 1:697, 1963

17. David, N. J., Klintworth, G. I~., Frieclbcrg. s. J., aud L)illon, M.: Fatal athcromttotts cerebral embolism associated \vith lrright plaques in the retinal arterioles. Report of a case, Neurology (Minnenp.) 13:708, 1963.

18. Report of the \‘eterans r\dministration Co- operative Study of Atherosclerosis, Neurology- Section: An evaluation of anticoagulant therapy, in the treatment of cerebrovascular disease, Neurology (Minneap.) 11 : No. 4, Part 2. 132, 1961.

19. Baker, R. N., Broward, J. .\., Fang, II. C., Fisher, C. M., Groch, S. N., Heyman, ,I., Karp, H. R., McDevitt, K., Scheinberg, I’.. Schwartz. W.. and ‘I‘oole. 1. F. : Anticoaeulant

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therapy in cerebral infarction. Report on co- operative study, Neurology (Minneap.) 12:823, 1962.

2.1. Leishman, r\. 1\‘. ID.: Merits of reducing high blood-pressure, Lancet 1:1284, 1963.

24. Marshall, J.: .\ trial of long-term hypotensive therapy in c.crcl,ro\-ascul;Ir disease, Lancet 1:lO. 1964.