ABSTRACT
The relationship of blood pressure to cognition in the elderly is a poorly understood topic. Many questions exist such as does treatment of hypertension prevent cognitive decline, the optimal timing of intervention and selecting the appropriate agent. In this review we will explore recent epidemiologic data and clinical trials addressing hypertension and cognition, review pathophysiology of chronic hypertension and effects of brain function, discuss the timing of intervention and finally review opportunities for future research.
Subject(s)
Blood Pressure , Cognition Disorders/psychology , Cognition , Cognitive Aging , Hypertension/physiopathology , Age Factors , Aged , Aged, 80 and over , Antihypertensive Agents/therapeutic use , Blood Pressure/drug effects , Brain/physiopathology , Cognition Disorders/epidemiology , Cognition Disorders/physiopathology , Cognition Disorders/prevention & control , Female , Geriatric Assessment , Humans , Hypertension/drug therapy , Hypertension/epidemiology , Hypertension/psychology , Male , Middle Aged , Prognosis , Risk FactorsABSTRACT
We carried out a quality improvement project utilizing the electronic medical record (EMR) to determine (1) the quality of vascular neurologists' recommendations for recurrent stroke prevention and (2) primary care provider (PCP) acknowledgement of the vascular neurologists' recurrent stroke prevention recommendations and their frequency of meeting the recommended metrics for risk factor control and lifestyle modification. We conducted a retrospective EMR chart review on a convenience sample of ischemic stroke patients during two epochs. Data collected included risk factors, stroke subtype, and process and outcome guidance metrics for recurrent ischemic stroke prevention according to American Heart Association/American Stroke Association (AHA/ASA) recommendations. Overall, vascular neurologists commonly recommended appropriate AHA/ASA risk factor management standards, but were less likely to do so for lifestyle management. Improvements in the EMR system over time, including the establishment of guideline-driven importable recurrent stroke prevention templates, led to a high frequency of proper risk factor and lifestyle recommendations made by vascular neurologists. Statistical analysis provided further evidence that the EMR positively influenced the delivery of proper recurrent stroke prevention guidance. Although PCPs infrequently acknowledged receipt of vascular neurology consultations, there was a relatively high frequency of achieved risk factor control. The latter may be attributed at least in part to pre-existent quality improvement programs implemented at primary care offices. Our exploratory findings suggest that proper use of the EMR may heighten efforts to provide appropriate and consistent recurrent stroke prevention recommendations in a primary care setting.
Subject(s)
Ambulatory Care , Brain Ischemia/prevention & control , Electronic Health Records , Neurologists , Referral and Consultation , Stroke/prevention & control , Aged , Ambulatory Care/methods , Female , Humans , Male , Middle Aged , Physicians, Primary Care , Quality Improvement , Retrospective Studies , Risk Reduction Behavior , Secondary PreventionABSTRACT
PURPOSE OF REVIEW: The purpose of this review is to discuss the prevention of venous thromboembolism (VTE) in stroke patients. We discuss use of oral anticoagulation and other interventions for the prevention of VTE. A new class of medications, non-vitamin K antagonist oral anticoagulants (NOACs), have been successfully trialed for the prevention of VTE. We review the data and guidance statements for VTE prevention. RECENT FINDINGS: Warfarin and vitamin K antagonist drugs have been the mainstay of VTE prevention for decades. More recently, NOACs have become available for both stroke and systemic embolism prevention in nonvalvular atrial fibrillation and for VTE treatment or prevention. NOACs have been shown to be at least noninferior for VTE prevention and treatment when compared with warfarin, and have a good safety profile. Other approaches include use of graduated compression stockings, intermittent compression stockings, inferior vena cava filters, and heparins. Selection of the appropriate VTE prophylaxis in stroke patients is important to reduce associated morbidity and mortality.
Subject(s)
Anticoagulants/therapeutic use , Stroke/drug therapy , Venous Thrombosis/prevention & control , Humans , Stroke/complications , Stroke/therapy , Venous Thrombosis/complicationsABSTRACT
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.
Subject(s)
Cognitive Dysfunction/drug therapy , Dementia, Vascular/drug therapy , Nootropic Agents/therapeutic use , Animals , Cholinesterase Inhibitors/therapeutic use , Cognitive Dysfunction/etiology , Cognitive Dysfunction/physiopathology , Dementia, Vascular/etiology , Dementia, Vascular/physiopathology , Executive Function/drug effects , Humans , Life Style , Risk FactorsABSTRACT
Cerebral hyperperfusion is a relatively rare syndrome with significant and potentially preventable clinical consequences. The pathophysiology of cerebral hyperperfusion syndrome (CHS) may involve dysregulation of the cerebral vascular system and hypertension, in the setting of increase in cerebral blood flow. The early recognition of CHS is important to prevent complications such as intracerebral hemorrhage. This review will focus on CHS following carotid endarterectomy and carotid artery stenting. We will discuss the typical clinical features of CHS, risk factors, pathophysiology, diagnostic modalities for detection, identification of patients at risk, and prevention and treatment. Although currently there are no specific guidelines for the management of CHS, identification of patients at risk for CHS and aggressive treatment of hypertension are recommended.
ABSTRACT
PURPOSE: This study determined the role of inducible nitric oxide synthase (iNOS) and nitric oxide (NO) in the resistance response of BALB/c mice to P. aeruginosa-induced keratitis. METHODS: RT-PCR, nitrite detection, iNOS inhibition, ELISA, and immunohistochemistry were used. RESULTS: Early after infection, iNOS mRNA expression and nitrite levels in cornea were elevated compared to levels in the uninfected cornea. Treatment with aminoguanidine sulfate (AG), an inhibitor of iNOS, resulted in extensive corneal destruction, reduced nitrite levels, and reduced nitrotyrosine staining. Infected mice also had increased bacterial burden and elevated levels of MIP-1alpha, IL-1beta, and MIP-2 in the cornea. Dual-labeling immunohistochemistry established the macrophage as the major source of iNOS in the infected cornea. CONCLUSIONS: These data provide evidence that iNOS is constitutively expressed in the BALB/c cornea; that iNOS-derived NO is required for bacterial killing/stasis; and that the macrophage is the major cell source of NO.