Epidemiology

Stroke is a major health concern worldwide. It accounts for 11% of all deaths in England and Wales.[3] Each year in England 2000 people have a first episode of TIA. The age-adjusted annual incidence rate for TIA in the UK has been estimated at 190 cases per 100,000 population.[9] This is slightly higher than the reported incidence in Spain (35-60/100,000) and Belgium (68 to 102 /100,000).[10][11]

Risk factors

In patients with atrial fibrillation without valvular disease, the relative risk for TIA is 2.5- to 5-fold higher than in patients without atrial fibrillation. There is a dramatically higher risk when associated with valve abnormality.[15][17]

Persistent atrial fibrillation appears to have a higher risk than intermittent fibrillation.[17]

Atrial fibrillation causes stasis in the left atrium, which increases the chance of thrombus formation in the left atrial appendage. Thrombus once formed inside the heart can embolise, creating TIA or stroke.

Odds ratio of 2.0 for TIA. Aortic valve disease has higher risk than mitral valve disease.[17]

The mechanism of association is likely to be due to valve abnormality forming a thrombogenic focus in the heart and thus predisposing to embolic events.

Strong for high-grade stenosis. Risk of stroke, TIA, or death in asymptomatic stenosis ranges from 11% to 21% with medical management only.[18] Higher rates of stenosis (>70%) are associated with significantly increased risk compared with moderate stenosis (50% to 69%).

This may be due either to stasis, leading to increased risk of cardioembolic events, or via common risk factors for cerebrovascular disease and ischaemic heart failure. The odds ratio for congestive heart failure and TIA is 2.4.[17]

The most common risk factor for cerebrovascular disease.

Relative risk for TIA is approximately 2- to 5-fold in the presence of hypertension.[15][17] The higher the chronic BP elevation, the more this risk factor is important for cerebral ischaemia, forming a continuous risk association.

Mechanism is via increasing likelihood of atherosclerotic vascular disease.

Diabetes is a potent risk factor for atherosclerotic disease and has been reported to be present in up to one third of patients who present with cerebral ischaemia.[19][20] The presence of diabetes increases the risk for TIA by an odds ratio of 1.5 to 2.[15][17][21]

Diabetes is frequently associated with other atherosclerotic risk factors in the metabolic syndrome. It is recommended that the patient with diabetes be recognised to be at greater than average risk for cerebrovascular disease. As a result, patients with diabetes are felt to merit aggressive management of other modifiable risk factors.

Tobacco abuse is one of the most important modifiable risk factors for cerebrovascular disease, and smokers have 1.5 to 2 times the risk of non-smokers for cerebrovascular events.[15][22]

Tobacco smoke may increase blood viscosity and increase coagulability.

The increased risk wanes with smoking cessation, but some increased risk remains, likely associated with lasting atherosclerotic vascular changes.

The association between smoking and ischaemic stroke is strongest in younger patients.[22]

Strong association for heavy use only. The relationship between alcohol use and stroke is non-linear with higher risk with heavy use, but a relative protective effect with moderate alcohol intake.[23]

Moderate alcohol use may increase protective levels of high-density lipoprotein (HDL) and decrease platelet aggregation. Intake of >60 g of alcohol daily is associated with an increased risk of ischaemic stroke with an odds ratio of 1.6.[23] Changes in blood pressure may also occur with drinking that may lead to a predisposition to stroke.[24]

TIAs are more common in middle age and in older people. Symptoms in a young patient increase the possibility of alternative diagnosis or a less common aetiology for ischaemia, such as congenital heart disease, paradoxical emboli, drug use, or hypercoagulability.

Another atherosclerotic risk factor, but more weakly associated with cerebrovascular disease than with cardiovascular disease.

In selected cases, such as the young TIA patient with a PFO, atrial septal aneurysm, and significant shunt, there may be an association with stroke.[25] For the unselected general population, the presence of a PFO does not significantly increase the risk of cerebral ischaemia. However, in patients with cryptogenic stroke, closure of PFOs has been shown to reduce recurrent stroke rates.[26]

The relationship between PFO and TIA is complicated by the commonness of PFO in the population. More than a quarter of the population will have this remnant of fetal circulation, and yet only a small fraction will have a TIA or stroke.

It appears that vigorous physical activity may be protective against later cerebrovascular events.[27] Overall, highly active patients have a 27% lower risk of stroke incidence.

Obesity, particularly abdominal obesity, is weakly associated with cerebrovascular disease. It is unclear the extent to which this is a direct association or mediated via comorbidities such as diabetes, hypertension, and hyperlipidaemia.

The majority of TIAs occur in patients who lack any hypercoagulability, with only 1% to 4.8% of strokes being due to coagulation disorders.[8]

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