Nocturnal hypoxemia and central apneas increase mortality, but not recurrent ischemic events after ischemic stroke

BackgroundThe aim of the study was to investigate whether findings in cardiorespiratory polygraphy had an association with stroke mortality or ischemic event recurrence after ischemic stroke.MethodsWe prospectively studied 204 ischemic stroke patients who underwent cardiorespiratory polygraphy within the first 48 h after the symptom onset. We followed all these patients for a median of 6.2 years. We evaluated mortality, time of survival, causes of death and new ischemic events.ResultsOf 204 ischemic stroke patients, 43 died and 48 had a new ischemic event during the follow-up. The lowest arterial oxyhemoglobin saturation (min SaO₂) (P = 0.007) was lower, the percentage of time spent below arterial oxyhemoglobin saturation less than 90% (T90) (P = 0.005) was higher, and central apnea index per hour (CAI/h) (P = 0.04) was higher among the deceased. Male gender, older age, diabetes mellitus, elevated modified Rankin scale (mRS) score, lower Glasgow Coma Scale (GCS) score and CAI/h independently predicted higher mortality. Peripheral arterial disease (PAD) and higher National Institutes of Health Stroke Scale (NIHSS) score were independent predictors for a recurrent ischemic event. Among those having respiratory event index (REI) at least 30, older age and lower GCS score independently predicted higher mortality. Only 21 stroke patients initiated continuous positive airway pressure (CPAP) treatment; of those, only one had a new ischemic event.ConclusionsThe non-survivors had more severe nocturnal hypoxemia and more central apneas than survivors. Among patients with REI at least 30/h, increased CAI predicted higher mortality, but not independently.Clinical trial registrationURL:http://www.clinicaltrials.gov. Unique identifier: NCT01861275</p

Obesity and the Risk of Cryptogenic Ischemic Stroke in Young Adults

Objectives: We examined the association between obesity and early-onset cryptogenic ischemic stroke (CIS) and whether fat distribution or sex altered this association. Materials and Methods: This prospective, multi-center, case-control study included 345 patients, aged 18-49 years, with first-ever, acute CIS. The control group included 345 age-and sex-matched stroke-free individuals. We measured height, weight, waist circumference, and hip circumference. Obesity metrics analyzed included body mass index (BMI), waist-to-hip ratio (WHR), waist-to-stature ratio (WSR), and a body shape index (ABSI). Models were adjusted for age, level of education, vascular risk factors, and migraine with aura. Results: After adjusting for demographics, vascular risk factors, and migraine with aura, the highest tertile of WHR was associated with CIS (OR for highest versus lowest WHR tertile 2.81, 95%CI 1.43-5.51; P=0.003). In sex-specific analyses, WHR tertiles were not associated with CIS. However, using WHO WHR cutoff values (>0.85 for women, >0.90 for men), abdominally obese women were at increased risk of CIS (OR 2.09, 95%CI 1.02-4.27; P=0.045). After adjusting for confounders, WC, BMI, WSR, or ABSI were not associated with CIS. Conclusions: Abdominal obesity measured with WHR was an independent risk factor for CIS in young adults after rigorous adjustment for concomitant risk factors.Peer reviewe

Nocturnal hypoxemia and central apneas increase mortality, but not recurrent ischemic events after ischemic stroke

Abstract Background: The aim of the study was to investigate whether findings in cardiorespiratory polygraphy had an association with stroke mortality or ischemic event recurrence after ischemic stroke. Methods: We prospectively studied 204 ischemic stroke patients who underwent cardiorespiratory polygraphy within the first 48 h after the symptom onset. We followed all these patients for a median of 6.2 years. We evaluated mortality, time of survival, causes of death and new ischemic events. Results: Of 204 ischemic stroke patients, 43 died and 48 had a new ischemic event during the follow-up. The lowest arterial oxyhemoglobin saturation (min SaO₂) (P = 0.007) was lower, the percentage of time spent below arterial oxyhemoglobin saturation less than 90% (T90) (P = 0.005) was higher, and central apnea index per hour (CAI/h) (P = 0.04) was higher among the deceased. Male gender, older age, diabetes mellitus, elevated modified Rankin scale (mRS) score, lower Glasgow Coma Scale (GCS) score and CAI/h independently predicted higher mortality. Peripheral arterial disease (PAD) and higher National Institutes of Health Stroke Scale (NIHSS) score were independent predictors for a recurrent ischemic event. Among those having respiratory event index (REI) at least 30, older age and lower GCS score independently predicted higher mortality. Only 21 stroke patients initiated continuous positive airway pressure (CPAP) treatment; of those, only one had a new ischemic event. Conclusions: The non-survivors had more severe nocturnal hypoxemia and more central apneas than survivors. Among patients with REI at least 30/h, increased CAI predicted higher mortality, but not independently

New insights into the genetic etiology of Alzheimer’s disease and related dementias

Characterization of the genetic landscape of Alzheimer’s disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/‘proxy’ AD cases and 677,663 controls. We found 75 risk loci, of which 42 were new at the time of analysis. Pathway enrichment analyses confirmed the involvement of amyloid/tau pathways and highlighted microglia implication. Gene prioritization in the new loci identified 31 genes that were suggestive of new genetically associated processes, including the tumor necrosis factor alpha pathway through the linear ubiquitin chain assembly complex. We also built a new genetic risk score associated with the risk of future AD/dementia or progression from mild cognitive impairment to AD/dementia. The improvement in prediction led to a 1.6- to 1.9-fold increase in AD risk from the lowest to the highest decile, in addition to effects of age and the APOE ε4 allele

New insights into the genetic etiology of Alzheimer’s disease and related dementias

Characterization of the genetic landscape of Alzheimer’s disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/‘proxy’ AD cases and 677,663 controls. We found 75 risk loci, of which 42 were new at the time of analysis. Pathway enrichment analyses confirmed the involvement of amyloid/tau pathways and highlighted microglia implication. Gene prioritization in the new loci identified 31 genes that were suggestive of new genetically associated processes, including the tumor necrosis factor alpha pathway through the linear ubiquitin chain assembly complex. We also built a new genetic risk score associated with the risk of future AD/dementia or progression from mild cognitive impairment to AD/dementia. The improvement in prediction led to a 1.6- to 1.9-fold increase in AD risk from the lowest to the highest decile, in addition to effects of age and the APOE ε4 allele