A multi-institution study published in Nature Communications reveals that iron drives fatty tissue formation in the heart and leads to chronic heart failure in roughly 50 percent of heart attack survivors.
While survival after a heart attack is possible for most, too many survivors have long-term complications such as heart failure. With this new research, doctors and scientists may be able to prevent these risks.
“For the first time, we have identified a root cause of chronic heart failure following a heart attack,” says Rohan Dharmakumar, PhD, executive director of Indiana University’s Krannert Cardiovascular Research Center and associate director for research at the Cardiovascular Institute.
Study Details
The multi-million-dollar study, which involved collaborators from institutions in the United States and Canada, followed large animal models over six months. Researchers found that in heart attacks that result in bleeding within the heart muscle — which is about half of them — scar tissue is slowly replaced by fat. Fatty tissue can’t push blood from the heart effectively, and this is what leads to heart failure and eventually to death in many survivors of hemorrhagic heart attacks, says Dharmakumar.
“Using noninvasive imaging, histology, and molecular biology techniques, and various other technologies, we have shown that iron from red blood cells is what drives this process,” explains Dharmakumar. “When we removed the iron, we reduced the amount of fat in the heart muscle. This finding establishes a pathway for clinical investigations to remedy or mitigate the effects associated with iron in hemorrhagic myocardial infarction patients.”
Dharmakumar and his team are currently testing iron chelation therapy to do just that in a recently launched clinical trial.
Conclusion
“Our studies provide insights into the pathophysiology and the means to mitigate post-[myocardial infarction, left ventricle] MI LV remodeling. Notably, we showed that not all MIs are the same; and that the residual iron from hemorrhagic MIs plays an important role in the progressive weakening of the heart in the post-MI period, independent of initial infarct size. Hence unlike MI size, which is permanent, reducing iron within MI to mitigate the progressive loss of cardiac function well after acute MI offers a new dimension in the development of disease-modifying therapies for [chronic heart failure] CHF.”
