An American has a heart attack about every 40 seconds. Many factors contribute to how well a patient does after a heart attack, or myocardial infarction, to use the technical term. The two biggest factors are the size of the initial infarction (the obstruction of the blood supply) and the efficiency of the recovery process.
One way to improve the recovery process might be to fine-tune inflammation after a heart attack, and researchers at the Texas A&M Institute of Biosciences and Technology uncovered a potential new approach in the journal Circulation. There are possible ways to improve recovery, and those are exciting because they significantly reduce heart attack patient mortality and the associated severe complications, such as arrhythmia and aneurysm, and make the healing process of the injured heart smoother.
“After a heart attack, there is a massive inflammatory response, which is a double-edged sword,” said Jiang Chang, MD, PhD, professor at the Institute of Biosciences and Technology Center for Translational Cancer Research and corresponding author of the paper. “The body built this inflammatory response to rescue tissue and repair injury, but many times, it is greater than it should be and actually causes harm. Balancing the inflammatory response is the key—and the challenge.”
Chang’s approach involves a protein called RhoE, which might be able to fine tune that response. Using an animal model that doesn’t have any RhoE, he and his team were able to show that lack of this protein causes an intense inflammatory response and poorer heart function.
In fact, the researchers created a patient-oriented model to test whether reducing RhoE could mimic what happens in patients with a poor prognosis after a heart attack and found that it could. This is likely due to the excessive inflammation, which leads to larger infarctions, decreased contractility of heart muscle and increased risk of death.
“This is a new biomarker that can help predict the patient’s outcome, but perhaps more importantly, it is also a potential new therapeutic target,” Chang said. “We hope to be able to finish these preclinical studies in the next four years, and then we may be able to move potential new drugs targeting RhoE into clinical trials.”
This research was supported, in part, by the National Institutes of Health through grants NIH-NHLBI R01HL102314, R01HL123953 and R01HL141215. Drs. Yuan Dai, Jiangping Song and Wenjiao Li are the co-lead authors of the study.
This article by Christina Sumners originally appeared in Vital Record.
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