Effect of chronic atrial fibrillation on regional cerebral blood flow.

Lavy, S; Stern, Shlomo; Melamed, Eldad; Cooper, Gerald R.; A, Keren; Levy, Paul S.

doi:10.1161/01.str.11.1.35

Cited by 132 publications

(80 citation statements)

References 21 publications

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“…5 8 10 15 Second, a previous study found a significant reduction in hemispheric cerebral blood flow in patients with AF compared with those with sinus rhythm. 21 The effect of the decreased hemispheric cerebral blood flow may contribute to the development of large infarcts and neurological severity in patients with AF.…”

Section: Discussionmentioning

confidence: 99%

Atrial fibrillation as a predictive factor for severe stroke and early death in 15 831 patients with acute ischaemic stroke

Kimura

2005

Journal of Neurology, Neurosurgery & Psychiatry

282

166

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Section: Discussionmentioning

confidence: 99%

Atrial fibrillation as a predictive factor for severe stroke and early death in 15 831 patients with acute ischaemic stroke

Kimura

2005

Journal of Neurology, Neurosurgery & Psychiatry

282

166

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“…140,141 In a meta-analysis including 77 668 patients, of whom 11 700 had AF, AF was associated with a 42% greater risk of dementia after adjustment for other known stroke-promoting conditions. 142 Hypothesized pathophysiological mechanisms include cerebral hypoperfusion, 143 microembolization, 144 inflammation, and platelet dysfunction. 145 Unfortunately 141,146 Consequently, the pathogenitic role of microemboli is uncertain, given the observation that antithrombotic therapy did not modify the association between AF and cognitive decline in these studies.…”

Section: Cognitive Dysfunctionmentioning

confidence: 99%

The Clinical Profile and Pathophysiology of Atrial Fibrillation

Andrade

Khairy

Dobrev

et al. 2014

Circulation Research

982

364

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Atrial fibrillation (AF) is the most common arrhythmia (estimated lifetime risk, 22%–26%). The aim of this article is to review the clinical epidemiological features of AF and to relate them to underlying mechanisms. Long-established risk factors for AF include aging, male sex, hypertension, valve disease, left ventricular dysfunction, obesity, and alcohol consumption. Emerging risk factors include prehypertension, increased pulse pressure, obstructive sleep apnea, high-level physical training, diastolic dysfunction, predisposing gene variants, hypertrophic cardiomyopathy, and congenital heart disease. Potential risk factors are coronary artery disease, kidney disease, systemic inflammation, pericardial fat, and tobacco use. AF has substantial population health consequences, including impaired quality of life, increased hospitalization rates, stroke occurrence, and increased medical costs. The pathophysiology of AF centers around 4 general types of disturbances that promote ectopic firing and reentrant mechanisms, and include the following: (1) ion channel dysfunction, (2) Ca 2+ -handling abnormalities, (3) structural remodeling, and (4) autonomic neural dysregulation. Aging, hypertension, valve disease, heart failure, myocardial infarction, obesity, smoking, diabetes mellitus, thyroid dysfunction, and endurance exercise training all cause structural remodeling. Heart failure and prior atrial infarction also cause Ca 2+ -handling abnormalities that lead to focal ectopic firing via delayed afterdepolarizations/triggered activity. Neural dysregulation is central to atrial arrhythmogenesis associated with endurance exercise training and occlusive coronary artery disease. Monogenic causes of AF typically promote the arrhythmia via ion channel dysfunction, but the mechanisms of the more common polygenic risk factors are still poorly understood and under intense investigation. Better recognition of the clinical epidemiology of AF, as well as an improved appreciation of the underlying mechanisms, is needed to develop improved methods for AF prevention and management.

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“…20 Another potential mechanism, although still not definitively proven, is brain hypoperfusion, which may depend on reduced cardiac output and on the beat-to-beat variability in the length of the cardiac cycle. 21 In AF patients, the ability to increase cardiac output during exercise seems to be limited, thus affecting the exercise-associated elevation in cerebral perfusion. 22 In a recent study, Alosco et al 23 evaluated cerebral perfusion, by means of cerebral blood flow velocity of the middle cerebral artery with transcranial Doppler ultrasonography, in 187 patients (mean age, 68.5±8.8 years), without history of stroke, who were enrolled in a National Institutes of Health study examining neurocognitive outcomes in older adults with heart failure.…”

mentioning

confidence: 99%