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1.
Neurosci Bull ; 2020 Feb 18.
Artigo em Inglês | MEDLINE | ID: mdl-32072450

RESUMO

To evaluate whether the polygenic profile modifies the development of sporadic Alzheimer's disease (sAD) and pathological biomarkers in cerebrospinal fluid (CSF), 462 sAD patients and 463 age-matched cognitively normal (CN) controls were genotyped for 35 single-nucleotide polymorphisms (SNPs) that are significantly associated with sAD. Then, the alleles found to be associated with sAD were used to build polygenic risk score (PRS) models to represent the genetic risk. Receiver operating characteristic (ROC) analyses and the Cox proportional hazards model were used to evaluate the predictive value of PRS for the sAD risk and age at onset. We measured the CSF levels of Aß42, Aß42/Aß40, total tau (T-tau), and phosphorylated tau (P-tau) in a subgroup (60 sAD and 200 CN participants), and analyzed their relationships with the PRSs. We found that 14 SNPs, including SNPs in the APOE, BIN1, CD33, EPHA1, SORL1, and TOMM40 genes, were associated with sAD risk in our cohort. The PRS models built with these SNPs showed potential for discriminating sAD patients from CN controls, and were able to predict the incidence rate of sAD and age at onset. Furthermore, the PRSs were correlated with the CSF levels of Aß42, Aß42/Aß40, T-tau, and P-tau. Our study suggests that PRS models hold promise for assessing the genetic risk and development of AD. As genetic risk profiles vary among populations, large-scale genome-wide sequencing studies are urgently needed to identify the genetic risk loci of sAD in Chinese populations to build accurate PRS models for clinical practice.

2.
Pacing Clin Electrophysiol ; 43(3): 297-307, 2020 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-32045008

RESUMO

AIMS: In this study, we investigated the characteristics and underlying mechanisms of the electrocardiographic (ECG) morphology during left bundle branch area pacing (LBBAP), which have not been systematically described. METHODS: Patients with indications for permanent cardiac pacing underwent LBBAP attempts. The ECGs of patients with confirmed left bundle branch (LBB) capture were compared with those of individuals with right bundle branch block (RBBB) on 12-lead ECG. Intracardiac electrograms recorded during implantation were analyzed in all patients who underwent pacing. RESULTS: LBBAP was successfully achieved in 87.5% (56/64) of patients. The QRS morphologies in lead V1 during LBBAP, which typically demonstrated Qr (60.7%), qR (19.6%), rSR' (7.1%), or QS (12.5%) patterns, differed from those of native RBBB, which featured rsR' (57.5%), M shape (23.7%), or monophasic R patterns (18.7%). The terminal R' wave duration in lead V1 was significantly shorter during LBBAP than during native RBBB (51 ± 12 ms vs 85 ± 19 ms, p < 0.001). LBB potentials were recorded in 66.1% (37/56) of the LBBAP patients. No significant differences in ECG characteristics were found between LBBAP with and without recorded LBB potentials. The presence of bundle branch block during LBBAP significantly prolonged QRS duration, R wave peak time, and terminal R' wave duration in lead V1 . CONCLUSION: LBBAP-ECG patterns are characterized by a shorter terminal R' wave duration in lead V1 compared with that of native RBBB configurations. Bundle branch conduction integrity has an impact on ECG characteristics during LBBAP.

4.
Neurosci Bull ; 36(2): 195-197, 2020 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-31494835
5.
Lancet Neurol ; 19(1): 81-92, 2020 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-31494009

RESUMO

China has the largest population of patients with dementia in the world, imposing a heavy burden on the public and health care systems. More than 100 epidemiological studies on dementia have been done in China, but the estimates of the prevalence and incidence remain inconsistent because of the use of different sampling methods. Despite improved access to health services, inadequate diagnosis and management for dementia is still common, particularly in rural areas. The Chinese Government issued a new policy to increase care facilities for citizens older than 65 years, but most patients with dementia still receive care at home. Western medicines for dementia symptoms are widely used in China, but many patients choose Chinese medicines even though they have little evidence supporting efficacy. The number of clinical trials of Chinese and western medicines has substantially increased as a result of progress in research on new antidementia drugs but international multicentre studies are few in number. Efforts are needed to establish a national system of dementia care enhance training in dementia for health professionals, and develop global collaborations to prevent and cure this disease.

6.
Inorg Chem ; 58(19): 12700-12706, 2019 Oct 07.
Artigo em Inglês | MEDLINE | ID: mdl-31556291

RESUMO

The highly porous luminescent metal-organic frameworks (MOFs) can act as fluorescent probes for the detection of nitro compounds and can also serve as containers and energy transfer platforms to construct the host-guest systems. Herein, two new three-dimensional MOFs with high porosity were prepared successfully by the electron-rich tetrakis(4-pyridylphenyl)ethylene (tppe) as ligands. Compound 1 shows the high sensitivity and selectivity toward nitro-antibiotics in an aqueous media, particularly showing the best detection efficiency for furazolidone (FZD) among the reported luminescent sensors. The highly efficient fluorescence quenching toward FZD may be attributed to the electron and energy transfer. Compound 2 has naphthalene-2,7-dicarboxylic acid (2,7-npd) and tppe as dual linkers, and the energy transfer between 2,7-npd and tppe leads to the emission band in a large scale. It is worth noting that the single-phased white-light materials can be obtained by the in situ encapsulation of different concentration of sulforhodamine 101 (SR101) into compound 2 matrix.


Assuntos
Antibacterianos/análise , Substâncias Luminescentes/química , Estruturas Metalorgânicas/química , Nitrocompostos/análise , Estilbenos/química , Cristalografia por Raios X , Luminescência , Medições Luminescentes , Modelos Moleculares , Rodaminas/química
7.
Aging (Albany NY) ; 11(17): 6762-6791, 2019 09 03.
Artigo em Inglês | MEDLINE | ID: mdl-31479419

RESUMO

p75 neurotrophin receptor (p75NTR) has been implicated in Alzheimer's disease (AD). However, whether p75NTR is involved in Tau hyperphosphorylation, one of the pathologies observed in AD, remains unclear. In our previous study, the extracellular domain of p75NTR blocked amyloid beta (Aß) toxicity and attenuated Aß-induced Tau hyperphosphorylation. Here we show that, in the absence of Aß, p75NTR regulates Tau phosphorylation in the transgenic mice with the P301L human Tau mutation (pR5). The knockout of p75NTR in pR5 mice attenuated the phosphorylation of human Tau. In addition, the elevated activity of kinases responsible for Tau phosphorylation including glycogen synthase kinase 3 beta; cyclin-dependent-kinase 5; and Rho-associated protein kinase was also inhibited when p75NTR is knocked out in pR5 mice at 9 months of age. The increased caspase-3 activity observed in pR5 mice was also abolished in the absence of p75NTR. Our study also showed that p75NTR is required for Aß- and pro-brain derived neurotrophin factor (proBDNF)-induced Tau phosphorylation, in vitro. Overall, our data indicate that p75NTR is required for Tau phosphorylation, a key event in the formation of neurofibrillary tangles, another hallmark of AD. Thus, targeting p75NTR could reduce or prevent the pathologic hyperphosphorylation of Tau.

8.
Neurobiol Dis ; 132: 104567, 2019 12.
Artigo em Inglês | MEDLINE | ID: mdl-31394202

RESUMO

Neurofibrillary tangles of hyperphosphorylated tau protein (p-tau) are a key pathological feature of Alzheimer's disease (AD). Tau phosphorylation is suggested to be secondary to amyloid-beta (Aß) accumulation. However, the mechanism by which Aß induces tau phosphorylation in neurons remains unclear. Neurotrophin receptor p75 (p75NTR) is a receptor for Aß and mediates Aß neurotoxicity, implying that p75NTR may mediate Aß-induced tau phosphorylation in AD. Here, we showed that Aß-induced tau hyperphosphorylation and neurodegeneration, including tau phosphorylation, synaptic disorder and neuronal loss, in the brains of both male wild-type (Wt) mice and male P301L transgenic mice (a mouse model of human tauopathy) were alleviated by genetic knockout of p75NTR in the both mouse models. We further confirmed that the activation or inhibition of cyclin-dependent kinase 5 (CDK5) and glycogen synthase kinase-3ß (GSK3ß) significantly changed Aß/p75NTR-mediated p-tau levels in neurons. Treatment of male P301L mice with soluble p75NTR extracellular domain (p75ECD-Fc), which antagonizes the binding of Aß to p75NTR, suppressed tau hyperphosphorylation. Taken together, our findings suggest that p75NTR meditates Aß-induced tau pathology and is a potential druggable target for AD and other tauopathies.

9.
Alzheimers Dement ; 15(9): 1208-1217, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31399333

RESUMO

INTRODUCTION: We aimed to estimate the frequency of each AT(N) (ß-amyloid deposition [A], pathologic tau [T], and neurodegeneration [N]) profile in different clinical diagnosis groups and to describe the longitudinal change in clinical outcomes of individuals in each group. METHODS: Longitudinal change in clinical outcomes and conversion risk of AT(N) profiles are assessed using linear mixed-effects models and multivariate Cox proportional-hazard models, respectively. RESULTS: Participants with A+T+N+ showed faster clinical progression than those with A-T-N- and A+T±N-. Compared with A-T-N-, participants with A+T+N± had an increased risk of conversion from cognitively normal (CN) to incident prodromal stage of Alzheimer's disease (AD), and from MCI to AD dementia. A+T+N+ showed an increased conversion risk when compared with A+T±N-. DISCUSSION: The 2018 research framework may provide prognostic information of clinical change and progression. It may also be useful for targeted recruitment of participants with AD into clinical trials.

11.
J Alzheimers Dis ; 70(2): 399-412, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31177213

RESUMO

Emerging evidence suggests that gut microbiota dysbiosis plays a role in neurodegenerative disorders. However, whether the composition and diversity of the gut microbiota are altered in tauopathies remains largely unknown. This study was aimed to examine the diversity and composition of the gut microbiota in tauopathies, as well as the correlation with pathological changes in the brain. We collected fecal samples from 32 P301L tau transgenic mice and 32 age- and gender-matched littermate mice at different ages. The 16S ribosomal RNA sequencing technique was used to analyze the microbiota composition in feces. Brain tau pathology levels were measured by immunohistochemistry. The diversity and composition of the gut microbiota significantly changed with aging. At the phylum level, the relative abundance of Bacteroidetes was increased, while Firmicutes were decreased in P301L mice compared with that in Wt mice after 3 months of age. In addition, Actinobacteria was decreased in P301L mice at 3 and 6 months of age, meanwhile Tenericutes was decreased in P301L mice at 10 months of age. Moreover, several specific macrobiota were highly associated with the levels of AT8-tau or pT231-tau protein in the brain. Our findings suggest that gut microbiota changed with aging, as well as in the tauopathy mice model. Modulation of the gut microbiota may be a potential strategy for treatment of tauopathy.

12.
Neurotox Res ; 36(3): 515-522, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31209785

RESUMO

Parkinson's disease (PD) is attributed to interactions among genes and environmental and lifestyle factors, but the genetic architecture of PD is complex and not completely understood. To evaluate whether the genetic profile modifies PD development and cerebrospinal fluid (CSF) pathological biomarkers, we enrolled 418 PD patients and 426 age- and sex-matched normal controls. Forty-six single nucleotide polymorphisms (SNPs) that were reported to be significantly associated with PD in large-scale genome-wide association studies (GWASs) were genotyped and analysed. The alleles associated with PD were used to build polygenic risk score (PRS) models to represent polygenic risk. The Cox proportional hazards model and receiver operating characteristic (ROC) analyses were used to evaluate the prediction value of the PRS for PD risk and age at onset. The CSF α-synuclein levels were measured in a subgroup of control subjects (n = 262), and its relationship with the PRS was analysed. We found that some SNPs identified from other populations had significant correlations with PD in our Chinese cohort. The PRS we built had prediction value for PD risk and age at onset. The CSF α-synuclein level had no correlation with the PRS in normal subjects.


Assuntos
Herança Multifatorial/genética , Doença de Parkinson/genética , alfa-Sinucleína/líquido cefalorraquidiano , Idade de Início , Idoso , Idoso de 80 Anos ou mais , Grupo com Ancestrais do Continente Asiático/genética , Estudos de Casos e Controles , China/epidemiologia , Feminino , Predisposição Genética para Doença/genética , Humanos , Incidência , Masculino , Pessoa de Meia-Idade , Polimorfismo de Nucleotídeo Único/genética , Modelos de Riscos Proporcionais , Curva ROC , Fatores de Risco
13.
Stroke Vasc Neurol ; 4(1): 22-27, 2019 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-31105975

RESUMO

Background: Capsular warning syndrome (CWS) is defined as recurrent episodes of transient ischaemic attacks ≥3 times during a short time frame. There is no effective therapy to stop these attacks. We, herein, report our experience of using intravenous tirofiban to treat CWS. Methods: All patients with CWS in our hospital from January 2013 to September 2017 were reviewed. Patients in tirofiban group (T-group) were treated by intravenous tirofiban at 0.4 µg/kg/min for 30 min followed by 0.1-0.15 µg/kg/min infusion. Other treatments (non-T-group) included thrombolytic, oral antiplatelet agents and anticoagulant. Intracerebral haemorrhage (ICH), systematic bleeding, new attacks after treatment, National Institutes of Health Stroke Scale (NIHSS) scores at 24 hours and modified Rankin Scales (mRSs) at 3 months were recorded. Descriptive statistics were used for analysis. Results: Of 23 patients qualified (15 in T-group, 8 in non-T-group), the duration of symptoms ranged from 2 to 100 min before treatments. After treatment, in T-group, four patients (26.7%) had recurrent attacks, and NIHSS scores were 0 in 11 patients (73.3%) at 24 hours. All patients reached a favourable outcome (mRS ≤2 at 3 months. In non-T-group, five patients (62.5%) had new attacks. NIHSS scores were 0 in two patients (25%) at 24 hours. At 3 months, seven patients (87.5%) reached a favourable outcome. Neither ICH nor systematic bleeding or thrombocytopaenia occurred in both groups of patients. Conclusions: Intravenous tirofiban can be a potentially effective and safe therapy to stop early symptomatic fluctuations and shorten the duration of functional deficits in patients with CWS.

14.
Am J Hypertens ; 32(9): 880-889, 2019 08 14.
Artigo em Inglês | MEDLINE | ID: mdl-31111864

RESUMO

BACKGROUND: Atherosclerosis is a chronic inflammatory disease triggered by endothelial dysfunction and exaggerated by macrophage infiltration. Although endothelin-1 (ET-1) plays an important role in vascular inflammation and reactive oxygen species production, the individual effect of ET-1 in atherogenesis remains unclear. METHODS AND RESULTS: ET-1 expression was increased in mouse atherosclerotic plaques and human umbilical vein endothelial cells (HUVECs) administrated by oxidized low-density lipoprotein stimulation. Moreover, the immunofluorescence co-staining showed upregulated ET-1 expression in endothelial cells. Real-time polymerase chain reaction demonstrated that ET-1 overexpression promoted adhesion molecules and chemokines secretion in HUVECs. Following this intervention, the migration of macrophages and the pro-inflammatory cytokines were increased. More importantly, the endothelial dysfunction regulated by ET-1 and subsequently the effect on macrophage activation were mediated by ETA receptor and largely reversed by protein kinase C (PKC) inhibitor. Eight-week-old male ApoE-/- mice and eET-1/ApoE-/- mice were fed with high-fat diet for 12 weeks. eET-1/ApoE-/- significantly increased atherosclerotic lesions in the whole aorta and aortic sinus, which accompanied by the induction of inflammatory cytokines and macrophages infiltration. CONCLUSIONS: ET-1 accelerates atherogenesis by promoting adhesion molecules and chemokines, as well as subsequent macrophage activation. Collected, these evidence suggest that ET-1 might be a potential target for the treatment of atherogenesis.

15.
Neurosci Bull ; 35(6): 1113-1115, 2019 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-31037579
16.
Ann Clin Transl Neurol ; 6(4): 788-794, 2019 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-31020003

RESUMO

Objective: Obstructive sleep apnea syndrome (OSAS) is characterized by nocturnal intermittent hypoxemia and can increase the risk of Parkinson's disease. This study aimed to investigate the association between plasma α-synuclein levels and hypoxia in the patients with OSAS. Methods: We recruited 42 OSAS patients and 46 controls with simple snoring matched for age and gender. OSAS was diagnosed on the basis of the clinical symptoms as well as the nighttime polysomnography. Plasma total α-synuclein and phosphorylated α-synuclein levels were measured by ELISA kits. Results: The OSAS patients had significant higher levels of plasma total α-synuclein and phosphorylated α-synuclein levels. Both of the above indexes were positively correlated with the apnea-hypopnea index and the oxygen desaturation index, while they were negatively correlated with the mean and lowest oxyhemoglobin saturations. Interpretation: This study suggests that chronic intermittent hypoxia can increase the α-synuclein levels, which may contribute to the pathogenesis of Parkinson's disease.


Assuntos
Hipóxia/sangue , Fosforilação/fisiologia , Apneia Obstrutiva do Sono/sangue , alfa-Sinucleína/sangue , Adulto , Índice de Massa Corporal , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Oxigênio/sangue , Plasma/metabolismo , Polissonografia/métodos , Apneia Obstrutiva do Sono/complicações , Ronco/complicações
17.
J Alzheimers Dis ; 69(1): 169-178, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-30958377

RESUMO

Brain amyloid-ß (Aß) deposition is a hallmark to define Alzheimer's disease (AD). We investigated the positive rate of brain amyloid deposition assessed with 11C-Pittsburgh compound (PiB)-PET and blood Aß levels in a cohort of probable AD patients who were diagnosed according to the 1984 NINCDS-ADRDA criteria. Eighty-four subjects with a clinical diagnosis of probable AD dementia, amnestic mild cognitive impairment (MCI), and cognitively normal (CN) status were subjected to PiB-PET and 18F-fluorodeoxyglucose (FDG)-PET scans. Plasma biomarkers of Aß42, Aß40, and T-tau were measured using single molecule array technology. The positive rate of PiB-PET, the associations between PiB-PET status and FDG-PET, plasma biomarkers, and clinical manifestations were analyzed. PiB-PET was positive in 77.36% of probable AD patients, 31.80% of MCI patients, and 0 of NC. Plasma Aß42/Aß40 ratio was associated with PiB-PET, the ROC curve analysis revealing an AUC of 0.77 (95% CI: 0.66-0.87), with a sensitivity of 82% and specificity of 64%. Some clinical manifestations were associated with PiB-PET imaging. Our findings indicate that only three-fourths of patients diagnosed with probable AD fit the pathological criteria, suggesting that we should be cautious regarding the accuracy of AD diagnosis when no biomarker evidence is available in our clinical practice.

18.
Neurotox Res ; 36(1): 101-107, 2019 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-30977102

RESUMO

The neurotrophin receptor p75 (p75NTR) plays important roles in regulating amyloid-beta (Aß) metabolism in the brain. The expression of p75NTR is altered in the brain of patients with Alzheimer's disease (AD). In this study, we aimed to evaluate whether p75NTR mRNA level in the peripheral blood cells is changed among AD patients and its potential to be a biomarker for AD. The study subjects included 26 patients with AD (PiB-PET positive) and 28 cognitively normal controls (PiB-PET negative). RNA was extracted from peripheral blood cells of fast blood. p75NTR mRNA was measured using quantitative real-time PCR assay. p75NTR mRNA levels in blood cells were comparable between AD patients and controls. p75NTR mRNA levels in blood cells were not correlated with MMSE scores, ApoE genotypes, gender, and age. p75NTR mRNA expression in blood cells is not changed in AD patients and is unlikely to be a biomarker for AD.


Assuntos
Doença de Alzheimer/sangue , Proteínas do Tecido Nervoso/sangue , Receptores de Fator de Crescimento Neural/sangue , Idoso , Idoso de 80 Anos ou mais , Doença de Alzheimer/genética , Apolipoproteínas E/genética , Biomarcadores/sangue , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , RNA Mensageiro/sangue
19.
Neurotox Res ; 36(3): 463-471, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-30941646

RESUMO

Parkinson's disease (PD) is a common neurodegenerative disease characterized by neuronal loss in the substantia nigra. The p75 neurotrophin receptor (p75NTR, encoded by NGFR) was found to play an important role in the selective neuronal death of dopamine neurons in the substantia nigra, as well as the pathogenesis and development of PD. To assess the association between NGFR gene polymorphism and the susceptibility of PD, this case-control study consisting of 414 PD patients and 623 age- and sex-matched controls in a Chinese Han cohort was conducted. Twelve tag-single nucleotide polymorphisms (tag-SNPs) were selected from the NGFR gene through the construction of linkage disequilibrium blocks. One tag-SNP from the ADAM17 gene was also selected owing to its function of encoding tumor necrosis factor α-converting enzyme, which is responsible for the shedding of the extracellular domain of p75NTR. A multiplex polymerase chain reaction-ligase detection reaction (PCR-LDR) method was applied for genotyping. The associations between tag-SNPs and the risk of PD with the adjustment for age and sex were analyzed by unconditional logistic regression, and five genetic models including codominant, dominant, recessive, over-dominant, and additive models were applied. The results showed that among the 13 tag-SNPs, rs741073 was associated with a reduced risk of PD in the codominant (OR = 0.71, 95% CI = 0.54-0.93, P = 0.037), dominant (OR = 0.76, 95% CI = 0.58-0.98, P = 0.033), and over-dominant models (OR = 0.71, 95% CI = 0.54-0.92, P = 0.010), and rs1804011 was also associated with a reduced risk of PD in the codominant (OR = 0.69, 95% CI = 0.50-0.95, P = 0.049), dominant (OR = 0.69, 95% CI = 0.50-0.93, P = 0.014), over-dominant (OR = 0.70, 95% CI = 0.51-0.96, P = 0.025), and additive models (OR = 0.72, 95% CI = 0.54-0.94, P = 0.016). However, these associations did not retain after Bonferroni correction. Conclusively, our study failed to reveal the association between the selected tag-SNPs within NGFR, ADAM17, and the susceptibility of PD. The role of p75NTR and its gene polymorphisms in the pathogenesis of PD needs to be further studied.


Assuntos
Proteína ADAM17/genética , Grupo com Ancestrais do Continente Asiático/genética , Proteínas do Tecido Nervoso/genética , Doença de Parkinson/genética , Polimorfismo de Nucleotídeo Único/genética , Receptores de Fator de Crescimento Neural/genética , Idoso , Estudos de Casos e Controles , China , Feminino , Estudos de Associação Genética , Predisposição Genética para Doença/genética , Humanos , Masculino
20.
J Cardiovasc Electrophysiol ; 30(6): 815-823, 2019 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-30891845

RESUMO

INTRODUCTION: Adenosine triphosphate (ATP)-provoked dormant conduction (DC) and pacing for unexcitability are used to identify conduction gaps along the ablation lines after circumferential pulmonary vein isolation (CPVI). We aim to determine whether ATP provocation and pacing are interchangeable as endpoints for ablation of paroxysmal atrial fibrillation (PAF). METHODS AND RESULTS: A total of 107 patients with PAF were randomly divided into two groups after completion of CPVI. In group I (A-P group, n = 53), ATP was administered first. If DC was uncovered, additional ablation was performed until ATP tests were negative. Bipolar pacing along the ablation line was performed subsequently. In group II (P-A group, n = 54), the same protocol was used, but the pacing and the ATP tests were performed in the opposite sequence. The 12-month ablation outcomes of all patients were compared with those of a historical control group of 107 patients with PAF in whom only ATP test was performed. Regardless of which test was performed first, the other modality still identified conduction gaps. In group I, pacing maneuvers identified gaps in 49% (n = 26) of patients who had negative ATP tests. In group II, ATP tests uncovered DC in 18.5% (n = 10) of patients in whom pacing identified no gaps. After 12 months, a higher proportion of patients (91.6%) were free from atrial tachyarrhythmias compared with the historical control group (81.3%; P = 0.031). CONCLUSION: Pacing along the ablation lines and ATP provocation are complementary tests for evaluating the durability of CPVI and can lead to better long-term outcomes when used in combination.

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