Priming Heart Before an Attack Could Limit Damage

Animal study shows preconditioning cardiac cells helps organ better tolerate loss of blood flow

By Carolyn Colwell
HealthDay Reporter

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THURSDAY, Jan. 10 (HealthDay News) -- Just as daily runs can prepare you to survive a marathon, blocking blood flow to the heart for brief spells could condition cardiac cells to better withstand the damage of a heart attack, a new animal study from the University of Cincinnati suggests.

Ultimately, if validated in humans, these findings could lead to a drug that "could be given to a patient where the heart is in stress, and it could [then] tolerate that stress better," explained study leader Dr. Karyn L. Butler. Such a drug might also protect the hearts of people with known cardiac problems who are about to undergo surgery.

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The findings show a new way to make use of a long-known phenomenon in which short-lived restrictions on blood flow, known as ischemia, could strengthen the heart's ability to recover from a heart attack, Butler added.

This preconditioning is "almost a form of exercise for the cell," explained Butler, who is an associate professor of surgery at the university. "For example, if you are going to run a marathon, you don't start with 20K, you start with a little bit at a time. If the heart is exposed to a brief period of ischemia -- maybe five minutes or a shorter period of time, and then exposed to a long period of time which we know as a heart attack -- hundreds of animal as well as human studies show that the heart can tolerate a heart attack better. It's almost as if the cell gets used to it and can prepare itself for handling a longer period of reduced blood flow."

Butler and her team shared two new insights into this protective, preconditioning phenomenon. They've identified in animals the molecular mechanisms behind preconditioning in a healthy heart, and they've demonstrated that the activating factor can be transferred to a healthy heart.

Their study examined the mechanism of a signaling pathway known as JAK-STAT in normal hearts, Butler explained. The next step, she said, will be to see if activating the same mechanism can work in hearts that have been exposed to high blood pressure.

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