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Abstract Heart disease is the major leading cause of death and disability in the world. 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.
Introduction It has been known since the Ebers papyrus [ 1 ] in BC, and probably even before then, that the brain and heart are intimately connected.
This belief was consolidated by religious and scientific dogma for centuries. Fast-forwarding to the 20th century, several researchers in the late s became aware of an intriguing link between a sick heart and the start of cognitive deterioration that often led to vascular dementia VaD [ 2 ].
The suggested link between cardiovascular deficits as a risk to AD was important not only because it has now been generally accepted to be true but because it implied that other extracardiac vascular risk factors might also play a crucial role in the initiation of this dementia by possibly sharing common pathological pathways or markers common in AD.
Moreover, the therapeutic implications of controlling such vascular risk factors to AD have become one of the most important inroads in the search to lower the rising prevalence of AD and VaD [ 34 ]. Cardiovascular disease affects the heart vessels which affect the structural tissue of the heart and The fundamental factors affecting the elderly in the society be classified as coronary the most commonvalvular, cardiomyopathic, arrhythmic, congenital, and heart failure [ 5 ].
Due to space constraints, only some forms of cardiovascular disease will be reviewed here although it is anticipated that most forms of heart disease which lower cerebral blood flow through an impairment in cardiac structure or physiology will also be found to increase AD risk.
Cardiovascular Disease, Cognition, and Cerebral Autoregulation The original association between cardiac pathology and cognitive dysfunction described above as cardiogenic dementia was based on the high incidence of cardiac dysrhythmias seen in patients with dementia solely due to vascular causes [ 6 ].
Thus, chronic heart block and dysrhythmias that were shown to lower cardiac output and lead to persistent cognitive dysfunction and dementia were rightly believed to stem from a diseased heart [ 6 ].
When arrhythmias were suspected to cause cognitive dysfunction, it was found that cognitive dysfunction could be attenuated or reversed with cardiac pacing [ 67 ].
Restoration of cognitive ability by pacing was attributed to bringing the impaired cerebral perfusion back to normal by maintaining an adequate heart rate [ 6 ]. At the present time, brain hypoperfusion that develops from low cardiac output or hypotension has been shown to cause cognitive deficits in attention and memory [ 8 ], and more recent studies propose that these deficits develop from brain hypoperfusion and can lead to AD [ 9 — 11 ].
When hypotension is involved, its link to cognitive decline has been generally ignored in clinical practice. One reason for this attitude is the current dogma that low systemic blood pressure does not cause brain dysfunction because compensatory cerebral autoregulation prevents brain hypoperfusion from being activated [ 12 ].
However, studies have confirmed, particularly in the elderly, that cerebral autoregulation does not necessarily protect the brain from chronic low blood pressure and low cardiac output, an outcome that can result in cerebral blood flow insufficiency and its accompanying consequences [ 913 — 15 ].
Evidence to support the concept linking cognitive function to cerebral perfusion also 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. Normally, cerebral autoregulation maintains a constant blood flow to the brain between 50— mm Hg mean arterial pressure.
The main function of cerebral autoregulation is to maintain cerebral perfusion pressure by signaling brain arterioles to dilate or constrict during changes in arterial blood pressure [ 17 ]. Cerebral autoregulation may become impaired with aging [ 18 ] but it is not clear why or how.
The long-term evolution for potential brain damage during aging can involve decades. It may develop from atherosclerosis, arterial stiffness, or cardiovascular disease which can impair cerebral autoregulation homeostasis and result in brain hypoperfusion Figure 2.
Brain hypoperfusion would preferentially affect the older brain which is already primed to neurometabolic dysfunction by decreased delivery of energy substrates to brain cells [ 19 — 21 ].
Glucose is the primary molecule used to create energy fuel for mammalian brain cells and the brain depends on a continuous and optimal flow of blood to maintain normal brain cell activity and structural integrity [ 28 ]. If impaired cerebral autoregulation is indeed one of the culprits that contributes to cognitive failure in the elderly following chronically evolving vascular insults, a number of cerebral vasoactive molecules may be coconspirators in the development of AD, among them vasodilators such as endothelial nitric oxide, adenosine, prostacyclin, and epoxygenases that yield epoxyeicosatrienoic acids and vasoconstrictors such as thromboxane A2, endothelin-1, and hydroxyeicosatetraenoic acids HETE.
Curiously, pharmacologic inhibition of HETE appears to impair cerebral autoregulation in vivo [ 29 ]. Another cyclic burden on the heart that generates reduced blood flow to the brain is the finding that cerebral hypoperfusion can impair cerebrovascular reactivity [ 3031 ], possibly as a result of reduced nitric oxide release from damaged endothelial cells [ 32 ].
Other vascular risk factors, such as chronic hypertension can shift the limits of autoregulation toward higher blood pressure levels [ 33 ].
This adaptative mechanism protects the brain against hypertension to some degree but can also render it more vulnerable to cerebral hypoperfusion in elderly individuals who are aggressively treated with antihypertensive medication that induces hypotension. For this reason, it has been argued that careful consideration should be exercised when elderly persons with mild or moderate hypertension are given anti-hypertensive therapy, since such a treatment may lead to unregulated hypotension and risk of dementia [ 3435 ].
Not surprisingly, when dynamic cerebral autoregulation is impaired from unilateral carotid artery stenosis, carotid endarterectomy, or stenting can reverse the effects of the brain dysautoregulation [ 36 ]. Recent evidence indicates that patients undergoing carotid artery stent placement for atherosclerosis showed either neurocognitive improvement at the end of 12 months or no worsening in status from baseline, suggesting that this procedure is safe and possibly effective [ 37 ].
Cerebral autoregulatory dysfunction can also occur with vertebral artery disease although little can be done surgically to correct impaired blood flow from these lesioned vessels [ 38 ]. Despite the obvious importance that connects some types of heart disease to cognitive impairment Figure 1it has been largely ignored by many researchers in the field and by most cardiologists as evidenced by the absence of presentations discussing this topic in Alzheimer or heart-related conferences.Everywhere, certain religious and social groups of persons can be found on the margins of society: immigrants, gypsies, the homeless, displaced persons, refugees, the untouchables in the caste system and those who are suffering from diseases which carry a social stigma.
The stress associated with caring for chronically ill family members may result in stress for the caregiver. Home care providers i.e. spouses, children of elderly parents and parents themselves contribute a huge sum in the national economy. In most parts, the economic contribution or quantification of home care providers is not accounted for.
This chapter examines some of the factors affecting health status that are driving health care spending among the Medicare population. The workshop presentations covered three such factors, which research shows are important to . FOUNDATION.
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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).