No abstract available.
Echocardiography, Transesophageal* ; Stroke*

BACKGROUND AND PURPOSE: The presence of dysphagia and aspiration in stroke patients is associated with increased mortality and morbidity. Early recognition and management of these two conditions via reliable, minimally invasive bedside procedures before complications arise remains challenging in everyday clinical practice. This study reviews the available bedside screening tools for detecting swallowing status and aspiration risk in acute stroke by qualitatively observing reference population study design, clinical flexibility, reliability and applicability to acute-care settings. METHODS: The primary search was conducted using the PubMed, Embase, and Cochrane Library databases. The search was limited to papers on humans written in English and published from 1991 to 2016. Eligibility criteria included the consecutive enrollment of acute-stroke inpatients and the development of a protocol for screening aspiration risk during oral feeding in this population. RESULTS: Of the 652 sources identified, 75 articles were reviewed in full however, only 12 fulfilled the selection criteria. Notable deficiencies in most of the bedside screening protocols included poor methodological designs and inadequate predictive values for aspiration risk which render clinicians to be more conservative in making dietary recommendations. CONCLUSIONS: The literature is dense with screening methods for assessing the presence of dysphagia but with low predictive value for aspiration risk after acute stroke. A standard, practical, and cost-effective screening tool that can be applied at the bedside and interpreted by a wide range of hospital personnel remains to be developed. This need is highlighted in settings where neither trained personnel in evaluating dysphagia nor clinical instrumentation procedures are available.
Deglutition Disorders ; Deglutition* ; Humans ; Inpatients ; Mass Screening* ; Mortality ; Patient Selection ; Personnel, Hospital ; Pliability ; Stroke

BACKGROUND AND PURPOSE: This study aimed was to measure the quality of life, fatigue, stress, and depression in a consecutive sample of caregivers of multiple sclerosis (MS) patients. METHODS: We included data from 131 consecutive caregivers of MS patients [age=51.2±12.8 years (mean±SD), males=53.4%, duration of caregiving=10.0±6.3 years]. We assessed the quality of life, fatigue, stress, and depression of the caregivers using the 36-item Short Form Health Survey, Krupp Fatigue Severity Scale, Kingston Caregiver Stress Scale, and Hamilton Scale for Depression, respectively. The disability status of the patients was assessed using the Kurtzke Expanded Disability Status Scale. We used linear regression models to identify possible correlations between all of the aforementioned scales, while multivariable logistic regression models were employed to assess the correlations of caregiver fatigue with caregiver characteristics and patient disability. RESULTS: The linear regression analyses revealed that caregiver fatigue was positively associated with stress and negatively correlated with both physical health status and mental health status. Caregiver stress was positively associated with depression and negatively correlated with both physical health status and mental health status. Depression was negatively correlated with both caregiver physical health status and mental health status. In multivariable logistic regression analysis, caregiver fatigue was found to be independently associated with education status [odds ratio (OR)=0.61, 95% CI=0.37 to 0.99], history of chronic disease (OR=5.52, 95% CI=1.48 to 20.55), other chronic diseases in the family (OR=7.48, 95% CI=1.49 to 37.47), and the disability status of the patient (OR=1.36, 95% CI=1.03 to 1.80). CONCLUSIONS: Fatigue, stress, and depression in caregivers of MS patients are negatively correlated with their physical health status and mental health status. Caregiver fatigue is independently associated with education status, history of chronic disease, other chronic disease in the family, and patient disability.
Anxiety ; Caregivers* ; Chronic Disease ; Depression ; Education ; Fatigue ; Health Surveys ; Humans ; Linear Models ; Logistic Models ; Mental Health ; Multiple Sclerosis* ; Quality of Life* ; Weights and Measures

Numerous observational studies have identified a decline in cerebro-/cardiovascular (CV) admissions during  the initial phase of the COVID-19 pandemic. Recent studies and meta-analyses indicated that the overall decrease was smaller than that found in initial studies during the first months of 2020. Two years later we still do not have clear evidence about the potential causes and impacts of the reduction of CV hospitalizations during the COVID-19 pandemic. It has becoming increasingly evident that collateral damage (i.e., incidental damage to the public and patients) from the COVID-19 outbreak is the main underlying cause that at least somewhat reflects the effects of imposed measures such as social distancing and self-isolation. However, a smaller true decline in CV events in the community due to a lack of triggers associated with such acute syndromes cannot be excluded. There is currently indirect epidemiological evidence about the immediate impact that the collateral damage had on excess mortality, but possible late consequences including a rebound increase in CV events are yet to be observed. In the present narrative review, we present the reporting milestones in the literature of the rates of CV admissions and collateral damage during the last 2 years, and discuss all possible factors contributing to the decline in CV hospitalizations during the COVID-19 pandemic. Healthcare systems need to be prepared so that they can cope with the increased hospitalization rates for CV events in the near future.

Background: and Purpose Lipoprotein(a) [Lp(a)] is a lipoprotein structurally similar to low-density lipoprotein and is considered a genetically determined risk factor for cardiovascular disease. Although Lp(a) has been linked to ischemic stroke, its role in secondary stroke prevention, particularly in stroke recurrence, remains unclear. Methods: A systematic search of MEDLINE and Scopus databases was conducted to identify randomized controlled trials (RCTs) and observational studies reporting Lp(a) levels in patients with ischemic stroke or transient ischemic attack. The primary outcome was stroke recurrence, and secondary outcomes included poor functional outcome, all-cause mortality, and recurrent vascular events. Pooled odds ratios (ORs) were calculated using a random-effects model. Results: A total of 12 studies, including one RCT post hoc analysis and 11 observational studies, comprising 17,903 patients (mean age 63 years, 38% female), were included. Elevated Lp(a) levels were significantly associated with increased stroke recurrence (OR: 1.69; 95% confidence interval [CI]: 1.09–2.63; P=0.020) and poor functional outcome (OR: 2.09; 95% CI: 1.40–3.11; P<0.001). No significant associations were found between Lp(a) levels and all-cause mortality (OR: 2.20; 95% CI: 0.89–5.43; P=0.088) or recurrent vascular events (OR: 2.66; 95% CI: 0.95–7.44; P=0.063). Conclusion Elevated Lp(a) levels are linked to increased stroke recurrence and poor functional outcome in stroke patients. Lp(a) may represent a novel therapeutic target in secondary stroke prevention in addition to a promising biomarker.

Background: and Purpose Lipoprotein(a) [Lp(a)] is a lipoprotein structurally similar to low-density lipoprotein and is considered a genetically determined risk factor for cardiovascular disease. Although Lp(a) has been linked to ischemic stroke, its role in secondary stroke prevention, particularly in stroke recurrence, remains unclear. Methods: A systematic search of MEDLINE and Scopus databases was conducted to identify randomized controlled trials (RCTs) and observational studies reporting Lp(a) levels in patients with ischemic stroke or transient ischemic attack. The primary outcome was stroke recurrence, and secondary outcomes included poor functional outcome, all-cause mortality, and recurrent vascular events. Pooled odds ratios (ORs) were calculated using a random-effects model. Results: A total of 12 studies, including one RCT post hoc analysis and 11 observational studies, comprising 17,903 patients (mean age 63 years, 38% female), were included. Elevated Lp(a) levels were significantly associated with increased stroke recurrence (OR: 1.69; 95% confidence interval [CI]: 1.09–2.63; P=0.020) and poor functional outcome (OR: 2.09; 95% CI: 1.40–3.11; P<0.001). No significant associations were found between Lp(a) levels and all-cause mortality (OR: 2.20; 95% CI: 0.89–5.43; P=0.088) or recurrent vascular events (OR: 2.66; 95% CI: 0.95–7.44; P=0.063). Conclusion Elevated Lp(a) levels are linked to increased stroke recurrence and poor functional outcome in stroke patients. Lp(a) may represent a novel therapeutic target in secondary stroke prevention in addition to a promising biomarker.

Background: and Purpose Lipoprotein(a) [Lp(a)] is a lipoprotein structurally similar to low-density lipoprotein and is considered a genetically determined risk factor for cardiovascular disease. Although Lp(a) has been linked to ischemic stroke, its role in secondary stroke prevention, particularly in stroke recurrence, remains unclear. Methods: A systematic search of MEDLINE and Scopus databases was conducted to identify randomized controlled trials (RCTs) and observational studies reporting Lp(a) levels in patients with ischemic stroke or transient ischemic attack. The primary outcome was stroke recurrence, and secondary outcomes included poor functional outcome, all-cause mortality, and recurrent vascular events. Pooled odds ratios (ORs) were calculated using a random-effects model. Results: A total of 12 studies, including one RCT post hoc analysis and 11 observational studies, comprising 17,903 patients (mean age 63 years, 38% female), were included. Elevated Lp(a) levels were significantly associated with increased stroke recurrence (OR: 1.69; 95% confidence interval [CI]: 1.09–2.63; P=0.020) and poor functional outcome (OR: 2.09; 95% CI: 1.40–3.11; P<0.001). No significant associations were found between Lp(a) levels and all-cause mortality (OR: 2.20; 95% CI: 0.89–5.43; P=0.088) or recurrent vascular events (OR: 2.66; 95% CI: 0.95–7.44; P=0.063). Conclusion Elevated Lp(a) levels are linked to increased stroke recurrence and poor functional outcome in stroke patients. Lp(a) may represent a novel therapeutic target in secondary stroke prevention in addition to a promising biomarker.

BACKGROUND AND PURPOSE: Current guidelines do not provide firm directions on atrial fibrillation (AF) screening after ischemic stroke (IS). We sought to investigate the association of implantable cardiac monitoring (ICM) duration with the yield of AF detection in IS patients. METHODS: We included studies reporting AF detection rates by ICM in IS patients with negative initial AF screening. We excluded studies reporting prolonged cardiac monitoring with devices other than ICM, not providing AF detection rates or monitoring duration, and reporting overlapping data for the same population. The random-effects model was used for all pooled estimates and meta-regression analyses. RESULTS: We included 28 studies (4,531 patients, mean age 65 years). In meta-regression analyses, the proportion of AF detection by ICM was independently associated with monitoring duration (coefficient=0.015; 95% confidence interval [CI], 0.005 to 0.024) and mean patient age (coefficient=0.009; 95% CI, 0.003 to 0.015). No associations were detected with other patient characteristics, including IS subtype (cryptogenic vs. embolic stroke of undetermined source) or time from IS onset to CM implantation. In subgroup analyses, significant differences (P<0.001) in the AF detection rates were found for ICM duration (<6 months: 5% [95% CI, 3% to 6%]; ≥6 and ≤12 months: 21% [95% CI, 16% to 25%]; >12 and ≤24 months: 26% [95% CI, 22% to 31%]; >24 months: 34% [95% CI, 29% to 39%]). CONCLUSIONS: Extended duration of ICM monitoring and increased patient age are factors that substantially increase AF detection in IS patients with initial negative AF screening.
Atrial Fibrillation ; Humans ; Mass Screening ; Stroke

Background: and Purpose Secondary progressive multiple sclerosis (SPMS) presents with a challenging clinical phenotype, and siponimod has a potential to treat the active clinical phenotype of this disease. This single-center longitudinal study aimed to determine the therapeutic effects of siponimod in patients with active SPMS over 12 months. Methods: The clinical and radiological parameters of 50 patients with active SPMS treated using siponimod were assessed at baseline and after a 1-year follow-up period using the annual relapse rate (ARR), the Expanded Disability Status Scale (EDSS), the occurrence of gadolinium-enhanced lesion (GdE+), the Modified Fatigue Impact Scale (MFIS), and the Symbol Digit Modalities Test. The urine bladder postvoid residual (PVR) volume was also measured in a subcohort of 39 participants. Participants with an EDSS score ≥5.0 at baseline were finally assessed separately in prespecified subgroup analyses. Results: There were significant reductions in ARR (p<0.001), GdE+ (p<0.001), and MFIS score (p=0.001) during the follow-up period. The progression of physical and cognitive disabilities remained stable (p>0.05). The PVR-volume analysis revealed a significant decrease in urine bladder PVR volume (p<0.001). These observations were consistent for the subgroup with EDSS score ≥5.0. Conclusions Siponimod demonstrated efficacy in reducing ARR, GdE+, fatigue levels, and PVR volume, while maintaining stability in the cognitive and physical disability statuses of patients with SPMS. Similar findings were documented in the subgroup with EDSS score ≥5.0.

Background: and Purpose Secondary progressive multiple sclerosis (SPMS) presents with a challenging clinical phenotype, and siponimod has a potential to treat the active clinical phenotype of this disease. This single-center longitudinal study aimed to determine the therapeutic effects of siponimod in patients with active SPMS over 12 months. Methods: The clinical and radiological parameters of 50 patients with active SPMS treated using siponimod were assessed at baseline and after a 1-year follow-up period using the annual relapse rate (ARR), the Expanded Disability Status Scale (EDSS), the occurrence of gadolinium-enhanced lesion (GdE+), the Modified Fatigue Impact Scale (MFIS), and the Symbol Digit Modalities Test. The urine bladder postvoid residual (PVR) volume was also measured in a subcohort of 39 participants. Participants with an EDSS score ≥5.0 at baseline were finally assessed separately in prespecified subgroup analyses. Results: There were significant reductions in ARR (p<0.001), GdE+ (p<0.001), and MFIS score (p=0.001) during the follow-up period. The progression of physical and cognitive disabilities remained stable (p>0.05). The PVR-volume analysis revealed a significant decrease in urine bladder PVR volume (p<0.001). These observations were consistent for the subgroup with EDSS score ≥5.0. Conclusions Siponimod demonstrated efficacy in reducing ARR, GdE+, fatigue levels, and PVR volume, while maintaining stability in the cognitive and physical disability statuses of patients with SPMS. Similar findings were documented in the subgroup with EDSS score ≥5.0.