Based on that, a possible correlation with the clinical outcome is that the damaging effects of Gαq sustained activation, such as cardiomyocytes apoptosis, vasoconstriction and cardiac hypertrophy could be prolonged, impairing the AT1R receptor signaling and eventually contributing to AF development (Adams et al., 1998; Adams et al., 2000). This evidence concerns the gene GNAQ and cardiac hypertrophy.