Stopping Heart Attacks at a Cellular Level

Cell regrowth reduction can prevent additional heart attacks

(RxWiki News) A protein embedded in blood vessel walls may be key to preventing second or third heart attacks. Researchers suspect that stopping dangerous cell growth after a vascular injury may be the key to prevention.

Protein AIF-1 stimulates undesirable formation of new cells after such an injury, while IRT-1 discourages new cell formation. The latter may be important in preventing additional heart attacks.

"Monitor your blood pressure and cholesterol to lower plaque in arteries."

Maria Gomez, a researcher from Lund University in Sweden, has already had success in animal experiments in collaboration with Temple University. Gomez noted that after an artery injury, inner layer artery cells start to regrow, which can be problematic.

Arterial injuries are commonly caused by angioplasty, a procedure to clear blocked arteries after a heart attack. Gomez said that while the procedure initially opens arteries, new cell formation afterwards can increase the risk of additional heart attacks.

Researchers used rats to prove the opposite effects of the pair of proteins. The carotid artery of rats was damaged with balloon dilation, much like angioplasty to simulate the procedure. Two weeks later there was considerably less cell formation in arteries that had more of the protein IRT-1. With AIF-1, the opposite effect was observed.

Gomez noted that researchers have found the mechanism to control the balance between the two proteins. She said a drug could be used to increase the amount of the "good" protein IRT-1. The medication is still in pre-clinical trials. Success has been reported in mice.

As part of the study, investigators also analyzed 150 fatty plaque deposits removed from the carotid arteries of patients. This revealed that unstable plaques that more easily rupture contain more AIF-1. Plaques with higher levels of IRT-1 were found to be less dangerous.

Cell regrowth in the arteries also can lead to potentially harmful changes in blood flow. It is possible that AIF-1 may play a role in forming plaques in arteries, researchers found.

The study was recently published in journal Cardiovascular Research.

Review Date: 
December 8, 2011