However, these reflections of increased cardiac hypertrophy in AKO mice were also associated with increases in end systolic and diastolic volumes (Table 1), suggesting that a possible reduction in alpha1A-AR-stimulated physiologic hypertrophy led instead to an increase in pathologic hypertrophy and subsequently to worsened post-MI ventricular dilatation. The gene discussed is ADRA1A; the disease is Ventriculomegaly.