Abstract
Heart disease is the major leading cause of death and disability in the world. Mainly affecting the elderly population, heart disease and its main outcome, cardiovascular disease, have become an important risk factor in the development of cognitive decline and Alzheimer's disease (AD). This paper examines the evidence linking chronic brain hypoperfusion induced by a variety of cardiovascular deficits in the development of cognitive impairment preceding AD. The evidence indicates a strong association between AD and cardiovascular risk factors, including ApoE4, atrial fibrillation, thrombotic events, hypertension, hypotension, heart failure, high serum markers of inflammation, coronary artery disease, low cardiac index, and valvular pathology. In elderly people whose cerebral perfusion is already diminished by their advanced age, additional reduction of cerebral blood flow stemming from abnormalities in the heart-brain vascular loop ostensibly increases the probability of developing AD. Evidence also suggests that a neuronal energy crisis brought on by relentless brain hypoperfusion may be responsible for protein synthesis abnormalities that later result in the classic neurodegenerative lesions involving the formation of amyloid-beta plaques and neurofibrillary tangles. Insight into how cardiovascular risk factors can induce progressive cognitive impairment offers an enhanced understanding of the multifactorial pathophysiology characterizing AD and ways at preventing or managing the cardiovascular precursors of this dementia.
Highlights
It has been known since the Ebers papyrus [1] in 1552 BC, and probably even before that the brain and heart are intimately connected
Fast-forwarding to the 20th century, several researchers in the late 1970s became aware of an intriguing link between a sick heart and the start of cognitive deterioration that often led to vascular dementia (VaD) [2]
Subtle cognitive changes may progress to global cognitive decline and dementia, this conclusion requires further work to prove or disprove. It provides a preventive guide when clinical testing detects elderly patients with low ejection fraction or cardiac output. These findings show that advancing age, cardiovascular pathology, and cognitive function are closely linked, and that novel interventions to correct impending cardiac hemodynamic homeotassis could make a difference in preventing or significantly slowing a potential pathway to dementia
Summary
It has been known since the Ebers papyrus [1] in 1552 BC, and probably even before that the brain and heart are intimately connected. Evidence to support the concept linking cognitive function to cerebral perfusion comes from studies showing that cerebral blood flow rises in healthy subjects following moderate exercise but cerebral perfusion may not increase if cardiac output is limited by cardiac pathology affecting, for example, heart rate from a dysrhythmia [16]. These findings indicate that cerebral autoregulation does not reverse brain hypoperfusion when cardiac output is compromised by specific cardiac pathology. The ultimate fallout from low cardiac output on the brain is that hemodynamic pump dysfunction in the older person can significantly lower blood flow to brain cells via cerebral hypoperfusion, thereby diminishing energy substrate supply needed for normal brain cell metabolism [46,47,48,49,50]
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