• The Cerebrovascular Disease Study Group was established in artº15º of the Portuguese Neurological Society estatutes, with the aim of studying, investigating and revealing the most relevant aspects of cerebrovascular diseases.
• To study the main problems which cerebrovascular diseases incite, undertaking collaborative actions at a national level.
• To work in cooperation with International Groups in the different and most relevant aspects of cerebrovascular diseases, thus contributing to a constant updating at a national level.
• To create and coordinate cultural and educational activities related with the practise and progress of knowledge on cerebrovascular diseases.
• To discuss and publish relevant work in its field of activity.
• To contribute to improve the quality of welfare.

The Group includes members of the Portuguese Neurological Society and is open for admission to emeritus or meritorious individuals or collective entities, who, although not members of the Portuguese Neurological Society, have an interest in the purposed aims.

STROKE RISK FACTORS

Definition: Risk factor - Characteristic or lifestyle of an individual, or in a population, which indicates that this individual or that population has an increased probability of suffering an stroke, as compared to an individual or population without that characteristic.

Most stroke patients have well known risk factors for cerebrovascular disease, some time before stroke. Thus, it is possible to decrease the stroke incidence by reducing the prevalence of risk factors in the population (mass strategy) and identifying "high risk" individuals, who can be treated.

A. Definite and non-modifiable risk factors

Age: most important risk factor for cerebral infarction and primary cerebral hemorrhage.

Sex: Slightly higher incidence of stroke in males (middle aged)

Genetic factors: In some cases can be the cause of stroke.

B. Definite and modifiable risk factors

Blood pressure: Arterial hypertension (diastolic and/or systolic) is a causal risk factor for all kinds of stroke in all age. There is an exponential relationship between "normal" diastolic arterial pressure values and CVA. There is no evidence of an diastolic arterial pressure limit below which the stroke risk is constant.

Smoking: Tobacco is an important stroke risk factor for stroke, particularly in extracraneal atheroma. After two or three years of not smoking, the risk for stroke becomes identical to that of a non smoker.

Diabetes Mellitus: Diabetes mellitus is a risk factor for vascular disease in general. The diabetic patient has a two fold stroke risk, as compared to a non-diabetic.

Heart Disease: Potentially emboligenous heart disease is a stroke risk factor, specially atrial fribrilation and valvular disease.

Stenosis of the pre-cerebral arteries: Stenosis of the origin of the internal carotid artery, as well as other pre-cerebral arteries is a stroke risk factor.

Transient ischemic attacks (TIA): A patient with TIA has about 5 to 10 fold times a higher stroke risk, as compared to a patient with the same age without TIA (at least during the first year).

&Alcohol: A low quantity of alcohol intake is not a stroke risk factor. It is established that an excessive alcohol intake is a stroke risk factor, particularly cerebral hemorrhage.

C. Probable risk factors for Cerebrovascular Disease

Lipids: Most studies indicate that high serum cholesterol levels slighty increase the risk of ischemic stroke.

Fibrinogen and Hematocrit: Elevated hematocrit and fibrinogen levels slightly increase the stroke risk.

Obesity: Abdominal obesity, although usually associated with other risk factors, is by itself a stroke risk factor.

Feminine sexual hormones: The absolute risk of important vascular events in women doing oral contraception (except if smoking and >30 yrs) is very low. Hormonal replacement therapy in post-menopausal women doesn't seem to increase the stroke risk though, having a protective role in some cases.

Sedentarism: Lack of regular physical exercise is a stroke risk factor.

CAROTID ENDARTECTOMY IN SECONDARY AND PRIMARY ISCHEMIC STROKE PREVENTION

General guidelines

• Every carotid endarterectomy candidate patient should be examined and have follow-up visits with a Neurologist.
• Carotid stenosis should be confirmed by angiography.
• Morbility and mortality monitoring is recommended - angiographic and pre-operatory - in every Centre where carotid endarterectomy is done.

A. Symptomatic patients

1. With indication for carotid endarterectomy

• Patients with Ischemic Transient Attacks (TIA) or non-disabling ischemic Cerebrovascular Infarcts, with stenosis of 70 to 99% in the ipsilateral internal carotid artery.

Endarterectomy should be done as soon as possible.

2. Without indication for carotid endarterectomy

• Patients with non-disabling TIA or ischemic stroke with stenosis of the ipsilateral internal carotid artery <30%.
• Patients with non-disabling TIA or ischemic stroke and occlusion of the ipsilateral internal carotid artery .

NOTE: These recommendations are not modified in the following cases:

• Presence of ipsilateral intracranial stenosis in a patient with extracranial stenosis of the internal carotid artery.

• Presence of assymptomatic intracranial aneurism.

B. Assymptomatic patients

Acceptable indication

• Stenosis of the internal carotid artery >70% in Centres with morbility and mortality - angiographic and per-operatory - <3%.

NON VALVULAR ARIAL FIBRILATION (AF)

Atrial fibrillation increases 5 times the stroke risk , being 75% of these accidents emboligenic and, in most cases, disabling. The role of associated carotid stenosis is lesser in AF. In fact, it's 12% prevalence, is similar in AF patients with or without stroke. The long term prognosis for a AF stroke patient is poor, since one third will have a major event: stroke, systemic embolism or death. The stroke risk in patients with AF is not the same.The clinical variables associated with increased risk are: age >65, high blood pressure, diabetes and TIA or previous stroke. The fact that the AF might be intermittent doesn't decrease the embolic risk. From an echocardiographic point of view, enlargement of the left atrium and left ventricular dysfunction increases the stroke risk.

Recent primary prevention studies have proved the protective role of oral anticoagulants (70% stroke reduction) and aspirin (25% reduction) in AF. The serious hemorrhagic risk associated with anticoagulants is about 1% per year, increasing, however, over 75 years of age, time in which it is advisable to keep the anticoagulation at a lower INR level. In relation to secondary prevention, the results of the European Atrial Fibrillation Trial (EAFT) show that the use of oral anticoagulants decreases by half the risk of a new stroke, while aspirin shows a much lower effect.The risk of oral anticoagulation under this indication is low (3% hemorrhage/year; 0.2% intracranial hemorrhage/year). It must be remembered however, that in this study the age limit for oral anticoagulation was 80 yrs.

NON VALVULAR ATRIAL FIBRILATION (AF)

APRIL 1996

Primary Prevention

• Patients under 75 years of age and with any of the following risk factors: hypertension, previous embolism, heart failure, left atrium enlargement, left ventricular dysfunction - are recommended for oral anticoagulation (INR 2-4.5).
• In the remaining and in patients with counter-indications for oral anticoagulants, aspirin is recommended (250-300mg/day)

Secondary Prevention

Patients with Atrial Fibrilation who suffered Transient Ischemic Attacks or Disabling Cerebral Infarction are recommended for oral anticoagulation (INR 2-4.5).

In patients with counter-indications for oral anticoagulation, aspirin is recommended (250-300mg/ dia).

Counter-indications for anticoagulation

• >80 years of age
• chronic alcoholism
• hepatic insufficiency
• Non controlled, chronic high arterial blood pressure: diastolic arterial pressure >100, systolic arterial pressure >180mmHg in at least two consecutive days.
• hemorrhagic rethinopathy
• previous intracraneal hemorrhage
• hemorrhagic diathesis
• peptic ulcer during the past 3 years
• gastrointestinal bleeding or hematuria in the last 6 months.
• pregnancy
• neurological or osteo-articular disease which may lead to frequent falls.
• dementia
• inability to take medication as prescribed or to regularly do the necessary control lab tests regularly.
• patients with symptoms which significantly restricts their lifestyles or prevents a totally indepedent existence (Rankin >3).

PLATELET ANTI-AGGREGATION IN PRIMARY AND SECONDARY ISCHEMIC STROKE PREVENTION

RECOMMENDATIONS

A. PRIMARY PREVENTION

Recommended anti-aggregation:

1. As alternative to anti-aggregants, in non rheumatismal atrial fibrilation (AF). Anti-aggregation is recommended as the first choice if the patient is under 75 years of age and doesn't suffer from any of the following conditions: high blood pressure, previous embolism, heart failure, left ventricular dysfunction or left auricle enlargement in echocardiogram.
2. Patients with evidence of arterial disease or thrombotic vascular events in other territories.

1. Assymptomatic carotid stenosis >50%.

B. SECONDARY PREVENTION

Anti-aggregant therapy in secondary prevention of vascular events decreases in 15% the vascular death risk, in 25% the major vascular risk event, in 32% the myocardial infarction risk and in 30% the stroke risk.

1. Definitive recommendation for platelet antiaggregation, based in several controlled clinical trials.

• Following TIA or stroke, except if the patient has anticoagulation indication.
• Following carotid endarterectomy.
• In emboligenous cardiopathies of high-medium risk an anti-aggregant agent should be added, if the patient suffers recurrency of embolic events in spite of correct anticogulation.

2. Recommendations for platelet antiaggregation - althoug in absence of several controlled clinical trials:

• Silent cerebral infarction.
• Vascular dementia, even without TIA/stroke episode.
• In patientes who have already suffered more than one TIA/stroke, with at least one being hemorrhagic.

Anti-aggregation should be initiated as soon as the physician establishes the stroke diagnosis. If clinically there is a reason to suspect intracranial hemorrhage, a CT scan should be previously performed. On the other hand, not performing a CT scan doesn't counter indicate the anti-aggregant prescription. Platelet anti-aggregation should continue along the years.

FINAL NOTES

The benefit of secondary prevention is independent of the anti-aggregant used, of those with proved efficacy: Aspirin, Ticlopidine, Dipiridamol.