Heart failure is a global health problem commonly complicated by sleep apnea, a comorbidity that further shortens a person’s lifespan. By targeting the neural activity that drives both heart failure and sleep apnea, a promising new drug has been developed that can treat heart failure and sleep apnea.
For patients with heart failure, the prognosis is poor and mortality is high despite recent therapeutic advances. According to the National Institutes of Health, heart failure affects more than 64 million people worldwide, making it a major global public health priority.
Heart failure occurs when the heart muscle becomes weak and cannot pump effectively. The brain responds to heart failure by activating the body’s sympathetic nervous system, causing a “fight or flight” response to stimulate the heart more effectively. However, long-term prolonged stimulation, coupled with sleep apnea, leads to a shortened life expectancy. Most patients die within five years of his diagnosis of heart failure.
The part of the brain that sends impulses to the heart also controls breathing. Central sleep apnea (CSA) – repetitive pauses in breathing during sleep because the brain does not send the proper signals to the respiratory muscles – is common in people with heart failure. Sleep apnea is thought to be caused by increased sensitivity of peripheral chemoreceptors found in the carotid arteries that detect changes in arterial blood oxygen (hypoxia) and initiate a reflex to bring oxygen levels back to normal. It is One receptor in particular, P2X3, is known to influence this reflex response.
Besides treating the underlying cause of CSA, including heart failure, current treatment for sleep apnea is limited to continuous positive airway pressure (CPAP), which uses mild air pressure to keep the airway open. I’m here. However, CPAP, which requires a tight-fitting mask to be worn while sleeping, is poorly tolerated.
Promising new drugs have now been developed that target the neural activity that drives both heart failure and sleep apnea. Researchers at the University of Auckland in New Zealand tested the drug, known as AF-130, in rats with chronic heart failure and sleep apnea. They found that AF-130 acted as a potent P2X3 receptor antagonist, normalizing the body’s respiratory response to hypoxia and significantly improving the amount of blood pumped by the heart (cardiac output). bottom. Respiratory disturbance resolved.
“This drug does work for heart failure, but it’s two for the price of one. It also relieves apnea for which there are currently no drugs and only poorly tolerated CPAP.”
AF-130 has also been found to reduce systemic inflammation, reduce heart weight, and prevent fluid from collecting in the lungs, a common side effect of heart failure. It was the first drug to control the neural activity from the brain to the heart that causes apnea.
The results of this study support the idea that carotid P2X3 receptors play an important role in the pathological mechanisms underlying cardiovascular and respiratory diseases.
“Several classes of drugs have been developed in recent decades to improve the prognosis of heart failure,” says cardiologist Dr. Martin Stiles. “But none of these drugs work like this new one. So it’s exciting to see new ways that might reverse some features of heart failure.”
Even more promising is that the drug will soon be approved by the FDA, albeit for another clinical use.
The study was published in a journal Nature Communications.
Source: University of Auckland
