The foregoing results also supported previous studies that the ACE D allele was associated with higher ACE activity [7-9], converting more angiotensin II and thus stimulating inflammatory/fibrogenic responses and scar formation during myocardial infarction, or inducing reactive oxygen species to cause myocardial damage in the border zones and enlargement of the infarct size [24]. Here, AGT is linked to myocardial infarction.