Washington, Jan 28 - Even though healthy men and women have similarly structured hearts, the US researchers have discovered genetic differences in diseased hearts.
The new genetic differences found by researchers from Washington University in St. Louis in diseased hearts could pave the way to personalised treatment of various heart ailments.
Generally, men are more susceptible to developing atrial fibrillation, an irregular, rapid heartbeat that may lead to stroke, while women are more likely to develop long-QT syndrome, a rhythm disorder that can cause rapid heartbeats and sudden cardiac death, the journal Public Library of Science ONE reports.
Igor Efimov, professor of biomedical engineering at the Washington University School of Engineering & Applied Science, and former doctoral student Christina Ambrosi analysed 34 human hearts, looking for genetic differences that might explain gender differences in heart disease, according to a Washington statement.
The team screened for 89 major genes in electrophysiology, ion channel subunits, calcium handling proteins and transcription factors important in cardiac conduction and in the development of arrhythmia - and the left atria - and ventricles - in human hearts.
What was striking in this study is that we expected very large gender differences in expression of genes in the ventricles, but we did not find such differences, says Efimov, also professor of medicine, radiology and cell biology and physiology at Washington School of Medicine.
Unexpectedly, we found huge gender differences in the atria, the professir said.
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.
When women have the highest levels of estrogen, they are least vulnerable to arrhythmia -- women are protected by estrogen, Efimov 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.