Author + information
- Received June 7, 2011
- Accepted June 21, 2011
- Published online October 25, 2011.
- Arantxa González, PhD⁎,
- Susana Ravassa, PhD⁎,
- Javier Beaumont, PhD⁎,
- Begoña López, PhD⁎ and
- Javier Díez, MD, PhD⁎,†,⁎ ()
- ↵⁎Reprint requests and correspondence:
Dr. Javier Díez, Division of Cardiovascular Sciences, Centre of Applied Medical Research, University of Navarra, Av. Pío XII, Pamplona 55 31008, Spain
Classical therapy of heart failure is based on treatment of its pre-disposing/triggering factors and of the neurohumoral activation secondary to the deterioration of cardiac function. A new view is emerging that proposes the direct intervention on the pathological structural remodeling of the myocardium as part of heart failure therapy. In fact, in conditions of chronic injury, the cardiomyocytic and the noncardiomyocytic components of the myocardium undergo a series of structural lesions (i.e., cardiomyocyte growth and death, inflammation, alterations of collagen matrix, and microvascular rarefaction) that are governed by a complex interplay of mechanisms. Our increasing knowledge of the role of these mechanisms in remodeling enables us not only to better understand how our more successful therapies work but also to explore novel therapies for the future. In this paper, we will examine recent insights from experimental and pilot clinical studies that have provided new targets for interventions to prevent or reverse inflammation, alterations of collagen matrix, and cardiomyocyte death.
This study was supported by funds from the agreement between the Foundation for Applied Medical Research and Unión Temporal de Empresas Project Centro de Investigación Médica Aplicada, the Instituto de Salud Carlos III, Ministry of Science and Innovation, Spain (grants PS09/02234 and PS09/02247), and the European Commission Project, The Metabolic Road to Diastolic Heart Failure, Brussels, Belgium (grant FP7-HEALTH-2010-261409). Dr. González is the recipient of a Ramón y Cajal contract from the Ministry of Science and Innovation, Madrid, Spain (RYC-2010-05797). The authors have reported they have no relationships relevant to the contents of this paper to disclose. Drs. González and Ravassa contributed equally to this work.
- Received June 7, 2011.
- Accepted June 21, 2011.
- American College of Cardiology Foundation