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Preconditioning stem cells for cardiovascular disease: an important step forward.

See related article, pages 545–555 

The promise of stem cell therapies to regenerate new myocardium and/or to enhance intrinsic repair processes has generated enthusiasm in the scientific and clinical communities, as well as among the public and its state and national representatives. This enthusiasm is based primarily on the limited inherent cardiac regeneration capability, the increased worldwide incidence of cardiovascular disease because of the aging of the population in the developed world and adverse consequences of lifestyle changes associated with industrialization and urbanization in developing countries, the fact that left ventricular dysfunction is the final common pathway for most forms of cardiovascular disease, and the fact that despite advances in medical and device therapies, mortality, repeated hospitalization rates, and quality of life limitations in patients with left ventricular dysfunction remain at unacceptable levels.

The cell type studied most extensively in the clinical setting of chronic left ventricular dysfunction is the skeletal myoblast (SkM). Advantages of this approach include demonstrated improved cardiac performance in animal models and relatively easy accessibility to large numbers of autologous stem cells in patient populations. However, the largest and most recent placebo-controlled, randomized trial (Myoblast Autologous Grafting in Ischemic Cardiomyopathy (MAGIC) Trial)1 did not demonstrate sustained efficacy as defined by the primary end point, global ejection fraction, although secondary end points of changes in left ventricular volumes were significantly improved in the high-dose (800 million cells) group. Efficacy for any cell product is certainly dependent on delivery to the intended region, an issue largely addressed with direct injection protocols, and then successful retention at that site. Retention is one of the most significant identified issues limiting efficacy in most studied models, with some estimating a greater than 90% cell loss2 because of necrosis or apoptosis within 24 hours of …