Monocytes: protagonists of infarct inflammation and repair after myocardial infarction.

Myocardial infarction (MI) is the most frequent cause of heart failure, which is an incapacitating disease with high prevalence and broad socioeconomic impact. In 2008 in the United States, 5.7 million people suffered from heart failure, and more than 287 000 people died.1 Timely revascularization of ischemic myocardium reduces acute infarct mortality, and current standard therapy with β blockers and angiotensin-converting enzyme (ACE) inhibitors curbs development of post-MI heart failure. For example, ACE inhibitor treatment reduced mortality from 25% to 20% in the Survival and Ventricular Enlargement (SAVE) trial.2 Although this is a major advance, long-term mortality remains high. The combination of reduced acute infarct mortality due to efficient acute care and insufficient options to treat infarct survivors chronically has contributed to an increased heart failure prevalence (Figure 1).3 Figure 1. Disease statistics. A, Deaths per 100 000 population for coronary heart disease in men, ages 35 to 74 years, United States, 1970 to 2005. B, Deaths due to heart failure, United States, 1970 to 2005. C, Hospitalizations per 100 000 population for heart failure, age ≥65 years, United States, 1971 to 2006. Adapted from National Heart, Lung, and Blood Institute Fact Book 2008.3 The need to understand and treat heart failure better has motivated clinicians and basic scientists to explore new therapeutic strategies to repair the failing heart, for instance, with stem cells.4,5 Augmentation of intrinsic wound healing that occurs during the first 1 to 2 weeks after MI is a prospective approach with the potential to prevent heart failure. During this period, the infarct is highly active biologically.6–8 Delicate granulation tissue undergoes rapid turnover of cells and of structural components such as the extracellular matrix. Preexisting collagen is digested and new matrix is laid down. During these extensive changes of tissue …