Symptom burden guiding invasive electrophysiological study in paroxysmal supraventricular tachycardia: The believe SVT registry.

BACKGROUND AND OBJECTIVE: Patients with palpitations clinically suggestive of paroxysmal supraventricular tachycardia (PSVT) are often managed conservatively until ECG-documentation of the tachycardia, leading to high impact on life quality and healthcare resource utilization. We evaluated results of electrophysiological study (EPS), and ablation when appropriate, among these patients, with special focus on gender differences in management. METHODS: BELIEVE SVT is a European multicenter, retrospective registry in tertiary hospitals performing EPS in patients with palpitations, without ECG-documentation of tachycardia or preexcitation, and considered highly suggestive of PSVT by a cardiologist or cardiac electrophysiologist. We analyzed clinical characteristics, results of EPS and ablation, complications, and clinical outcomes during follow-up. RESULTS: Six-hundred eighty patients from 20 centers were included. EPS showed sustained tachycardia in 60.9% of patients, and substrate potentially enabling AVNRT in 14.7%. No major/permanent complications occurred. Minor/transient complications were reported in 0.84% of patients undergoing diagnostic-only EPS and 1.8% when followed by ablation. During a 3.4-year follow-up, 76.2% of patients remained free of palpitations recurrence. Ablation (OR: 0.34, P < .01) and male gender (OR: 0.58, P = .01) predicted no recurrence. Despite a higher female proportion among patients with recurrence, (77.2% vs 63.5% among those asymptomatic during follow-up, P < .01), 73% of women in this study reported no recurrence of palpitations after EPS. CONCLUSIONS: EPS and ablation are safe and effective in preventing recurrence of nondocumented palpitations clinically suggestive of PSVT. Despite a lower efficacy, this strategy is also highly effective among women and warrants no gender differences in management.

Differences in the prognostic value of the electrocardiographic pattern after cardiac resynchronization therapy according to age.

OBJECTIVES: In this cohort study, we analyzed if a specific pattern in three leads of the electrocardiogram (Rs in V1, Qr in aVL, or rS in I) was associated with outcomes after cardiac resynchronization therapy (CRT) depending on age. METHODS: Patients with CRT devices were included from January 2012 to April 2019. We divided the sample into 2 groups, those with age ≥ 75 years old and those younger. The primary endpoint was a composite of all-cause death and heart failure (HF) hospitalization at 1 year. RESULTS: We included 111 patients. Patients older than 75 years (26.1%, n = 29) had a significantly higher rate of hypertension and atrial fibrillation and received less frequently optimal medical therapy. The patterns were observed in 32 (39.0%) younger patients and 11 (37.9%) older patients. Patients who presented any of them had a lower incidence of the primary endpoint in the younger group (0 vs. 14%, p = 0.029), but not in the older group (9.1 vs. 27.8%, p = 0.24). The presence of a basal QRS duration greater than 160 ms was associated with a higher rate of the primary endpoint in the elderly (50 vs. 13%, p = 0.015), but not in the younger group (16.7 vs. 7.1%, p = 0.254). CONCLUSIONS: The presence of the selected patterns after CRT is associated with a lower incidence of all-cause death and hospitalization for HF in patients younger than 75 years, but not in those older than 75 years. Conversely, baseline QRS duration was associated with worse outcomes in older patients, but not in the younger group.

A Differential Profile of Biomarkers between Patients with Atrial Fibrillation and Healthy Controls.

Atrial fibrillation (AF) is explained by anatomical and electrophysiological changes in the atria determined by high pressure, dilatation, infiltration and inflammation in the myocardium. There are some biomarkers implicated in these processes, namely, NT-proBNP, high sensitivity troponin (Hs-Tn), urate, galectin-3, ST2, C reactive protein and fibrinogen. The aim of this study was to assess differences in these biomarkers between patients with AF and healthy controls. We designed a cross-sectional study consecutively including all patients undergoing electrical cardioversion in our hospital for persistent AF and matched healthy controls. We included 115 patients with persistent non-valvular AF and 33 healthy subjects. The biomarkers NT-proBNP, ST2 and Hs-Tn T were significantly related to the presence of AF (1054 ± 833.30 vs. 58.31 ± 59.40, p < 0.001; 35.43 ± 15.89 vs. 27.43 ± 10.95, p < 0.001 and 10.25 ± 6.11 vs. 8.42 ± 6.85, p < 0.001, respectively). NT-proBNP was the best biomarker differentiating AF patients (area under the curve 0.995). The best NT-proBNP cut-off point to differentiate AF was 102 pg/mL; for Hs-Tn T it was 11.5 ng/L and for ST2 it was 37.7 ng/mL. It is possible that these biomarkers intervene at the onset of AF and have no role in AF maintenance.

Influence of Baseline Physical Activity as a Modifying Factor on COVID-19 Mortality: A Single-Center, Retrospective Study.

INTRODUCTION: The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection causes a severe respiratory disease with a 3% global mortality. In the absence of effective treatment, controlling of risk factors that predispose to severe disease is essential to reduce coronavirus disease 2019 (COVID-19) mortality. Large observational studies suggest that exercise can reduce the risk of all-cause and disease-specific mortality. The aim of this study was to analyze the influence of the baseline physical activity level on COVID-19 mortality METHODS: This is a retrospective cohort study that included patients between 18 and 70 years old, diagnosed with COVID-19 and hospitalized in our center between February 15 and April 15, 2020. After discharge all the patients included in the study were contacted by telephone. Baseline physical activity level was estimated using the Rapid Assessment of Physical Activity Scale questionnaire and patients were divided into two groups for comparison: sedentary patients (group 1) and active patients (group 2). RESULTS: During the study period 552 patients were admitted to our hospital and met the inclusion criteria. Global mortality in group 1 was significantly higher than in group 2 (13.8% vs 1.8%; p < 0.001). Patients with a sedentary lifestyle had increased COVID-19 mortality independently of other risk factors previously described (hazard ratio 5.91 (1.80-19.41); p = 0.003). CONCLUSION: A baseline sedentary lifestyle increases the mortality of hospitalized patients with COVID-19. This finding may be of great utility in the prevention of severe COVID-19 disease.

sST2 and Galectin-3 genotyping in patients with persistent atrial fibrillation.

Genotyping of ST2 and galectin-3 in atrial fibrillation (AF) is not well analyzed. The aim of our study was to analyze the possible relationship between levels of sST2 and galectin-3 and three polymorphisms in patients with AF. We included 125 patients with persistent AF undergoing electric cardioversion. We analyzed sST2 and galectin-3 levels and three polymorphisms in peripheral blood samples. Rs2274273 was significantly related with levels of galectin-3. Rs1558648 was associated with levels of sST2 but rs13019803 were not. None of the polymorphisms were connected to the variation of biomarkers levels during the follow up. We found a relationship between rs2274273 and galectin-3 levels and rs1558648 and sST2 levels in patients with AF.

Ivabradina para el control crónico de la frecuencia cardiaca en fibrilación auricular permanente. Diseño del proyecto BRAKE-AF / Ivabradine for chronic heart rate control in persistent atrial fibrillation. Design of the BRAKE-AF project

INTRODUCCIÓN Y OBJETIVOS: La ivabradina es un inhibidor de la corriente If, principal determinante de la función marcapasos del nódulo sinusal, aprobado como antianginoso y para tratar la insuficiencia cardiaca. Existen indicios sobre su capacidad para inhibir la conducción a través del nódulo auriculoventricular (NAV). Sobre esta base, el proyecto BRAKE-AF plantea el uso de ivabradina como agente cronotrópico negativo en fibrilación auricular (FA). MÉTODOS: Se realizará un ensayo clínico multicéntrico de fase III, aleatorizado, abierto, en paralelo, con diseño de no inferioridad, para comparar la ivabradina frente a la digoxina en 232 pacientes con FA permanente no controlada con bloqueadores beta o antagonistas del calcio; el objetivo primario es la reducción de la frecuencia cardiaca media diurna en un Holter de 24 h a los 3 meses. El ensayo se apoyará en un estudio electrofisiológico que analizará el efecto de la ivabradina en el potencial de acción del NAV humano, utilizando un modelo experimental en células de ovario de hámster chino transfectadas con el ADN que codifica la expresión de los distintos canales que componen dicho potencial de acción, registrando las corrientes iónicas mediante la técnica del parche de membrana. RESULTADOS: Se obtendrá información tanto del efecto de la ivabradina en las corrientes iónicas y el potencial de acción del NAV como de su eficacia y su seguridad en pacientes con FA permanente. CONCLUSIONES: Los resultados del proyecto BRAKE-AF podrían permitir que la ivabradina se incluyera en el limitado arsenal de fármacos disponibles actualmente para el control de frecuencia en la FA

INTRODUCTION AND OBJECTIVES: Ivabradine is an inhibitor of the If channel, the main determinant of the pacemaker function of the sinus node. The drug has been approved for the treatment of angina and heart failure. There is some evidence of its role as an inhibitor of atrial-ventricular node (AVN) conduction. The aim of the BRAKE-AF project is to assess ivabradine use for rate control in atrial fibrillation (AF). METHODS: A multicenter, randomized, parallel, open-label, noninferiority phase III clinical trial will be conducted to compare ivabradine vs digoxin in 232 patients with uncontrolled permanent AF despite beta-blockers or calcium channel blockers. The primary efficacy endpoint is the reduction in daytime heart rate measured by 24-hour Holter monitoring at 3 months. This clinical trial will be supported by an electrophysiological study of the effect of ivabradine on the action potential of the human AVN. To do this, an experimental model will be used with Chinese hamster ovarium cells transfected with the DNA encoding the expression of the t channels involved in this action potential and recording of the ionic currents with patch clamp techniques. RESULTS: New data will be obtained on the effect of ivabradine on the human AVN and its safety and efficacy in patients with permanent AF. CONCLUSIONS: The results of the BRAKE-AF project might allow inclusion of ivabradine within the limited arsenal of drugs currently available for rate control in AF

Biomarkers in atrial fibrillation and heart failure with non-reduced ejection fraction: Diagnostic application and new cut-off points.

BACKGROUND: Atrial fibrillation (AF) and heart failure (HF) with non-reduced left ventricle ejection fraction (LVEF) present a diagnostic overlap. In this paper, we analyze differences in biomarkers between patients with and without HF, in a cohort of patients presenting with symptomatic AF. Differences in biomarkers between patients with medium range ejection fraction HF (HFmrEF) and those with preserved ejection fraction HF (HFpEF) are also analyzed. METHODS: A total of 115 patients with symptomatic persistent AF were included. Seven biomarkers were measured: NT-proBNP, high sensitivity T troponin (hsTNT), galectin-3, ST2, fibrinogen, urate and C-reactive protein. RESULTS: Patients with non-reduced LVEF HF had significantly higher NT-proBNP levels than those without HF. This biomarker was the only variable independently related with the presence of non-reduced LVEF HF. Troponin was the only factor independently related with the presence of HFmrEF. CONCLUSIONS: NT-proBNP showed the best diagnostic accuracy for detecting the presence of non-reduced LVEF HF. We found higher diagnostic NT-proBNP cut-off values than those previously reported. Troponin was the most accurate biomarker differentiating HFmrEF from HFpEF.

Ivabradine for chronic heart rate control in persistent atrial fibrillation. Design of the BRAKE-AF project.

INTRODUCTION AND OBJECTIVES: Ivabradine is an inhibitor of the If channel, the main determinant of the pacemaker function of the sinus node. The drug has been approved for the treatment of angina and heart failure. There is some evidence of its role as an inhibitor of atrial-ventricular node (AVN) conduction. The aim of the BRAKE-AF project is to assess ivabradine use for rate control in atrial fibrillation (AF). METHODS: A multicenter, randomized, parallel, open-label, noninferiority phase III clinical trial will be conducted to compare ivabradine vs digoxin in 232 patients with uncontrolled permanent AF despite beta-blockers or calcium channel blockers. The primary efficacy endpoint is the reduction in daytime heart rate measured by 24-hour Holter monitoring at 3 months. This clinical trial will be supported by an electrophysiological study of the effect of ivabradine on the action potential of the human AVN. To do this, an experimental model will be used with Chinese hamster ovarium cells transfected with the DNA encoding the expression of the t channels involved in this action potential and recording of the ionic currents with patch clamp techniques. RESULTS: New data will be obtained on the effect of ivabradine on the human AVN and its safety and efficacy in patients with permanent AF. CONCLUSIONS: The results of the BRAKE-AF project might allow inclusion of ivabradine within the limited arsenal of drugs currently available for rate control in AF. CLINICAL TRIAL REGISTRATION: http://www.clinicaltrials.gov. Identifier: NCT03718273.

Impacto de la primera ola de la pandemia de SARS-CoV-2 en la tasa de implante de marcapasos con indicación preferente/urgente. Estudio español / Impact of the first wave of the SARS-CoV-2 pandemic on preferential/emergent pacemaker implantation rate. Spanish study

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An elderly Jervell and Lange-Nielsen patient heterozygous compound for two new KCNQ1 mutations.

We present the case of a 66-year-old female with early onset deafness and seizures, who was diagnosed with epilepsy at the age of 2 years. She received antiepileptic drugs and was free of syncope episodes for 32 years. After a syncope at the age of 34, the ECG was characteristic of long-QT syndrome and was treated with antiarrhythmic drugs. Sequencing of the KCNQ1 gene identified two novel KCNQ1 variants interpreted to be pathogenic, and the patient was finally diagnosed with Jervell and Lange-Nielsen syndrome. © 2016 Wiley Periodicals, Inc.

Truncating FLNC Mutations Are Associated With High-Risk Dilated and Arrhythmogenic Cardiomyopathies.

BACKGROUND: Filamin C (encoded by the FLNC gene) is essential for sarcomere attachment to the plasmatic membrane. FLNC mutations have been associated with myofibrillar myopathies, and cardiac involvement has been reported in some carriers. Accordingly, since 2012, the authors have included FLNC in the genetic screening of patients with inherited cardiomyopathies and sudden death. OBJECTIVES: The aim of this study was to demonstrate the association between truncating mutations in FLNC and the development of high-risk dilated and arrhythmogenic cardiomyopathies. METHODS: FLNC was studied using next-generation sequencing in 2,877 patients with inherited cardiovascular diseases. A characteristic phenotype was identified in probands with truncating mutations in FLNC. Clinical and genetic evaluation of 28 affected families was performed. Localization of filamin C in cardiac tissue was analyzed in patients with truncating FLNC mutations using immunohistochemistry. RESULTS: Twenty-three truncating mutations were identified in 28 probands previously diagnosed with dilated, arrhythmogenic, or restrictive cardiomyopathies. Truncating FLNC mutations were absent in patients with other phenotypes, including 1,078 patients with hypertrophic cardiomyopathy. Fifty-four mutation carriers were identified among 121 screened relatives. The phenotype consisted of left ventricular dilation (68%), systolic dysfunction (46%), and myocardial fibrosis (67%); inferolateral negative T waves and low QRS voltages on electrocardiography (33%); ventricular arrhythmias (82%); and frequent sudden cardiac death (40 cases in 21 of 28 families). Clinical skeletal myopathy was not observed. Penetrance was >97% in carriers older than 40 years. Truncating mutations in FLNC cosegregated with this phenotype with a dominant inheritance pattern (combined logarithm of the odds score: 9.5). Immunohistochemical staining of myocardial tissue showed no abnormal filamin C aggregates in patients with truncating FLNC mutations. CONCLUSIONS: Truncating mutations in FLNC caused an overlapping phenotype of dilated and left-dominant arrhythmogenic cardiomyopathies complicated by frequent premature sudden death. Prompt implantation of a cardiac defibrillator should be considered in affected patients harboring truncating mutations in FLNC.

Respuesta al ECG de noviembre de 2016 / Response to ECG, November 2016

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ECG de noviembre de 2016 / ECG, November 2016

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