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1.
Heart Rhythm ; 2022 Apr 04.
Artigo em Inglês | MEDLINE | ID: mdl-35381379

RESUMO

BACKGROUND: The interaction of the pulmonary vein (PV) and putative nonpulmonary triggers of atrial fibrillation (AF) remains unclear and has yet to translate into patient-tailored ablation strategies. OBJECTIVE: The purpose of this study was to use noncontact mapping to detail the global conduction patterns in paroxysmal and persistent AF and how they are modified during PV ablation. METHODS: Forty patients during AF ablation underwent mapping using a noncontact catheter (AcQMap, Acutus Medical, Inc., Carlsbad, CA) before and after PV isolation (PVI). Propagation history maps were analyzed postprocedure for each patient to categorize conduction patterns into focal, organized reentrant, and disorganized patterns (F-Patterns, O-Patterns, and D-Patterns, respectively). RESULTS: Activation patterns identified by using a noncontact mapping system can be subclassified from 3 main patterns into subtypes (macroreentrant and localized reentrant [MR and LR] subtypes and disorganized 1 and disorganized 2 [D1 and D2] subtypes). Persistent AF demonstrated more D-Patterns and less O-Patterns and F-Patterns than did paroxysmal AF. In addition, patients with PAF inducible after PVI demonstrated a higher region number and higher prevalence of MR subtypes than did those noninducible. PVs remained the critical region and included almost one-third of all patterns across any AF types. PVI was effective to eliminate PV-related functional phenotypes and affected recurrence with other patterns. CONCLUSION: Activation patterns identified using AcQMap can be classified into 3 main patterns (F-Patterns, O-Patterns, and D-Patterns) as well as subtypes (MR and LR subtypes and D1 and D2 subtypes). PerAF was different from PAF in demonstrating a higher region number and higher prevalence of D-Patterns but a lower region number and lower prevalence of O-Patterns and F-Patterns.

2.
Front Cardiovasc Med ; 9: 842885, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-35252406

RESUMO

Hypertension is a major cardiovascular risk factor for atrial fibrillation (AF) worldwide. However, the role of mechanical stress caused by hypertension on downregulating the L-type calcium current (ICa,L), which is vital for AF occurrence, remains unclear. Therefore, the aim of the present study was to investigate the role of Piezo1, a mechanically activated ion channel, in the decrease of ICa,L in response to high hydrostatic pressure (HHP, one of the principal mechanical stresses) at 40 mmHg, and to elucidate the underlying pathways. Experiments were conducted using left atrial appendages from patients with AF, spontaneously hypertensive rats (SHRs) treated with valsartan (Val) at 30 mg/kg/day and atrium-derived HL-1 cells exposed to HHP. The protein expression levels of Piezo1, Calmodulin (CaM), and Src increased, while that of the L-type calcium channel a1c subunit protein (Cav1.2) decreased in the left atrial tissue of AF patients and SHRs. SHRs were more vulnerable to AF, with decreased ICa,L and shortened action potential duration, which were ameliorated by Val treatment. Validation of these results in HL-1 cells in the context of HHP also demonstrated that Piezo1 is required for the decrease of ICa,L by regulating Ca2+ transient and activating CaM/Src pathway to increase the expression of paired like homeodomain-2 (Pitx2) in atrial myocytes. Together, these data demonstrate that HHP stimulation increases AF susceptibility through Piezo1 activation, which is required for the decrease of ICa,L via. the CaM/Src/Pitx2 pathway in atrial myocytes.

3.
Clin Exp Pharmacol Physiol ; 49(1): 25-34, 2022 01.
Artigo em Inglês | MEDLINE | ID: mdl-34438468

RESUMO

Atrial fibrillation (AF) is associated with atrial conduction disturbances caused by electrical and/or structural remodelling. In the present study, we hypothesized that connexin might interact with the calcium channel through forming a protein complex and, then, participates in the pathogenesis of AF. Western blot and whole-cell patch clamp showed that protein levels of Cav1.2 and connexin 43 (Cx43) and basal ICa , L were decreased in AF subjects compared to sinus rhythm (SR) controls. In cultured atrium-derived myocytes (HL-1 cells), knocking-down of Cx43 or incubation with 30 mmol/L glycyrrhetinic acid significantly inhibited protein levels of Cav1.2 and Cav3.1 and the current density of ICa , L and ICa , T . Incubation with nifedipine or mibefradil decreased the protein level of Cx43 in HL-1 cells. Moreover, Cx43 was colocalized with Cav1.2 and Cav3.1 in atrial myocytes. Therefore, Cx43 might regulate the ICa , L and ICa , T through colocalization with calcium channel subunits in atrial myocytes, representing a potential pathogenic mechanism in AF.


Assuntos
Remodelamento Atrial , Canais de Cálcio/fisiologia , Conexina 43/fisiologia , Átrios do Coração/metabolismo , Miócitos Cardíacos/metabolismo , Animais , Fibrilação Atrial/metabolismo , Remodelamento Atrial/fisiologia , Western Blotting , Canais de Cálcio/metabolismo , Canais de Cálcio Tipo L/metabolismo , Canais de Cálcio Tipo L/fisiologia , Linhagem Celular , Células Cultivadas , Conexina 43/metabolismo , Átrios do Coração/efeitos dos fármacos , Átrios do Coração/fisiopatologia , Humanos , Mibefradil/farmacologia , Camundongos , Camundongos Endogâmicos BALB C , Microscopia Confocal , Miócitos Cardíacos/efeitos dos fármacos , Miócitos Cardíacos/fisiologia , Nifedipino/farmacologia , Técnicas de Patch-Clamp
4.
J Geriatr Cardiol ; 18(7): 523-533, 2021 Jul 28.
Artigo em Inglês | MEDLINE | ID: mdl-34404989

RESUMO

OBJECTIVE: To investigate the prevalence and modifiable risk factors of degenerative valvular heart disease (DVHD) among elderly population in southern China. METHODS: A stratified multistage sampling method was used to recruit subjects. The contents of the survey included the questionnaire, laboratory examination, echocardiography, and other auxiliary examinations. The possible risk factors of DVHD were analyzed by logistic regression analysis. RESULTS: A total of 3538 subjects ≥ 65 years of age were enrolled. One thousand three hundred and seven subjects (36.9%) were diagnosed with DVHD. Degenerative was the most common etiology of VHD. Prevalence of DVHD increased with advancing age. The prevalence of DVHD differed by living region (χ 2 = 45.594, P < 0.001), educational level ( χ 2 = 50.557, P < 0.001), and occupation ( χ 2 = 36.961, P < 0.001). Risk factors associated with DVHD included age (two-fold increased risk for each 10-year increase in age), elevated level C-reactive protein (OR = 1.346, 95% CI: 1.100-1.646), elevated level low density lipoprotein (OR = 1.243, 95% CI: 1.064-1.451), coronary artery disease (OR = 1.651, 95% CI: 1.085-2.513), smoking (OR = 1.341, 95% CI: 1.132-1.589), and hypertension (OR = 1.414, 95% CI: 1.221-1.638). Other significant risk factors included reduced or elevated level red blood cell (OR = 1.347, 95% CI: 1.031-1.761; OR = 1.599, 95% CI: 1.097-2.331; respectively), elevated level platelets (OR = 1.891, 95% CI: 1.118-3.198), elevated level uric acid (OR = 1.282, 95% CI: 1.112-1.479), and stroke (OR: 1.738, 95% CI = 1.085-2.513). CONCLUSIONS: The survey characterized the baseline conditions of DVHD cohort of elderly population in Guangzhou city. The established and emerging risk factors for DVHD may represent challenges and opportunities for therapy.

5.
Cell Death Dis ; 12(2): 216, 2021 02 26.
Artigo em Inglês | MEDLINE | ID: mdl-33637715

RESUMO

Mitochondrial dysfunction and impaired Ca2+ handling are involved in the development of diabetic cardiomyopathy (DCM). Dynamic relative protein 1 (Drp1) regulates mitochondrial fission by changing its level of phosphorylation, and the Orai1 (Ca2+ release-activated calcium channel protein 1) calcium channel is important for the increase in Ca2+ entry into cardiomyocytes. We aimed to explore the mechanism of Drp1 and Orai1 in cardiomyocyte hypertrophy caused by high glucose (HG). We found that Zucker diabetic fat rats induced by administration of a high-fat diet develop cardiac hypertrophy and impaired cardiac function, accompanied by the activation of mitochondrial dynamics and calcium handling pathway-related proteins. Moreover, HG induces cardiomyocyte hypertrophy, accompanied by abnormal mitochondrial morphology and function, and increased Orai1-mediated Ca2+ influx. Mechanistically, the Drp1 inhibitor mitochondrial division inhibitor 1 (Mdivi-1) prevents cardiomyocyte hypertrophy induced by HG by reducing phosphorylation of Drp1 at serine 616 (S616) and increasing phosphorylation at S637. Inhibition of Orai1 with single guide RNA (sgOrai1) or an inhibitor (BTP2) not only suppressed Drp1 activity and calmodulin-binding catalytic subunit A (CnA) and phosphorylated-extracellular signal-regulated kinase (p-ERK1/2) expression but also alleviated mitochondrial dysfunction and cardiomyocyte hypertrophy caused by HG. In addition, the CnA inhibitor cyclosporin A and p-ERK1/2 inhibitor U0126 improved HG-induced cardiomyocyte hypertrophy by promoting and inhibiting phosphorylation of Drp1 at S637 and S616, respectively. In summary, we identified Drp1 as a downstream target of Orai1-mediated Ca2+ entry, via activation by p-ERK1/2-mediated phosphorylation at S616 or CnA-mediated dephosphorylation at S637 in DCM. Thus, the Orai1-Drp1 axis is a novel target for treating DCM.


Assuntos
Glicemia/metabolismo , Cardiomiopatias Diabéticas/metabolismo , Dinaminas/metabolismo , Hipertrofia Ventricular Esquerda/metabolismo , Mitocôndrias Cardíacas/metabolismo , Dinâmica Mitocondrial , Miócitos Cardíacos/metabolismo , Proteína ORAI1/metabolismo , Animais , Sinalização do Cálcio , Células Cultivadas , Cardiomiopatias Diabéticas/genética , Cardiomiopatias Diabéticas/patologia , Cardiomiopatias Diabéticas/fisiopatologia , Modelos Animais de Doenças , MAP Quinases Reguladas por Sinal Extracelular/metabolismo , Hipertrofia Ventricular Esquerda/genética , Hipertrofia Ventricular Esquerda/patologia , Hipertrofia Ventricular Esquerda/fisiopatologia , Masculino , Camundongos , Mitocôndrias Cardíacas/genética , Mitocôndrias Cardíacas/ultraestrutura , Miócitos Cardíacos/ultraestrutura , Proteína ORAI1/genética , Fosforilação , Ratos Sprague-Dawley , Ratos Zucker , Função Ventricular Esquerda , Remodelação Ventricular
6.
Clin Exp Pharmacol Physiol ; 48(3): 435-442, 2021 03.
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.


Assuntos
Fator de Necrose Tumoral alfa , Animais , Átrios do Coração/metabolismo , Camundongos , Miócitos Cardíacos , Proteína Quinase C-alfa/metabolismo , Ratos
8.
J Geriatr Cardiol ; 17(3): 155-159, 2020 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-32280332

RESUMO

OBJECTIVE: To determine the risk factors for thromboembolism in lower risk patients with non-valvular atrial fibrillation (AF) and low CHA2DS2-VASc scores, which remain undefined. METHODS: We retrospectively analyzed the baseline clinical characteristics, routine laboratory parameters, and echocardiographic measurements of 705 patients (71.1% male; mean age: 52.10 ± 9.64 years) with low CHA2DS2-VASc score (0 or 1; 1 point for female sex) out of 1346 consecutive patients with non-valvular AF who underwent transesophageal echocardiography (TEE) at Guangdong Cardiovascular Institute between January 2013 and December 2015. RESULTS: Patients with left atrial thrombus (LAT) or spontaneous echo contrast (SEC) on TEE (24/705, 4%) showed a higher incidence rate of vascular disease (54.2% vs. 32.9%, P = 0.045) and non-paroxysmal AF (79.2% vs. 29.4%, P < 0.001), larger left atrial diameter (43.08 ± 4.59 vs. 36.02 ± 5.53 mm, P < 0.001), and lower left ventricular ejection fraction (58.23 ± 8.82% vs. 64.15 ± 7.14%, P < 0.001) than those without. Multivariate logistic regression analysis identified left atrial diameter [odds ratio (OR) = 1.171, 95% confidence interval (CI): 1.084-1.265, P < 0.001] and non-paroxysmal AF (OR = 3.766, 95% CI: 1.282-11.061, P = 0.016) as independent risk factors for LAT/SEC. In ROC curve analysis, a left atrial dimeter cutoff of 37.5 mm yielded 95.0% sensitivity and 62.7% specificity (AUC: 0.847, P < 0.0001, 95% CI: 0.793-0.914). CONCLUSION: In patients with non-valvular AF with low CHA2DS2-VASc score, the presence of LAT or SEC was associated with left atrial enlargement, which had moderate predictive value, and non-paroxysmal AF.

9.
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.


Assuntos
Aorta/fisiopatologia , Sinalização do Cálcio , Cálcio/metabolismo , Diabetes Mellitus Experimental/fisiopatologia , Contração Muscular/fisiologia , Músculo Liso Vascular/fisiopatologia , Miócitos de Músculo Liso/patologia , Animais , Biomarcadores/metabolismo , Canais de Cálcio/metabolismo , Diabetes Mellitus Experimental/sangue , Técnicas de Silenciamento de Genes , Concentração Inibidora 50 , Masculino , Fenótipo , Fenilefrina/farmacologia , Ratos Zucker , Molécula 1 de Interação Estromal/metabolismo , Vasoconstrição , Vasodilatação/fisiologia
10.
J Cardiovasc Electrophysiol ; 31(4): 960-963, 2020 04.
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.


Assuntos
Potenciais de Ação , Fascículo Atrioventricular/fisiopatologia , Estimulação Cardíaca Artificial , Eletrocardiografia , Técnicas Eletrofisiológicas Cardíacas , Frequência Cardíaca , Taquicardia Ventricular/diagnóstico , Adulto , Feminino , Humanos , Valor Preditivo dos Testes , Taquicardia Ventricular/fisiopatologia , Fatores de Tempo
11.
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.


Assuntos
Angiotensina II/metabolismo , Angiotensina I/metabolismo , Remodelamento Atrial/efeitos dos fármacos , Quinase 1 de Adesão Focal/metabolismo , Fragmentos de Peptídeos/metabolismo , Regulação para Cima/efeitos dos fármacos , Quinases da Família src/metabolismo , Animais , Antiarrítmicos/farmacologia , Apêndice Atrial/metabolismo , Fibrilação Atrial/patologia , Linhagem Celular Tumoral , Humanos , Pressão Hidrostática , Camundongos , Miócitos Cardíacos/metabolismo , Ratos , Ratos Endogâmicos SHR , Receptor Tipo 1 de Angiotensina/metabolismo , Valsartana/farmacologia
12.
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
13.
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.


Assuntos
Fibrilação Atrial/epidemiologia , Glicemia/análise , Diabetes Mellitus Tipo 2/epidemiologia , Intolerância à Glucose/epidemiologia , Adulto , Fatores Etários , Idoso , Fibrilação Atrial/diagnóstico , Biomarcadores/sangue , China/epidemiologia , Estudos Transversais , Diabetes Mellitus Tipo 2/sangue , Diabetes Mellitus Tipo 2/diagnóstico , Feminino , Intolerância à Glucose/sangue , Intolerância à Glucose/diagnóstico , Humanos , Masculino , Pessoa de Meia-Idade , Prevalência , Prognóstico , Medição de Risco , Fatores de Risco , Fatores Sexuais , Fatores de Tempo , Regulação para Cima
14.
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
15.
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
16.
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
17.
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
18.
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
20.
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.

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