According to a report from the Global Burden of Disease (GBD) 2016 Lifetime Risk of Stroke Collaborators,1 the estimated global lifetime risk of stroke in 2016 for those aged 25 years or older was ...24·9%, an increase from 22·8% in 1990. In a policy statement crafted by an American Heart Association working group, it was concluded that, by 2030, almost 4% of US adults will have had a stroke, accounting for total direct annual stroke-related medical costs increasing from US$71·55 billion in 2012 to $183·13 billion by 2030.2 Driving the upswing in stroke prevalence rates is a projected increase in stroke attributed to a growing and ageing population and lower stroke case fatality rates associated with better acute ischaemic stroke care and improved recurrent stroke prevention strategies.2 These findings point to the importance of continued surveillance of stroke case fatality, incidence, and recurrence rates.1,2 In The Lancet Neurology, the GBD 2016 Stroke Collaborators3 provide a systematic analysis of the global, regional, and national burden of stroke from 1990 to 2016 in terms of incidence, prevalence, deaths, years lived with disability, years of life lost, and disability-adjusted life-years (DALYs). ...metabolic factors (high systolic blood pressure, body-mass index, fasting plasma glucose, and total cholesterol and low glomerular filtration rate) accounted for 72% of stroke DALYs, behavioural factors (smoking, poor diet, and physical inactivity) accounted for 66%, and environmental risks (air pollution and lead exposure) accounted for about 28%.
Inflammation may be an important mechanism underlying dementia and cognitive decline in the elderly. Inflammation has been implicated in the neuropathological cascade leading to the development of ...Alzheimer's disease and other common forms of dementia in later life. These observations have led to observational epidemiological study to define the association of systemic and brain inflammatory markers on cognitive impairment and dementia. Furthermore, clinical trials have been carried out to better elucidate the possible role of nonsteroidal anti‐inflammatory drugs (NSAIDs) in the prevention or slowing of progression of Alzheimer's disease. In this review, we discuss the observational epidemiological and clinical trial evidence of the role of inflammation on the occurrence and prevention of dementia or cognitive decline. NSAIDs hold promise to prevent dementia if given in an appropriate time window during the induction phase of dementia and to subjects with apolipoprotein E (APOE) e4 alleles. Also, immunotherapy may prove beneficial.
Community engagement is a means to help overcome challenges to the delivery of health care and preventative services. On the occasion of the 2021 International Stroke Conference Edgar J. Kenton III ...Lecture, I review community engagement strategies utilized in the AAASPS trial (African-American Antiplatelet Stroke Prevention Study) and SDBA (Studies of Dementia in the Black Aged) observational studies that I directed. The main community engagement strategies included use of home visits (bringing the study to the community), engagement of churches, community advisors, community physicians, other healthcare providers, major Black community organizations, and utilization of diversity training. Community engagement strategies were a major component of AAASPS and SDBA that helped to ensure successful recruitment and retention of an underrepresented community in clinical trial and observational studies. Lessons learned from these studies largely carried out in the 1980s and 1990s helped to dispel myths that Blacks could not be recruited into large-scale clinical trials, emphasized the importance of studying underrepresented groups with adequate statistical power to test primary study hypotheses, and provided foundational recruitment and retention methods for future consideration.
Cardiovascular risk is increased in patients with gout. We compared cardiovascular outcomes associated with febuxostat, a nonpurine xanthine oxidase inhibitor, with those associated with allopurinol, ...a purine base analogue xanthine oxidase inhibitor, in patients with gout and cardiovascular disease.
We conducted a multicenter, double-blind, noninferiority trial involving patients with gout and cardiovascular disease; patients were randomly assigned to receive febuxostat or allopurinol and were stratified according to kidney function. The trial had a prespecified noninferiority margin of 1.3 for the hazard ratio for the primary end point (a composite of cardiovascular death, nonfatal myocardial infarction, nonfatal stroke, or unstable angina with urgent revascularization).
In total, 6190 patients underwent randomization, received febuxostat or allopurinol, and were followed for a median of 32 months (maximum, 85 months). The trial regimen was discontinued in 56.6% of patients, and 45.0% discontinued follow-up. In the modified intention-to-treat analysis, a primary end-point event occurred in 335 patients (10.8%) in the febuxostat group and in 321 patients (10.4%) in the allopurinol group (hazard ratio, 1.03; upper limit of the one-sided 98.5% confidence interval CI, 1.23; P=0.002 for noninferiority). All-cause and cardiovascular mortality were higher in the febuxostat group than in the allopurinol group (hazard ratio for death from any cause, 1.22 95% CI, 1.01 to 1.47; hazard ratio for cardiovascular death, 1.34 95% CI, 1.03 to 1.73). The results with regard to the primary end point and all-cause and cardiovascular mortality in the analysis of events that occurred while patients were being treated were similar to the results in the modified intention-to-treat analysis.
In patients with gout and major cardiovascular coexisting conditions, febuxostat was noninferior to allopurinol with respect to rates of adverse cardiovascular events. All-cause mortality and cardiovascular mortality were higher with febuxostat than with allopurinol. (Funded by Takeda Development Center Americas; CARES ClinicalTrials.gov number, NCT01101035 .).
The Maintenance of brain health is a lifelong process whereby potentially deleterious exposures such as cardiovascular risks, amyloid beta, and phosphorylated tau may adversely affect the brain ...decades before there are clinical manifestations. Thus, the early structural and neuropathological foundation for the development of cognitive impairment and its allied features later in life may provide precursor targets such that interventions may be applied to prevent or slow cognitively impairing processes if the underlying mechanism(s) can be addressed in time.
Cognitive impairment of later life is an important medical and public health challenge. Worldwide it is estimated that the number of persons with dementia will continue to increase, especially in ...low‐ and middle‐income countries. An important public health challenge relates to the prevention of cognitive decline and dementia. Specifically, is it possible to maintain cognitive vitality or prevent or slow cognitive decline? In this opinion‐based piece, I review United States‐based guidance statements for maintenance of cognition and select single and multidomain trials designed to preserve cognitive function. Guidance statements now recommend that we treat or prevent cardiovascular risks in hopes of preventing cognitive impairment or decline. I discuss potential gaps between guidance statements and interventional studies, and provide comments on where windows of opportunity may exist to close potential gaps in our quest to maintain cognitive vitality.
This article is part of the Special Issue “Vascular Dementia”.
Worldwide, dementia prevalence is expected to triple over the next 30 years. Strategies to prevent or slow cognitive decline in older persons have not been successful. More recently, however, we have begun to think more broadly about the antecedents of the dementias of later life and have begun to recognize the importance of modifiable cardiovascular risk factors and the occurrence of coexistent stroke, a preventable condition, in patients with Alzheimer's disease. In this opinion‐piece I review United States‐based guidance statements for maintenance of cognitive vitality, recent clinical trials to prevent cognitive impairment, and potential gaps in relation to clinical strategies to prevent cognitive impairment. The graphic depicts steps to be taken to preserve cognitive vitality in line with recommendations from the Institute of Medicine report.
This article is part of the Special Issue “Vascular Dementia”.
Age-related dementia, most commonly caused by Alzheimer disease or cerebrovascular factors (vascular dementia), is a major public health threat. Chronic arterial hypertension is a well-established ...risk factor for both types of dementia, but the link between hypertension and its treatment and cognition remains poorly understood. In this scientific statement, a multidisciplinary team of experts examines the impact of hypertension on cognition to assess the state of the knowledge, to identify gaps, and to provide future directions.
Authors with relevant expertise were selected to contribute to this statement in accordance with the American Heart Association conflict-of-interest management policy. Panel members were assigned topics relevant to their areas of expertise, reviewed the literature, and summarized the available data.
Hypertension disrupts the structure and function of cerebral blood vessels, leads to ischemic damage of white matter regions critical for cognitive function, and may promote Alzheimer pathology. There is strong evidence of a deleterious influence of midlife hypertension on late-life cognitive function, but the cognitive impact of late-life hypertension is less clear. Observational studies demonstrated a cumulative effect of hypertension on cerebrovascular damage, but evidence from clinical trials that antihypertensive treatment improves cognition is not conclusive.
After carefully reviewing the literature, the group concluded that there were insufficient data to make evidence-based recommendations. However, judicious treatment of hypertension, taking into account goals of care and individual characteristics (eg, age and comorbidities), seems justified to safeguard vascular health and, as a consequence, brain health.
Vascular cognitive impairment and dementia Gorelick, Philip B.; Counts, Scott E.; Nyenhuis, David
Biochimica et biophysica acta,
05/2016, Letnik:
1862, Številka:
5
Journal Article
Recenzirano
Odprti dostop
Vascular contributions to cognitive impairment are receiving heightened attention as potentially modifiable factors for dementias of later life. These factors have now been linked not only to ...vascular cognitive disorders but also Alzheimer's disease. In this chapter we review 3 related topics that address vascular contributions to cognitive impairment: 1. vascular pathogenesis and mechanisms; 2. neuropsychological and neuroimaging phenotypic manifestations of cerebrovascular disease; and 3. prospects for prevention of cognitive impairment of later life based on cardiovascular and stroke risk modification. This article is part of a Special Issue entitled: Vascular Contributions to Cognitive Impairment and Dementia edited by M. Paul Murphy, Roderick A. Corriveau and Donna M. Wilcock.
•Age-related cerebrovascular factors and pathological events precipitate VCID.•Neuropsychological and neuroimaging manifestations of cerebrovascular disorders•Current thinking on CVD and VCID risk factors and prevention•A variety of animal models have been developed to replicate vascular pathology.•Neuroimaging and neuropsychology advances provide more complete understanding of VCI.
Vascular cognitive impairment (VCI) is the second most common type of dementia after Alzheimer's disease (AD). Stroke and cardiovascular risk factors have been linked to both AD and VCI and ...potentially can affect cognitive function in mid and later life. Various pharmacological agents, including donepezil, galantamine, and memantine, approved for the treatment of AD have shown modest cognitive benefits in patients with vascular dementia (VaD). However, their functional and global benefits have been inconsistent. Donepezil has shown some cognitive benefit in patients with VaD only, and galantamine has shown some benefit in mixed dementia (AD/VaD). The benefits of other drugs such as rivastigmine, memantine, nimodipine, and piracetam are not clear. Some other supplements and herbal therapies, such as citicoline, actovegin, huperzine A, and vinpocetine, have also been studied in patients with VaD, but their beneficial effects are not well established. Non-drug therapies and lifestyle modifications such as diet, exercise, and vascular risk factor control are important in the management of VCI and should not be ignored. However, there is a need for more robust clinical trials focusing on executive function and other cognitive measures and incorporation of newer imaging modalities to provide additional evidence about the utility of these strategies in patients with VCI.
Alzheimer disease and vascular cognitive impairment are important causes of cognitive decline in the elderly. It has now been shown that vascular risk factors have measurable negative effects on the ...brain and are associated with cognitive impairment. We review vascular factors that might be responsible to cognitive decline in Alzheimer disease and vascular cognitive impairment and the corresponding interventions that might prevent cognitive impairment as we age.