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1.
Transl Res ; 218: 1-15, 2020 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-32032554

RESUMO

Etiology-based diagnosis of dilated cardiomyopathy (DCM) is challenging. We evaluated whether peripheral microRNAs (miRNAs) could be used to characterize the DCM etiology. We investigated the miRNA plasma profiles of 254 subjects that comprised 5 groups: Healthy subjects (n = 70), idiopathic DCM patients (n = 55), ischemic DCM patients (n = 60) and 2 groups of patients with pathogenic variants responsible for familial DCM in the LMNA (LMNAMUT, n = 37) and BAG3 (BAG3MUT, n = 32) genes. Diagnostic performance was assessed using receiver operating characteristic curves. In a screening study (n = 30), 179 miRNAs robustly detected in plasma samples were profiled in idiopathic DCM and carriers of pathogenic variants. After filtering, 26 miRNA candidates were selected for subsequent quantification in the whole study population. In the validation study, a 6-miRNA panel identified familial DCM with an AUC (95% confidence interval [CI]) of 87.8 (82.0-93.6). The 6-miRNA panel also distinguished between specific DCM etiologies with AUCs ranging from 85.9 to 89.9. Only 1 to 10 of the subjects in the first and second tertiles of the 6-miRNA panel were patients with familial DCM. Additionally, a 5-miRNA panel showed an AUC (95% CI) of 87.5 (80.4-94.6) for the identification of carriers with pathogenic variants who were phenotypically negative for DCM. The 5-miRNA panel discriminated between carriers and healthy controls with AUCs ranging from 83.2 to 90.8. Again, only 1 to 10 of the subjects in the lowest tertiles of the 5-miRNA panel were carriers of pathogenic variants. In conclusion, miRNA signatures could be used to rule out patients with pathogenic variants responsible for DCM.

4.
Am Heart J ; 220: 213-223, 2020 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-31864099

RESUMO

BACKGROUND: Cardiogenic syncope in Brugada syndrome (BrS) increases the risk of major events. Nevertheless, clinical differentiation between cardiogenic and vasovagal syncope can be challenging. We characterized the long-term incidence of major events in a large cohort of BrS patients who presented with syncope. METHODS: From a total of 474 patients, syncope was the initial manifestation in 135 (28.5%) individuals (43.9 ±â€¯13.9 years, 71.1% male). The syncope was classified prospectively as cardiogenic, vasovagal, or undefined if unclear characteristics were present. Clinical, electrocardiographic, genetic, and electrophysiologic features were analyzed. Cardiogenic syncope, sustained ventricular arrhythmias, and sudden death were considered major events in follow-up. RESULTS: In 66 patients (48.9%), the syncope was cardiogenic; in 51 (37.8%), vasovagal and in 18 (13.3%); undefined. The electrophysiology study (EPS) inducibility was more frequent in patients with cardiogenic syncope and absent in all patients with undefined syncope (28 [53.8%] vs 5 [12.2%] vs 0 [0%]; P < .01). During follow-up (7.7 ±â€¯5.6 years), only patients with cardiogenic syncope presented major events (16 [11.9%]). Among patients with inducible EPS, 7 (21.2%) presented major events (P = .04). The negative predictive value of the EPS for major events was 92.4%. The incidence rate of major events was 2.6% person-year. Parameters associated with major events included cardiogenic syncope (hazard ratio [HR] 6.3; 95% CI 1.1-10.4; P = .05), spontaneous type 1 electrocardiogram (HR 3.7; 95% CI 1.3-10.5; P = .01), and inducible EPS (HR 2.8; 95% CI 1.1-8.8; P = .05). CONCLUSIONS: An accurate syncope classification is crucial in BrS patients for risk stratification. In patients with syncope of unclear characteristics, the EPS may be helpful to prevent unnecessary implantable cardioverter defibrillators.

5.
J Electrocardiol ; 56: 85-89, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31326859

RESUMO

Supraventricular tachycardias (SVT) are the most common arrhythmias in the perinatal period. Permanent junctional reciprocating tachycardia (PJRT) is a rare form of SVT, often incessant and refractory to pharmacological treatments. Our goal was to analyze the clinical features and treatment of PJRT in patients younger than 2 months and to describe their long-term outcomes. METHODS: Retrospective descriptive observational study of patients diagnosed between 2000 and 2015 in the NICU of a referral center for the treatment of pediatric arrhythmias. History of pregnancy, neonatal period, pharmacological treatment, electrophysiological study and long-term follow-up were reviewed. RESULTS: 129 of the 10.198 (1.26%) patients admitted to the NICU had SVT, sixteen of them (12.3%) being diagnosed as PJRT. Ten cases had a prenatal diagnosis. For those six patients postnatally diagnosed, the tachycardia was detected either during a routine check-up or because of acute hemodynamic instability. The majority of patients required combinations of drugs, despite that the tachycardia was poorly controlled. Fifteen patients underwent cardiac ablation, nine patients (60%) in the neonatal period and six during childhood. The procedure was completely effective in all cases. One patient had a transient complete AV block that resolved spontaneously 24 hours after the procedure. No other complications were seen. After a mean follow-up of 10.9 years, no patient has presented recurrence, cardiac dysfunction, signs of ischemia or EKG abnormalities, they all have a normal life. CONCLUSIONS: When PJRT is refractory to multiple drugs, cardiac ablation should be taken into account at early stages even in very young patients.

6.
J Clin Med ; 8(7)2019 Jul 16.
Artigo em Inglês | MEDLINE | ID: mdl-31315195

RESUMO

Short QT syndrome, one of the most lethal entities associated with sudden cardiac death, is a rare genetic disease characterized by short QT intervals detected by electrocardiogram. Several genetic variants are causally linked to the disease, but there has yet to be a comprehensive analysis of variants among patients with short QT syndrome. To fill this gap, we performed an exhaustive study of variants currently catalogued as deleterious in short QT syndrome according to the American College of Medical Genetics and Genomics and the Association for Molecular Pathology. Analysis of the 32 variants described in the literature determined that only nine (28.12%) have a conclusive pathogenic role. All definitively pathogenic variants are located in KCNQ1, KCNH2, or KCNJ2; three genes encoding potassium channels. Other variants located in genes encoding calcium or sodium channels are associated with electrical alterations concomitant with shortened QT intervals but do not guarantee a diagnosis of short QT syndrome. We recommend caution regarding previously reported variants classified as pathogenic. An exhaustive re-analysis is necessary to clarify the role of each variant before routinely translating genetic findings to the clinical setting.

7.
J Cardiovasc Transl Res ; 12(4): 389-390, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-31309403

RESUMO

The name of author M. Alejandra Restrepo-Cordoba was parsed incorrectly (in such a way as to suggest that her surname is "Alejandra Restrepo-Cordoba") in this article as published.

9.
Front Genet ; 10: 450, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31156706

RESUMO

Cardiomyopathies are a heterogeneous group of inherited cardiac diseases characterized by progressive myocardium abnormalities associated with mechanical and/or electrical dysfunction. Massive genetic sequencing technologies allow a comprehensive genetic analysis to unravel the cause of disease. However, most identified genetic variants remain of unknown clinical significance due to incomplete penetrance and variable expressivity. Therefore, genetic interpretation of variants and translation into clinical practice remain a current challenge. We performed retrospective comprehensive clinical assessment and genetic analysis in six families, four diagnosed with arrhythmogenic cardiomyopathy, and two diagnosed with hypertrophic cardiomyopathy (HCM). Genetic testing identified three rare variants (two non-sense and one small indel inducing a frameshift), each present in two families. Although each variant is currently classified as pathogenic and the cause of the diagnosed cardiomyopathy, the onset and/or clinical course differed in each patient. New genetic technology allows comprehensive yet cost-effective genetic analysis, although genetic interpretation, and clinical translation of identified variants should be carefully done in each family in a personalized manner.

10.
Int J Mol Sci ; 20(8)2019 Apr 23.
Artigo em Inglês | MEDLINE | ID: mdl-31018519

RESUMO

Epilepsy is a common neurological disorder associated with increased morbidity and mortality. Sudden unexpected death in epilepsy, also known as SUDEP, is the main cause of death in patients with epilepsy. SUDEP has an incidence of 1.2 per 1000 person-years in adults and 0.2 per 1000 person-years in children. SUDEP accounts for 8-17% of deaths in patients with epilepsy. It is commonly associated with a history of generalized tonic-clonic seizures, and its risk may be increased by other factors such as postictal electroencephalographic suppression, prone sleeping position, altered heart rate variability, conduction abnormalities, gender, or antiepileptic medications. Recently, electrocardiograms, electroencephalograms, and imaging markers have helped clinicians stratify SUDEP risk and identify patients in need of close monitoring. However, the pathophysiology of SUDEP is likely multifactorial and still unknown. Improving the knowledge of SUDEP incidence, risk factors, and biomarkers can help design and implement effective prevention strategies.


Assuntos
Morte Súbita/epidemiologia , Epilepsia/genética , Animais , Arritmias Cardíacas/complicações , Arritmias Cardíacas/genética , Arritmias Cardíacas/patologia , Arritmias Cardíacas/fisiopatologia , Morte Súbita/patologia , Epilepsia/epidemiologia , Epilepsia/patologia , Epilepsia/fisiopatologia , Predisposição Genética para Doença , Humanos , Fatores de Risco
11.
Hum Mutat ; 40(6): 749-764, 2019 06.
Artigo em Inglês | MEDLINE | ID: mdl-30821013

RESUMO

Brugada syndrome (BrS) is an inherited arrhythmogenic disease associated with sudden cardiac death. The main gene is SCN5A. Additional variants in 42 other genes have been reported as deleterious, although these variants have not yet received comprehensive pathogenic analysis. Our aim was to clarify the role of all currently reported variants in minor genes associated with BrS. We performed a comprehensive analysis according to the American College of Medical Genetics and Genomics guidelines of published clinical and basic data on all genes (other than SCN5A) related to BrS. Our results identified 133 rare variants potentially associated with BrS. After applying current recommendations, only six variants (4.51%) show a conclusive pathogenic role. All definitively pathogenic variants were located in four genes encoding sodium channels or related proteins: SLMAP, SEMA3A, SCNN1A, and SCN2B. In total, 33.83% of variants in 19 additional genes were potentially pathogenic. Beyond SCN5A, we conclude definitive pathogenic variants associated with BrS in four minor genes. The current list of genes associated with BrS, therefore, should include SCN5A, SLMAP, SEMA3A, SCNN1A, and SCN2B. Comprehensive genetic interpretation and careful clinical translation should be done for all variants currently classified as potentially deleterious for BrS.

12.
Curr Cardiol Rev ; 15(1): 30-37, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-30210005

RESUMO

BACKGROUND: Sudden death of a newborn is a rare entity, which may be caused by genetic cardiac arrhythmias. Among these diseases, Long QT syndrome is the most prevalent arrhythmia in neonates, but other diseases such as Brugada syndrome, Short QT syndrome and Catecholaminergic Polymorphic Ventricular Tachycardia also cause sudden death in infants. All these entities are characterized by well-known alterations in the electrocardiogram and the first symptom of the disease may be an unexpected death. Despite the low prevalence of these diseases, the performance of an electrocardiogram in the first hours or days after birth could help identify these electrical disruptions and adopt preventive measures. In recent years, there has been an important impulse by some experts in the scientific community towards the initiation of a newborn electrocardiogram-screening program, for the detection of these electrocardiographic abnormalities. In addition, the use of genetic analysis in neonates could identify the cause of these heart alterations. Identification of relatives carrying the genetic alteration associated with the disease allows adoption of measures to prevent lethal episodes. CONCLUSION: Recent technological advances enable a comprehensive genetic screening of a large number of genes in a cost-effective way. However, the interpretation of genetic data and its translation into clinical practice are the main challenges for cardiologists and geneticists. However, there is important controversy as to the clinical value, and cost-effectiveness of the use of electrocardiogram as well as of genetic testing to detect these cases. Our review focuses on these current matters of argue.


Assuntos
Morte Súbita Cardíaca/patologia , Eletrocardiografia/métodos , Testes Genéticos/métodos , Síndrome do QT Longo/diagnóstico , Humanos , Lactente , Recém-Nascido , Síndrome do QT Longo/patologia
13.
Minerva Anestesiol ; 85(2): 173-188, 2019 02.
Artigo em Inglês | MEDLINE | ID: mdl-30394071

RESUMO

Brugada Syndrome is characterized by arrhythmogenic risk that may be exacerbated by different metabolic and pharmacological factors. Since its first description, knowledge of this syndrome and its detection by physicians belonging to different specialties have gradually increased. The risk of arrhythmias is well known to increase in the postoperative period, and this risk is particularly accentuated in patients with Brugada Syndrome. The purpose of this review is to analyze the relationship between this syndrome and anesthesia; establish recommendations for the safe management of these patients in the surgical setting; and update the relevant concepts regarding the safety of drug administration in individuals with Brugada Syndrome.

14.
J Am Coll Cardiol ; 72(22): 2747-2757, 2018 12 04.
Artigo em Inglês | MEDLINE | ID: mdl-30497561

RESUMO

BACKGROUND: The prevalence and significance of structural abnormalities in Brugada syndrome (BrS) are still largely debated. OBJECTIVES: The authors investigated the relationship between genetic background, electroanatomic abnormalities, and pathologic substrate in BrS. METHODS: They performed 3-dimensional electroanatomic unipolar and bipolar mapping in 30 patients with BrS. Twenty patients underwent 3-dimensional electroanatomic unipolar and bipolar mapping-guided right ventricular outflow tract (RVOT) endomyocardial biopsy. Programmed ventricular stimulation and genetic analysis were performed in all patients. RESULTS: Low-voltage areas (LVAs) were observed at unipolar map in 93% of patients and at bipolar map in 50% of cases. Unipolar LVAs were always larger than bipolar LVAs, were always colocalized, and in all cases included RVOT. Disease-causing mutations were detected in 10 (33%) patients. Programmed ventricular stimulation was positive in 16 cases (53%). In 75% of patients, RVOT histology showed pathologic findings with myocardial inflammation in 80% of them. Among patients with abnormal bipolar map submitted to endomyocardial biopsy, 9 (81%) showed evidence of myocardial inflammation. Conversely, bipolar map was abnormal in 83% of patients with myocardial inflammation. Myocardial inflammation was also more prevalent among inducible patients (83% vs. 25% in noninducible; p = 0.032). CONCLUSIONS: BrS is characterized by electroanatomical and structural abnormalities localized to RVOT with a gradient of the pathologic substrate from epicardium to endocardium possibly driven by myocardial inflammation. These findings reclassify BrS as a combination of structural and electrical defects opening the way to new risk stratification and therapeutic strategies.


Assuntos
Mapeamento Potencial de Superfície Corporal/métodos , Síndrome de Brugada/diagnóstico por imagem , Síndrome de Brugada/fisiopatologia , Imagem Tridimensional/métodos , Obstrução do Fluxo Ventricular Externo/diagnóstico por imagem , Obstrução do Fluxo Ventricular Externo/fisiopatologia , Adulto , Síndrome de Brugada/terapia , Desfibriladores Implantáveis , Eletrocardiografia/métodos , Feminino , Seguimentos , Humanos , Masculino , Pessoa de Meia-Idade , Obstrução do Fluxo Ventricular Externo/terapia
15.
Front Cardiovasc Med ; 5: 149, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-30420954

RESUMO

Short QT syndrome is a highly malignant inherited cardiac disease characterized by ventricular tachyarrhythmias leading to syncope and sudden cardiac death. It is responsible of lethal episodes in young people, mainly infants. International guidelines establish diagnostic criteria with the presence of a QTc ≤ 340 ms in the electrocardiogram despite clinical diagnostic values remain controversial. In last years, clinical diagnosis, risk stratification as well as preventive therapies have been improved due to identification of pathophysiological mechanisms. The only effective option is implantation of a defibrillator despite Quinidine may be at times an effective option. Currently, a limited number of rare variants have been identified in seven genes, which account for nearly 20-30% of families. However, some of these variants are associated with phenotypes showing a shorter QT interval but no conclusive diagnosis of Short QT syndrome. Therefore, an exhaustive interpretation of each variant and a close genotype-phenotype correlation is necessary before clinical translation. Here, we review the main clinical and genetic hallmarks of this rare entity.

16.
J Am Coll Cardiol ; 72(9): 1046-1059, 2018 08 28.
Artigo em Inglês | MEDLINE | ID: mdl-30139433

RESUMO

The Brugada syndrome is an inherited disorder associated with risk of ventricular fibrillation and sudden cardiac death in a structurally normal heart. Diagnosis is based on a characteristic electrocardiographic pattern (coved type ST-segment elevation ≥2 mm followed by a negative T-wave in ≥1 of the right precordial leads V1 to V2), observed either spontaneously or during a sodium-channel blocker test. The prevalence varies among regions and ethnicities, affecting mostly males. The risk stratification and management of patients, principally asymptomatic, still remains challenging. The current main therapy is an implantable cardioverter-defibrillator, but radiofrequency catheter ablation has been recently reported as an effective new treatment. Since its first description in 1992, continuous achievements have expanded our understanding of the genetics basis and electrophysiological mechanisms underlying the disease. Currently, despite several genes identified, SCN5A has attracted most attention, and in approximately 30% of patients, a genetic variant may be implicated in causation after a comprehensive analysis.


Assuntos
Síndrome de Brugada/diagnóstico , Síndrome de Brugada/terapia , Síndrome de Brugada/etiologia , Humanos
17.
Forensic Sci Int Genet ; 37: 54-63, 2018 11.
Artigo em Inglês | MEDLINE | ID: mdl-30086531

RESUMO

Sudden infant death syndrome is the leading cause of death during the first year of life. A large part of cases remains without a conclusive cause of death after complete autopsy. In these situations, cardiac arrhythmia of genetic origin is suspected as the most plausible cause of death. Our aim was to ascertain whether genetic variants associated with sudden cardiac death might be the cause of death in a cohort of infants died suddenly. We analyzed 108 genes associated with sudden cardiac death in 44 post-mortem samples of infants less than 1 year old of age who died at rest. Definite cause of death was not conclusive in any case after a complete autopsy. Genetic analysis identified at least one rare variant in 90.90% of samples. A total of 121 rare genetic variants were identified. Of them, 33.05% were novel and 39.66% were located in genes encoding ion channels or associated proteins. A comprehensive genetic analysis in infants who died suddenly enables the unraveling of potentially causative cardiac variants in 2045% of cases. Molecular autopsy should be included in forensic protocols when no conclusive cause of death is identified. Large part genetic variants remain of uncertain significance, reinforcing the crucial role of genetic interpretation before clinical translation but also in early identification of relatives at risk.


Assuntos
Variação Genética , Sequenciamento de Nucleotídeos em Larga Escala , Análise de Sequência de DNA , Morte Súbita do Lactente/genética , Estudos de Coortes , Variações do Número de Cópias de DNA , Feminino , Frequência do Gene , Humanos , Lactente , Recém-Nascido , Masculino , Reação em Cadeia da Polimerase
18.
J Mol Med (Berl) ; 96(8): 845-856, 2018 08.
Artigo em Inglês | MEDLINE | ID: mdl-30008018

RESUMO

Lamin A/C gene (LMNA)-related familial dilated cardiomyopathy (fDCM) is an aggressive heart disease that often leads to transplantation and sudden death. The aim of our study was to evaluate the circulating microRNA (miRNA) profiles of patients with LMNA pathogenic mutations. The study population (N = 75) included (i) patients with pathogenic LMNA mutations responsible for fDCM (LMNAMUT), (ii) age- and sex-matched LMNA wild-type controls (LMNAWT control), and (iii) LMNA wild-type idiopathic DCM (iDCM) patients (LMNAWT iDCM). Detailed clinical information was obtained from each participant. A panel of 179 plasma miRNAs was evaluated using RT-qPCR. An initial screening study was performed in LMNAMUT carriers and age-matched LMNAWT controls (N = 16). Forty-four miRNAs were specifically deregulated in LMNAMUT carriers. Ten miRNA candidates were selected for subsequent validation after coexpression analyses and filtered for expression levels and statistical significance. Among the candidates, let-7a-5p, miR-142-3p, miR-145-5p and miR-454-3p levels were significantly increased in LMNAMUT carriers compared to LMNAWT controls and iDCM patients (P < 0.050). These circulating miRNAs, and their combination, were also associated with the presence of pathogenic mutations in regression and ROC analyses. This signature also discriminates between LMNAWT healthy subjects and LMNAMUT carriers who are phenotypically negative for DCM and between LMNAWT iDCM and LMNA-related DCM patients. Correlation and functional enrichment analyses supported their association with the pathophysiology of the disease. We demonstrated for the first time that a specific miRNA signature could serve as a novel non-invasive tool to assist in the diagnosis of patients with fDCM caused by LMNA pathogenic mutations. KEY MESSAGES: Let-7a-5p, miR-142-3p, miR-145-5p and miR-454-3p are differentially expressed in LMNAMUT carriers. A composite score based on these miRNAs is a biomarker of mutations in the LMNA gene. This miRNA signature can be associated with the pathophysiology of familial DCM. The circulating miRNA profile can assist in the diagnosis of familial DCM.


Assuntos
Cardiomiopatia Dilatada/sangue , Cardiomiopatia Dilatada/etiologia , MicroRNA Circulante , Lamina Tipo A/genética , MicroRNAs/genética , Adulto , Alelos , Substituição de Aminoácidos , Biomarcadores , Cardiomiopatia Dilatada/diagnóstico , Biologia Computacional , Ecocardiografia , Feminino , Perfilação da Expressão Gênica , Predisposição Genética para Doença , Genótipo , Testes de Função Cardíaca , Humanos , Masculino , MicroRNAs/sangue , Pessoa de Meia-Idade , Mutação , Curva ROC , Transcriptoma
19.
Arch Cardiol Mex ; 88(4): 306-312, 2018.
Artigo em Espanhol | MEDLINE | ID: mdl-30030015

RESUMO

Currently, there are a significant percentage of autopsies left without a conclusive diagnosis of death, especially when this lethal event occurs suddenly. Genetic analysis has been recently incorporated into the field of forensic medicine, especially in patients with sudden death and where no conclusive cause of death is identified after a complete medical-legal autopsy. Inherited arrhythmogenic diseases are the main cause of death in these cases. To date, more than 40 genes have been associated with arrhythmogenic disease, and causing sudden cardiac death has been described. The main arrhythmogenic diseases are Long QT Syndrome, Catecholaminergic Polymorphic Ventricular Tachycardia, Brugada Syndrome, and Short QT Syndrome. These post-mortem genetic studies, not only allow a diagnosis of the cause of death, but also allow a clinical translation in relatives, focusing on the early identification of individuals at risk of syncope, as well as adopting personalised therapeutic measures for the prevention of a lethal arrhythmic episode.


Assuntos
Arritmias Cardíacas/complicações , Autopsia/métodos , Morte Súbita Cardíaca/etiologia , Arritmias Cardíacas/genética , Humanos , Síncope/etiologia
20.
PLoS One ; 13(7): e0200756, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-30020974

RESUMO

BACKGROUND: Patients with end-stage renal disease have very high mortality. In individuals on hemodialysis, cardiovascular deaths account for ~50% of all deaths in this population, mostly due to arrhythmia. To determine the causes of these arrhythmic deaths is essential in order to adopt preventive strategies. The main objective of this study was to investigate whether, the presence of QTc interval alterations, from electrolyte abnormalities or presence of rare genetic variants, could have a relationship with sudden arrhythmogenic deaths in end-stage renal disease patients. METHODS: We recorded the pre- and post-dialysis QTc interval in 111 patients undergoing hemodialysis. In 47 of them, we analyzed 24 SCD-related genes including the most prevalent genes associated with long QT syndrome using a custom resequencing panel. RESULTS: We found a positive although not significant association between the presence of long QTc and mortality in a subset of end-stage renal disease patients. In addition, in five patients with long QTc only after dialysis (21.7%) we detected rare potentially pathogenic genetic variants. Three out of these five carriers subsequently died suddenly. CONCLUSIONS: Genetic background may be determinant in the risk of sudden cardiac death in these patients. We recommend evaluating the QTc interval before and after hemodialysis, and performing a genetic analysis of individuals with long QTc after hemodialysis.


Assuntos
Arritmias Cardíacas/metabolismo , Arritmias Cardíacas/fisiopatologia , Morte Súbita Cardíaca/patologia , Eletrólitos/metabolismo , Falência Renal Crônica/metabolismo , Falência Renal Crônica/fisiopatologia , Síndrome do QT Longo/fisiopatologia , Idoso , Biologia Computacional , Eletrocardiografia , Feminino , Humanos , Masculino , Pessoa de Meia-Idade
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