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Copyright of Revista Española de Cardiología (18855857) is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Revista Española de Cardiología (18855857) is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

In Brugada syndrome, even within the same family where all affected individuals share the same mutation, phenotypic variation is prominent, with variable penetrance and expressivity, presenting different degrees of involvement. It is difficult to establish a direct correlation between genotype and phenotype to predict prognosis in complications and risk of sudden death. The factors that modulate this inter- and intra-familial phenotypic variability remain to be determined. With the intention of testing whether other genetic factors, in addition to the causal mutation in SCN5A, may have a modulating effect on the Brugada phenotype and the risk of sudden death, we have studied 8 families with a causal variant in SCN5A with at least two affected individuals, one of whom has suffered cardiac arrest or sudden death. Whole exome sequencing was performed looking for additional variants that modify the phenotype and allow us to predict a better or worse prognosis for the evolution of the disease. The results did not show any clear genetic modifier; nevertheless, highlight the possible implication of the cholesterol and fibrosis pathways, as well as the circadian rhythm, as possible modulators of Brugada syndrome phenotype.

Introduction and objectives: To report medium- and long-term results following a single second-generation cryoballoon (CB2)-based ablation procedure in patients with paroxysmal (PAF) and persistent (PeAF) atrial fibrillation. Methods: A retrospective study was performed of consecutive patients undergoing a first CB2-based ablation procedure in a tertiary center. Cryoenergy was applied for 3 min if a time to effect 30 s beyond a three-month blanking period. The clinical impact of recurrences was classified using a severity score. Results: A total of 172 patients (134 PAF and 38 PeAF) were included, of whom 25 (14.5%) had structural heart disease and 120 (69.7%) had a normal or mildly dilated left atrium. Acute success was achieved in 167 (97.1%). After a median follow-up of 27 (14-41) months, 100 patients (58.1%) remained free of atrial arrhythmias (64.2% for PAF and 36.8% for PeAF, p=0.006). Left atrial size (p=0.05) and clinical presentation as PeAF (p=0.006) were predictors of recurrence. Of patients with recurrences, 11.1% did not require further therapies and an additional 16.7% had good control with antiarrhythmic drugs. Conclusions: A single CB2 procedure resulted in 58.1% of patients remaining free of atrial arrhythmias at 27-month follow-up. Conservative management was useful in 27.8% of patients with recurrences. Resumo: Introdução e objectivos: Relatar os resultados a médio e longo prazo após um único procedimento de crioablação com um sistema de segunda geração (CB2) em doentes com fibrilhação auricular paroxística (PAF) e persistente (pAF). Métodos: Estudaram-se retrospetivamente doentes consecutivos referidos para uma primeira ablação com CB2 num centro terciário. A ablação foi efetuada com crioenergia aplicada durante 3 minutos se o tempo do efeito foi < 60 s, ou então foi aplicada durante 4 mim, com uma aplicação extra em caso de isolamento tardio ou temperatura subótima. Realizou-se o acompanhamento por meio do registo do sistema de saúde eletrónico regional e pelo telefone ou com entrevistas pessoais. A recorrência foi definida como qualquer arritmia auricular > 30 segundos depois dum período de três meses. O impacto clínico das recorrências foi classificado utilizando uma pontuação de gravidade. Resultados: Foram estudados 172 doentes (134 PAF e 38 pAF). Vinte cinco (14,5%) tinham doença cardíaca estrutural e 120 (69,7%) tinham uma aurícula esquerda (LA) normal ou levemente dilatada (LA). Foi obtido sucesso agudo em 167 (97,1%). Após um seguimento médio de 27 [14-41] meses, 100 doentes (58,1%) permaneceram livres de arritmias auriculares (64,2% para PAF e 36,8% para pAF, p = 0,006). O tamanho da LA (p = 0,05) e a apresentação clínica de pAF (p = 0,006) foram preditores das recorrências. Dos doentes com recorrências 11,1% não precisaram de terapias adicionais e 16,7% foram bem controlados com medicamentos antiarrítmicos. Conclusões: Dos doentes, 58% ficaram livres de arritmias após um único procedimento CB2, até 27 meses de acompanhamento. Uma estratégia conservadora foi útil nos 27,8% dos doentes com recorrências. Keywords: Atrial fibrillation, Catheter ablation, Cryoballoon, Outcome, Palavras-chave: Fibrilhação auricular, Ablação por cateter, Cryoballoon, Resultado

Copyright of Revista Española de Cardiología (18855857) is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Revista Española de Cardiología (18855857) is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Summary: Recent research into the prevalence of Leishmania infantum infection in the Mediterranean basin points to the involvement of cats as a reservoir host, but only sporadic cases of feline leishmaniosis have been reported. Feline leishmaniosis presents primarily as cutaneous disease and diagnosis is based on the demonstration of the parasite by skin biopsy. The present report describes the microscopical changes in tissue biopsies from 15 cats with leishmaniosis. The biopsies were derived from the skin, ocular tissue and mucocutaneous junctions. The most common histopathological feature was diffuse granulomatous inflammation with macrophages containing numerous amastigotes. Other patterns included granulomatous perifolliculitis and lichenoid interface dermatitis, where there were fewer parasitized macrophages. The presence of amastigotes was confirmed by immunohistochemistry in each case. The results of the study confirm the value of histopathological and immunohistochemical techniques for the diagnosis of feline leishmaniosis. [ABSTRACT FROM AUTHOR]

Copyright of Revista Española de Cardiología (18855857) is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Revista Española de Cardiología (18855857) is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Revista Española de Cardiología (18855857) is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

In Brugada syndrome, even within the same family where all affected individuals share the same mutation, phenotypic variation is prominent, with variable penetrance and expressivity, presenting different degrees of involvement. It is difficult to establish a direct correlation between genotype and phenotype to predict prognosis in complications and risk of sudden death. The factors that modulate this inter- and intra-familial phenotypic variability remain to be determined. With the intention of testing whether other genetic factors, in addition to the causal mutation in SCN5A, may have a modulating effect on the Brugada phenotype and the risk of sudden death, we have studied 8 families with a causal variant in SCN5A with at least two affected individuals, one of whom has suffered cardiac arrest or sudden death. Whole exome sequencing was performed looking for additional variants that modify the phenotype and allow us to predict a better or worse prognosis for the evolution of the disease. The results did not show any clear genetic modifier; nevertheless, highlight the possible implication of the cholesterol and fibrosis pathways, as well as the circadian rhythm, as possible modulators of Brugada syndrome phenotype., Competing Interests: The authors have declared that no competing interests exist.

A 39-year-old woman with no structural heart disease and frequent episodes of sudden onset palpitations was referred for the electrophysiological study. During the study, a slightly irregular narrow QRS tachycardia with AV dissociation was repeatedly induced and spontaneously terminated. Apparently, irregular cycles and termination of the tachycardia were related to the dissociated sinus rhythm: atrial depolarizations timed when the AV junction was refractory were able to reset the tachycardia, while early atrial depolarizations caused its termination. This observation was enough to diagnose the tachycardia mechanism in our case., (© 2012 Wiley Periodicals, Inc.)

A 62-year-old woman who underwent heart transplantation 6 years later presented a regular atrial tachycardia. Electrophysiologic evaluation showed an atrial arrhythmia in the recipient atrium with 2:1 conduction to the donor atrium, with a confusing electroanatomical map. With the suspect of alternant conduction through two different breakthroughs, the map was split in two concordant maps, corresponding to two connections that were successfully ablated. Later on, a third connection was detected and therefore ablated., (©2011, The Authors. Journal compilation ©2011 Wiley Periodicals, Inc.)

An episode of device-related proarrhythmia is reported. Ventricular tachycardia was induced by ventricular pacing in a dual-chamber implantable cardioverter-defibrillator due to an inappropriate interaction of programmed device settings with the atrial preference pacing, an automatic algorithm designed to prevent atrial tachyarrhythmias.

Introduction and Objectives: Anemia is a common finding in outpatients with heart failure (HF) and is associated with increased mortality. The aims of this study were to identify determinants of the hemoglobin level in a large group of hospitalized patients with systolic HF and to investigate the medium-term prognostic value of the hemoglobin level., Methods: The study included 460 consecutive patients (age 68.3 [12.3] years, 74% male) who were hospitalized with a diagnosis of HF and left ventricular systolic dysfunction (i.e., a left ventricular ejection fraction <45%). At hospital discharge, biochemical and hematological parameters were measured and clinical and echocardiographic variables were recorded. Patients were followed up for 16.8[9.7] months., Results: Anemia, as defined by World Health Organization criteria, was present in 189 (41.1%) patients. The following independent determinants of the hemoglobin level were identified: age (relative risk [RR]=1.035, 95% CI, 1.011-1.060; P=.004), female sex (RR=1.843, 95% CI, 1.083-3.135; P=.024), diabetes mellitus (RR=1.413, 95% CI, 1.087-1.838; P=.010), plasma urea level (RR=1.013, 95% CI, 1.005-1.022; P=.001), and loop diuretic use (RR=2.801, 95% CI, 1.463-5.364; P=.002). A decrease in hemoglobin level was associated with increased risks of death (RR per g/dL=1.232, 95% CI, 1.103-1.375; P<.001) and death or HF readmission (RR per g/dL=1.152, 95% CI, 1.058-1.255; P<.001), but not with readmission for non-fatal HF (RR per g/dL=1.081, 95% CI, 0.962-1.215; P=.265). Blood transfusion during hospitalization did not alter the increased risk of death (RR=2.19, 95% CI 1.40-3.41; P=.001)., Conclusions: In hospitalized patients with systolic HF, the hemoglobin level at hospital discharge was an independent predictor of death in the medium term, but not of readmission for non-fatal HF. The main determinants of the hemoglobin level were age, sex, renal function, diabetes, and the need for diuretics.