Clinical Utilization of Skeletal Myoblasts

Clinical and Scientific Background The current pharmacotherapy for congestive heart failure,1 including neurohormonal inhibition, with angiotensin-converting enzyme (ACE) inhibitors and β-blockers, improves the clinical outcome, but fails to stop the progression of the disease. Similarly, despite the best available treatment, the cumulative incidence of mortality and heart failure increases time-dependently in patients with a previous myocardial infarction.2Therefore, novel treatment methods that improve cardiac function and prevent heart failure are in demand. The mechanisms leading to congestive heart failure after an acute myocardial infarction are only partially understood,3 and, according to current belief, a progressive decrease in the number of viable myocytes after an acute myocardial infarction could at least partially explain this transition. Therefore, myocardial infarction and subsequent heart failure can be viewed as a disease of cellular deficiency.4