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Myocardial contractility is enhanced in transgenic (TG) mice with cardiac-restricted overexpression of the alpha1A-adrenergic receptors (alpha1A-AR). We tested the hypothesis that this enhanced inotropy protects against dysfunction and remodeling after myocardial infarction (MI).

Transgenic α1A-adrenergic activation limits post-infarct ventricular remodeling and dysfunction and improves survival