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Dive into the research topics where Rubén A. Cabo is active.

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Featured researches published by Rubén A. Cabo.


Revista Espanola De Cardiologia | 2005

Reparación valvular en la insuficiencia mitral crónica

Evaristo Castedo; Vanessa Moñivas; Rubén A. Cabo; Emilio Monguió; Carlos García Montero; Raul Burgos; Santiago Serrano-Fiz; Gabriel Téllez de Peralta; Magdalena González; Miguel A. Cavero; Juan Ugarte

La reparacion valvular es el tratamiento quirurgico ideal de la insuficiencia mitral. En este trabajo presentamos los resultados de la reparacion valvular en pacientes con insuficiencia mitral cronica operados en nuestro centro durante los ultimos 8 anos. Analizamos el grado de correccion de la insuficiencia, el beneficio funcional, la morbimortalidad hospitalaria, la evolucion posquirurgica de la funcion ventricular y la supervivencia global y libre de reoperacion a medio plazo.


Cardiovascular Surgery | 2003

Left atrial thrombosis after heart transplantation

Evaristo Castedo; Raul Burgos; Alfonso Cañas; Rubén A. Cabo; Santiago Serrano-Fiz; J Segovia; Juan Ugarte

Left atrial thrombosis in the absence of rheumatic heart disease and atrial fibrillation is a rare occurrence. We report two cases of left atrial pedunculated thrombus formation after orthotopic heart transplantation. Despite an uneventful post-operative course, sinus rhythm and normal contractility of the heart, large thrombi could be found several months following transplantation. Surgical thrombectomy was performed under cardiopulmonary bypass. Operative technique is proposed as one of the main factors that can contribute to left atrial thrombosis after heart transplantation.


The Annals of Thoracic Surgery | 2015

Type A Aortic Dissection: The Controversy of the Root Replacement

María Martín; Daniel García Iglesias; José Rozado; Remigio R. Padrón; Ana García-Campos; César Morís; Rubén A. Cabo

M IS C E L L A N E O U S Postoperative care was driven by standardized evidence-based protocols. Antifibrinolytic agents, aminocaproic acid, were used routinely in all patients, whereas aprotinin was used in a highly selective fashion in patients at risk for bleeding, such as urgent or emergent cases requiring high doses of clopidogrel, IIB/IIIA antagonists, or both. All patients in the study cohort, without absolute contraindications,were taking aspirinpreoperatively, and aspirinwas given to all patients in stable condition on the first postoperative day, and was rarely held as a result of excessive chest tube output because most of the hemorrhagic complications were addressed aggressively, typically within the first 24 hours postoperatively. Indeed, only 9 patients returned, to the operating room for bleeding (7 of whom received red blood cell transfusions, and only 4 of the 9 had graft occlusion at catheterization). Given the small number of reoperations for bleeding and a similar overall graft occlusion rate, we doubt that the association of transfusion with occlusion is biased by these few patients. We fully concur that poor coronary targets are associated with an increased risk of graft failure, but unfortunately, we do not have data on target vessel size or characteristics; thus, these elements were not included in our risk models. Despite this, we would expect the transfusion rate to be independent of the target quality and hence similar between patients with poor or good targets. Arguably, given the increased technical complexity associated with poor coronary targets, this might increase cardiopulmonary bypass time and hence result in a greater likelihood of transfusion. We did adjust for this possibility by including cardiopulmonary bypass time in our analyses, and we found that transfusion remained associated with graft occlusion [2]. We did not analyze the effects of either platelet or fresh frozen plasma transfusions individually or in combination with red blood cell transfusion on graft durability. Although our retrospective analysis documents a clear and tantalizing association between blood transfusions and graft failure, in the absence of corroborating studies it should be regarded as hypothesis generating, serving as another reason to thoughtfully consider the indications and specific trigger point for the administration of homologous blood products, and serve to identify areas requiring focused basic science research or randomized trials to elucidate the mechanisms underlying our observational findings.


Revista Espanola De Cardiologia | 2004

Surgical Treatment for Hypertrophic Obstructive Cardiomyopathy

Evaristo Castedo; Rubén A. Cabo; Iván Núñez; Emilio Monguió; Carlos García Montero; Raul Burgos; Santiago Serrano-Fiz; Gabriel Téllez; Magdalena González; Miguel A. Cavero; Juan Ugarte

Introduction and objectives Five percent of the patients with hypertrophic obstructive cardiomyopathy (HOCM) have symptoms unresponsive to medical treatment and are candidates for invasive therapy. The objective of this study was to analyze our results with surgical treatment of HOCM during the last 10 years. Patients and method Between July 1993 and January 2004 26 patients with HOCM refractory to drug therapy were operated on. An extended septal myectomy was performed, in combination with anterior mitral leaflet plication in 19 cases (73%) and with mitral valve replacement in 5 (19%). Evolution of the grade of dyspnea, left ventricle outflow tract gradient (LVOTG), mitral regurgitation, and systolic anterior motion after surgery was analyzed. Results Mean follow-up was 63 (37) months. After surgery, a significant reduction in LVOTG (from 96.5 to 19.5 mmHg; P P P Conclusions Surgery in patients with HOCM yields great clinical improvements with low morbidity and mortality. Simultaneous intervention for both myocardial and valvular components of the disease allows not only reduction in the LVOTG but also correction of mitral regurgitation and abolition of systolic anterior motion.


International Journal of Cardiology | 2016

Nonsyndromic thoracic aortic aneurysm and dissection: Finally answers.

María Martín; Vicente Barriales; José Rozado; Ana Fidalgo; Daniel García Iglesias; Guillermo Solache-Berrocal; César Morís; Rubén A. Cabo; Isabel Rodríguez

a Area del Corazón del Hospital Universitario Central de Asturias, Avda Roma s/n, Oviedo, Spain b Bone andMineral ResearchUnit, IRSIN, Hospital Universitario Central de Asturias, REDinREN from ISCIII, Area del CorazónHospital Universitario Central de Asturias, AvdaRoma s/n, Oviedo, Spain c Cardiac Surgery, Hospital Universitario Central de Asturias, Area del Corazón Hospital Universitario Central de Asturias, Avda Roma s/n, Oviedo, Spain


Journal of Cardiovascular Translational Research | 2017

Thoracic Aneurysms and Dissections: Towards a Further and Better Knowledge

María Martín; Laura Díaz-Chirón; José Rozado; Luis Gutiérrez de la Varga; José Julián Rodríguez Reguero; Rubén A. Cabo; César Morís

Dear Editor, We have read with great interest the manuscript recently published in your journal by Landis et al. about candidate genetic modifiers of syndromic and familial thoracic aneurysms and dissections [1]. This is a welcome, necessary, and very useful study that can improve the diagnosis of this probably underdiagnosed entity. As it is well known, type A aortic dissection is a potentially lethal condition requiring early diagnosis and treatment as well as an adequate and thorough follow-up. Although hypertension is a frequently associated risk factor, it may be the first manifestation of syndromes such as Marfan, bicuspid aortopathy, or part of the entity known as thoracic aortic aneurysms and dissections (TAAD). The latter is associated histologically with cystic medial necrosis (currently encompassed in the term MEMA, which refers to mucoid extracellular matrix accumulation) [2]. Given the familial implications of recognizing these entities, reaching an etiological diagnosis is fundamental. In this sense, in our opinion two aspects are of special interest. First of all, the relevance of molecular testing when the postmortem exam provides no conclusive results in order to diagnose arrhythmogenic diseases such as Brugada or long QT syndrome with serious family involvement [3, 4]. Next, in specific cases of aortic dissection, both the histological analysis and genetic testing are fundamental. Marfan syndrome and bicuspid disease are well-recognized, hereditary disorders; however, TAAD is an emerging entity probably underdiagnosed. It is histologically associated with cystic medial degeneration and elastic fiber loss and or fragmentation, so in the absence of an available genetic test, the presence of these alterations should lead us to a family screening and follow-up [2]. In conclusion, all the initiatives that favor the diffusion and the better knowledge of this aortic pathology are welcome. The genetic study, if available, is essential since it avoids unnecessary follow-up in non-affected relatives, but in its absence, periodic follow-up will allow an early diagnosis avoiding catastrophic consequences. We must not forget that, according to the evidence available so far, these patients should be treated as Marfan syndrome [5].


Clinical Cardiology | 2016

Response to Survivors of Aortic Dissection: Activity, Mental Health, and Sexual Function; and Exercise and Physical Activity for the Post–Aortic Dissection Patient: The Clinician's Conundrum

María Martín; Jesús M. de la Hera; José Rozado; Daniel García Iglesias; César Morís; Juan Ignacio Pérez Calvo; Rubén A. Cabo

Chaddha A et al. Clin Cardiol. 2015;38:652–659.


Revista Espanola De Cardiologia | 2005

Valve Repair for Chronic Mitral Regurgitation

Evaristo Castedo; Vanessa Moñivas; Rubén A. Cabo; Emilio Monguió; Carlos García Montero; Raul Burgos; Santiago Serrano-Fiz; Gabriel Téllez de Peralta; Magdalena González; Miguel A. Cavero; Juan Ugarte

Valve repair is the best surgical treatment for mitral regurgitation. In the present article we describe the results of mitral valve repair in patients with chronic mitral regurgitation treated at our center during the last eight years. The degree of correction of valve insufficiency, functional benefit, in-hospital morbidity and mortality, postoperative outcome of ventricular function, and middle-term overall and reoperation-free survival are analyzed.


Revista Espanola De Cardiologia | 2003

Feocromocitoma de aurícula derecha

Rubén A. Cabo; Evaristo Castedo; Miguel Pastrana; Ricardo Crespo; Carlos García Montero; Juan Ugarte

El feocromocitoma es un tumor productor de catecolaminas y una causa infrecuente de hipertension arterial. La mayoria estan localizados en la glandula suprarrenal, siendo la localizacion intrapericardica una rareza. Describimos el caso de una paciente de 46 anos, hipertensa de un ano de evolucion, a la que tras una crisis hipertensiva se le diagnostico un feocromocitoma de auricula derecha mediante gammagrafia con 131 I-metaiodobencilguanidina y resonancia magnetica. El tumor fue resecado con exito mediante circulacion extracorporea y la pared auricular, reconstruida con un parche de pericardio bovino. Palabras clave: Tumores cardiacos. Feocromocitoma. Cirugia.


The Annals of Thoracic Surgery | 2003

Edge-to-edge tricuspid repair for redeveloped valve incompetence after DeVega’s annuloplasty

Evaristo Castedo; Alfonso Cañas; Rubén A. Cabo; Raul Burgos; Juan Ugarte

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Evaristo Castedo

Autonomous University of Madrid

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Juan Ugarte

Autonomous University of Madrid

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Raul Burgos

Autonomous University of Madrid

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Carlos García Montero

Autonomous University of Madrid

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Santiago Serrano-Fiz

Autonomous University of Madrid

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María Martín

European Bioinformatics Institute

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Gabriel Téllez

Autonomous University of Madrid

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Alfonso Cañas

Autonomous University of Madrid

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