A myocardial infarction involves the blockage of a coronary artery that supplies the heart muscle with the oxygen and nutrients necessary for normal function.
Several natural biological response mechanisms are then triggered. Previous studies have shown that the heart attempts to dilate other arteries—and even build new ones—to serve as a bypass, though these reactions are usually neither fast nor effective enough to prevent heart damage or a fatal outcome.
A team of researchers from the University of Chinese Academy of Sciences discovered that an alternative bypass mechanism is actually at work, involving tiny capillaries that connect arteries to veins.
In a study published in the journal Science, the scientists describe in detail—for the first time—how this natural repair system functions and how it might be artificially stimulated to improve recovery prospects following a heart attack.
“Collectively, these findings redefine the cellular origins and formation mechanisms of coronary collaterals and highlight their role in facilitating effective cardiac tissue repair,” the researchers write.
They began the study by employing a more precise cell-tracking technique than those used in previous research, enabling them to observe the movement of endothelial cells (which line blood vessels) in both large arteries and much smaller connecting capillaries.
Experiments on mice simulating a myocardial infarction yielded an unexpected result.
The primary work of rerouting blood flow was carried out by endothelial cells in the smaller capillaries rather than in the larger arteries.
Essentially, the capillaries attempt to remodel themselves into structures more resembling arteries as a repair mechanism. This is a sort of workaround, similar to a process seen in newborn mice while their hearts are still developing.
“This process mirrors a developmental program in which capillary endothelial cells fuse to form small-diameter coronary artery branches during heart growth in newborns,” the researchers write.
As a next step, the scientists wanted to see if this bypass mechanism could be enhanced in some way, potentially leading to better future treatments.
They identified the signaling protein VEGF-A—which stimulates blood vessel growth—as a promising candidate. When administered to mice for a short period, this protein triggered a chemical chain reaction that strengthened the shunting arteries.
Mice receiving the optimized VEGF-A treatment showed improved blood flow around the injury site, reduced cardiac scarring, and better heart function.
“Modest supplementation with VEGF-A can also restore microcirculatory function, suggesting that targeting the vascular microenvironment is a valuable therapeutic strategy,” the researchers note.
It is worth noting that these studies were conducted on mice rather than humans; however, it is highly likely that similar processes occur in the human heart following injury.
Now that the mechanism behind this natural backup system has been detailed, researchers can begin exploring how it might aid in the development of therapies for heart attack patients.
In the United States, the survival rate for hospitalized heart attack patients currently exceeds 90 percent; however, these events often leave behind long-term damage that can lead to further cardiovascular complications. We may be able to address this by using treatments that improve blood flow and reduce scarring immediately after a heart attack.
The good news is that we are making progress in understanding the underlying causes of heart attacks and the best ways to treat them, and one such approach could involve supporting the body’s own repair processes.
“These results identify capillary arterialization as a central mechanism of endogenous revascularization and represent a potential therapeutic strategy for treating ischemic heart disease,” the researchers write.
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