The renin increases the production of an enzyme called angiotensin-converting enzyme, or ACE, which in turn activates a hormone called angiotensin. The angiotensin increases blood pressure by constricting blood vessels, enlarges the heart and boosts pumping action by stimulating the release of adrenaline. That helps relieve the blood-starved kidneys in the short term, but in the long run inflicts greater damage on the heart. Doctors now routinely prescribe drugs called ACE inhibitors to interrupt that cascade and reduce strain on the heart. But that's not enough for all patients.
All people have two copies of most genes.
Heart failure patients who don't have this mutated ACE gene or have only one copy seem to respond well to ACE inhibitors, McNamara said. But several studies, including an early one by Bristow, have shown that patients who have two copies of the mutation fare poorly, even with the help of ACE inhibitors. In the Pitt study, McNamara and his colleagues found that 32 percent of 328 heart failure patients at UPMC had two copies of the mutated ACE gene. The Pitt researchers observed that simply increasing the dosage of ACE inhibitors had no effect on the survival of these patients. Bristow said that's because there's a limit to how much of the enzyme can be blocked.