Thorax Institute

Barcelona, Spain

Thorax Institute

Barcelona, Spain
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Penela D.,Thorax Institute | Heras M.,University of Barcelona
European Cardiology | Year: 2011

Treatment with antiplatelet therapy is mandatory in acute coronary syndrome. The effectiveness of aspirin and clopidogrel both in the acute phase and in secondary prevention has been clearly demonstrated, although some problems have also arisen, such as variability of platelet inhibition with clopidogrel or increased bleeding in patients undergoing urgent surgery. New antiplatelet drugs have been tested and are currently incorporated into the therapeutic armamentarium. Their different pharmacokinetic and pharmacodynamic properties are a good addition to the classic antiplatelet therapy, overcoming some of its limitations. In this context, the choice of appropriate antiplatelet therapy requires an individualised approach. The aim of this article is to summarise existing evidence and highlight the main features of the new antiplatelet drugs, as well as offering a vision of some challenges in the use of this therapy. © TOUCH BRIEFINGS 2011.

Vestbo J.,University of Southern Denmark | Vestbo J.,University of Manchester | Hurd S.S.,Global Initiative for Chronic Obstructive Lung Disease | Rodriguez-Roisin R.,Thorax Institute | And 2 more authors.
Clinical Respiratory Journal | Year: 2012

Introduction: The Global Initiative for Chronic Obstructive Lung Disease (GOLD) has published a strategy for diagnosis and for management of chronic obstructive pulmonary disease (COPD) since 2001 and this has formed the basis for numerous national and regional guidelines. Objectives: We describe the background for the 2011 revision of the GOLD document. Methods: The GOLD document is updated annually and revised every 5 years based on published research as well as an evaluation by an expert panel of how to best formulate and disseminate knowledge on COPD. Results: The GOLD 2011 revision states that spirometry is required for making a clinical diagnosis of COPD. At the same time, the document has less emphasis on spirometric evaluation of disease severity and launches a combined assessment taking symptoms, spirometry and history of exacerbations into account. This is matched with initial treatment for COPD where smoking cessation, pulmonary rehabilitation and physical activity in general are given high priority followed by pharmacologic treatment guided by the novel assessment scheme. Comorbidities are often present in COPD and the GOLD 2011 revision gives some guidance in how to manage these as well as how to manage COPD in the presence of comorbidities. Conclusion: A more clinically oriented GOLD document will hopefully improve assessment and management of COPD. © 2012 Blackwell Publishing Ltd.

Agusti A.,University of Barcelona | Agusti A.,CIBER ISCIII | Agusti A.,Thorax Institute | Gea J.,CIBER ISCIII | And 3 more authors.
Respirology | Year: 2016

Chronic obstructive pulmonary disease (COPD) is a complex and heterogeneous disease, so its clinical management needs to be personalized as much as possible. 'Complex' means that COPD has several components with non-linear dynamic interactions, whereas 'heterogeneous' indicates that not all these components are present in all patients or, in a given patient, at all time points. This complexity and heterogeneity explains and justifies the need for personalizing the assessment and treatment of patients with COPD. We propose here that the implementation of a 'control panel' will facilitate the deployment of personalized COPD medicine in clinical practice. Such a control panel should provide the practicing clinician complementary and relevant information on treatable clinical characteristics in a single patient at a given time point. For the purpose of this discussion, we consider these variables to be 'biomarkers'. Which treatable clinical characteristics should the COPD control panel include has not yet been formally validated. The review below suggests and discusses which ones might be considered in the future and should be viewed as a working proposal. © 2015 Asian Pacific Society of Respirology.

Li Bassi G.,Thorax Institute | Li Bassi G.,Institute dInvestigacions Biomediques August Pi i Sunyer | Li Bassi G.,Research Center Biomedica en Red Enfermedades Respiratorias | Marti J.D.,Thorax Institute | And 23 more authors.
Critical Care Medicine | Year: 2014

OBJECTIVE:: In the semirecumbent position, gravity-dependent dissemination of pathogens has been implicated in the pathogenesis of ventilator-associated pneumonia. We compared the preventive effects of a ventilatory strategy, aimed at decreasing pulmonary aspiration and enhancing mucus clearance versus the Trendelenburg position. DESIGN:: Prospective randomized animal study. SETTING:: Animal research facility, University of Barcelona, Spain. SUBJECTS:: Twenty-four Large White-Landrace pigs. INTERVENTIONS:: Pigs were intubated and on mechanical ventilation for 72 hours. Following surgical preparation, pigs were randomized to be positioned: 1) in semirecumbent/prone position, ventilated with a duty cycle (TITTOT) of 0.33 and without positive end-expiratory pressure (control); 2) as in the control group, positive end-expiratory pressure of 5cm H2O and TITTOT to achieve a mean expiratory-inspiratory flow bias of 10L/min (treatment); 3) in Trendelenburg/prone position and ventilated as in the control group (Trendelenburg). Following randomization, Pseudomonas aeruginosa was instilled into the oropharynx. MEASUREMENTS AND MAIN RESULTS:: Mucus clearance rate was measured through fluoroscopic tracking of tracheal markers. Microspheres were instilled into the subglottic trachea to assess pulmonary aspiration. Ventilator-associated pneumonia was confirmed by histological/microbiological studies. The mean expiratory-inspiratory flow in the treatment, control, and Trendelenburg groups were 10.7±1.7, 1.8±3.7 and 4.3±2.8L/min, respectively (p < 0.001). Mucus clearance rate was 11.3±9.9mm/min in the Trendelenburg group versus 0.1±1.0 in the control and 0.2±1.0 in the treatment groups (p = 0.002). In the control group, we recovered 1.35% ± 1.24% of the instilled microspheres per gram of tracheal secretions, whereas 0.22% ± 0.25% and 0.97% ± 1.44% were recovered in the treatment and Trendelenburg groups, respectively (p = 0.031). Ventilator-associated pneumonia developed in 66.67%, 85.71%, and 0% of the animals in the control, treatment, and Trendelenburg groups (p < 0.001). CONCLUSIONS:: The Trendelenburg position predominates over expiratory flow bias and positive end-expiratory pressure in the prevention of gravity-dependent translocation of oropharyngeal pathogens and development of ventilator-associated pneumonia. These findings further substantiate the primary role of gravity in the pathogenesis of ventilator-associated pneumonia. © 2014 by the Society of Critical Care Medicine and Lippincott Williams and Wilkins.

Brugada J.,Thorax Institute | Pappone C.,University of Milan | Berruezo A.,Thorax Institute | Vicedomini G.,University of Milan | And 4 more authors.
Circulation: Arrhythmia and Electrophysiology | Year: 2015

Whether Brugada syndrome (BrS) depends on functional epicardial substrates, which may be definitively eliminated by radiofrequency ablation, remains unknown. Methods and Results-Patients with BrS underwent epicardial mapping to identify areas of abnormal electrograms as target for radiofrequency ablation. Substrate identification consisted in mapping right ventricle epicardial surface before and after flecainide (2 mg/kg per 10 minutes). After radiofrequency ablation, flecainide and remap confirmed elimination of abnormal substrate, BrS ECG pattern, and ventricular tachycardia/ventricular fibrillation inducibility. Flecainide testing was performed at each follow-up visits ≤6 months. Fourteen patients with BrS, median age 39 years (30.3-42.3) with implantable cardioverter-defibrillator were enrolled. Low-voltage areas (<1.5 mV) were commonly identified on the anterior right free wall and right ventricular outflow tract, which increased after flecainide from 17.6 cm2 (12.1-24.2) to 28.5 cm2 (21.6-30.2; P=0.001). Similarly, areas with abnormal electrograms increased after flecainide from 19.0 (17.5-23.6) to 27.3 cm2 (24.0-31.2; P=0.001). After 23.8 minutes (18.1-28.5) of radiofrequency ablation, abnormal electrograms disappeared, whereas low-voltage areas were replaced by scar areas (<0.5 mV) of 25.9 cm2 (19.6-31.0). Substrate elimination resulted in BrS ECG pattern disappearance and no ventricular tachycardia/ventricular fibrillation inducibility without complications. After a median follow-up of 5 months (3.8-5.3), ECG remained normal despite flecainide. Conclusions-In patients with BrS, there is a relationship between abnormal ECG pattern, the extent of abnormal epicardial substrate, and ventricular tachycardia/ventricular fibrillation inducibility. Ablation of the substrate identified in the presence of flecainide can eliminate the BrS phenotype and warrants further study. © 2015 American Heart Association, Inc.

Arbelo E.,Thorax Institute | Arbelo E.,University of Barcelona | Arbelo E.,Institute dInvestigacions Biomediques August Pi I Sunyer IDIBAPS | Brugada J.,Thorax Institute | And 2 more authors.
Current Cardiology Reports | Year: 2014

The Brugada syndrome (BS) is a hereditary disease characterized by typical electrocardiographic alterations (elevation of the ST segment in right precordial leads) that affects young individuals without structural heart disease, predisposing them to ventricular arrhythmias and sudden death (SD). Several genetic mutations of different subunits of the sodium, calcium and potassium channel have been involved. The majority of patients with BS remain asymptomatic; however, the most frequent symptoms are syncope and/or SD secondary to polymorphic ventricular tachycardia (PVT) or ventricular fibrillation (VF). Electrocardiographic manifestations of the BS are typically dynamic and occasionally only become apparent after the administration of a sodium channel blocker or with fever. Risk stratification is mainly based on symptoms and the surface electrocardiogram. However, in asymptomatic patients, risk evaluation is still controversial and requires further studies. This review provides an updated summary of the BS from the point of view of genetic, clinical manifestations, risk stratification and management. © 2014 Springer Science+Business Media.

Andreu D.,Thorax Institute | Berruezo A.,Thorax Institute | Ortiz-Perez J.T.,Thorax Institute | Silva E.,Thorax Institute | And 7 more authors.
Circulation: Arrhythmia and Electrophysiology | Year: 2011

Background-Scar heterogeneity identified with contrast-enhanced cardiac magnetic resonance (CE-CMR) has been related to its arrhythmogenic potential by using different algorithms. The purpose of the study was to identify the algorithm that best fits with the electroanatomic voltage maps (EAM) to guide ventricular tachycardia (VT) ablation. Methods and Results-Three-dimensional scar reconstructions from preprocedural CE-CMR study at 3T were obtained and compared with EAMs of 10 ischemic patients submitted for a VT ablation. Three-dimensional scar reconstructions were created for the core (3D-CORE) and border zone (3D-BZ), applying cutoff values of 50%, 60%, and 70% of the maximum pixel signal intensity to discriminate between core and BZ. The left ventricular cavity from CE-CMR (3D-LV) was merged with the EAM, and the 3D-CORE and 3D-BZ were compared with the corresponding EAM areas defined with standard cutoff voltage values. The best match was obtained when a cutoff value of 60% of the maximum pixel signal intensity was used, both for core (r 2=0.827; P<0.001) and BZ (r 2=0.511; P=0.020), identifying 69% of conducting channels (CC) observed in the EAM. Matching improved when only the subendocardial half of the wall was segmented (CORE: r 2=0.808; P<0.001 and BZ: r 2=0.485; P=0.025), identifying 81% of CC. When comparing the location of each bipolar voltage intracardiac electrogram with respect to the 3D CE-CMR-derived structures, a Cohen κ coefficient of 0.70 was obtained. Conclusions-Scar characterization by means of high resolution CE-CMR resembles that of EAM and can be integrated into the CARTO system to guide VT ablation. © 2011 American Heart Association, Inc.

Bellera M.N.,Thorax Institute | Ortiz J.T.,Thorax Institute | Perez-Rodon J.,Hospital Josep Trueta | Mercader J.,Hospital Of Granollers | And 3 more authors.
International Journal of Cardiology | Year: 2010

Background: The presence of small areas of necrosis has been occasionally reported immediately following apical ballooning syndrome (ABS). However, their persistence at later stages and impact on long-term prognosis are currently unknown. Methods: Twenty consecutive patients admitted for ABS between 2004 and 2007 were prospectively evaluated. Demographic, clinical, angiographic, and echocardiographic data were collected during hospital admission. At a mean of 11 ± 9 months follow-up, a contrast enhanced cardiac magnetic resonance (ce-CMR) study was performed in 17 cases. The presence of hyperenhancement on ce-CMR images, reflecting irreversible myocardial damage, was recorded by two independent observers. Results: Two of 3 patients with hyperenhancement on ce-CMR images presented in worse condition, including pulmonary edema or cardiogenic shock, compared to just 2 of 14 patients without hyperenhancement (p = 0.052). Segmental wall motion substantially improved in both of those cases; the third patient continued to have hypokinesis in a segment showing hyperenhancement. Segmental wall motion also significantly improved in all patients with no hyperenhancement. At a mean of 20 ± 12 months follow-up, no deaths or major adverse cardiac events were documented among patients with or without hyperenhancement. Conclusions: Despite segmental wall motion recovery, an area of irreversible myocardial damage can sometimes be identified long after ABS. However, in this limited series of patients, the presence of scar, even when presenting with heart failure and a higher troponin release, was not associated with adverse long-term outcomes as compared to patients with intact myocardium. © 2008 Elsevier Ireland Ltd. All rights reserved.

Mas S.,University of Barcelona | Mas S.,Institute dInvestigacions Biomediques August Pi i Sunyer IDIBAPS | Mas S.,Research Center Biomedica En Red Of Salud Mental Cibersam | Gasso P.,University of Barcelona | And 15 more authors.
Pharmacogenetics and Genomics | Year: 2011

Background and Objective: Dry cough is the most common reason for stopping angiotensin-converting enzyme inhibitors (ACEi) therapy. The role of ACE in the metabolism of bradykinin has been proposed as a pathogenic mechanism. This study included a complete analysis of the variability of the genes involved in bradykinin metabolism (ACE and XPNPEP2) and bradykinin receptors (BDKRB2). We included two polymorphisms in the ABO (related to ACE levels); two polymorphisms in the AGTR1, and one polymorphism in the BKRB1 (related to ACEi response). Methods: A total of 281 patients who had been treated with ACEi were retrospectively recruited [102 patients were considered as cases (cough) and 179 patients were considered as controls (no cough)], and 56 polymorphisms were tested for association. Results: We found that genetic polymorphisms in BDKRB2 [rs8016905; P=0.003; odds ratio (OR)=2.21] and ABO (rs495828; P=0.001; OR=2.45) are associated with ACEi-induced cough after correction for multiple testing. The effect of polymorphisms in ABO was sex specific (female patients; P=0.0006; OR=3.26). When we analyzed the subgroup of patients homozygous GG for rs4343, two polymorphisms in the ACE were found to have protective properties (rs4459610 and rs4267385; P=0.005 and 0.004; OR=0.25). We also found a strong interaction between the ABO polymorphisms, rs495828 and rs8176746 (P<0.0001; OR=3.7). Conclusion: These results highlight the importance of genetic determinants of ACE levels as good predictors of the ACEi response, and provide ABO as a good candidate gene for pharmacogenetic studies of ACEi-related cough. Moreover, our results also confirm the importance of bradykinin in the pathogenesis of this adverse effect. © 2011 Wolters Kluwer Health | Lippincott Williams & Wilkins.

PubMed | Thorax Institute and Professor of Cardiology and Head of Reference Center for Hereditary Arrhythmia
Type: Journal Article | Journal: Arrhythmia & electrophysiology review | Year: 2016

Brugada syndrome (BrS) is a clinical entity characterised by an incomplete right bundle branch block associated with an ST segment elevation in the right precordial leads and a risk of ventricular arrhythmia and sudden death in the absence of structural abnormalities. Patients with a personal history of sudden death have an annual arrhythmia risk of recurrence as high as 10 %. Similarly, the presence of syncope is consistently associated with an increased arrhythmic risk. This risk can be estimated at about 1.5 % per year. The risk is lower in asymptomatic patients. Regarding the relatively high rate of complication of Implantable cardioverter defibrillator (ICD) implantation, in most of the cases, asymptomatic patients with a Brugada syndrome revealed during ajmaline challenge do not need to be implanted. The situation is more complex in patients with a spontaneous type 1 aspect since the risk could be estimated to be around 0.8 % per year. For these patients, a careful evaluation of the arrhythmic risk using all the different tools available is mandatory.

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