Deletion of PARP-1 in mice or pharmacological inhibition of PARP activity decreases cardiac hypertrophy induced by angiotensin II (Pillai et al., 2006) or pressure overload (Pillai et al., 2005a; Xiao et al., 2005), delays the progression from hypertensive cardiomyopathy to HF (Bartha et al., 2009), decreases cell death and HF after MI (Palfi et al., 2006) and diminishes myocardial ischemia/reperfusion injury (Szabo et al., 2002). This evidence concerns the gene PARP1 and myocardial infarction.