Another life-saving application for beta blockers
Oral drug used for long-term treatment of heart disease may also help after attack
Long-hailed superdrug for treating chronic heart disease, beta blockers may have another life-saving effect on the organ, new research suggests.
A team of scientists at York University has discovered that this class of drugs, considered miraculous for easing the workload of a damaged, but functioning heart, may also help the organ’s muscle cells survive an acute attack.
Damage and death of the cardiomyocyte, which contract to make the heart pump, could lead to heart failure.
“This is a new aspect of beta-blocker function that wasn’t known before,” says York University department of biology professor John McDermott, the study’s lead author.
“It’s exciting to have a potential application of one of the discoveries we’ve made.”
Currently, doctors only prescribe beta blockers as a long-term treatment for heart disease. It’s not used in critical or acute care.
But the study, published this month in the journal Cell Death Discovery, suggests that an immediate dose of beta blockers in the hours following a heart attack could stop these crucial cells from dying in the short term — and down the road.
The beta blockers, which are taken orally, slow heart rate and ease pressure on a struggling circulatory sys- tem, enabling a damaged heart to continue to do its duty.
Now, it appears that in rat and mouse tissue, these drugs promote the activity of Mef2, a protein molecule found in the heart’s muscle. Mef2 protects cells, which have become stressed in one way or another, from dying, McDermott says.
That is vital because heart cells can’t regenerate.
And they become particularly vulnerable during a heart attack when a surge of hormones, particuladrenalinaline, block Mef2’s protective action, he says.
McDermott’s team discovered that the beta blockers seem to block those nefarious hormonal signals, enabling Mef2 to continue its important work of helping the heart’s muscle cells stay alive and operating smoothly.
“If you lose those (heart muscle) cells, you can’t get them back,” he says. “And then the heart can’t function very well to push blood around your body.”
The next step in the research, McDermott says, is to find out whether the beta blockers have the same effect on human tissue as they do in the rodent cells.
McDermott, who has been studying muscle gene expression for more than 25 years, has recently collaborated with a research group at the Toronto General Hospital, which studies human heart tissue.
If all goes well, he says, it may not be too long before beta blockers, which are well tested and have been widely prescribed since the 1970s, are used in this new application.