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1.
Artigo em Inglês | MEDLINE | ID: mdl-32966616

RESUMO

The atrial-specific ultra-rapid delayed rectifier K+ current (Ikur) plays an important role in the progression of atrial fibrillation (AF). Because inflammation is known to lead to the onset of AF, we aimed to investigate whether tumour necrosis factor-α (TNF-α) played a role in regulating Ikur and the potential signalling pathways involved. Whole-cell patch-clamp and biochemical assays were used to study the regulation and expression of Ikur in myocytes and in tissues from left atrial appendages (LAAs) obtained from patients with sinus rhythm (SR) or AF, as well as in rat cardiomyocytes (H9c2 cells) and mouse atrial myocytes (HL-1 cells). Ikur current density was markedly reduced in atrial myocytes from AF patients compared with SR controls. Reduction of Kv1.5 protein levels was accompanied by increased expression of TNF-α and protein kinase C (PKC)α activation in AF patients. Treatment with TNF-α dose-dependently reduced Ikur and protein expression of Kv1.5 but not Kv3.1b in H9c2 cells and HL-1 cells. TNF-α also increased activity of PKCα. Specific PKCα inhibitor Gö6976 alleviated the reduction in Ikur induced by TNF-α, but not the reduction in Kv1.5 protein. TNF-α was involved in the electrical remodelling associated with AF, probably by depressing Ikur in atrial myocytes via activation of PKCα.

2.
J Mol Cell Cardiol ; 141: 82-92, 2020 04.
Artigo em Inglês | MEDLINE | ID: mdl-32222458

RESUMO

Vascular dysfunction is a common pathological basis for complications in individuals affected by diabetes. Previous studies have established that endothelial dysfunction is the primary contributor to vascular complications in type 2 diabetes (T2DM). However, the role of vascular smooth muscle cells (VSMCs) in vascular complications associated with T2DM is still not completely understood. The aim of this study is to explore the potential mechanisms associated with Ca2+ handling dysfunction and how this dysfunction contributes to diabetic vascular smooth muscle impairment. The results indicated that endothelium-dependent vasodilation was impaired in diabetic aortae, but endothelium-independent vasodilation was not altered. Various vasoconstrictors such as phenylephrine, U46619 and 5-HT could induce vasoconstriction in a concentration-dependent manner, such that the dose-response curve was parallel shifted to the right in diabetic aortae, compared to the control. Vasoconstrictions mediated by L-type calcium (Cav1.2) channels were attenuated in diabetic aortae, but effects mediated by store-operated calcium (SOC) channels were enhanced. Intracellular Ca2+ concentration ([Ca2+]i) in VSMCs was detected by Fluo-4 calcium fluorescent probes, and demonstrated that SOC-mediated Ca2+ entry was increased in diabetic VSMCs. VSMC-specific knockout of STIM1 genes decreased SOC-mediated and phenylephrine-induced vasoconstrictive response in mice aortae. Additionally, Orai1 expression was up-regulated, Cav1.2 expression was downregulated, and the phenotypic transformation of diabetic VSMCs was determined in diabetic aortae. The overexpression of Orai1 markedly promoted the OPN expression of VSMCs, whereas SKF96365 (SOC channel blocker) reversed the phenotypic transformation of diabetic VSMCs. Our results demonstrated that the vasoconstriction response of aortic smooth muscle was weakened in type 2 diabetic rats, which was related to the downregulation of the Cav1.2 channel and the up-regulation of the SOC channel signaling pathway.

3.
J Mol Cell Cardiol ; 140: 10-21, 2020 03.
Artigo em Inglês | MEDLINE | ID: mdl-32006532

RESUMO

Hypertension is an independent risk factor for atrial fibrillation (AF), although its specific mechanisms remain unclear. Previous research has been focused on cyclic stretch, ignoring the role of high hydrostatic pressure. The present study aimed to explore the effect of high hydrostatic pressure stimulation on electrical remodeling in atrial myocytes and its potential signaling pathways. Experiments were performed on left atrial appendages from patients with chronic AF or sinus rhythm, spontaneously hypertensive rats (SHRs) treated with or without valsartan (10 mg/kg/day) and HL-1 cells were exposed to high hydrostatic pressure using a self-developed device. Whole-cell patch-clamp recordings and western blots demonstrated that the amplitudes of ICa,L, Ito, and IKur were reduced in AF patients with corresponding changes in protein expression. Angiotensin protein levels increased and Ang1-7 decreased, while focal adhesion kinase (FAK) and Src kinase were enhanced in atrial tissue from AF patients and SHRs. After rapid atrial pacing, AF inducibility in SHR was significantly higher, accompanied by a decrease in ICa,L, upregulation of Ito and IKur, and a shortened action potential duration. Angiotensin upregulation and FAK/Src activation in SHR were inhibited by angiotensin type 1 receptor inhibitor valsartan, thus, preventing electrical remodeling and reducing AF susceptibility. These results were verified in HL-1 cells treated with high hydrostatic pressure, and demonstrated that electrical remodeling regulated by the FAK-Src pathway could be modulated by valsartan. The present study indicated that high hydrostatic pressure stimulation increases AF susceptibility by activating the renin-angiotensin system and FAK-Src pathway in atrial myocytes.

4.
J Cardiovasc Electrophysiol ; 31(4): 960-963, 2020 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-32077548

RESUMO

We present a case of wide-complex tachycardia in which the clinical electrophysiological diagnosis was considered to be bundle branch re-entry ventricular tachycardia. A series of ventricular entrainment attempts were performed from the left and right ventricular septum to confirm the diagnosis. Entrainment pacing with a general current output (10 mA) was performed from the right ventricular septum with manifest fusion and a post-pacing interval similar to tachycardia cycle length. Thereafter, another entrainment attempt with a greater current output (20 mA) was performed from the same site. Paradoxically, concealed fusion was demonstrated by selective RB capture only, though there was no clear "RB" potential seen. In this case, we attempt to explain and illustrate the mechanism of paradoxical near-field inability to capture with increasing current strength.

5.
Life Sci ; 242: 117209, 2020 Feb 01.
Artigo em Inglês | MEDLINE | ID: mdl-31870776

RESUMO

AIMS: Hypertension is an independent risk factor for atrial fibrillation (AF). However, the direct effect of hydrostatic pressure on atrial electrical remodeling is unclear. The present study investigated whether hydrostatic pressure is responsible for atrial electrical remodeling and addressed a potential role of inflammation in this pathology. MAIN METHODS: Whole-cell patch-clamp recordings and biochemical assays were used to study the regulation and expression of ion channels in left atrial appendages in patients with AF, spontaneously hypertensive rats (SHRs), and atrium-derived cells (HL-1 cells) exposed to standard (0 mmHg) and elevated (20, 40 mmHg) hydrostatic pressure. KEY FINDINGS: Both TNF-α and MIF were highly expressed in patients with AF and SHRs. AF inducibility in SHRs was higher after atrial burst pacing, accompanied by a decrease in the L-type calcium current (ICa,L), an increase in the transient outward K+ current (Ito) and ultra-rapid delayed rectifier K+ current (IKur), and a shortened action potential duration (APD), which could be inhibited by atorvastatin. Furthermore, exposure to elevated pressure was associated with electrical remodeling of the HL-1 cells. The peak current density of ICa,L was reduced, while Ito and IKur were increased. Moreover, the expression levels of Kv4.3, Kv1.5, TNF-α, and MIF were upregulated, while the expression of Cav1.2 was downregulated in HL-1 cells after treatment with high hydrostatic pressure (40 mmHg). Atorvastatin alleviated the electrical remodeling and increased inflammatory markers in HL-1 cells induced by high hydrostatic pressure. SIGNIFICANCE: Elevated hydrostatic pressure led to atrial electrical remodeling and increased AF susceptibility by upregulating inflammation.


Assuntos
Remodelamento Atrial , Citocinas/metabolismo , Pressão Hidrostática/efeitos adversos , Adulto , Animais , Western Blotting , Feminino , Átrios do Coração/metabolismo , Humanos , Masculino , Pessoa de Meia-Idade , Miócitos Cardíacos/metabolismo , Técnicas de Patch-Clamp , Ratos Endogâmicos SHR , Ratos Wistar , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Regulação para Cima
6.
BMC Cardiovasc Disord ; 19(1): 270, 2019 11 28.
Artigo em Inglês | MEDLINE | ID: mdl-31779588

RESUMO

BACKGROUND: To estimate the prevalence of elevated blood glucose level (EBG, including type 2 diabetes mellitus and impaired fasting glucose), and its association with non-valvular atrial fibrillation (NVAF) in Guangzhou, China. METHODS: The population-based follow-up Guangzhou Heart Study collected baseline data from July 2015 to August 2017 among 12,013 permanent residents aged > 35 from 4 Guangzhou districts. Two streets (Dadong and Baiyun) in the Yuexiu District, and one street (Xiaoguwei) and two towns (Xinzao and Nancun) in the Panyu District were chosen as representative of urban and rural areas, respectively. Each participant completed a comprehensive questionnaire, and underwent physical examination, blood sample collection for laboratory testing, electrocardiography, and other evaluations. Multivariable logistic regression analyses were used to estimate the independent association between hyperglycemia and NVAF prevalence. RESULTS: The prevalence of EBG in overall study population was 29.9%. Compared with residents without EBG, the odds ratio (OR) for AF among residents with EBG was significantly higher (1.94, 95% confidence interval [CI]: 1.40-2.70, P <  0.001), even after multivariate adjustment for metabolic abnormalities (OR = 1.60, 95% CI: 1.14-2.25, P = 0.007), and driven by women (OR = 1.80, 95% CI: 1.12-2.91, P = 0.016). CONCLUSIONS: In Guangzhou, China, prevalence of EBG is high among residents aged > 35 years and associated with a multivariate adjusted increase in prevalence of NVAF overall and in women.

7.
BMJ Open ; 9(5): e028007, 2019 05 29.
Artigo em Inglês | MEDLINE | ID: mdl-31147367

RESUMO

OBJECTIVES: There are country and regional variations in the prevalence of hyperuricaemia (HUA). The prevalence of HUA and non-valvular atrial fibrillation (NVAF) in southern China is unknown. DESIGN: A cross-sectional study. SETTING AND PARTICIPANTS: A total of 11 488 permanent residents aged 35 or older from urban and rural areas of Guangzhou, China were enrolled. A questionnaire was used to compile each participant's demographic information and relevant epidemiological factors for HUA and NVAF. All participants were assessed using a panel of blood tests and single-lead 24-hour ECG. MAIN OUTCOME MEASURES: HUA was defined as serum uric acid level >420 µmol/L in men and >360 µmol/L in women. NVAF was diagnosed as per guidelines. RESULTS: The prevalence of HUA was 39.6% (44.8% in men and 36.7% in women), and 144 residents (1.25%) had NVAF. Prevalence of HUA increased with age in women but remained stably high in men. After adjusting for potential confounders, age, living in urban areas, alcohol consumption, central obesity, elevated fasting plasma glucose level, elevated blood pressure, lower high-density lipoprotein cholesterol level and elevated triglycerides level were associated with increased risk of HUA. Residents with HUA were at higher risk for NVAF. Serum uric acid level had a modest predictive value for NVAF in women but not men. CONCLUSIONS: HUA was highly prevalent among citizens of southern China and was a predictor of NVAF among women.


Assuntos
Fibrilação Atrial/epidemiologia , Hiperuricemia/epidemiologia , Distribuição por Idade , China/epidemiologia , Análise por Conglomerados , Estudos Transversais , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Prevalência , Fatores de Risco , Saúde da População Rural/estatística & dados numéricos , Distribuição por Sexo , Saúde da População Urbana/estatística & dados numéricos
8.
BMC Cardiovasc Disord ; 19(1): 90, 2019 04 15.
Artigo em Inglês | MEDLINE | ID: mdl-30987582

RESUMO

BACKGROUND: The ECG characteristics of the distal coronary venous system ventricular arrhythmias (VAs) share common features with VAs arising from the aortic cusps or the endocardial left ventricular outflow tract (LVOT) beneath the cusps. The purpose of this study was to identify specific electrocardiographic and electrophysiological characteristics of VAs originating from the distal great cardiac vein (GCV). METHODS: Based on the successful ablation site, patients with idiopathic VAs from the distal GCV, left coronary cusp (LCC) or the subvalvular left ventricular outflow tract (LVOT) area were included in the present study. RESULTS: The final population consisted of 39 patients (35 males, mean age 51 ± 23 years). All VAs displayed a right bundle branch block (RBBB) morphology with inferior axis. Among these patients, 15 were successfully ablated at the GCV, 15 at the LCC and 9 at the subvalvular region. A "w" pattern in lead I was present in 12 out of 15 (80%) VAs originating from the distal GCV compared to none of VAs arising from the other two sites (p < 0.01). VAs with a GCV origin exhibited more commonly increased intrinsicoid deflection time, higher maximum deflection index and wider QRS duration compared to LCC and subvalvular sites (p < 0.05). Acceptable pace mapping at the successful ablation site was achieved in 10 patients. After an average of 36 ± 24 months follow up, 14 (93.3%) patients were free from VAs recurrence. CONCLUSION: A "w" pattern in lead I may distinguish distal GCV VAs from VAs arising from the LCC or the subvalvular region.


Assuntos
Potenciais de Ação , Arritmias Cardíacas/diagnóstico , Bloqueio de Ramo/diagnóstico , Seio Coronário/fisiopatologia , Eletrocardiografia , Ventrículos do Coração/fisiopatologia , Adulto , Idoso , Arritmias Cardíacas/fisiopatologia , Arritmias Cardíacas/cirurgia , Bloqueio de Ramo/fisiopatologia , Bloqueio de Ramo/cirurgia , Ablação por Cateter , Seio Coronário/cirurgia , Técnicas Eletrofisiológicas Cardíacas , Feminino , Frequência Cardíaca , Ventrículos do Coração/cirurgia , Humanos , Masculino , Pessoa de Meia-Idade , Valor Preditivo dos Testes , Intervalo Livre de Progressão , Fatores de Tempo
9.
Heart Vessels ; 34(5): 860-867, 2019 May.
Artigo em Inglês | MEDLINE | ID: mdl-30599061

RESUMO

To investigate the safety and midterm outcome of concomitant left atrial appendage (LAA) closure and catheter ablation (CA) as a one-stage hybrid procedure for non-valvular atrial fibrillation (AF) in a multicenter registry. A total of 50 consecutive patients with symptomatic drug-resistant non-valvular AF with CHA2DS2-VASc score ≥ 2 and contraindications for antithrombotic therapy were included in the prospectively established LAA closure registry, and underwent concomitant LAA closure (48 for WATCHMAN and 2 for ACP) and CA procedure (40 for radiofrequency and 10 for cryoballoon CA). Two cardiac tamponades, one peripheral vascular complications and one mild air embolism were observed during perioperative period. After mean follow-up of 20.2 ± 11.5 months, 18 (36%) patients presented with atrial arrhythmia relapse and 45 (91.8%) patients presented with complete sealing; furthermore, there were two transient ischemic attacks and one ischemic stroke under an off-oral anticoagulant situation, respectively. Concomitant CA and LAA closure as a one-stage hybrid procedure might be feasible and potentially decrease costs in patients with symptomatic non-valvular AF with high stroke risk and contraindication to antithrombotic treatment, and as safe as LAA closure procedure only during the perioperative period. However, it was necessary to further validate the mid-term safety.


Assuntos
Apêndice Atrial/cirurgia , Fibrilação Atrial/cirurgia , Ablação por Cateter , Dispositivo para Oclusão Septal , Idoso , Anticoagulantes/uso terapêutico , Fibrilação Atrial/tratamento farmacológico , Ecocardiografia Transesofagiana , Feminino , Seguimentos , Humanos , Masculino , Pessoa de Meia-Idade , Sistema de Registros , Fatores de Tempo , Resultado do Tratamento
10.
Int Heart J ; 60(1): 71-77, 2019 Jan 25.
Artigo em Inglês | MEDLINE | ID: mdl-30518718

RESUMO

The incidence of atrial tachycardia (AT) after rheumatic mitral valvular (RMV) surgery has been well described. However, there have been few reports on the characteristics, mechanism, and long-term ablation outcome of ATs after RMV surgery and concomitant Cox-MAZE IV procedure.The present study reviewed consecutive patients who underwent AT ablation between May 2008 and July 2013. All patients were refractory to antiarrhythmic drugs (AADs) and had a history of RMV surgery and Cox-MAZE IV procedure. A total of 34 patients underwent AT ablation after RMV surgery and concomitant Cox-MAZE IV procedure, and presented 57 mappable and 2 unmappable ATs. The 57 mappable ATs included 14 focal-ATs and 43 reentry-ATs. Ten of the 14 focal-like ATs were located at the pulmonary vein (PV) antrum and border of a box lesion. Of the 43 reentry-ATs, 16 were marco-reentrant around the mitral annulus (MA) and 16 around the tricuspid annulus. There were 41 atypical ATs (non-cavotricuspid isthmus related) including 16 ATs related to the box lesion and 21 ATs related to other Cox-MAZE IV lesions. The AT were successfully terminated in 33 (97.1%) patients. After mean follow-up of 46.9 ± 15.7 months, 25 (73.5%) patients maintained sinus rhythm without AADs after a single procedure and 28 (82.4%) patients after repeated procedures.The recurrent ATs after RMV surgery and concomitant Cox-MAZE IV were mainly reentry mechanism, and largely related to LA. An incomplete lesion or re-conductive gaps in a prior lesion might be the predominant mechanisms for these ATs. Catheter-based mapping and ablation of these ATs seems to be effective and safe during a long-term follow-up.


Assuntos
Procedimentos Cirúrgicos Cardíacos/efeitos adversos , Valva Mitral/cirurgia , Cardiopatia Reumática/cirurgia , Taquicardia Atrial Ectópica/epidemiologia , Taquicardia Atrial Ectópica/cirurgia , Adulto , Idoso , Ablação por Cateter , Mapeamento Epicárdico/instrumentação , Feminino , Seguimentos , Frequência Cardíaca , Humanos , Incidência , Masculino , Pessoa de Meia-Idade , Valva Mitral/fisiopatologia , Cardiopatia Reumática/fisiopatologia , Taquicardia Atrial Ectópica/etiologia , Taquicardia Atrial Ectópica/fisiopatologia , Resultado do Tratamento
11.
Naunyn Schmiedebergs Arch Pharmacol ; 392(1): 19-28, 2019 01.
Artigo em Inglês | MEDLINE | ID: mdl-30182188

RESUMO

Statins are widely used in the treatment of hypercholesterolemia. Studies have demonstrated that statins could maintain vascular contractile function through inhibiting the transformation of vascular smooth muscle cells (VSMCs) from the contractile phenotype to the synthetic phenotype. However, the underlying mechanisms have not been fully elucidated. The effect of atorvastatin on the thoracic aorta of Sprague-Dawley rats cultured in serum-free conditions in vitro was evaluated. Aortic constriction was induced by high potassium, phenylephrine, and CaCl2. The protein expression levels of α1 adrenoceptor; inositol 1,4,5-trisphosphate (IP3) receptor; protein kinase Cδ (PKCδ); stromal interaction molecule 1 (STIM1); high-voltage activated dihydropyridine-sensitive (L type, Cav1.2) channels; and two contractile phenotype marker proteins [α-smooth muscle actin (α-SMA) and myosin (SM-MHC)] were determined by western blotting. Compared with the fresh control, the constriction of rat aorta was impaired after culture in serum-free medium for 24 h. The impaired contraction of cultured aortas was mediated by Cav1.2 and store-operated Ca2+ (SOC) channel, which could be improved by atorvastatin at 20 µM. The protein expression levels of α1 adrenoceptor, IP3 receptor, PKCδ, STIM1, Cav1.2, α-SMA, and SM-MHC in the aortas cultured in serum-free conditions were decreased significantly. Atorvastatin partially prevented the reduction in the contractility and the downregulation of these proteins in cultured aortas. The transformation of the VSMC phenotype is associated with the vasoconstriction dysfunction of cultured aortas. Atorvastatin may protect vascular function by modulating calcium signaling pathways.


Assuntos
Aorta Torácica/efeitos dos fármacos , Atorvastatina/farmacologia , Inibidores de Hidroximetilglutaril-CoA Redutases/farmacologia , Actinas/metabolismo , Animais , Aorta Torácica/fisiologia , Canais de Cálcio Tipo L/metabolismo , Receptores de Inositol 1,4,5-Trifosfato/metabolismo , Masculino , Miosinas/metabolismo , Técnicas de Cultura de Órgãos , Proteína Quinase C-delta/metabolismo , Ratos Sprague-Dawley , Receptores Adrenérgicos alfa 1/metabolismo , Molécula 1 de Interação Estromal/metabolismo , Vasoconstrição/efeitos dos fármacos
12.
J Geriatr Cardiol ; 15(6): 408-412, 2018 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-30108612

RESUMO

Objective: To evaluate the predictive value of red cell distribution width (RDW) on left atrial thrombus (LAT) or left atrial spontaneous echo contrast (LASEC) in patients with non-valvular atrial fibrillation (AF). Methods: We reviewed 692 patients who were diagnosed as non-valvular AF and underwent transesophageal echocardiography (TEE) in Guangdong Cardiovascular Institute from April 2014 to December 2015. The baseline clinical characteristics, laboratory test of blood routine, electrocardiograph measurements were analyzed. Results: Eighty-four patients were examined with LAT/LASEC under TEE. The mean RDW level was significantly higher in LAT/LASEC patients compared with the non-LAT/LASEC patients (13.59% ± 1.07% vs. 14.34% ± 1.34%; P < 0.001). Receiver-operating characteristic curve analysis was performed and indicated the best RDW cut point was 13.16%. Furthermore, multivariate logistic regression analysis indicated that RDW level > 13.16% could be an independent risk factor for LAT/LASEC in patients with AF. Conclusion: Elevated RDW level is associated with the presence of LAT/LASEC and could be with moderate predictive value for LAT/LASEC in patients with non-valvular AF.

14.
Cardiology ; 140(2): 87-95, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-29920487

RESUMO

OBJECTIVES: The aim of the study was to examine the association of CHADS2/CHA2DS2-VASc scores with left atrial thrombus (LAT) and spontaneous echocardiographic contrast (SEC) in non-anticoagulated nonvalvular atrial fibrillation (NVAF) spontaneous patients, and to develop a new scoring system for LAT/SEC prediction. METHODS: Consecutive non-anticoagulated NVAF patients with or without LAT/SEC by transesophageal echocardiography were identified in the Guangdong General Hospital. RESULTS: Among 2,173 patients, the prevalence of LAT/SEC was 4.9%. Both predictive values of CHADS2 and CHA2DS2-VASc scores for the presence of LAT/SEC were low-to-moderate (receiver operating characteristic [ROC] = 0.591 and 0.608, respectively, p = 0.90). By multivariate analysis, non-paroxysmal AF, decreased left ventricular ejection fraction, and left atrial enlargement were positively associated with LAT/SEC, while CHADS2/CHA2DS2VASc scores were not. A new scoring system based on these 3 factors above significantly improved the discrimination for LAT/SEC (ROC = 0.792). CONCLUSIONS: CHADS2/CHA2DS2-VASc scores had limited value in predicting LAT/SEC; a new scoring system that combines AF type and echocardiographic parameters may better predict LAT/SEC as a surrogate for cardioembolic risk in NVAF patients.


Assuntos
Medição de Risco/métodos , Tromboembolia/diagnóstico por imagem , Tromboembolia/epidemiologia , Trombose/epidemiologia , Idoso , Idoso de 80 Anos ou mais , Fibrilação Atrial/complicações , Fibrilação Atrial/diagnóstico por imagem , Função do Átrio Esquerdo , China/epidemiologia , Meios de Contraste , Ecocardiografia Transesofagiana , Cardiopatias , Humanos , Masculino , Pessoa de Meia-Idade , Análise Multivariada , Fatores de Risco , Acidente Vascular Cerebral/etiologia , Trombose/complicações , Trombose/diagnóstico por imagem
16.
Int J Cardiol ; 258: 103-108, 2018 05 01.
Artigo em Inglês | MEDLINE | ID: mdl-29467096

RESUMO

OBJECTIVES: To investigate the relationship between hyperuricemia and left atrial thrombus (LAT)/spontaneous echo contrast (SEC) and to determine the predictive value of hyperuricemia in non-valvular (NV) atrial fibrillation (AF) patients. METHODS: The study retrospectively reviewed 1198 consecutive patients (male 801, female 397, and mean age of 56.84 ±â€¯12.22) who were diagnosed with AF and accepted transesophageal echocardiography (TEE) prior to catheter ablation, appendage occlusion and electrical cardioversion using a single-center database. The clinical baseline characteristics were collected from medical record review and analyzed. Patients were categorized into an LAT/SEC group and a normal group. RESULTS: According to the TEE examination, there were 97 (8.1%) patients with abnormality; of these, 49 were with LAT and 48 with SEC. The mean serum uric acid (SUA) level and hyperuricemia proportion were markedly higher in patients with LAT/SEC. The significant predictive effect was observed in the SUA level (OR = 1.006) and hyperuricemia (OR = 2.04). After adjustment for persistent/permanent-AF, age, gender, LA dimension > 40 mm, previous stroke, hypertension and diabetes, the SUA level (OR = 1.004) and hyperuricemia (OR = 1.69) were independent predictors for LAT/SEC. The SUA level (OR = 1.004) and hyperuricemia (OR = 1.69) were independent predictors for LAT/SEC, Further subgroup analysis in different CHA2DS2-VASc categories, it might be helpful to refine the LAT/SEC risk via combination area CHA2DS2-VASc score and hyperuricemia, especially in those with CHA2DS2-VASc score < 2. CONCLUSIONS: The SUA level and hyperuricemia proportion are closely associated with LA stasis. Hyperuricemia might independently predict and refine LA stasis risk among NVAF patients, especially in those with CHA2DS2-VASc score < 2.


Assuntos
Fibrilação Atrial/sangue , Fibrilação Atrial/diagnóstico por imagem , Átrios do Coração/diagnóstico por imagem , Hiperuricemia/sangue , Hiperuricemia/diagnóstico por imagem , Adulto , Idoso , Fibrilação Atrial/epidemiologia , Ecocardiografia/tendências , Feminino , Humanos , Hiperuricemia/epidemiologia , Masculino , Pessoa de Meia-Idade , Valor Preditivo dos Testes , Estudos Retrospectivos , Ácido Úrico/sangue
17.
Mol Med Rep ; 17(2): 3425-3431, 2018 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-29257298

RESUMO

Atrial fibrosis is the fundamental characteristic of the structural pathology associated with atrial fibrillation (AF). Inflammation can contribute to atrial fibrosis, engendering AF. The present study aimed to investigate the role of macrophage migration inhibitory factor (MIF), a pleiotropic cytokine, in the regulation of proliferation and function of cardiac fibroblasts (CFs). Biochemical assays were performed to examine the expression of extracellular matrix (ECM) in human atrial tissues, and the proliferation and regulation of ECM induced by MIF in CFs. The expression of ECM, including collage type 3, α1 (Col­3A1), matrix metalloproteinase (MMP)­2/-9 and transforming growth factor (TGF)­ß was higher in patients with permanent AF, compared with patients in sinus rhythm (SR), and the expression levels of MIF were also increased in AF. Treatment of CFs with mouse recombinant MIF (rMIF; 40 nM) for 48 h was found to promote the proliferation of CFs. The MIF­induced CF proliferation was completely inhibited by tyrosine kinase inhibitor­PP1. rMIF treatment also stimulated the activation of Src kinase in CFs. In addition, MIF treatment upregulated the expression levels of fibrosis­related proteins, Col­1, Col­3, MMP­2/-9 and TGF­ß, in the CFs. These results suggested that MIF was involved in the structural remodeling that accompanies AF, possibly by promoting the proliferation of CFs and increasing the expression of ECM. These data implicate inflammation as a potential driver of CF.


Assuntos
Arritmia Sinusal/patologia , Fibrilação Atrial/patologia , Proliferação de Células , Fibroblastos/patologia , Oxirredutases Intramoleculares/metabolismo , Fatores Inibidores da Migração de Macrófagos/metabolismo , Transdução de Sinais , Quinases da Família src/metabolismo , Adulto , Animais , Arritmia Sinusal/metabolismo , Fibrilação Atrial/metabolismo , Colágeno/análise , Colágeno/metabolismo , Matriz Extracelular/metabolismo , Matriz Extracelular/patologia , Feminino , Fibroblastos/metabolismo , Átrios do Coração/metabolismo , Átrios do Coração/patologia , Humanos , Oxirredutases Intramoleculares/análise , Fatores Inibidores da Migração de Macrófagos/análise , Masculino , Metaloproteinase 2 da Matriz/análise , Metaloproteinase 2 da Matriz/metabolismo , Metaloproteinase 9 da Matriz/análise , Metaloproteinase 9 da Matriz/metabolismo , Camundongos , Pessoa de Meia-Idade
18.
Oncotarget ; 8(54): 92079-92089, 2017 Nov 03.
Artigo em Inglês | MEDLINE | ID: mdl-29190899

RESUMO

The role of microRNA-92b-3p (miR-92b-3p) in cardiac hypertrophy was not well illustrated. The present study aimed to investigate the expression and potential target of miR-92b-3p in angiotensin II (Ang-II)-induced mouse cardiac hypertrophy. MiR-92b-3p was markedly decreased in the myocardium of Ang-II-infused mice and of patients with cardiac hypertrophy. However, miR-92b-3p expression was revealed increased in Ang-II-induced neonatal mouse cardiomyocytes. Cardiac hypertrophy was shown attenuated in Ang-II-infused mice received tail vein injection of miR-92b-3p mimic. Moreover, miR-92b-3p inhibited the expression of atrial natriuretic peptide (ANP), skeletal muscle α-actin (ACTA1) and ß-myosin heavy chain (MHC) in Ang-II-induced mouse cardiomyocytes in vitro. Myocyte-specific enhancer factor 2D (MEF2D), which was increased in Ang-II-induced mouse hypertrophic myocardium and cardiomyocytes, was identified as a target gene of miR-92b-3p. Functionally, miR-92b-3p mimic, consistent with MEF2D siRNA, inhibited cell size increase and protein expression of ANP, ACTA1 and ß-MHC in Ang-II-treated mouse cardiomyocytes. Taken together, we demonstrated that MEF2D is a novel target of miR-92b-3p, and attenuation of miR-92b-3p expression may contribute to the increase of MEF2D in cardiac hypertrophy.

19.
Front Physiol ; 8: 659, 2017.
Artigo em Inglês | MEDLINE | ID: mdl-28919866

RESUMO

Introduction: T wave oversensing (TWOS) is a major drawback of implantable cardioverter defibrillator (ICD) and data on predictors of TWOS in ICD is limited. We aimed to calculate a novel index of T wave safety margin (TWSM) and assess its potential for evaluating TWOS during the procedure of ICD implantation. Methods and Results: Thirty-two consecutive patients with ICD implantation were enrolled. During each procedure of ICD implantation, different ICD generators were connected to implanted sensing lead through active-fixation leads and bridging cables. R and T wave amplitudes were measured on ICD printouts according to the gain. The ICDs were programed to the most sensitive settings to reveal possible TWOS. A novel index TWSM was calculated according to the corresponding sensing algorithm of ICD. There was discrepancy of R wave amplitudes measured by different ICDs (P < 0.01). In Fortify and Teligen ICDs, T wave amplitudes showed no difference (P > 0.05) and TWSMs were sufficiently high (post sensing: 13.0 ± 7.6 and 28.3 ± 16.5, respectively, post pacing: 5.0 ± 2.2 and 4.6 ± 0.9, respectively). In nine patients with 10 TWOS episodes detected during the procedure of ICD implantation, generators with the highest TWSM were chosen. Only one TWOS episode during pacing was recorded during the 25 ± 7 mo follow-up period. Conclusions: We first propose the index of TWSM during ICD implantation as a potentially efficient predictor for TWOS. Evaluation of TWSM might help to reduce TWOS episodes in patients with high risk of TWOS. Prospective studies are warranted to validate this index and its potential to reduce TWOS episodes.

20.
Clin Exp Pharmacol Physiol ; 44(7): 771-778, 2017 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-28429502

RESUMO

Connexin 43 (Cx43) plays an important role in the pathogenesis of atrial fibrillation (AF). The present study sought to investigate the effect of macrophage migration inhibitory factor (MIF), a pleiotropic cytokine, on Cx43 expression and activity and determine the intracellular signalling pathways. Cx43 protein and mRNA levels were assayed using immunofluorescence, real-time polymerase chain reaction (PCR), and western blot. We found that increased MIF and extracellular regulated protein kinases (ERK) expression was accompanied by a significant reduction in Cx43 protein expression in atrial tissues from patients with AF compared with those with sinus rhythm. In cultured atrium-derived myocytes (HL-1 cells), mouse recombinant-MIF (rMIF, 20 or 40 nmol/L, 24 hours) down-regulated gene and protein expression of Cx43 in a concentration-dependent manner. U0126, a specific inhibitor of mitogen-activated protein kinase kinase (MAPKK) could reverse the decrease in expression of Cx43 protein induced by rMIF. Further studies revealed that rMIF (40 nmol/L, 15, 30, and 45 minutes) was able to stimulate phospho-Erk1/2 (Thr202/Tyr204) production in a time-dependent manner. These results suggest that MIF is involved in the pathogenesis of AF, probably by down-regulating the protein and gene expression of Cx43 via ERK1/2 kinase activation. Our findings represent a potential pathogenic mechanism in AF.


Assuntos
Conexina 43/metabolismo , Átrios do Coração/citologia , Fatores Inibidores da Migração de Macrófagos/metabolismo , Proteína Quinase 1 Ativada por Mitógeno/metabolismo , Proteína Quinase 3 Ativada por Mitógeno/metabolismo , Miócitos Cardíacos/metabolismo , Adulto , Animais , Fibrilação Atrial/genética , Fibrilação Atrial/metabolismo , Fibrilação Atrial/patologia , Conexina 43/genética , Feminino , Regulação Enzimológica da Expressão Gênica/efeitos dos fármacos , Átrios do Coração/patologia , Humanos , Fatores Inibidores da Migração de Macrófagos/farmacologia , Masculino , Camundongos , Pessoa de Meia-Idade , Miócitos Cardíacos/citologia , Miócitos Cardíacos/patologia , Inibidores de Proteínas Quinases/farmacologia , RNA Mensageiro/genética , RNA Mensageiro/metabolismo , Transdução de Sinais/efeitos dos fármacos , Nó Sinoatrial/efeitos dos fármacos , Nó Sinoatrial/fisiologia , Nó Sinoatrial/fisiopatologia
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