A new study in swine (pigs) has found that sermorelin can reduce scarring of heart muscle after a heart attack. This information confirms previous findings from research in rat models of heart attack. In the future, sermorelin and other GHRH agonists may be useful for treating post-infarction (after a heart attack) patients. These peptides have the potential to reduce long-term damage, speed recovery, and reduce complication rates.
The Scale of the Problem
Survival following a heart attack has improved with advances in care, but damage to the heart muscle often leads to a weakened pump function and heart failure. This is a serious condition, as 50% of individuals die within 5 years of a diagnosis of heart failure1. Clearly, reducing long-term consequences of a heart attack can improve survival. It can also improve morbidity as heart failure is an extremely debilitating condition.
The immediate damage caused by a heart attack is only one part of a larger problem that eventually leads to fatal heart failure. Other components of the problem include scar formation as well as generalized inflammation. Scar formation occurs secondary to wound healing. It can weaken the walls of the heart and interfere with the normal conduction of electrical signals. Post-infarction inflammation can weaken both the mechanical structure and electrical functioning of the heart as well. Without proper muscle structure, the heart cannot contract with enough force. Without proper electrical functioning, contractions are not coordinated or efficient and flow becomes turbulent. The ability to reduce inflammation and cardiac remodeling could drastically reduce the long-term consequences of heart attack2.
The Role of GHRH Agonists in Myocardial Repair
The current management of heart failure aims to maximize the effectiveness of whatever heart function remains. Unfortunately, morbidity and mortality remain high because the heart, in its weakened state, is more vulnerable to the effects of aging. New therapies aim to prevent remodeling, the change in heart structure that occurs secondary to scar formation and inflammation and which ultimately makes the heart weaker and less able to withstand the effects of aging.… Read the rest....