Fig. 7.

LRT does not reduce infarct size (Boyle and Weisman 1993; Hale and Kloner 1988; Hochman and Choo 1987; Jugdutt 1997), significantly alter collagen content (Connelly et al. 1992; Fang et al. 2007; Knowlton et al. 1992; Lerman et al. 1983), or increase uniaxial metrics of stiffness when compared to PO models (Connelly et al. 1985, 1992; Fang et al. 2007), but may reduce MMP activity (Carlyle et al. 1997; Fang et al. 2007) and improve the myocardium’s resistance to rupture (Connelly et al. 1985, 1992) during post-MI inflammation. All axes rely on arbitrary units, and all curves are qualitative representations of the studies summarized within this review. The start of inflammation (${\mathbf{A}}_{\mathit{I}\mathit{n}\mathit{f}}$) is defined as immediately following MI and before the application of LRT. The end of inflammation (${\mathbf{\Omega }}_{\mathit{I}\mathit{n}\mathit{f}}$) is defined by mass migration and proliferation of fibroblasts in the infarcted region