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Background and Purpose This scientific statement provides an overview of the evidence on vascular contributions to cognitive impairment and dementia. Vascular contributions to cognitive impairment and dementia of later life are common. Definitions of vascular cognitive impairment (VCI), neuropathology, basic science and pathophysiological aspects, role of neuroimaging and vascular and other associated risk factors, and potential opportunities for prevention and treatment are reviewed. This statement serves as an overall guide for practitioners to gain a better understanding of VCI and dementia, prevention, and treatment. Methods Writing group members were nominated by the writing group co-chairs on the basis of their previous work in relevant topic areas and were approved by the American Heart Association Stroke Council Scientific Statement Oversight Committee, the Council on Epidemiology and Prevention, and the Manuscript Oversight Committee. The writing group used systematic literature reviews (primarily covering publications from 1990 to May 1, 2010), previously published guidelines, personal files, and expert opinion to summarize existing evidence, indicate gaps in current knowledge, and, when appropriate, formulate recommendations using standard American Heart Association criteria. All members of the writing group had the opportunity to comment on the recommendations and approved the final version of this document. After peer review by the American Heart Association, as well as review by the Stroke Council leadership, Council on Epidemiology and Prevention Council, and Scientific Statements Oversight Committee, the statement was approved by the American Heart Association Science Advisory and Coordinating Committee. Results The construct of VCI has been introduced to capture the entire spectrum of cognitive disorders associated with all forms of cerebral vascular brain injury—not solely stroke—ranging from mild cognitive impairment through fully developed dementia. Dysfunction of the neurovascular unit and mechanisms regulating cerebral blood flow are likely to be important components of the pathophysiological processes underlying VCI. Cerebral amyloid angiopathy is emerging as an important marker of risk for Alzheimer disease, microinfarction, microhemorrhage and macrohemorrhage of the brain, and VCI. The neuropathology of cognitive impairment in later life is often a mixture of Alzheimer disease and microvascular brain damage, which may overlap and synergize to heighten the risk of cognitive impairment. In this regard, magnetic resonance imaging and other neuroimaging techniques play an important role in the definition and detection of VCI and provide evidence that subcortical forms of VCI with white matter hyperintensities and small deep infarcts are common. In many cases, risk markers for VCI are the same as traditional risk factors for stroke. These risks may include but are not limited to atrial fibrillation, hypertension, diabetes mellitus, and hypercholesterolemia. Furthermore, these same vascul...

†Professor Zanchetti died during the development of these Guidelines, in March 2018. He contributed fully to the redaction of these Guidelines, as a member of the Guidelines' Task Force and as a section coordinator. He will be sadly missed by colleagues and friends.

Table 2 Factors influencing prognosis Risk factors Subclinical Organ Damage Systolic and diastolic BP levels Electrocardiographic LVH (Sokolow-Lyon > 38 mm; Cornell > 2440 mm M ms) or: Levels of pulse pressure (in the elderly) Echocardiographic LVH8 (LVMI M ! 125 g/m 2 , W ! 110 g/m 2 ) Age (M > 55 years; W > 65 years) Carotid wall thickening (IMT > 0.9 mm) or plaque Smoking Carotid-femoral pulse wave velocity >12 m/s Dyslipidaemia Ankle/brachial BP index < 0.9 -TC > 5.0 mmol/l (190 mg/dl) or:Slight increase in plasma creatinine:-LDL-C > 3.0 mmol/l (115 mg/dl) or: M: 115-133 mmol/l (1.3-1.5 mg/dl); -HDL-C: M < 1.0 mmol/l (40 mg/dl), W < 1.2 mmol/l (46 mg/dl) or:Low estimated glomerular filtration rate y (< 60 ml/min/1.73 m 2 ) or creatinine clearance^(< 60 ml/min) -TG > 1.7 mmol/l (150 mg/dl) Fasting plasma glucose 5.6-6.9 mmol/L (102-125 mg/dl) Microalbuminuria 30-300 mg/24 h or albumin-creatinine ratio: ! 22 (M); or ! 31(W) mg/g creatinine Abnormal glucose tolerance test Abdominal obesity (Waist circumference > 102 cm (M), > 88 cm (W)) Family history of premature CV disease (M at age < 55 years; W at age < 65 years) Diabetes Mellitus Established CV or renal disease Fasting plasma glucose ! 7.0 mmol/l (126 mg/dl) on repeated measurements, or Cerebrovascular disease: ischaemic stroke; cerebral haemorrhage; transient ischaemic attack Postload plasma glucose > 11.0 mmol/l (198 mg/dl) Heart disease: myocardial infarction; angina; coronary revascularization; heart failure Renal disease: diabetic nephropathy; renal impairment (serum creatinine M > 133, W > 124 mmol/l); proteinuria (> 300 mg/24 h) Peripheral artery disease Advanced retinopathy: haemorrhages or exudates, papilloedema Note: the cluster of three out of 5 risk factors among abdominal obesity, altered fasting plasma glucose, BP > --130/85 mmHg, low HDL-cholesterol and high TG (as defined above) indicates the presence of metabolic syndrome M: men; W: women; CV: cardiovascular disease; IMT: intima-media thickness; BP: blood pressure; TG: triglycerides; C: cholesterol;^Cockroft Gault formula; y MDRD formula; 8Risk maximal for concentric LVH (left ventricular hypertrophy): increased LVMI (left ventricular mass index) with a wall thickness/radius ratio ! 0.42.

Stiffness of elastic arteries like the aorta predicts cardiovascular risk. By directly reflecting arterial stiffness, having the best predictive value for cardiovascular outcome and the ease of its measurement, carotid-femoral pulse wave velocity is now considered the gold standard for arterial stiffness assessment in daily practice. Many different measurement procedures have been proposed. Therefore, standardization of its measurement is urgently needed, particularly regarding the distance measurement. This consensus document advises on the measurement procedures in general and provides arguments for the use of 80% of the direct carotid-femoral distance as the most accurate distance estimate. It also advises the use of 10 m/s as new cut-off value for carotid-femoral pulse wave velocity.

Abstract-Arterial stiffness may predict coronary heart disease beyond classic risk factors. In a longitudinal study, we assessed the predictive value of arterial stiffness on coronary heart disease in patients with essential hypertension and without known clinical cardiovascular disease. Aortic stiffness was determined from carotid-femoral pulse wave velocity at baseline in 1045 hypertensives. The risk assessment of coronary heart disease was made by calculating the Framingham risk score according to the categories of gender, age, blood pressure, cholesterol, diabetes, and smoking. Mean age at entry was 51 years, and mean follow-up was 5.7 years. Coronary events (fatal and nonfatal myocardial infarction, coronary revascularization, and angina pectoris) and all cardiovascular events served as outcome variables in Cox proportional-hazard regression models. Fifty-three coronary events and 97 total cardiovascular events occurred. In univariate analysis, the relative risk of follow-up coronary event or any cardiovascular event increased with increasing level of pulse wave velocity; for 1 SD, ie, 3.5 m/s, relatives risks were 1.