Role of gene and stem cell therapy in coronary artery diseases

Prof. Dr. Stefan Janssens obtained his medical degree in 1984 from the University of Leuven, Belgium and finished his clinical cardiology fellowship at Gasthuisberg University Hospital, Leuven, Belgium in 1989. He subsequently obtained an international John E. Fogarty fellowship fromthe NIH (Bethesda, MD, USA) to continue his studies in cardiovascular medicine at Massachusetts General Hospital, Harvard University in Boston between 1989–1992. He received his PHD degree from the University of Leuven in 1993 where he subsequently became associate professor of medicine in 1997 and professor of medicine in 2002. He was appointed head of clinic and directorof the coronary care unit and became an independent group leader at the renowned Flemish Interuniversity Institute for Biotechnology in 1996. He is directing multiple research projects spanning the entire spectrum from basic transgenic animal models to large animal proof-of-principle gene and cell transfer studies to early translational cell transfer studies. Dr. Janssens served as deputy editorfor the European Heart Journal from 2002-2008 and is an active board member of several European and American professional cardiology societies.

A variety of progenitor cell types residing in bone marrow or circulating in the blood are capable of improving function of the infarcted heart in preclinical models but underlying mechanisms remain incompletely understood. A growing body of evidence suggests that improvement in cardiac function is largely independent of cardiac muscle regeneration but rather associated with paracrine effects of the transferred progenitor cells. Recent doubleblind, placebo-controlled randomized trials of autologous bone marrow cell transfer inmyocardial infarction patients have shown modestly augmented recovery of LV functionafter cell transfer (absolute increase in left ventricular ejection fraction ranging from 1.2 to2.5%) and were associated with a favorable effect on myocardial perfusion or metabolism, infarct remodeling with a greater reduction in infarct size and greater recovery of regional LV function. However, the number of cells which home to the injured heart after being applied in animal models or post-infarction patients is limited and less than 10% in most studies and some of the most recent clinical trials have failed to confirm cardioprotection.