hemodynamic parameters correlate poorly with LVM in humans3, 33, 34 and the rat. 35–37 Although limited, there are compelling examples of genes that have been identified through genomic analyses of remodeling that are now targets for therapeutic intervention, and we provide 2 examples of this. The first example is that of periostin, which was shown to be markedly upregulated in the first microarray study of post–myocardial infarction (MI) remodeling. 19 Subsequent studies revealed that periostin is important for post-MI remodeling and repair of the LV, 38 which has led to the idea that exogenous periostin may be useful for limiting LV remodeling. 39 The second example is Nix, a proapoptotic mitochondrial protein that is upregulated in genetic and pressure overload–induced models of cardiac hypertrophy in the mouse. 40 Overexpression of Nix results in cardiomyopathy, whereas cardiac-specific deletion of Nix protects the heart from adverse remodeling, prevents apoptotic cell death, and preserves LV function. 40, 41

State of the Art: Combined Genetic and Correlation Analyses of Gene Expression