6,963 publications from this institution
Background Several studies have compared surface electrocardiographic changes following different self-expandable (SE) (Evolut (Medtronic, USA); Acurate (Boston Scientific, USA); Portico (Abbott, USA); and Allegra (NVT, Germany)) and balloon-expandable (BE) Sapien-3 (Edwards Lifesciences, USA) transcatheter heart valves. We aimed to compare these prosthesis with the novel Myval BE prosthesis (Meril Life, India). Methods Academic European registry of consecutive patients with severe aortic stenosis who received any of the 6 aforementioned valves. Baseline, post-procedural, and discharge 12‑leads electrocardiograms (ECG) were centrally analyzed and compared. Results A total of 1131 patients were included: 135 Myval (11.9%), 290 Sapien-3 (25.6%), 298 Evolut (26.3%), 180 Acurate (15.9%), 125 Portico (11.1%), and 103 Allegra (9.1%). There were no baseline differences in intraventricular conduction disturbances rate. Compared to the novel BE Myval, there were similar procedural and in-hospital outcomes. Similar rates of early new permanent pacemaker implant (PPI) were observed amongst Myval (7.4%), Sapien-3 (13.4%), and Acurate (9.1%), but Evolut, Portico, and Allegra presented significantly higher rates (18.5%, p = 0.003; 29.5% p < 0.001 and 22%, p = 0.001, respectively). Central analysis of ECGs, unraveled significant prolongation of the PR segment with Evolut, Portico and Allegra whereas Evolut, Acurate, and Portico showed significant QRS widening compared to Myval. However, at discharge no differences in PR segment duration were observed while, Evolut, and Portico– but not Acurate, Allegra or Sapien-3 – still presented significant widening of QRS segment compared to Myval. Conclusions After blinded central ECG analysis, the novel Myval balloon-expandable prosthesis was associated with a low rate of early conduction disturbances.
Chronic obstructive pulmonary disease (COPD) is an increasing global health problem and cause of death. COPD is a chronic inflammatory disease predominantly affecting small airways and lung parenchyma that leads to progressive airway obstruction. However, current therapies fail to prevent either disease progression or mortality. The mainstay of current drug therapy is long-acting bronchodilators. Several once daily inhaled β2-agonists and muscarinic antagonists (and combinations) are now in development. No treatments effectively suppress chronic inflammation in COPD lungs. With better understanding of the inflammatory and destructive process in the pathophysiology of COPD, several new therapeutic targets have been identified. Several mediator antagonists or inhibitors tested in COPD have so far been disappointing, but CXCR2 antagonists that block pulmonary neutrophil and monocyte recruitment are more promising. Broad spectrum anti-inflammatory drugs may be more effective, and include inhibitors of the proinflammatory enzymes phosphodiesterase-4, p38 mitogen-activated protein kinase, Janus kinases, NF-κB kinase and PI3 kinase-γ and -δ, but side effects after oral administration are a major limitation so that in future inhaled delivery may be necessary. A new promising approach is reversal of corticosteroid resistance through increasing histone deacetylase-2 (HDAC2) activity. This might be achieved by existing treatments such as theophylline, nortriptyline and macrolides, or more selectively by PI3 kinase-δ inhibitors. Thus although there have been major advances in the development of long-acting bronchodilators for COPD, it has proved difficult to find anti-inflammatory treatments that are safe and effective.
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With the high initial success rates that are regularly reported for coronary angioplasty it has become increasingly difficult to demonstrate methods or techniques that are able to provide more beneficial acute results than can be achieved by conventional angioplasty. On the other hand, the incidence of late restenosis has remained much the same over the 10 years that angioplasty has been part of clinical practice [1] and there is still no proven intervention which modifies the restenosis process. The problem of restenosis has therefore assumed increasing relevance in determining the clinical value of coronary angioplasty, and accordingly, studies that address the problem of restenosis have needed to become more exacting. Although there have numerous articles addressing the problem of restenosis in the clinical setting, with many defining certain factors associated with restenosis and possible interventions to reduce the incidence of restenosis, there is surprisingly little consensus. Most of the discrepancies can be attributed to three factors: 1) the selection of patients, 2) the method of analyis, 3) the definition of restenosis employed. The purpose of this review is to show that these three factors influence the outcome and conclusions of restenosis studies.
The landmark Synergy between Percutaneous Coronary Intervention with Taxus and Cardiac Surgery (SYNTAX) Trial has aided in reducing the area of uncertainty in decision-making between percutaneous coronary intervention (PCI) and coronary artery bypass graft (CABG) surgery in patients with complex coronary artery disease. As part of the SYNTAX Trial, quantification of the coronary artery disease burden was prospectively undertaken by the Heart Team – consisting of at least an interventional cardiologist and cardiac surgeon – utilising the anatomical SYNTAX Score (www.syntaxscore.com) as a clinical tool in order to agree that equivalent anatomical revascularisation could be achieved. The anatomical SYNTAX Score is now advocated in both European and US revascularisation guidelines to guide decision-making between CABG and PCI as part of the SYNTAX pioneered Heart Team approach. In addition, the SYNTAX Trial has lead to the development and validation of the SYNTAX Score II, in which the anatomical SYNTAX Score was augmented with clinical variables, to allow for more objective and tailored decision making for the individual patient. Prospective validation of the SYNTAX Score II tool is currently ongoing in the SYNTAX II (ClinicalTrials.gov Identifier: NCT02015832) and EXCEL (ClinicalTrials.gov identifier: NCT01205776) trials. The present paper presents lessons learned from SYNTAX, including the development and/or validation of several SYNTAX based clinical tools, and the potential implications for current and future clinical practice.