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1.
S D Med ; 73(3): 112-115, 2020 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-32142229

RESUMO

Advancements in clinical informatics and translational genomics are changing the way we practice medicine. Automated decision support currently helps providers adjust prescribing patterns to reduce the likelihood of QT prolongation based upon drug-drug interaction. A similar approach is being explored for drug-gene interaction. Like many adverse drug reactions, QT prolongation can be influenced by variability in genetic factors. However, drug-induced QT prolongation can occur in the absence of any known ion channel gene abnormalities. We therefore review differences between congenital long QT syndrome and drug-induced long QT syndrome, and we underscore the need for decision support that integrates EKG data.


Assuntos
Sistemas de Apoio a Decisões Clínicas , Efeitos Colaterais e Reações Adversas Relacionados a Medicamentos , Síndrome do QT Longo , Torsades de Pointes , Automação , Interações de Medicamentos , Eletrocardiografia , Humanos , Síndrome do QT Longo/induzido quimicamente , Síndrome do QT Longo/diagnóstico
2.
Zhonghua Yi Xue Yi Chuan Xue Za Zhi ; 37(3): 289-294, 2020 Mar 10.
Artigo em Chinês | MEDLINE | ID: mdl-32128746

RESUMO

Long Q-T syndrome (LQTS) is an ion channel disease of the heart featuring single gene inheritance. It is characterized by prolonged QT interval, abnormal T wave, torsade de points (TdP) on electrocardiogram, with recurrent syncope, convulsion and even sudden death. Although the overall prevalence of LQTS is not high, the disease has attracted attention of cardiologists for its high incidence of sudden cardiac death. The compilation of this guideline has referred to the consensus of basic and clinical research, guidelines of other countries, and summarized the clinical manifestations, molecular basis, diagnostic criteria, treatment and prognosis, and genetic counseling of LQTS, with an aim to standardize its clinical diagnosis and treatment.


Assuntos
Canalopatias/diagnóstico , Canalopatias/terapia , Síndrome do QT Longo/diagnóstico , Síndrome do QT Longo/terapia , Guias de Prática Clínica como Assunto , Morte Súbita Cardíaca , Eletrocardiografia , Humanos , Canais Iônicos , Prognóstico
3.
Herz ; 45(1): 3-9, 2020 Feb.
Artigo em Alemão | MEDLINE | ID: mdl-31820028

RESUMO

Molecular genetic analysis is an important component in the diagnostics of some cardiovascular diseases; however, genetic testing should not be used as a screening technique as the diagnostic value strongly depends on anamnestic and clinical factors, such as a positive family history and the disease phenotype. In cardiovascular diseases with high mutation detection rates, e.g. hypertrophic cardiomyopathy and primary arrhythmia syndromes (long QT syndrome, catecholaminergic polymorphic ventricular tachycardia) genetic testing should be included in the diagnostic work-up. Family screening of first-degree relatives (cascade screening) is a particularly important application of genetic diagnostics for a timely identification of asymptomatic mutation carriers and initiation of preventive treatment. A molecular autopsy, also known as postmortem molecular genetic DNA testing, is a special indication for genetic diagnostics. It is particularly useful in the analysis of sudden cardiac death victims for the identification of disease-specific gene mutations. Therefore, given a selective use and a thorough evaluation of the test results, molecular genetic analyses can make a meaningful diagnostic and prognostic contribution. Potential applications of genetic analyses in the future are polygenic cardiovascular diseases. The use of new high-throughput technologies enables the analysis of multiple genetic variants, which can then be included in the calculation of a polygenic risk score for the prediction of the probability of a specific disease.


Assuntos
Testes Genéticos , Síndrome do QT Longo , Taquicardia Ventricular , Arritmias Cardíacas/diagnóstico , Arritmias Cardíacas/genética , Morte Súbita Cardíaca , Predisposição Genética para Doença , Humanos , Síndrome do QT Longo/diagnóstico , Síndrome do QT Longo/genética , Mutação , Taquicardia Ventricular/diagnóstico , Taquicardia Ventricular/genética
4.
Zhonghua Er Ke Za Zhi ; 57(9): 700-704, 2019 Sep 02.
Artigo em Chinês | MEDLINE | ID: mdl-31530356

RESUMO

Objective: To analyze and summarize the diagnosis and treatment experience of common inherited cardiac arrhythmia syndrome in pediatric patients, and explore the most appropriate therapy. Methods: A retrospective review identified 30 pediatric cases (19 males, 11 females) diagnosed with long QT syndrome (LQTS), Brugada syndrome (BrS), catecholaminergic polymorphic ventricular tachycardia (CPVT), hypertrophic cardiomyopathy (HCM), arrhythmogenc right ventricular cardiomyopathy (ARVC) from January 2008 to December 2018 in the Pediatric Cardiology Department, Guangdong Provincial People's Hospital. Data obtained included the diagnosis, treatment and follow-up outcome. Results: The most common inherited cardiac arrhythmia syndromes were LQTS (n=14) including 1 case with epilepsy, CPVT (n=5), HCM (n=7), ARVC (n=1), and BrS (n=3). Twenty-seven cases were admitted to hospital due to syncope, whereas the remaining 3 cases of BrS had not presented with syncope before admission. The average onset age of inherited arrhythmia was (10.0±3.3) years. Genetic testing was performed on 20 patients. The median follow-up time was 40 months. Among 15 patients who underwent implantable cardioverter defibrillator (ICD) and survived, 2 patients had frequent ICD discharge. One patient underwent radiofrequency ablation, and the other one received left cardiac sympathetic denervation and an increased ICD defibrillation threshold, and the number of ICD discharge was significantly reduced. Among 10 patients who received drug therapy, 4 patients including two patients who discontinued treatment without advices died. Two patients whose parents refused treatment died, 1 case diagnosed with unexplained sudden cerebral death, and the remaining 2 cases without indication for drug therapy survived without any treatment. Conclusions: Mortality rate is high in pediatric patients with inherited cardiac arrhythmia and syncope. The therapeutic effect of drugs are not satisfactory, ICD implantation is the most effective treatment to prevent sudden cardiac death currently, but the postoperative frequent discharge should be brought to the forefront and handled in time.


Assuntos
Displasia Arritmogênica Ventricular Direita/genética , Síndrome de Brugada/genética , Cardiomiopatia Hipertrófica/genética , Síndrome do QT Longo/genética , Taquicardia Ventricular/genética , Arritmias Cardíacas , Displasia Arritmogênica Ventricular Direita/diagnóstico , Displasia Arritmogênica Ventricular Direita/mortalidade , Displasia Arritmogênica Ventricular Direita/terapia , Síndrome de Brugada/diagnóstico , Síndrome de Brugada/mortalidade , Síndrome de Brugada/terapia , Cardiomiopatia Hipertrófica/diagnóstico , Cardiomiopatia Hipertrófica/mortalidade , Cardiomiopatia Hipertrófica/terapia , Criança , Morte Súbita Cardíaca , Desfibriladores Implantáveis , Feminino , Seguimentos , Testes Genéticos , Humanos , Síndrome do QT Longo/diagnóstico , Síndrome do QT Longo/mortalidade , Síndrome do QT Longo/terapia , Masculino , Estudos Retrospectivos , Síncope , Taquicardia Ventricular/diagnóstico , Taquicardia Ventricular/mortalidade , Taquicardia Ventricular/terapia , Resultado do Tratamento
5.
Cardiol Young ; 29(10): 1300-1301, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31475669

RESUMO

A female neonate with in utero selective serotonin reuptake inhibitor exposure presented with bradycardia shortly after birth. Electrocardiography showed severe QT prolongation and second-degree atrioventricular block. Over time QT-times spontaneously normalised and genetic testing did not show mutations associated with long QT syndrome making maternal selective serotonin reuptake inhibitor usage the most likely explanation for the observed severe transient neonatal QT prolongation.


Assuntos
Síndrome do QT Longo/induzido quimicamente , Exposição Materna/efeitos adversos , Paroxetina/efeitos adversos , Efeitos Tardios da Exposição Pré-Natal/induzido quimicamente , Eletrocardiografia , Feminino , Humanos , Recém-Nascido , Síndrome do QT Longo/diagnóstico , Gravidez , Efeitos Tardios da Exposição Pré-Natal/diagnóstico , Inibidores de Captação de Serotonina/efeitos adversos , Índice de Gravidade de Doença
6.
J Stroke Cerebrovasc Dis ; 28(11): 104308, 2019 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-31416760

RESUMO

Stroke involving some areas of the cerebral hemisphere, such as insula, amygdala, and lateral hypothalamus, may cause changes in autonomic control of cardiac function. A 58-year-old woman presented to the emergency department for acute onset of left facial-brachial-crural hemiparesis and dysarthria. A brain CT scan showed subacute ischemic lesion with hemorrhagic infarction in right insular-rolandic cortex. Over the next few days ECG showed severe bradycardia with elongation of QTc, significative pauses (5 seconds), runs of nonsustained ventricular tachycardia and torsades de pointes. Drug induced and other several possible causes of elongation of QT and bradycardia such as hypokalemia, a history of heart failure, and structural heart disease were ruled out. The case confirms that insular cortex plays a major role in stroke-induced cardiovascular changes.


Assuntos
Córtex Cerebral/irrigação sanguínea , Sistema de Condução Cardíaco/fisiopatologia , Frequência Cardíaca , Síndrome do QT Longo/etiologia , Acidente Vascular Cerebral/complicações , Torsades de Pointes/etiologia , Potenciais de Ação , Bradicardia/etiologia , Bradicardia/fisiopatologia , Estimulação Cardíaca Artificial , Córtex Cerebral/diagnóstico por imagem , Feminino , Humanos , Síndrome do QT Longo/diagnóstico , Síndrome do QT Longo/fisiopatologia , Síndrome do QT Longo/terapia , Pessoa de Meia-Idade , Marca-Passo Artificial , Acidente Vascular Cerebral/diagnóstico por imagem , Acidente Vascular Cerebral/fisiopatologia , Acidente Vascular Cerebral/terapia , Taquicardia Ventricular/etiologia , Taquicardia Ventricular/fisiopatologia , Torsades de Pointes/diagnóstico , Torsades de Pointes/fisiopatologia , Torsades de Pointes/terapia , Resultado do Tratamento
7.
Pediatr Cardiol ; 40(7): 1419-1430, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31440766

RESUMO

Long QT syndrome (LQTS) is an inherited primary arrhythmia syndrome that may present with malignant arrhythmia and, rarely, risk of sudden death. The clinical symptoms include palpitations, syncope, and anoxic seizures secondary to ventricular arrhythmia, classically torsade de pointes. This predisposition to malignant arrhythmia is from a cardiac ion channelopathy that results in delayed repolarization of the cardiomyocyte action potential. The QT interval on the surface electrocardiogram is a summation of the individual cellular ventricular action potential durations, and hence is a surrogate marker of the abnormal cellular membrane repolarization. Severely affected phenotypes administered current standard of care therapies may not be fully protected from the occurrence of cardiac arrhythmias. There are 17 different subtypes of LQTS associated with monogenic mutations of 15 autosomal dominant genes. It is now possible to model the various LQTS phenotypes through the generation of patient-specific induced pluripotent stem cell-derived cardiomyocytes. RNA interference can silence or suppress the expression of mutant genes. Thus, RNA interference can be a potential therapeutic intervention that may be employed in LQTS to knock out mutant mRNAs which code for the defective proteins. CRISPR/Cas9 is a genome editing technology that offers great potential in elucidating gene function and a potential therapeutic strategy for monogenic disease. Further studies are required to determine whether CRISPR/Cas9 can be employed as an efficacious and safe rescue of the LQTS phenotype. Current progress has raised opportunities to generate in vitro human cardiomyocyte models for drug screening and to explore gene therapy through genome editing.


Assuntos
Síndrome do QT Longo/genética , Eletrocardiografia , Ventrículos do Coração/fisiopatologia , Humanos , Células-Tronco Pluripotentes Induzidas/metabolismo , Síndrome do QT Longo/diagnóstico , Síndrome do QT Longo/metabolismo , Mutação , Miócitos Cardíacos/metabolismo
8.
Int Heart J ; 60(5): 1189-1191, 2019 Sep 27.
Artigo em Inglês | MEDLINE | ID: mdl-31447465

RESUMO

The first onset of cardiac event of long QT syndrome (LQTS) was at young age and caused by emotional or physical triggers. We presented a 64-year-old woman who experienced recurrent ventricular arrhythmia after hemodialysis initiation because of end-stage renal disease. Persistent prolonged QTc interval and diagnosis of inherited LQT2 were missed at her first 3 years of hemodialysis. The patient was beta-blocker nonresponder for ventricular arrhythmias suppression and experienced multiple ICD discharge. We reported an inherited LQT2 case with uncommon clinical manifestations and the successful experience of mexiletine use in such a patient.


Assuntos
Falência Renal Crônica/terapia , Síndrome do QT Longo/genética , Mexiletina/uso terapêutico , Diálise Renal/efeitos adversos , Taquicardia Ventricular/tratamento farmacológico , Taquicardia Ventricular/etiologia , Antiarrítmicos/uso terapêutico , Eletrocardiografia/métodos , Feminino , Seguimentos , Humanos , Falência Renal Crônica/complicações , Falência Renal Crônica/diagnóstico , Síndrome do QT Longo/diagnóstico , Pessoa de Meia-Idade , Doenças Raras , Recidiva , Diálise Renal/métodos , Medição de Risco , Taquicardia Ventricular/diagnóstico , Resultado do Tratamento
9.
Int Heart J ; 60(4): 979-982, 2019 Jul 27.
Artigo em Inglês | MEDLINE | ID: mdl-31257342

RESUMO

Congenital long QT syndrome (LQTS) is a cardiac channelopathy that leads to the prolongation of the QT interval. This prolongation can lead to ventricular tachyarrhythmia, syncope, and sudden cardiac death. There are various types of LQTS. Treatment of LQT1 and LQT2 is mainly based on antiadrenergic therapy. LQT3, on the other hand, is a result of a mutation of the SCN5A gene, which encodes the sodium channels. In this type, patients are sensitive to vagal stimuli and episodes tend to occur at rest. Sodium channel blocking compounds, such as ranolazine, mexiletine, and flecainide, have been found to be effective in selective mutations.In this case report, we report the case of a child with congenital LQT3 (V411M) who presented first with sudden cardiac death and three weeks later with an implantable cardioverter defibrillator storm. Knowing the specific mutation and understanding the mechanism at the molecular level through an in vitro study yielded a clinically meaningful result. The patient's arrhythmia burden was totally eliminated following successful treatment with flecainide.


Assuntos
DNA/genética , Eletrocardiografia , Flecainida/uso terapêutico , Síndrome do QT Longo/tratamento farmacológico , Mutação , Canal de Sódio Disparado por Voltagem NAV1.5/genética , Criança , Análise Mutacional de DNA , Feminino , Humanos , Síndrome do QT Longo/diagnóstico , Síndrome do QT Longo/genética , Canal de Sódio Disparado por Voltagem NAV1.5/metabolismo , Bloqueadores do Canal de Sódio Disparado por Voltagem/uso terapêutico
10.
Pediatr Int ; 61(9): 852-858, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31283864

RESUMO

BACKGROUND: Human calmodulin (CALM) gene mutation has been reported to be related to inherited arrhythmia syndromes, but the genotype-phenotype relationship remains unclear. METHODS AND RESULTS: We report here a 4-year-old boy who had cardiac arrest while playing in a kindergarten playground. Cardiopulmonary resuscitation was initiated immediately. Eleven minutes after the cardiac arrest, ambulance crews arrived and an automated external defibrillator was attached. His heart rhythm, which was ventricular fibrillation (VF), was returned to sinus rhythm after only one shock delivery. The boy was brought to hospital by air ambulance. During transfer, electrocardiogram (ECG) showed transient VF. On arrival, chest radiograph showed a cardiothoracic ratio of 55% without pulmonary congestion. A 12-lead ECG showed a normal sinus rhythm, biphasic T wave, and prolongation of the corrected QT interval. On ECG, VF was preceded by torsade de pointes or frequent polymorphic premature ventricular contractions (PVC). Echocardiography showed a normal heart structure with decreased cardiac function. On the second day of hospitalization, ECG showed remarkable QT prolongation, T-wave alternans, and frequent PVC. Thereafter, propranolol was started. The ECG showed rapid improvement of QT prolongation and T-wave abnormality. Genetic test indicated a CALM2 mutation, and he was diagnosed with long QT syndrome-15 (LQT15). CONCLUSIONS: CALM mutations cause long QT syndrome (LQTS), catecholaminergic polymorphic ventricular tachycardia (CPVT) and idiopathic VF. This patient with a CALM2 p.N98S mutation had both phenotypes of LQTS and CPVT.


Assuntos
Calmodulina/genética , Síndrome do QT Longo/diagnóstico , Síndrome do QT Longo/genética , Mutação , Pré-Escolar , Marcadores Genéticos , Humanos , Masculino
11.
Taiwan J Obstet Gynecol ; 58(4): 552-556, 2019 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-31307750

RESUMO

OBJECTIVE: Patients with Long QT syndrome (LQTS) P may present with torsades de pointes, ventricular tachycardia (VT), or ventricular fibrillation (VF) and are at risk of sudden cardiac death. MATERIALS AND METHODS: A 38 y/o female patient with uterus myoma developed VF during laparoscopic assisted vaginal hysterectomy surgery. Defibrillation was delivered and the electrocardiogram (ECG) returned to sinus rhythm after CPR. RESULTS: Patient survived and implantable cardioverter-defibrillator was implanted and received beta-blocker therapy. ECG obtained in out-patient clinic still showed QT interval prolongation, but revealed no prolongation few months after persistent beta-blocker therapy. LQTS type 8 (CACNA1C E768del mutation) was identified by genetic DNA sequencing study. CONCLUSIONS: Patients with concealed LQTS may have normal QT interval unless exposing to stress or specific stimuli. Unexpected ventricular arrhythmia may happen during any medical management. We should avoid triggers of QT prolongation, and get familiar with management of the episode.


Assuntos
Morte Súbita Cardíaca , Cardioversão Elétrica/métodos , Histerectomia/métodos , Leiomioma/cirurgia , Síndrome do QT Longo/complicações , Neoplasias Uterinas/cirurgia , Adulto , Anestesia Geral/efeitos adversos , Anestesia Geral/métodos , Reanimação Cardiopulmonar/métodos , Desfibriladores Implantáveis , Eletrocardiografia/métodos , Feminino , Humanos , Laparoscopia/métodos , Leiomioma/complicações , Leiomioma/diagnóstico , Síndrome do QT Longo/congênito , Síndrome do QT Longo/diagnóstico , Prognóstico , Medição de Risco , Índice de Gravidade de Doença , Taquicardia Ventricular/diagnóstico , Taquicardia Ventricular/etiologia , Taquicardia Ventricular/terapia , Resultado do Tratamento , Neoplasias Uterinas/complicações , Neoplasias Uterinas/diagnóstico
12.
Clin J Sport Med ; 29(4): 285-291, 2019 07.
Artigo em Inglês | MEDLINE | ID: mdl-31241530

RESUMO

BACKGROUND: Because sudden cardiac death (SCD) in the young mainly occurs in individuals with structurally normal hearts, improved screening techniques for detecting inherited arrhythmic diseases are needed. The QT interval is an important screening measurement; however, the criteria for detecting an abnormal QT interval are based on Bazett formula and older populations. OBJECTIVE: To define the normal upper limits for QT interval from the electrocardiograms (ECGs) of healthy young individuals, compare the major correction formula and propose new QT interval thresholds for detecting those at risk of SCD. METHODS: Young active individuals underwent ECGs as part of routine preparticipation physical examinations for competitive sports or community screening. This was a nonfunded study using de-identified data with no follow-up. RESULTS: There were 31 558 subjects: 2174 grade school (7%), 18 547 high school (59%), and 10 822 college (34%). Mean age was 17 (12-35 years), 45% were female, 67% white, and 11% of African descent. Bazett performed least favorably for removing the effect of heart rate (HR), whereas Fridericia performed the best. Fridericia correction also closely fit the raw data best (R of 0.65), and at percentile values applicable to screening. The recommended risk cut points using Bazetts correction identified less than half of the athletes in the 99th or 99.5th percentiles of the uncorrected QT by HR range. Use of Fridericia correction increased capture rates by over 50%. CONCLUSION: Our results support the application of the Fridericia-corrected threshold of 460 for men and 470 milliseconds for women (and 485 milliseconds for marked prolongation) rather than Bazett correction for the preparticipation examination.


Assuntos
Síndrome do QT Longo/diagnóstico , Programas de Rastreamento/normas , Medição de Risco , Adolescente , Adulto , Atletas , Morte Súbita Cardíaca/prevenção & controle , Eletrocardiografia , Feminino , Frequência Cardíaca , Humanos , Masculino , Valores de Referência , Adulto Jovem
13.
Am J Health Syst Pharm ; 76(14): 1059-1070, 2019 Jul 02.
Artigo em Inglês | MEDLINE | ID: mdl-31185072

RESUMO

PURPOSE: We aimed to construct a dynamic model for predicting severe QT interval prolongation in hospitalized patients using inpatient electronic health record (EHR) data. METHODS: A retrospective cohort consisting of all adults admitted to 2 large hospitals from January 2012 through October 2013 was established. Thirty-five risk factors for severe QT prolongation (defined as a Bazett's formula-corrected QT interval [QTc] of ≥500 msec or a QTc increase of ≥60 msec from baseline) were operationalized for automated EHR retrieval; upon univariate analyses, 26 factors were retained in models for predicting the 24-hour risk of QT events on hospital day 1 (the Day 1 model) and on hospital days 2-5 (the Days 2-5 model). RESULTS: A total of 1,672 QT prolongation events occurred over 165,847 days of risk exposure during the study period. C statistics were 0.828 for the Day 1 model and 0.813 for the Days 2-5 model. Patients in the upper 50th percentile of calculated risk scores experienced 755 of 799 QT events (94%) allocated in the Day 1 model and 804 of 873 QT events (92%) allocated in the Days 2-5 model. Among patients in the 90th percentile, the Day 1 and Days 2-5 models captured 351 of 799 (44%) and 362 of 873 (41%) QT events, respectively. CONCLUSION: The risk models derived from EHR data for all admitted patients had good predictive validity. All risk factors were operationalized from discrete EHR fields to allow full automation for real-time identification of high-risk patients. Further research to test the models in other health systems and evaluate their effectiveness on outcomes and patient care in clinical practice is recommended.


Assuntos
Eletrocardiografia/efeitos dos fármacos , Registros Eletrônicos de Saúde/estatística & dados numéricos , Síndrome do QT Longo/diagnóstico , Modelos Biológicos , Idoso , Feminino , Hospitalização/estatística & dados numéricos , Humanos , Síndrome do QT Longo/induzido quimicamente , Síndrome do QT Longo/epidemiologia , Masculino , Pessoa de Meia-Idade , Prognóstico , Estudos Retrospectivos , Medição de Risco/métodos , Fatores de Risco , Índice de Gravidade de Doença
14.
Pediatrics ; 144(1)2019 07.
Artigo em Inglês | MEDLINE | ID: mdl-31167936

RESUMO

We present the case of a girl aged 17 years and 10 months who has a strong family history of long QT syndrome and genetic testing confirming the diagnosis of long QT syndrome in the patient also. She was initially medically treated with ß-blocker therapy; however, after suffering 1 episode of syncope during exertion, she underwent placement of an implantable cardioverter defibrillator. Since then, she has never had syncope. However, during the few months before this presentation, she experienced shocks on multiple occasions without any underlying arrhythmias. These shocks are disconcerting for her, and she is having significant anxiety about them. She requests the defibrillator to be inactivated. However, her mother, who also shares the diagnosis of long QT syndrome, disagrees and wants the defibrillator to remain active. The ethics team is consulted in this setting of disagreement between an adolescent, who is 2 months shy of the age of maturity and medical decision-making, and her mother, who is currently responsible for her medical decisions. The question for the consultation is whether it would be ethically permissible for the doctors to comply with the patient's request to turn off the defibrillator or whether the doctors should follow the mother's wishes until the patient is 18 years of age.


Assuntos
Desfibriladores Implantáveis/ética , Consentimento Informado por Menores/ética , Síndrome do QT Longo/terapia , Consentimento dos Pais/ética , Participação do Paciente , Adolescente , Fatores Etários , Desfibriladores Implantáveis/efeitos adversos , Desfibriladores Implantáveis/psicologia , Feminino , Humanos , Consentimento Informado por Menores/psicologia , Síndrome do QT Longo/diagnóstico , Síndrome do QT Longo/psicologia , Relações Mãe-Filho/psicologia , Consentimento dos Pais/psicologia , Participação do Paciente/psicologia , Relações Médico-Paciente/ética , Relações Profissional-Família/ética
15.
Cardiol Young ; 29(5): 697-698, 2019 May.
Artigo em Inglês | MEDLINE | ID: mdl-31169106

RESUMO

The coexistence of long QT syndrome with 2:1 or complete atrioventricular blocks has been reported in the literature, but, to the best of our knowledge, this is the first pediatric case of long QT syndrome coexisting with first-degree atrioventricular blocks( 1 - 3 ).


Assuntos
Bloqueio Atrioventricular/complicações , Síndrome do QT Longo/complicações , Bloqueio Atrioventricular/diagnóstico , Eletrocardiografia , Humanos , Lactente , Síndrome do QT Longo/diagnóstico , Masculino
16.
Int J Chron Obstruct Pulmon Dis ; 14: 1053-1061, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31190790

RESUMO

Objectives: COPD is the fourth-leading cause of mortality worldwide. Prolonged QTc has been found to be a long-term negative prognostic factor in ambulatory COPD patients. The aim of this study was to evaluate the extent of prolonged-QTc syndrome in COPD patients upon admission to an internal medicine department, its relationship to hypomagnesemia, hypokalemia, and hypocalcemia, and the effect of COPD treatment on mortality during hospital stay. Methods: This prospective cohort study evaluated COPD patients hospitalized in an internal medicine department. The study evaluated QTc, electrolyte levels, and known risk factors during hospitalization of COPD patients. Results: A total of 67 patients were recruited. The median QTc interval was 0.441 seconds and 0.434 seconds on days 0 and 3, respectively. Prolonged QTc was noted in 35.8% of patients on admission and 37.3% on day 3 of hospitalization. The median QTc in the prolonged-QTc group on admission was 0.471 seconds and in the normal-QTc group 0.430 seconds. There was no significant difference in age, sex, electrolyte levels, renal function tests, or blood gases on admission between the two groups. Mortality during the hospital stay was significantly higher in the prolonged-QTc group (3 deaths, 12%) than in the normal QTc group (no deaths) (P=0.04). A subanalysis was performed, removing known causes for prolonged QTc. We found no differences in age, electrolytes, or renal functions. There was a small but significant difference in bicarbonate levels. Conclusion: Our findings demonstrated that there was no correlation between QTc prolongation in hospitalized COPD patients and electrolyte levels, comorbidities, or relevant medications. A higher rate of mortality was noted in patients with prolonged QTc in comparison to normal QTc. As such, it is suggested that prolonged QTc could serve as a negative prognostic factor for mortality during hospitalization in COPD patients.


Assuntos
Hospitalização , Síndrome do QT Longo/mortalidade , Doença Pulmonar Obstrutiva Crônica/mortalidade , Desequilíbrio Hidroeletrolítico/mortalidade , Potenciais de Ação , Idoso , Idoso de 80 Anos ou mais , Biomarcadores/sangue , Cálcio/sangue , Causas de Morte , Progressão da Doença , Feminino , Sistema de Condução Cardíaco/fisiopatologia , Frequência Cardíaca , Mortalidade Hospitalar , Humanos , Hipocalcemia/sangue , Hipocalcemia/mortalidade , Hipopotassemia/sangue , Hipopotassemia/mortalidade , Síndrome do QT Longo/diagnóstico , Síndrome do QT Longo/fisiopatologia , Magnésio/sangue , Masculino , Pessoa de Meia-Idade , Potássio/sangue , Prognóstico , Estudos Prospectivos , Doença Pulmonar Obstrutiva Crônica/diagnóstico , Doença Pulmonar Obstrutiva Crônica/fisiopatologia , Medição de Risco , Fatores de Risco , Fatores de Tempo , Desequilíbrio Hidroeletrolítico/sangue , Desequilíbrio Hidroeletrolítico/diagnóstico
18.
Prog Cardiovasc Dis ; 62(3): 227-234, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31078562

RESUMO

Sudden cardiac death (SCD) accounts for 230,000 to 350,000 deaths per year in the United States. While many who suffer SCD possess underlying structural heart disease, inherited arrhythmia syndromes are also important contributors to SCD. In patients without structural heart disease, inherited arrhythmia syndromes are identified in >50% of the remaining patients. In this review, we will focus on the presentation and management of three major inherited syndromes that lead to SCD in patients without structural heart disease: long QT syndrome (LQTS), Brugada syndrome, and catecholaminergic polymorphic ventricular tachycardia (CPVT). All these syndromes can present in patients who are asymptomatic or, at the other extreme, with syncope and even SCD. LQTS syndrome and Brugada are the most common inherited arrhythmogenic syndromes, while CPVT is much rarer. Determining which patients need pharmacologic treatment and those who would benefit from more aggressive treatment such as sympathectomies and implantable defibrillators is not always clear.


Assuntos
Síndrome de Brugada , Morte Súbita Cardíaca/etiologia , Síndrome do QT Longo , Taquicardia Ventricular , Síndrome de Brugada/complicações , Síndrome de Brugada/diagnóstico , Síndrome de Brugada/terapia , Desfibriladores Implantáveis , Eletrocardiografia , Humanos , Síndrome do QT Longo/complicações , Síndrome do QT Longo/diagnóstico , Síndrome do QT Longo/terapia , Medição de Risco , Taquicardia Ventricular/complicações , Taquicardia Ventricular/diagnóstico , Taquicardia Ventricular/terapia
19.
Rev Soc Bras Med Trop ; 52: e20180453, 2019 May 16.
Artigo em Inglês | MEDLINE | ID: mdl-31141053

RESUMO

INTRODUCTION: Concern regarding the cardiotoxicity of antimalarials has been renewed because of their potential to cause QT/QTc interval prolongation related to torsade de pointes (TdP). Artemisinin-piperaquine (AP) is considered an effective artemisinin-based combination therapy (ACT) for malaria. METHODS: This study involved a retrospective analysis of clinical data of 93 hospitalized malaria patients who had received AP orally. Electrocardiograms (ECGs) were obtained at specific time points in the original study. RESULTS: Some cases of QT prolongation were observed. However, no TdP was found. CONCLUSIONS: AP may cause QT interval prolongation in some malaria patients but may not lead to TdP.


Assuntos
Antimaláricos/efeitos adversos , Artemisininas/efeitos adversos , Síndrome do QT Longo/induzido quimicamente , Malária Falciparum/tratamento farmacológico , Quinolinas/efeitos adversos , Adulto , Antimaláricos/uso terapêutico , Artemisininas/uso terapêutico , Quimioterapia Combinada , Eletrocardiografia , Feminino , Humanos , Síndrome do QT Longo/diagnóstico , Masculino , Pessoa de Meia-Idade , Quinolinas/uso terapêutico , Estudos Retrospectivos
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