Molecular ‘glitch’ leads to post-op heart failure
March 1, 2000
Molecular glitch’ leads to post-op heart failure
Research into the cause of a nearly universal heart failure that occurs after open-heart surgery could lead to preventive measures that might impact ICU staff, says Anne Murphy, MD, a pediatric cardiologist at Johns Hopkins University, who led the research team.
Murphy’s team found a small molecular glitch that leads to "cardiac stunning," an acquired heart failure that affects nearly anyone who has the blood supply to the heart temporarily shut down through open heart surgery or use of a heart-lung machine.
Researchers note that cardiac stunning is the reason that heart patients must spend an entire day in intensive care after surgery.
Research focuses on abnormal protein
In the study, published in the Jan. 21 issue of the journal Science, scientists looked at an abnormal form of a protein, troponin I (TrI), that is part of the heart muscle cell’s contracting machinery. The damaged protein is missing amino acid building blocks.
Through experiments with mice, the team showed that insertion of the damaged TrI actually caused the mice to develop enlarged hearts, a response to weakened heart muscle.
Murphy says heart cells deprived of oxygen have a sudden increase in calcium, which sets up production of enzymes that shorten the TrI protein molecules. That, in turn, causes heart contraction problems.
The disorder can last anywhere from hours to days. Patients usually are given adrenaline or a similar drug to strengthen the heart beat. Some patients, particularly those with complications, can die.
Although the research so far has not produced a treatment for the condition, Murphy says it points the way toward possible future prevention. She says that if clinicians can anticipate stunning, then perhaps they could pretreat surgery patients to avert TrI shortening.
Such therapies are at least a few years away, she says. "I think what that means for the future is that this can now be a therapeutic target. Both our group and I’m sure pharmaceutical groups can actually target therapeutics toward avoiding injury to the troponin I protein or ways to avoid the cardiac dysfunction when the protein is injured, in order to devise a specific therapy for myocardial stunning."
Condition common in ICUs
Murphy says ICU staff may have been aware of the syndrome for years without knowing what it was called.
"Obviously, the ICU is where you see it frequently," she says. "Nurses know that when their cardiacs come back from the operating room, they’re most likely going to have some cardiac dysfunction.
"Now, they can be aware that there are specific abnormalities that may be targeted in the future, so that when patients get to the ICU after open-heart surgery or after an aborted heart attack, they’ll be in better shape."
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