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1.
J Am Heart Assoc ; 13(3): e030587, 2024 Feb 06.
Article in English | MEDLINE | ID: mdl-38240252

ABSTRACT

BACKGROUND: Cerebral embolic protection devices (CEPD) capture embolic material in an attempt to reduce ischemic brain injury during transcatheter aortic valve replacement. Prior reports have indicated mixed results regarding the benefits of these devices. With new data emerging, we performed an updated meta-analysis examining the effect of CEPD during transcatheter aortic valve replacement on various clinical, neurological, and safety parameters. METHODS AND RESULTS: A comprehensive review of electronic databases was performed comparing CEPD and no-CEPD in transcatheter aortic valve replacement. Primary clinical outcome was all-cause stroke. Secondary clinical outcomes were disabling stroke and all-cause mortality. Neurological outcomes included worsening of the National Institutes of Health Stroke Scale score, Montreal Cognitive Assessment score from baseline at discharge, presence of new ischemic lesions, and total lesion volume on neuroimaging. Safety outcomes included major or minor vascular complications and stage 2 or 3 acute kidney injury. Seven randomized controlled trials with 4016 patients met the inclusion criteria. There was no statistically significant difference in the primary clinical outcome of all-cause stroke; secondary clinical outcomes of disabling stroke, all-cause mortality, neurological outcomes of National Institutes of Health Stroke Scale score worsening, Montreal Cognitive Assessment worsening, presence of new ischemic lesions, or total lesion volume on diffusion-weighted magnetic resonance imaging between CEPD versus control groups. There was no statistically significant difference in major or minor vascular complications or stage 2 or 3 acute kidney injury between the groups. CONCLUSIONS: The use of CEPD in transcatheter aortic valve replacement was not associated with a statistically significant reduction in the risk of clinical, neurological, and safety outcomes.


Subject(s)
Acute Kidney Injury , Aortic Valve Stenosis , Embolic Protection Devices , Intracranial Embolism , Stroke , Transcatheter Aortic Valve Replacement , Humans , Transcatheter Aortic Valve Replacement/methods , Aortic Valve Stenosis/complications , Aortic Valve Stenosis/surgery , Treatment Outcome , Intracranial Embolism/etiology , Intracranial Embolism/prevention & control , Stroke/etiology , Stroke/prevention & control , Stroke/surgery , Aortic Valve/surgery , Risk Factors
2.
Neuroscientist ; 26(2): 134-155, 2020 04.
Article in English | MEDLINE | ID: mdl-31092147

ABSTRACT

Traumatic brain injury (TBI) is a major health problem in the United States, which affects about 1.7 million people each year. Glial cells, T-cells, and mast cells perform specific protective functions in different regions of the brain for the recovery of cognitive and motor functions after central nervous system (CNS) injuries including TBI. Chronic neuroinflammatory responses resulting in neuronal death and the accompanying stress following brain injury predisposes or accelerates the onset and progression of Alzheimer's disease (AD) in high-risk individuals. About 5.7 million Americans are currently living with AD. Immediately following brain injury, mast cells respond by releasing prestored and preactivated mediators and recruit immune cells to the CNS. Blood-brain barrier (BBB), tight junction and adherens junction proteins, neurovascular and gliovascular microstructural rearrangements, and dysfunction associated with increased trafficking of inflammatory mediators and inflammatory cells from the periphery across the BBB leads to increase in the chronic neuroinflammatory reactions following brain injury. In this review, we advance the hypothesis that neuroinflammatory responses resulting from mast cell activation along with the accompanying risk factors such as age, gender, food habits, emotional status, stress, allergic tendency, chronic inflammatory diseases, and certain drugs can accelerate brain injury-associated neuroinflammation, neurodegeneration, and AD pathogenesis.


Subject(s)
Alzheimer Disease/pathology , Alzheimer Disease/physiopathology , Brain Injuries, Traumatic/physiopathology , Brain/metabolism , Inflammation/metabolism , Animals , Blood-Brain Barrier/metabolism , Brain/pathology , Brain Injuries, Traumatic/metabolism , Disease Models, Animal , Humans , Inflammation/physiopathology
3.
Cureus ; 11(11): e6139, 2019 Nov 12.
Article in English | MEDLINE | ID: mdl-31886074

ABSTRACT

Fucosidosis is a lysosomal storage disease, resulting from a deficiency of the enzyme alpha-L-fucosidase. We present the case of an affected female with numerous manifestations, clinically and radiographically. In fucosidosis, advanced interventions are not always necessary to have rewarding outcomes. In fact, early diagnosis and management of the symptoms with a multi-systemic supportive care approach can improve the quality of life and may also prolong the life of those patients diagnosed with fucosidosis.

4.
Mo Med ; 116(5): 400-403, 2019.
Article in English | MEDLINE | ID: mdl-31645793

ABSTRACT

Intracerebral hemorrhage occurs when a diseased blood vessel within the brain bursts. We present a case of 69-year-old patient with two sequential episodes of lobar intracerebral hemorrhage occurring during sexual intercourse. Both episodes were associated with the use of phosphodiesterase-5 inhibitors. This is the first case reported which is temporally associated with isolated bilateral lobar bleeds with appropriate use of phosphodiesterase-5 inhibitor on two different occasions associated with sexual intercourse.


Subject(s)
Cerebral Hemorrhage/etiology , Phosphodiesterase 5 Inhibitors/adverse effects , Sildenafil Citrate/adverse effects , Tadalafil/adverse effects , Aged , Cerebral Hemorrhage/diagnostic imaging , Coitus , Erectile Dysfunction/drug therapy , Humans , Male , Phosphodiesterase 5 Inhibitors/administration & dosage , Sildenafil Citrate/administration & dosage , Tadalafil/administration & dosage , Tomography, X-Ray Computed
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