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Showing papers by "Guillermo Torre-Amione published in 2006"



Journal ArticleDOI
TL;DR: Almost 33% of patients with systolic heart failre have evidence of abnormal electrical activation on urface electrocardiogram (ECG), seen as a QRS duraion of 120 milliseconds, most commonly as a left undle branch block (LBBB).
Abstract: egardless of underlying etiology, heart failure may be ssociated with an abnormal sequence of ventricular ontractions, referred to as cardiac or ventricular dysynchrony. This abnormality may be due to both disurbed electrical activation and regional abnormalities n contraction due to ischemia, myocardial scarring or eplacement of myocardium by infiltrative diseases. pproximately 33% of patients with systolic heart failre have evidence of abnormal electrical activation on urface electrocardiogram (ECG), seen as a QRS duraion of 120 milliseconds, most commonly as a left undle branch block (LBBB). The ventricular contracion pattern associated with LBBB results in the followng abnormalities: abnormal ventricular septal motion ith movement paradoxical to the lateral wall of the eft ventricle, and thus a decrease in regional left entricular ejection fraction (LVEF); a delay in mitral alve opening and aortic valve closure resulting in a hortened left ventricular (LV) filling time; and mitral egurgitation, caused or aggravated by dyssynchronous ctivation of papillary muscles and the surrounding yocardium and incomplete closure of the mitral valve aused by late ventricular contraction. In addition to dyssynchrony resulting from underlyng cardiac pathologies, some data suggest that cariac dyssynchrony induced by a pacemaker (right entricular [RV] or combined right atrial [RA] and

78 citations


Journal ArticleDOI
TL;DR: A group of investigators and clinician scientists with expertise in the field of heart failure met for 2 days in Woodstock, VT, to discuss the status of the current heart failure nomenclature and to seek a consensus on whether and how this nomenClature might be changed.
Abstract: The understanding of the pathomechanisms leading to heart failure has evolved from the simplistic pump-failure concept to the more complex syndrome involving neurohormonal and inflammatory systems. Anti-inflammatory therapy targeting specific cytokines, however, such as tumor necrosis factor-alpha, has failed to show clinical benefit. As a result, the focus has turned toward more broad-spectrum anti-inflammatory strategies. This review examines the various broad-spectrum anti-inflammatory modalities that have been used in heart failure: IV immunoglobulin administration, immune modulation therapy, immune adsorption, and plasmapheresis.

24 citations


Journal ArticleDOI
TL;DR: Increased MAC expression in failing human hearts indicates that the complement system is activated in the heart failure milieu, and its removal after hemodynamic normalization is evidence of dynamic regulation, suggesting a pathogenic role for the MAC.
Abstract: Inflammatory cytokine-mediated pathways are activated in heart failure and participate in the pathogenesis and progression of the disease. Another major response to inflammation is mediated through the complement system with the production of the membrane attack complex (MAC), a protein known to cause cell lysis and mediate apoptosis. It was postulated that the complement system is activated in patients with heart failure, and this study investigated whether hemodynamic conditions regulate this pathway. The expression of the MAC was assessed in myocardial biopsy samples of normal and failing hearts by immunohistochemistry and Western blot analysis. Myocardial samples from failing hearts were obtained before and after left ventricular assist device implantation. Immunohistochemical staining and Western blot analysis identified increased MAC expression in failing but not normal myocardium. After hemodynamic unloading with left ventricular assist device support, MAC expression returned to levels found in normal controls. In failing hearts, MAC expression did not differ between ischemic and nonischemic causes of heart failure. In conclusion, increased MAC expression in failing human hearts indicates that the complement system is activated in the heart failure milieu. Its removal after hemodynamic normalization is evidence of dynamic regulation, suggesting a pathogenic role for the MAC. These findings identify the complement system as part of a novel pathophysiologic path in heart failure that can potentially be targeted by future therapy.

16 citations