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1.
Ren Fail ; 42(1): 54-65, 2020 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-31878817

RESUMO

Cardiovascular disease (CVD) is the leading cause of morbidity and mortality in chronic kidney disease (CKD) patients. QT interval prolongation is a congenital or acquired condition that is associated with an increased risk of torsade de pointes (TdP), sudden cardiac death (SCD), and all-cause mortality in the general population. The prevalence of acquired long QT syndrome (aLQTS) is high, and various acquired conditions contribute to the prolonged QT interval in patients with CKD. More notably, the prolonged QT interval in CKD is an independent risk factor for SCD and all-cause mortality. In this review, we focus on the epidemiological characteristics, risk factors, underlying mechanisms and treatments of aLQTS in CKD, promoting the management of aLQTS in CKD patients.

3.
Genes Genet Syst ; 94(4): 181, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31666448

RESUMO

The article appeared in Genes & Genetic Systems Vol. 94, No. 1 (p. 23-34) was listed under the incorrect category. We apologize for this error. The correction is as follows:   Incorrect: Mini review   Identification of atrial fibrillation-associated microRNAs in left and right atria of rheumatic mitral valve disease patients Yang Yan, Rui Shi, Xiaojiang Yu, Chaofeng Sun, Weijin Zang and Hongyan Tian   Correct: Full paper   Identification of atrial fibrillation-associated microRNAs in left and right atria of rheumatic mitral valve disease patients Yang Yan, Rui Shi, Xiaojiang Yu, Chaofeng Sun, Weijin Zang and Hongyan Tian.

5.
Braz J Med Biol Res ; 52(9): e8446, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31482999

RESUMO

Left atrial diameter (LAD) has been considered an independent risk factor for atrial fibrillation (AF) relapse after pulmonary vein isolation (PVI). However, whether LAD or other factors are more predictive of late recurrence in patients with paroxysmal AF remains unclear. We aimed to evaluate the value of pulmonary vein (PV) parameters for predicting AF relapse 1 year after patients underwent cryoablation for paroxysmal AF. Ninety-seven patients with paroxysmal AF who underwent PVI successfully were included. PV parameters were measured through computed tomography scans prior to PVI. A total of 28 patients had recurrence of AF at one-year follow-up. The impact of several variables on recurrence was evaluated in multivariate analyses. LAD and the time from first diagnosis of AF to ablation maintained its significance in predicting the relapse of AF after relevant adjustments in multivariate analysis. When major diameter of right inferior pulmonary vein (RIPV) (net reclassification improvement (NRI) 0.179, CI=0.031-0.326, P<0.05) and cross-sectional area (CSA) of RIPV (NRI: 0.122, CI=0.004-0.240, P<0.05) entered the AF risk model separately, the added predictive capacity was large. The accuracy of the two parameters in predicting recurrence of AF were not inferior (AUC: 0.665 and 0.659, respectively) to echocardiographic LAD (AUC: 0.663). The inclusion of either RIPV major diameter or CSA of RIPV in the model increased the C-index (0.766 and 0.758, respectively). We concluded that major diameter of RIPV had predictive capacity similar to or even better than that of LAD for predicting AF relapse after cryoablation PVI.


Assuntos
Fibrilação Atrial/etiologia , Átrios do Coração/anatomia & histologia , Veias Pulmonares/anatomia & histologia , Idoso , Fibrilação Atrial/cirurgia , Ablação por Cateter/métodos , Criocirurgia/métodos , Feminino , Átrios do Coração/diagnóstico por imagem , Humanos , Masculino , Pessoa de Meia-Idade , Estudos Prospectivos , Veias Pulmonares/diagnóstico por imagem , Recidiva , Fatores de Risco , Sensibilidade e Especificidade , Tomografia Computadorizada por Raios X , Resultado do Tratamento
6.
Mol Med Rep ; 20(2): 1541-1550, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-31257466

RESUMO

Recovery of the blood supply is the most effective treatment against ischemic heart disease; however, it is also a major cause of myocardial ischemia/reperfusion injury in clinical therapy. Curcumin has been reported to possess beneficial effects against hypoxia/reoxygenation (H/R)­induced cardiomyocyte injury by regulating cell proliferation, apoptosis and antioxidant enzyme activity. The aim of the present study was to investigate the molecular mechanisms underlying the effects of curcumin on H/R­injured cardiomyocytes. H9C2 cardiomyocytes were pretreated with curcumin, and then cultured under H/R conditions. The viability of H9C2 cells was measured using a Cell Counting kit­8 assay, and the levels of intracellular lactate dehydrogenase (LDH), malondialdehyde (MDA) and superoxide dismutase (SOD) were measured to assess cell injury. Levels of reactive oxygen species (ROS) and apoptosis were evaluated by flow cytometry. The expression levels of Notch intracellular domain (NICD) and numerous downstream genes were analyzed via reverse transcription­quantitative polymerase chain reaction and western blotting. The results revealed that curcumin protected H9C2 cells against H/R­induced injury, reversing the H/R­induced increases in LDH and MDA levels, and decreases in SOD levels. ROS levels in H/R­induced cells were also significantly downregulated by curcumin treatment (P<0.01), and the apoptotic rate was significantly decreased from 15.13% in the H/R group to 7.7% in the H/R + curcumin group (P<0.01). The expression levels of NICD, hairy and enhancer of split (Hes)­1, Hes­5 and hairy/enhancer­of­split related with YRPW motif protein 1 (Hey­1) were significantly decreased in H/R­treated cells following curcumin treatment. Treatment with Jagged1 attenuated the effects of curcumin on cell viability, ROS levels and apoptosis; the Notch pathway was also reactivated. The present study indicated that there was a role for the Notch pathway in the protective effects of curcumin against H/R­induced cardiomyocyte injury, suggesting that downregulation of the Notch pathway may alleviate H/R­induced injury in H9C2 cells.


Assuntos
Antioxidantes/farmacologia , Curcumina/farmacologia , Miócitos Cardíacos/efeitos dos fármacos , Oxigênio/farmacologia , Receptores Notch/genética , Transdução de Sinais/efeitos dos fármacos , Animais , Apoptose/efeitos dos fármacos , Apoptose/genética , Fatores de Transcrição Hélice-Alça-Hélice Básicos/genética , Fatores de Transcrição Hélice-Alça-Hélice Básicos/metabolismo , Hipóxia Celular , Linhagem Celular , Sobrevivência Celular/efeitos dos fármacos , Regulação da Expressão Gênica , Proteína Jagged-1/farmacologia , L-Lactato Desidrogenase/genética , L-Lactato Desidrogenase/metabolismo , Malondialdeído/antagonistas & inibidores , Malondialdeído/metabolismo , Miócitos Cardíacos/metabolismo , Miócitos Cardíacos/patologia , Ratos , Espécies Reativas de Oxigênio/antagonistas & inibidores , Espécies Reativas de Oxigênio/metabolismo , Receptores Notch/antagonistas & inibidores , Receptores Notch/metabolismo , Proteínas Repressoras/genética , Proteínas Repressoras/metabolismo , Transdução de Sinais/genética , Superóxido Dismutase/genética , Superóxido Dismutase/metabolismo , Fatores de Transcrição HES-1/genética , Fatores de Transcrição HES-1/metabolismo
7.
Pharm Biol ; 57(1): 245-249, 2019 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-30929547

RESUMO

CONTEXT: Allicin is a potential antiarrhythmic agent. The antiarrhythmic properties of allicin rely on its blockade of various cardiac ion channels. The l-type calcium (Cav1.2) channel provides a pivotal substrate for cardiac electrophysiologic activities. The mechanism of allicin on Cav1.2 remains unclear. OBJECTIVE: This study evaluated the potential of allicin on the synthesis and trafficking of Cav1.2 channels. MATERIALS AND METHODS: Primary cardiomyocytes (CMs) from neonatal Sprague-Dawley (SD) rats were exposed to allicin (0, 0.0001, 0.001, 0.01, 0.1, 1, 10, 100 µg/mL) for 24 and 48 h. The CellTiter-Glo assay was performed to measure CM viability. Western blot with grayscale analysis and confocal laser scanning microscopy were used to evaluate the effects of allicin on the synthesis and trafficking of Cav1.2 channel proteins in primary CMs. RESULTS: There was no significant difference in apoptotic toxicity from the actual cell viability (p > 0.05) in any group (0, 0.0001, 0.001, 0.01, 0.1, 1, 10, 100 µg/mL allicin), except that viability in the 0.001 and 0.01 µg/mL groups at 24 h were significantly greater (137.37 and 135.96%) (p < 0.05). Western blot with grayscale analysis revealed no substantial inhibition by allicin of the synthesis of Cav1.2 proteins. Confocal laser scanning microscopy revealed trafficking dysfunction of Cav1.2 channels caused by allicin in primary CMs. CONCLUSION: This study is the first to demonstrate that allicin inhibits cardiac Cav1.2 channels by disrupting trafficking, possibly mediating its antiarrhythmic benefits. Therefore, allicin might serve as a new antiarrhythmic agent in the future.


Assuntos
Antiarrítmicos/farmacologia , Canais de Cálcio Tipo L/metabolismo , Miócitos Cardíacos/efeitos dos fármacos , Ácidos Sulfínicos/farmacologia , Animais , Sobrevivência Celular/efeitos dos fármacos , Masculino , Miócitos Cardíacos/metabolismo , Cultura Primária de Células , Transporte Proteico/efeitos dos fármacos , Ratos , Ratos Sprague-Dawley
8.
J Investig Med ; 67(6): 971-976, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-30765501

RESUMO

Research on atrial histology of humans without cardiovascular disease is scarce. Therefore, our aim was to study human atrial histology in subjects without cardiovascular disease. Histology of the right atrium, left atrium or atrial septum was studied in eight patients (one newborn infant and seven adults) who died of a non-cardiac cause and who were not known to suffer from any cardiovascular pathology. Staining with hematoxylin phloxine saffron or Masson's trichrome was performed to have a better identification of fibrosis and H&E for better identification of lymphocytes. Atrial histology was compared with the histology of the left ventricle and was taken from a collection of standard glass slides. Common light microscopic examination and numeric image processing was performed in all samples. Left atrial histology showed a substantial amount of adipocytes and interstitial fibrosis, associated with replacement fibrosis in some of these cases including one case of lymphocytic infiltrates, similar to the histologic changes of the right ventricle (RV) known in patients with arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVD). Furthermore, we identified a perpendicular orientation of atrial myocardial fibres, which is also a feature of the thin RV free wall. A similar histologic substrate to the RV myocardium known in ARVD is found in the atria of humans without an overt cardiovascular pathology. This may explain the high prevalence of atrial fibrillation in the general population.

9.
Clin Cardiol ; 42(4): 452-458, 2019 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-30801746

RESUMO

BACKGROUND: Atrial fibrillation (AF) is the most common cardiac arrhythmia, with its incidence making up nearly one-third of all hospital admissions. Atrioventricular block (AVB) is a conduction abnormality along the atrioventricular node or the His-Purkinje system. The relationship between atrioventricular conduction block and AF is controversial. HYPOTHESIS: This study is designed to observe whether there is a correlation between AVB and AF, and which type of AVB has the most obvious correlation with AF. METHODS: This study retrospectively reviewed 1345 patients. We classified the AVB according to the AVB classification criteria. One hundred and two patients were excluded, and the final total sample size was 1243 patients, including 679 patients in the AF group (378, 55.7% males) and 564 patients in the non-AF group (287, 50.8% males). AF group and non-AF group were compared to observe the relationship between AVB and AF. RESULTS: The I AVB have a relative statistical risk of 1.927 (95% confidence interval [CI]: 1.160-3.203, P < 0.05) with the occurrence of AF. II AVB occupied the largest proportion, accounting for 67 cases (9.87%), and the statistical risk of II AVB in AF is 16.845 (95% CI: 6.099-46.524, P < 0.000). III AVB has a comparative statistical risk of 17.599 (95% CI: 4.212-73.541, P < 0.000). CONCLUSIONS: The three types of AVB in the AF group were significantly higher than that in the non-AF group. II AVB has the highest incidence rate compared with other types of AVB in the AF group. AVB can be used as a risk factor for AF occurrence.


Assuntos
Fibrilação Atrial/etiologia , Bloqueio Atrioventricular/complicações , Nó Atrioventricular/fisiopatologia , Medição de Risco/métodos , Adolescente , Adulto , Idoso , Idoso de 80 Anos ou mais , Fibrilação Atrial/epidemiologia , Fibrilação Atrial/fisiopatologia , Bloqueio Atrioventricular/epidemiologia , Bloqueio Atrioventricular/fisiopatologia , China/epidemiologia , Feminino , Seguimentos , Humanos , Incidência , Masculino , Pessoa de Meia-Idade , Prognóstico , Estudos Retrospectivos , Fatores de Tempo , Adulto Jovem
10.
Int J Mol Med ; 43(3): 1253-1262, 2019 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-30628647

RESUMO

Congenital long QT syndrome (LQTS) is a cardiac channelopathy that often results in fatal arrhythmias. LQTS mutations not only lead to abnormal myocardial electrical activities but are associated with heart contraction abnormalities, cardiomyopathy and congenital heart defects. In vivo and in vitro studies have found that LQTS mutations are associated with cardiomyocyte apoptosis, cardiac developmental disorders and even embryonic mortality. Cardiac delayed rectifier potassium channel dysfunction due to the human ether­à­go­go­related gene (hERG) mutation causes congenital LQTS type 2. The majority of LQTS 2 mutations are characterized by mutant protein accumulation in the endoplasmic reticulum (ER). Unfolded or misfolded protein retention in the ER causes an unfolded protein reaction, which is characteristic of ER stress (ERS). Therefore, the present study hypothesized that LQTS mutations can cause cardiac structural abnormalities via ERS­mediated cardiomyocyte apoptosis. To test this hypothesis, 293 cells were transiently transfected with an L539fs/47­hERG plasmid to generate an LQTS 2 model. L539fs/47­hERG is an LQTS 2 mutation, which consists of a 19­bp deletion at 1619­1637 and a point mutation at 1692. Using confocal laser scanning microscopy analysis, it was verified that the L539fs/47­hERG protein was retained in the ER. Hoechst 33342 apoptosis staining indicated that apoptosis was increased in the L539fs/47­hERG­transfected cells, and this be reversed by treatment with 4­phenyl butyric acid. Western blot analysis revealed increased expression levels of the ERS chaperone glucose regulated protein 78 and pro­apoptotic ERS­induced factors, including protein kinase R­like endoplasmic reticulum kinase, eukaryotic translation­initiation factor­2α and C/EBP homologous protein, in the L539fs/47­hERG­transfected cells. The B­cell lymphoma (Bcl­2)­associated X protein/Bcl­2 ratio and caspase­12 were also increased in the mutated cells. These results demonstrate that L539fs/47­hERG induces cell apoptosis and the potential molecular mechanism involves the activation of ERS and ERS­mediated cell apoptosis.


Assuntos
Apoptose/genética , Estresse do Retículo Endoplasmático/genética , Mutação , Substituição de Aminoácidos , Sequência de Bases , Retículo Endoplasmático/genética , Retículo Endoplasmático/metabolismo , Células HEK293 , Humanos , Síndrome do QT Longo/genética , Síndrome do QT Longo/metabolismo , Modelos Biológicos , Análise de Sequência de DNA , Regulador Transcricional ERG/química , Regulador Transcricional ERG/genética , Regulador Transcricional ERG/metabolismo , Resposta a Proteínas não Dobradas
11.
Oxf Med Case Reports ; 2019(1): omy122, 2019 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-30697438

RESUMO

The risk factors of acquired long QT syndrome (aLQTS) are sometimes overlooked in clinics. Drugs, hypokalemia, age and female sex are well-known risk factors of QT prolongation-dependent torsade de pointes (TdP), which explains the high incidence of sudden cardiac death in LQT patients. Here, we report a case of an elderly female patient with lung cancer who was in poor condition, for whom amiodarone was mistakenly prescribed to rectify premature ventricular contractions. QT prolongation-dependent TdP immediately followed intravenous injection of amiodarone. Fortunately, the patient survived aborted sudden cardiac arrest after effective cardio-pulmonary resuscitation and electric defibrillation. Upon reviewing the clinical information, several pre-existing risk factors of aLQTS and TdP were identified. The mistaken prescription of amiodarone provoked TdP after these risk factors were overlooked in this case and thus predisposed this patient to a high susceptibility of drug-induced TdP.

12.
J Cell Biochem ; 120(6): 10155-10163, 2019 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-30635942

RESUMO

Finding ways to reduce myocardial ischemia/reperfusion injury in the process of myocardial infarction has been an area of intense study in the field of heart disease. Recent studies have shown that long noncoding RNA (lncRNA) and autophagy play important roles in cardiovascular diseases. In our study, software analysis and dual-luciferase reporter assays have shown that miR-30a has binding sites on both AK088388 and Beclin-1. Continuing experiments found that miR-30a expression is downregulated, while the expressions of AK088388, Beclin-1, and LC3-II are upregulated in hypoxia/reoxygenation (H/R) cardiomyocytes; miR-30a inhibits the expression of AK088388, Beclin-1, and LC3-II in H/R cardiomyocytes, while AK088388 promotes the expression of Beclin-1 and LC3-II and inhibits miR-30a expression. AK088388 small interfering RNA and miR-30a mimics can promote the viability of H/R cardiomyocytes, reduce lactate dehydrogenase release, and reduce apoptosis. Mutations of the miR-30a binding site in AK088388 could not block the effects of miR-30a mentioned above. Therefore, AK088388 can competitively bind to miR-30a, promoting the expression of Beclin-1 and LC3-II, autophagy, and eventually cell damage. This finding provides new evidence for understanding the role of lncRNA in myocardial ischemia/reperfusion injury.

13.
J Investig Med ; 67(2): 289-294, 2019 02.
Artigo em Inglês | MEDLINE | ID: mdl-30367011

RESUMO

Patients with chronic kidney disease (CKD) have a high risk of fatal arrhythmias. The extended severe corrected QT (QTc) interval is a hallmark of ventricular arrhythmias and sudden cardiac death. The objective of this study was to evaluate the prevalence of acquired long QT syndrome (aLQTS) in hospitalized patients with CKD and search for potential risk factors to improve clinical risk stratification in patients with CKD. Information about patients with CKD was retrospectively collected in our hospital between January 2013 and June 2017. The prevalence of aLQTS in different stages of CKD was evaluated. The common risk factors for QTc prolongation in patients with CKD were compiled, and multivariable logistic regression analysis was used to evaluate how each factor was related to aLQTS in CKD. A total of 804 patients with CKD (299 females, 37.2%) participated in our study. The prevalence of aLQTS among all 804 patients was 56.97%, and the prevalence of QTc prolongation (>500 ms) was 10.07%. Among the elderly, impaired kidney function, hemodialysis, low serum potassium and low left ventricular ejection fraction (LVEF) were associated with QTc prolongation in patients with CKD. The prevalence of aLQTS is much higher and increases with the decline of kidney function in hospitalized patients with CKD, which is related to older age, impaired kidney function, hemodialysis, serum potassium and low LVEF.

14.
Genes Genet Syst ; 94(1): 23-34, 2019 Apr 09.
Artigo em Inglês | MEDLINE | ID: mdl-30584185

RESUMO

MicroRNA (miRNA) is associated with the development and pathology of atrial fibrillation (AF). In this study, we performed miRNA profiling of left and right atrium samples from individuals with AF-associated rheumatic mitral valve disease (RMVD) to identify miRNAs that are differentially expressed between RMVD patients with AF and RMVD with sinus rhythm (SR) as controls, as well as between left and right atrium samples from RMVD with AF patients. We performed hematoxylin and eosin staining as well as scanning and transmission electron microscopy to examine in detail any morphological and physiological changes in cardiomyocytes from RMVD patients with AF or SR. Raman spectroscopy was performed to identify molecular and structural information of left and right atrium samples from RMVD with AF and SR. We also performed miRNA array profiling to separately profile miRNA expression patterns of right and left atrium samples from three independent RMVD patients with AF and in a mixed pool of 10 RMVD patients with SR. Morphological and physiological analysis showed distinct shapes and structures of cardiomyocytes from the left and right atria of RMVD patients with AF or SR. The intensity of Raman spectroscopy of atrial tissues from RMVD patients with AF and with SR was different. miRNA profiling showed differential miRNA expression between RMVD patients with AF or SR, and between the left and right atria of RMVD patients with AF. Importantly, miRNAs showed consistent expression changes among all three patients, suggesting that these miRNAs have potential as markers for AF pathology. Our results revealed potential biomarker miRNAs for atrial fibrillation pathology in patients with RMVD. Meanwhile, our data suggested that miR-10b and miR-138-2, which were both significantly increased in the left atrium, are responsible for morphological and physiological phenotype differences between the left and right atria.


Assuntos
Fibrilação Atrial/genética , Átrios do Coração/metabolismo , Doenças das Valvas Cardíacas/genética , MicroRNAs/genética , Valva Mitral/metabolismo , Cardiopatia Reumática/genética , Fibrilação Atrial/metabolismo , Fibrilação Atrial/patologia , Feminino , Doenças das Valvas Cardíacas/metabolismo , Doenças das Valvas Cardíacas/patologia , Humanos , Masculino , MicroRNAs/metabolismo , Pessoa de Meia-Idade , Miócitos Cardíacos/metabolismo , Cardiopatia Reumática/metabolismo , Cardiopatia Reumática/patologia
15.
Braz. j. med. biol. res ; 52(9): e8446, 2019. tab, graf
Artigo em Inglês | LILACS-Express | ID: biblio-1019563

RESUMO

Left atrial diameter (LAD) has been considered an independent risk factor for atrial fibrillation (AF) relapse after pulmonary vein isolation (PVI). However, whether LAD or other factors are more predictive of late recurrence in patients with paroxysmal AF remains unclear. We aimed to evaluate the value of pulmonary vein (PV) parameters for predicting AF relapse 1 year after patients underwent cryoablation for paroxysmal AF. Ninety-seven patients with paroxysmal AF who underwent PVI successfully were included. PV parameters were measured through computed tomography scans prior to PVI. A total of 28 patients had recurrence of AF at one-year follow-up. The impact of several variables on recurrence was evaluated in multivariate analyses. LAD and the time from first diagnosis of AF to ablation maintained its significance in predicting the relapse of AF after relevant adjustments in multivariate analysis. When major diameter of right inferior pulmonary vein (RIPV) (net reclassification improvement (NRI) 0.179, CI=0.031-0.326, P<0.05) and cross-sectional area (CSA) of RIPV (NRI: 0.122, CI=0.004-0.240, P<0.05) entered the AF risk model separately, the added predictive capacity was large. The accuracy of the two parameters in predicting recurrence of AF were not inferior (AUC: 0.665 and 0.659, respectively) to echocardiographic LAD (AUC: 0.663). The inclusion of either RIPV major diameter or CSA of RIPV in the model increased the C-index (0.766 and 0.758, respectively). We concluded that major diameter of RIPV had predictive capacity similar to or even better than that of LAD for predicting AF relapse after cryoablation PVI.

16.
J Int Med Res ; 46(11): 4845-4851, 2018 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-30282519

RESUMO

Wellens' syndrome is characterised by particular changes in electrocardiogram (ECG) precordial lead T-waves accompanied by proximal stenosis of the left anterior descending (LAD) artery. Two cases of electrocardiographic changes associated with Wellens' syndrome are presented here. Case 1, a 55-year-old female, was transferred to the First Affiliated Hospital of Xi'an Jiaotong University with intermittent and laborious angina pectoris. Her first ECG on admission revealed T-wave inversion in leads V1-V3 and biphasic T-waves in V4. Case 2, an 85-year-old female, presented with dyspnoea and paroxysmal chest pain. Her admission ECG displayed asymmetrical T-wave inversion in leads V1-V3, I, and aVL, and depressed ST segments in leads V2-V5. In this patient, drug-eluting stents were placed on a LAD artery lesion and right coronary artery occlusion. The potential of ECGs to aid decision-making in severe myocardial infarction is straightforward, particularly in patients with characteristic ECGs, however, Wellens' syndrome has a wide spectrum of clinical manifestations and the ECG patterns may manifest itself persistently over a period of weeks. Therefore, ECG parameters should be combined with coronary angiography to confirm the presence of lesions.


Assuntos
Eletrocardiografia , Idoso de 80 Anos ou mais , Feminino , Humanos , Processamento de Imagem Assistida por Computador , Pessoa de Meia-Idade , Síndrome
17.
Clin Sci (Lond) ; 132(19): 2135-2146, 2018 10 15.
Artigo em Inglês | MEDLINE | ID: mdl-30190284

RESUMO

Background: Atrial fibrillation (AF) is the most common cardiac arrhythmia whose incidence is on the rise globally. However, the pathophysiologic mechanism of AF remains poorly understood and there has been a lack of circulatory markers to diagnose and predict prognosis of AF. In the present study, by measuring metabolic profile and analyzing plasma amino acid levels in AF patients, we sought to determine whether amino acid metabolism was correlated to the occurrence of AF. Methods: Consecutive patients admitted to hospital for AF were enrolled. Plasma samples were obtained after overnight fast and a profile of 61 amino acids was then measured using gas chromatography/mass spectrometry (GC/MS). Results: Twenty-three AF and thirty-seven control patients were enrolled in the study. A number of plasma amino acids were altered in AF, which showed significant prediction value for AF. Intriguingly, circulating 4-hydroxypyrrolidine-2-carboxylic was gradually lowered with the persistence of AF. Plasma amino acid levels were more strongly correlated with each other in AF as compared with control. Conclusion: By utilizing non-target metabolic profile surveys, we have found a number of altered amino acids, which exhibit diagnostic value for AF. Enhanced amino acids correlation network further identified AF as a metabolism disorder.


Assuntos
Aminoácidos/metabolismo , Fibrilação Atrial/metabolismo , Metaboloma , Metabolômica/métodos , Idoso , Aminoácidos/sangue , Fibrilação Atrial/diagnóstico , Fibrilação Atrial/fisiopatologia , Biomarcadores/sangue , Feminino , Cromatografia Gasosa-Espectrometria de Massas , Humanos , Masculino , Pessoa de Meia-Idade , Fatores de Risco
18.
J Cell Biochem ; 119(12): 10239-10249, 2018 12.
Artigo em Inglês | MEDLINE | ID: mdl-30145795

RESUMO

The dysregulation of long noncoding RNAs (lncRNAs) and microRNAs (miRNAs) participates in the remodeling of electrophysiological/ion channel in cardiomyocytes during arrhythmia. The lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is reported to be highly expressed in myocardial ischemia-reperfusion injury and offsets cardioprotective effects of fentanyl. However, the roles of MALAT1 and its related miRNAs during arrhythmia are poorly understood. In this study, the overexpression of MALAT1 was firstly indicated in cardiomyocytes from arrhythmic model rats. After downregulation of MALAT1 by RNA interference, transient outward potassium current (Ito), peak current density, and the levels of Kv4.2 and Kv4.3 channel proteins were increased in rat cardiomyocytes. Then, miR-200c was predicted and convinced to be a direct target of MALAT1, and high-mobility group box 1 (HMGB1) was verified to be a target of miR-200c during arrhythmia. HMGB1 expression reduced by the knockdown of MALAT1 was further decreased by miR-200c overexpression. In addition, cardiac Ito, peak current density, and the levels of Kv4.2 and Kv4.3 in arrhythmic model rats were detected to be negatively correlated with the expression of HMGB1, and to be positively with miR-200c expression. Taken together, these results suggested that MALAT1 may act as a competing endogenous RNA for miR-200c to upregulate the expression of HMGB1 and downregulate cardiac Ito.


Assuntos
Arritmias Cardíacas/genética , Proteína HMGB1/genética , MicroRNAs/genética , RNA Longo não Codificante/genética , Animais , Apoptose , Arritmias Cardíacas/metabolismo , Arritmias Cardíacas/patologia , Proliferação de Células , Modelos Animais de Doenças , Regulação da Expressão Gênica , Humanos , Miócitos Cardíacos/metabolismo , Miócitos Cardíacos/patologia , Potássio/metabolismo , Ratos , Canais de Potássio Shal/genética , Canais de Potássio Shal/metabolismo , Transdução de Sinais
19.
Int Immunopharmacol ; 62: 203-211, 2018 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-30015240

RESUMO

Monocytes recruited and adhering to the inflamed arteries are crucial for atherosclerosis development. Here, we report the role of zinc (Zn2+) homeostasis in monocyte adhesion and recruitment. By comparing the expression levels of Zn2+ transporters between non-adhering and adhering monocytes, we found that the Zn2+ importer ZIP8 was specifically upregulated in monocytes adhering to the aortas ex-vivo. Although the overexpression of ZIP8 increased the absorption of Zn2+, Fe2+ and Cd2+ in monocytes, only Zn2+ supplementation was demonstrated capable of promoting the adhesion of monocytes to endothelial monolayers in vitro. In addition, we confirmed the role of ZIP8-dependent Zn2+ influx in promoting monocyte adhesion to the aortas ex-vivo. More importantly, the enforced expression of ZIP8 increased monocyte adhesion and recruitment to the nascent atherosclerotic lesions in ApoE-/- mice. Overall, our results suggest that the Zn2+ influx in monocytes regulated by ZIP8 is a novel factor determining their adhesion and recruitment to atherosclerotic lesions, and that targeting ZIP8 or Zn2+ homeostasis may represent a novel strategy to interfere these activities.


Assuntos
Aorta/metabolismo , Proteínas de Transporte de Cátions/metabolismo , Adesão Celular , Doença da Artéria Coronariana/metabolismo , Monócitos/metabolismo , Zinco/metabolismo , Animais , Aorta/patologia , Apolipoproteínas E/genética , Proteínas de Transporte de Cátions/genética , Adesão Celular/genética , Linhagem Celular , Doença da Artéria Coronariana/genética , Doença da Artéria Coronariana/patologia , Modelos Animais de Doenças , Camundongos Endogâmicos C57BL , Camundongos Knockout , Monócitos/patologia , Regulação para Cima
20.
Exp Biol Med (Maywood) ; 243(10): 852-863, 2018 06.
Artigo em Inglês | MEDLINE | ID: mdl-29806494

RESUMO

The voltage-gated sodium channel 1.5 (Nav1.5), encoded by the SCN5A gene, is responsible for the rising phase of the action potential of cardiomyocytes. The sodium current mediated by Nav1.5 consists of peak and late components (INa-P and INa-L). Mutant Nav1.5 causes alterations in the peak and late sodium current and is associated with an increasingly wide range of congenital arrhythmias. More than 400 mutations have been identified in the SCN5A gene. Although the mechanisms of SCN5A mutations leading to a variety of arrhythmias can be classified according to the alteration of INa-P and INa-L as gain-of-function, loss-of-function and both, few researchers have summarized the mechanisms in this way before. In this review article, we aim to review the mechanisms underlying dysfunctional Nav1.5 due to SCN5A mutations and to provide some new insights into further approaches in the treatment of arrhythmias. Impact statement The field of ion channelopathy caused by dysfunctional Nav1.5 due to SCN5A mutations is rapidly evolving as novel technologies of electrophysiology are introduced and our understanding of the mechanisms of various arrhythmias develops. In this review, we focus on the dysfunctional Nav1.5 related to arrhythmias and the underlying mechanisms. We update SCN5A mutations in a precise way since 2013 and presents novel classifications of SCN5A mutations responsible for the dysfunction of the peak (INa-P) and late (INa-L) sodium channels based on their phenotypes, including loss-, gain-, and coexistence of gain- and loss-of function mutations in INa-P, INa-L, respectively. We hope this review will provide a new comprehensive way to better understand the electrophysiological mechanisms underlying arrhythmias from cell to bedside, promoting the management of various arrhythmias in practice.


Assuntos
Potenciais de Ação , Proteínas Mutantes/genética , Proteínas Mutantes/metabolismo , Mutação , Miócitos Cardíacos/fisiologia , Canal de Sódio Disparado por Voltagem NAV1.5/genética , Canal de Sódio Disparado por Voltagem NAV1.5/metabolismo , Humanos , Sódio/metabolismo
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