The results showed that women with failing hearts have a weaker system of gene expression than men males showed overall higher expression levels of nearly all of the 89 genes than women.
Women showed particularly lower atrial expression levels of several important genes encoding for potassium channels, including Kv4.3, KChIP2, Kv1.5 and Kir3.1. In fact, the atria of women with heart disease had less than half of the KChIP2 mRNA than atria in men.
Results of the research were published in PLOS ONE.
Efimov says while there are still many questions that need to be answered to explain these molecular differences, one factor that could be contributing to the difference is estrogen.
"When women have the highest levels of estrogen, they are least vulnerable to arrhythmia women are protected by estrogen," he says. "But after menopause, women develop atrial fibrillation at the same rate as men. We don't understand this and need to study this in humans."
Another potential factor is circadian rhythm, Efimov says.
"Humans are much more likely to die suddenly from heart disease early in the morning, between 5-7 a.m.," he says. "In the cardiac system in mice, it has been shown that there is an oscillation of gene expression, so certain genes expressed at 5 a.m. could be different by threefold at 5 p.m."
Efimov says the study on human hearts is unique to Washington University, as much cardiac research elsewhere is done mostly in animal models. In the future, the team would like to expand the research into pediatric hearts, taking advantage of Washington University's leading pediatric heart transplant program to learn more about pediatric physiology.
|Contact: Igor Efimov|
Washington University in St. Louis