ABSTRACT
Myocardial infarction (MI) induces left ventricular (LV) dysfunction and remodeling as a consequence of a healing process during which necrotic cardiomyocytes are removed by an inflammatory reaction and replaced with connective tissue scar.1,2 Although early revascularization reduces myocardial damage and improves survival after MI, approximately 30-35% of patients with successful restoration of epicardial flow demonstrate adverse cardiac remodeling, which is associated with worse long-term clinical outcomes.3,4
Novel strategies to replace lost myocardium, protect at-risk cardiomyocytes, or augment vascularity may preserve LV function and limit remodeling. Cytokine therapy has emerged as a non-invasive modality due to its potential ability to regenerate cardiomyoctyes, prevent cardiomyoctye loss through inhibition of apoptosis, induce neovascularization, and possibly improve interstitial matrix characteristics. These salutary effects of cytokine therapy can have a favorable impact on LV remodeling. Cytokine therapy may be applicable in conjunction with mechanical or cellular therapies or particularly for “no-option” patients – those with disabling ischemia despite optimal medical treatment, after all possibilities for conventional mechanical revascularization have been exhausted.
