Epidemiology
There are more than 100,000 strokes in the UK each year causing 38,000 deaths, making it a leading cause of death and disability.[5][6][7] People are most likely to have a stroke over the age of 55.[6][8] Ischaemic stroke prevalence can be further sub-divided according to pathophysiological mechanism: extracranial atherosclerosis (10%), intracranial atherosclerosis (10%), cardioembolic (25%), lacunar infarction ([small vessel disease] 15%), indeterminate aetiology ([i.e., cryptogenic] 30%), or other defined causes (10%). Ischaemic stroke is more common in older people and people with lower levels of education. In the UK, ischaemic stroke is more common in people who are black or South Asian.[9] In the US, ischaemic stroke is more common in African-American or Hispanic people.[10][11][12][13]
The overall incidence of stroke as well as stroke mortality has been decreasing over the last few decades in high-income countries; this is thought to be driven by effective primary prevention and improvements in stroke care.[14] However, there is some evidence of increasing incidence among young adults.[14][15] The bulk of the global stroke burden (86% of deaths and 89% of disability-adjusted life-years, or DALYs) is in lower-income and lower-middle-income countries where stroke incidence has increased.[16][17][18][19] Between 1990 and 2016, the highest risks for stroke were seen in East Asia, Central Europe, and Eastern Europe, and the lowest risk was in eastern sub-Saharan Africa.[18]
Risk factors
Even after controlling for other age-related conditions such as hypertension, this remains a strong non-modifiable risk factor.[11]
Stroke-causing genetic disorders with mendelian inheritance are rare. However, twin studies show that a significant portion of stroke risk is heritable, and epidemiological studies show that family history of stroke is a risk factor.[21]
Numerous candidate genes have been proposed, but none have yet been consistently replicated as a strong risk factor for stroke.[22]
History of previous ischaemic stroke indicates that the patient may sustain more ischaemic strokes in the future (particularly if risk factors, e.g., hypertension, are not corrected). Stroke rate has been reported as 1.5%, 2.1%, 2.8%, 3.7%, and 5.1% on days 2, 7, 30, 90, and 365, respectively, after transient ischaemic attack (TIA).[23] Studies show that the rate of post-TIA stroke might have decreased slightly since 1999, likely related to advances in cardiovascular risk prevention.[24][25]
Strongly associated with increased incidence of ischaemic stroke.[26]
Strongly associated with increased incidence of ischaemic stroke.[27]
Strongly associated with increased incidence of ischaemic stroke.[28]
Strongly implicated in the risk of cardioembolic stroke but not other ischaemic stroke sub-types.[29]
Several other cardiac conditions have been reported as potential causes of cardioembolism, with varying degrees of evidence. These conditions include myocardial infarction with regional wall motion abnormalities or decreased left ventricular ejection fraction, valvular disease, patent foramen ovale with or without atrial septal aneurysm, mitral valve prolapse, prosthetic heart valve, and cardiomyopathy.[30]
Associated with vascular stenosis, brain ischaemia, and Moyamoya disease (vascular occlusion affecting circle of Willis).[34]
Large prospective studies have shown that increased serum total cholesterol is modestly associated with an increased risk of ischaemic stroke.[35]
There are few studies on the association of low-density lipoprotein cholesterol with stroke, and the results are conflicting.[30] A meta-analysis showed that increased high-density lipoprotein is protective against ischaemic stroke.[36]
Have been associated with increased incidence of ischaemic stroke.[37][38] In the UK, ischaemic stroke is more common in black people, who have 1.5 to 2.5 times greater risk of having a stroke than white people. People who are South Asian also have a risk for stroke about 1.5 times greater than white people, particularly those in the Pakistani and Bangladeshi ethnic groups. In contrast, people of Chinese ethnicity have lower risk of stroke than white people.[9] In the US, compared with white people, the risk of having a first stroke is nearly twice as high for black people, and black people are twice as likely to die from stroke.[11][39] Higher rates of hypertension, obesity, and diabetes mellitus among black people might account for some of this disparity.[38][40]
Epidemiological studies show a relationship between decreased stroke risk and increased consumption of fruits and vegetables, decreased consumption of sodium, and increased consumption of potassium.[41][42][43][44]
The effects of decreased sodium and increased potassium intake may be mediated by a lower risk of hypertension.
Decreased physical activity has been associated with increased risk of ischaemic stroke.[45]
Severe obstructive sleep apnoea doubles the risk for incident stroke, especially in young to middle-aged people. Continuous positive airway pressure (CPAP) may reduce stroke risk, but trials have not provided a high level of evidence to support the benefits of CPAP for primary stroke prevention.[52][53]
Several drugs may influence stroke risk. Cocaine and other drugs may cause changes in blood pressure or vasculitic-type changes in the intracranial circulation.
Unsafe intravenous injections may lead to infective endocarditis with subsequent cardioembolism, or paradoxical embolism of injected foreign material.
Case-control studies show an elevated risk of stroke associated with migraine, particularly in younger women and in those with migraine with aura.[54]
Prospective and case-control studies show that higher serum homocysteine levels are associated with a higher risk of ischaemic stroke. However, a randomised trial of homocysteine lowering to prevent stroke showed no benefit of therapy.[55] Subsequent studies with stroke as a secondary endpoint have shown varying results.[56][57] Therefore, although homocysteine is clearly a marker of ischaemic stroke risk, it remains unclear whether homocysteine itself causes stroke.
Most studies of lipoprotein(a) and ischaemic stroke show increased risk with higher lipoprotein(a) levels. Lipoprotein(a) levels can be lowered with niacin, but it is not known whether lipoprotein(a) reduction reduces the risk of ischaemic stroke.
Elevated anti-cardiolipin or anti-beta2-glycoprotein-1 antibody levels have been associated with stroke.
Hereditary conditions associated with venous thromboembolism (e.g., antithrombin III deficiency, protein C deficiency, protein S deficiency, factor V Leiden mutation, or prothrombin gene mutations) have not been found to be risk factors for ischaemic stroke but are related to the risk of cerebral venous sinus thrombosis.[30][58]
The possibility that hypercoagulable states may be more strongly associated with certain stroke sub-groups, including stroke in young people, is plausible but has not been evaluated in large studies.
Associated with an increased risk of stroke after controlling for other risk factors.[59] Whether it directly causes stroke or is merely a marker of risk is uncertain.
Aortic arch plaques may be a risk factor for recurrent stroke and death. In cases of cryptogenic strokes, further diagnostic tests are warranted to search for large aortic plaques.[60]
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