To determine whether variations in the APOE, AGT, AT1R, and ACE genes contribute to the risk for early MI, we genotyped 220 Spanish male MI patients and 200 healthy controls younger than 55 years.
The 1166 A/C polymorphism in the 3' region of the AT1R gene and the 287-bp insertion/ deletion (I/D) polymorphism in the ACE gene were analyzed as described previously (29).
AGT, ACE, and AT1R allele and genotype frequencies did not differ between patients and controls.
The APOE genotype did not modify the risk associated with the ACE or AT1R genotypes (Table 3).
We also investigated a synergistic effect between the APOE and the AGT, AT1R, and ACE polymorphisms.
The published results are variable with respect to the association between polymorphisms of ACE, AGT, AT1R, and APOE with CAD, hypertension, and MI.
Howard Rockman, in collaboration with Trevena, showing that -arrestin biased AT1R ligands can protect cardiac tissue from injury.
The article, entitled "-Arrestin-biased AT1R stimulation promotes cell survival during acute cardiac injury" waspublished online ahead of print on August 10th 2012 in the American Journal of Physiology: Heart and Circulation Physiology.
These data further support the benefits of targeting the AT1R with a -arrestin biased ligand.