PRKG1 and cardiac hypertrophy: At the microvascular level, the decrease in the bioavailability of NO, alterations in the sGC-cGMP-PKG pathway, accumulation of ROS, and chronic low-grade inflammation are the main actions involved in the alteration of vascular function both at the systemic circulation and in the coronary territory, promoting a functional decrease in cardiomyocytes, evidenced by delayed myocardial relaxation, increased myocardial stiffness, cardiac hypertrophy, and interstitial fibrosis.