After additional adjustment for symptomatic stroke or MRI findings of infarcts, the association disappeared ( Table 4). However, the association was weakened after additional adjustment for cardiovascular risk factors and prevalent heart diseases. Individuals with AF had larger WMH volumes than those without after adjustment for TIV. In women, there were no significant associations between AF and symptomatic stroke, lacunes, and silent brain infarcts, but there was a trend toward an association between AF and large infarcts. In stratified analyses by sex, AF was associated with symptomatic stroke, large infarcts, lacunes, and silent brain infarcts in men. However, after exclusion of individuals with dementia, the interaction for AF and sex in relation to silent brain infarcts had a value of p = 0.121. No interactions were found between AF and sex in relation to symptomatic stroke ( p = 0.399 in the adjusted model), large infarcts ( p = 0.932), lacunes ( p = 0.313), or silent brain infarcts ( p = 0.410). Excluding individuals with dementia (and TIA for the analysis of silent brain infarcts) did not affect the results. Data AvailabilityĪF was associated with a history of symptomatic stroke (odds ratio 4.5, 95% confidence interval 2.1–9.5), large infarcts (OR 5.0, 95% CI 1.5–5.9), lacunes (OR 2.7, 95% CI 1.2–5.6), and silent brain infarcts (OR 3.5, 95% CI 1.6–7.4) ( Table 3). Individuals with missing data were omitted from the analyses. Purposeful variable selection was applied in all adjusted models 22 that is, all potential covariates were included in univariable models and thereafter in the multivariable models if the values of p were 15%. In analyses including WMHs and CMBs, stroke and infarcts were also considered possible covariates. Sex, education, heart disease, hypertension, diabetes, hypercholesterolemia, BMI, smoking, alcohol risk consumption, and the APOE ε4 allele were considered possible covariates. The analyses including silent brain infarcts were repeated after the additional exclusion of individuals with TIA. For analyses including silent brain infarcts, individuals with a history of symptomatic stroke (n = 44) were excluded. Definition of Diagnoses Used for ExclusionĪnalyses including stroke/infarcts and WMHs were repeated after the exclusion of individuals with dementia. Hypercholesterolemia was defined as present treatment with lipid-lowering medication, total cholesterol >6.2 mmol/L, low-density lipoprotein cholesterol ≥4.1 mmol/L, triglycerides >5.6 mmol/L, or high-density lipoprotein cholesterol 98 g alcohol/wk based on self-reported consumption during the last month. 18 Diabetes mellitus was defined as present treatment with insulin or antidiabetic drug, fasting glucose ≥7.0 mmol/L, or nonfasting glucose ≥11.1 mmol/L. Hypertension was defined as present medical treatment for hypertension, systolic blood pressure ≥150 mm Hg, or diastolic blood pressure ≥90 mm Hg as suggested by the Eight Joint National Committee in 2014. Myocardial infarction was defined through self-report, the NPR (ICD10-SE I21–I23, I24.1, I25.2, I25.6), or major or moderate Q waves on ECG (MC 1.1–1.2, excluding 1.2.6 and 1.2.8).

Heart failure was defined through self-report or the NPR (ICD10-SE I11.0, I13.0, I13.2, I50). Heart diseases included heart failure and myocardial infarction. 11 Because AF is associated with both symptomatic stroke and silent infarcts (i.e., infarcts on brain imaging without clinical symptoms), it is important to also consider the influence of stroke and silent infarcts when studying the effects of AF on the brain.Įducation level was defined as mandatory (corresponding to 7–8 years) or less vs more than mandatory. 10 For CMBs, different topography has been linked to different etiologies lobar CMBs have been associated with CAA, while CMBs in the infratentorial and deep brain regions have been associated with atherosclerosis and hypertension. 9 Lacunes are highly correlated with WMHs 6 and are associated with advanced age and vascular risk factors such as hypertension, smoking, and diabetes. 7 The most established risk factors for WMHs are hypertension and advanced age, 8 but other cardiovascular risk factors may also play a role. 6 Markers of cSVD on brain MRI includes white matter hyperintensities (WMHs), lacunes of presumed vascular origin, and cerebral microbleeds (CMBs). 6, 7 Different pathologic processes may lead to cSVD such as arteriosclerosis, cerebral amyloid angiopathy (CAA), venous collagenosis, and inflammation.

Const CHARSET_LOWER = 'abcdefghijklmnopqrstuvwxyz' Ĭonst CHARSET_UPPER = 'ABCDEFGHIJKLMNOPQRSTUVWXYZ' Ĭonst CHARSET_ALPHA = CHARSET_LOWER + CHARSET_UPPER Ĭonst CHARSET_ALNUM = CHARSET_ALPHA + CHARSET_NUM Ĭonst CHARSET_ALNUM_SANE = CHARSET_ALNUM.Cerebral small vessel disease (cSVD) affects small arteries, arterioles, capillaries, and small veins 6and has been related to cognitive decline, vascular dementia, and stroke.

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