ABSTRACT
Background@#It has become important to identify and manage risk factors for subclinical atrial fibrillation (AF) with an increase in its detection rate. Thus, this research aimed to investigate whether alcohol consumption contrib‑ utes to the development of subclinical AF. @*Methods@#This prospective study enrolled 467 patients without AF from a multicenter pacemaker registry. The incidence of subclinical AF (episodes of atrial rate > 220 beats per minute without symptoms) was compared between alcohol-drinking and non-drinking groups. @*Results@#During followup (median 18 months), the incidence and risk of long-duration atrial high-rate episodes (AHRE) ≥ 24 h were increased in the alcohol group compared to the non-alcohol group [5.47 vs. 2.10 per 100 personyears, adjusted hazard ratio (HR), 2.83; 95% confidence interval (CI), 1.14–7.04; P = 0.03]. After propensity score match‑ ing, the incidence and risk of long-duration AHRE were higher in the alcohol group (6.97 vs. 1.27 per 100 personyears, adjusted HR, 7.84; 95% CI, 1.21–50.93; P = 0.03). The mean burden of long-duration subclinical AF was higher in the alcohol group than in the non-alcohol group (0.18 vs. 1.61% during follow-up, P = 0.08). @*Conclusion@#Alcohol consumption was associated with an increased risk of subclinical AF. Long-duration AHRE inci‑ dence and AHRE burden were higher in alcohol drinkers than in non-drinkers.
ABSTRACT
Background@#Sudden cardiac arrest (SCA) has not been well studied in Asian countries. This study investigated the temporal trends in the incidence and outcomes of SCA and the impact of age, gender, economic state, and urbaniza‑ tion on SCA using a nationwide population-based sample cohort of South Korea. @*Methods@#In the Korean National Health Insurance Service—Sample Cohort consisting of one million persons from 2003 through 2013, we identified 5,675 (0.56%) patients with SCA using ICD-10 code I46 and I49.0. We evaluated the impact of the age, gender, household income, and urbanization level on the incidence and outcome of SCA. @*Results@#During the study period, the overall age- and gender-adjusted annual incidence of SCA increased by 46.9% from 30.9 in 2003 to 45.4 in 2013 (per 100,000 person-years, p < 0.001 for trend). The medical cost per 100,000 personyears also greatly increased about four times (p < 0.001 for trend). The overall adjusted survival to hospital discharge rate increased from 8.9% in 2003 to 13.2% in 2013 (adjusted rate ratio per year 1.05; p < 0.001 for trend). Old age and low household incomes of the population was related to increased SCA and poor survival to hospital discharge rate. The proportion of patients with intensive or advanced therapeutic modalities after SCA greatly increased from 1.6% in 2003 to 10.0% in 2013 (p < 0.001 for trend). This increase was consistent regardless of age, gender, economic state, and urbanization level. @*Conclusions@#Although the incidence of SCA was increased, the outcome was improved for the decade. However, in the elderly and low-income population, the incidence of SCA continued to rise and survival outcome was not improved.
ABSTRACT
For almost 20 years, data regarding the effect of rhythm control therapy for atrial fibrillation (AF) on cardiovascular prognosis in comparison with rate control therapy has not been conclusive. The safety of rhythm control and anticoagulation therapy has generally improved. Recently, it was revealed that a rhythm-control strategy reduced the risk of adverse cardiovascular events than usual rate control in patients with recent AF (diagnosed within 1 year). Within 1 year after the AF diagnosis, early initiation of rhythm control led to more favorable cardiovascular outcomes than rate control. Early rhythm control reduced the risks of stroke and heart failure-related admission than rate control. Moreover, rhythm control was associated with lower dementia risk than rate control. Finally, early rhythm control treatment was also effective in patients with asymptomatic AF but less effective in older adults. Therefore, in patients with AF, rhythm control should be considered at earlier stages, regardless of symptom.
ABSTRACT
Atrial fibrillation (AF) is the most common form of arrhythmia in the elderly population and increases stroke risk by a factor of 4- to 5-fold. There is increasing evidence to suggest that incident AF may contribute to the development of dementia, independent of overt stroke. In particular, relatively younger patients with AF are more prone to dementia development than older patients with AF. Evidence is accumulating regarding the possible treatment strategies for preventing dementia in patients with AF. Oral anticoagulation may be effective for reducing the risk of dementia, even in patients with low stroke risks. Among oral anticoagulants, the use of non-vitamin K antagonists have been associated with a considerably decreased risk of dementia than warfarin. Moreover, successful catheter ablation for AF has also been associated with decreased dementia risk compared to medical therapy, suggesting that restoration of sinus rhythm, and not the ablation procedure itself, as the important mechanism in the prevention of AF-associated dementia. Among midlife patients with AF, there appeared to be a U-shaped association of blood pressure (BP) and a linear association of hypertension with dementia risk.A BP of 120 to 129/80 to 84 mmHg has been identified as the optimal range. Finally, integrated management of AF was associated with a reduced risk of dementia in AF patients.
ABSTRACT
Atrial fibrillation (AF), the most common cardiac arrhythmia in the elderly population, has been associated with an impairment of cognitive function and an increased risk of dementia. Even though there does not appear to be solid evidence that any specific treatment prevents or delays AF-associated cognitive decline, evidence is accumulating regarding the possible treatment strategies for preventing dementia. Oral anticoagulation, especially non-vitamin K antagonist oral anticoagulants rather than warfarin use, has been suggested to be associated with reduced risk of dementia. Successfully maintaining sinus rhythm using catheter ablation might be also helpful in preventing subsequent dementia in patients with AF. In this review, we critically appraise the proposed treatment strategies for preventing AF-associated cognitive decline.
ABSTRACT
Background@#We aimed to investigate the comparative risk of fracture among patients with atrial fibrillation (AF) treated with warfarin or non-vitamin K antagonist oral anticoagulants (NOACs). @*Methods@#Using the Korean National Health Insurance Service database, patients with AF who received a prescrip‑ tion for apixaban, dabigatran, rivaroxaban, or warfarin between 2013 and 2016 were included. Risk of major fractures (osteoporotic hip, vertebral, or pelvic fractures) were compared using inverse probability of treatment weighting. @*Results@#There were 70,481 patients identified (41.3% women; mean [SD] age 70.5 [11.3] years); 16,992 apixaban, 22,514 dabigatran, 27,998 rivaroxaban, and 29,390 warfarin users. During a median follow-up of 390 days, 2412 major fractures occurred with weighted incidences per 100 patient-years of 2.56 for apixaban, 2.39 for dabigatran, 2.78 for rivaroxaban, and 3.43 for warfarin. NOAC use was associated with a lower risk for fracture than warfarin use: HR 0.70 (95% confidence interval [CI] 0.57–0.86) for apixaban, HR 0.69 (95% CI 0.60–0.78) for dabigatran, and HR 0.79 (95% CI 0.70–0.90) for rivaroxaban. In head-to-head comparisons between NOACs, there was no significant difference between apixaban and dabigatran. Rivaroxaban was associated with a higher risk for fracture than dabigatran (HR 1.15, 95% CI 1.02–1.31). @*Conclusion@#In patients with AF, NOAC use may result in a lower risk for osteoporotic fracture compared with warfa‑ rin use. Fracture risk does not seem to be altered by the choice of NOAC type, except for rivaroxaban. These associa‑ tions may help inform benefit–risk assessments when choosing between the different anticoagulant types.
ABSTRACT
Atrial fibrillation (AF), the most common cardiac arrhythmia in the elderly population, has been associated with an impairment of cognitive function and an increased risk of dementia. Even though there does not appear to be solid evidence that any specific treatment prevents or delays AF-associated cognitive decline, evidence is accumulating regarding the possible treatment strategies for preventing dementia. Oral anticoagulation, especially non-vitamin K antagonist oral anticoagulants rather than warfarin use, has been suggested to be associated with reduced risk of dementia. Successfully maintaining sinus rhythm using catheter ablation might be also helpful in preventing subsequent dementia in patients with AF. In this review, we critically appraise the proposed treatment strategies for preventing AF-associated cognitive decline.
ABSTRACT
Background@#We aimed to investigate the comparative risk of fracture among patients with atrial fibrillation (AF) treated with warfarin or non-vitamin K antagonist oral anticoagulants (NOACs). @*Methods@#Using the Korean National Health Insurance Service database, patients with AF who received a prescrip‑ tion for apixaban, dabigatran, rivaroxaban, or warfarin between 2013 and 2016 were included. Risk of major fractures (osteoporotic hip, vertebral, or pelvic fractures) were compared using inverse probability of treatment weighting. @*Results@#There were 70,481 patients identified (41.3% women; mean [SD] age 70.5 [11.3] years); 16,992 apixaban, 22,514 dabigatran, 27,998 rivaroxaban, and 29,390 warfarin users. During a median follow-up of 390 days, 2412 major fractures occurred with weighted incidences per 100 patient-years of 2.56 for apixaban, 2.39 for dabigatran, 2.78 for rivaroxaban, and 3.43 for warfarin. NOAC use was associated with a lower risk for fracture than warfarin use: HR 0.70 (95% confidence interval [CI] 0.57–0.86) for apixaban, HR 0.69 (95% CI 0.60–0.78) for dabigatran, and HR 0.79 (95% CI 0.70–0.90) for rivaroxaban. In head-to-head comparisons between NOACs, there was no significant difference between apixaban and dabigatran. Rivaroxaban was associated with a higher risk for fracture than dabigatran (HR 1.15, 95% CI 1.02–1.31). @*Conclusion@#In patients with AF, NOAC use may result in a lower risk for osteoporotic fracture compared with warfa‑ rin use. Fracture risk does not seem to be altered by the choice of NOAC type, except for rivaroxaban. These associa‑ tions may help inform benefit–risk assessments when choosing between the different anticoagulant types.
ABSTRACT
Atrial fibrillation (AF) is the most common form of arrhythmia in the elderly population and increases stroke risk by a factor of 4- to 5-fold. There is increasing evidence to suggest that incident AF may contribute to the development of dementia, independent of overt stroke. In particular, relatively younger patients with AF are more prone to dementia development than older patients with AF. Evidence is accumulating regarding the possible treatment strategies for preventing dementia in patients with AF. Oral anticoagulation may be effective for reducing the risk of dementia, even in patients with low stroke risks. Among oral anticoagulants, the use of non-vitamin K antagonists have been associated with a considerably decreased risk of dementia than warfarin. Moreover, successful catheter ablation for AF has also been associated with decreased dementia risk compared to medical therapy, suggesting that restoration of sinus rhythm, and not the ablation procedure itself, as the important mechanism in the prevention of AF-associated dementia. Among midlife patients with AF, there appeared to be a U-shaped association of blood pressure (BP) and a linear association of hypertension with dementia risk.A BP of 120 to 129/80 to 84 mmHg has been identified as the optimal range. Finally, integrated management of AF was associated with a reduced risk of dementia in AF patients.
ABSTRACT
Background@#Despite various strategies designed for preventing pain from propofol injection, it is still common and distressing to the patients. The purpose of the present study was to investigate the adequate effect-site concentration (Ce) of remifentanil to prevent pain due to propofol injection. @*Methods@#A total of 160 adults scheduled for elective surgery were randomly assigned to one of four groups receiving normal saline (group S) or remifentanil at a Ce of 2 (group R2), 3 (group R3), or 4 (group R4), administered via target-controlled infusion, followed by the injection of 2 mg/kg of propofol (delivered with 1% lipid propofol). The severity and incidence of injection pain were assessed on a four-point scale. @*Results@#The incidence of propofol injection pain was significantly lower in group R2, R3, or R4 than in group S (30%, 5%, or 2.5% vs. 70%, respectively). Moreover, the intensity of the pain was lesser in group R2, R3, or R4 than in group S. However, the incidence or severity of injection was not different between groups R3 and R4. @*Conclusions@#During the induction of balanced anesthesia using propofol injection, pretreatment with remifentanil at a target Ce of 3 ng/ml effectively reduced propofol injection pain in adults.
ABSTRACT
An interaction between ribosomal protein S3 (rpS3) and nuclear factor kappa B or macrophage migration inhibitory factor in non-small-cell lung cancer is responsible for radioresistance. However, the role of rpS3 in glioblastoma (GBM) has not been investigated to date. Here we found that in irradiated GBM cells, rpS3 translocated into the nucleus and was subsequently ubiquitinated by ring finger protein 138 (RNF138). Ubiquitin-dependent degradation of rpS3 consequently led to radioresistance in GBM cells. To elucidate the apoptotic role of rpS3, we analyzed the interactome of rpS3 in ΔRNF138 GBM cells. Nuclear rpS3 interacted with DNA damage inducible transcript 3 (DDIT3), leading to DDIT3-induced apoptosis in irradiated ΔRNF138 GBM cells. These results were confirmed using in vivo orthotopic xenograft models and GBM patient tissues. This study aims to clarify the role of RNF138 in GBM cells and demonstrate that rpS3 may be a promising substrate of RNF138 for the induction of GBM radioresistance, indicating RNF138 as a potential target for GBM therapy.
Subject(s)
Humans , Apoptosis , DNA Damage , Fingers , Glioblastoma , Heterografts , Lung Neoplasms , Macrophages , NF-kappa B , Ribosomal Proteins , Ubiquitin , UbiquitinationABSTRACT
Complete hardware removal is recommended in the case of patients with cardiovascular implantable electronic device (CIED) infections. However, the complete extraction of chronically implanted leads is not always achieved. The outcomes and optimal management of CIED infections with retained material after lead extractions have not been elucidated. In this case report, we present five patients with CIED infections with remnant lead tips even after lead extractions. Two patients had localized pocket infections, and were managed with antibiotics for a period of more than two weeks. The other three patients had infective endocarditis, and were managed with antibiotics for a period of more than four weeks. In one patient, the lead tip migrated to the right pulmonary artery, but did not produce any symptoms or complications. Only one of five patients experienced a resurgence of an infection.
Subject(s)
Humans , Anti-Bacterial Agents , Device Removal , Endocarditis , Pacemaker, Artificial , Pulmonary ArteryABSTRACT
As a new humanized monoclonal antibody against the interleukin-6 receptor, tocilizumab is currently used for the treatment of rheumatoid arthritis (RA) patients. Tocilizumab was reported to provoke drug-related liver toxicity, although there have been no reports on significant liver toxicity from tocilizumab in Korean patients with RA to date. Here, we describe the first case of tocilizumab-related liver toxicity in a patient with complicated RA, accompanied with macrophage activation syndrome, who had received tacrolimus and prednisolone and in whom both conventional disease modifying anti-rheumatic drugs, including methotrexate, leflunomide and sulfasalazine or tumor necrotizing factor-alpha blockades, were contraindicated due to drug eruption and a history of lung cancer.
Subject(s)
Humans , Antirheumatic Agents , Arthritis, Rheumatoid , Drug Eruptions , Interleukin-6 , Liver , Lung Neoplasms , Macrophage Activation Syndrome , Macrophage Activation , Macrophages , Methotrexate , Prednisolone , Sulfasalazine , Tacrolimus , Tranexamic AcidABSTRACT
TFAP2C (transcription factor-activating enhancer-binding protein 2C) expression has been positively correlated with poor prognosis in patients with certain types of cancer, but the mechanisms underlying TFAP2C-mediated tumorigenesis in non-small-cell lung cancer (NSCLC) are still unknown. We previously performed a microarray analysis to identify TFAP2C regulation genes, and TGFBR1 (transforming growth factor-β receptor type 1) was found to be upregulated by TFAP2C. We observed that TFAP2C or TGFBR1 overexpression led to oncogenic properties, such as cell viability, proliferation and cell cycle progression. TGFBR1 upregulation induced by TFAP2C also promoted cell motility and migration, leading to malignant development. We also found that PAK1 (p21 protein (Cdc42/Rac)-activated kinase 1) signaling was involved in TFAP2C/TGFBR1-induced tumorigenesis. These results were confirmed by an in vivo xenograft model and patient tissue samples. This study shows that TFAP2C promoted tumor progression by upregulation of TGFBR1 and consequent activation of PAK1 signaling.