Study sheds light on why women have faster heartbeats than men

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Doctors and researchers have puzzled for decades about a fundamental rhythm mystery: Why do women tend to have faster heartbeats while men are more likely to develop irregular rhythms like atrial fibrillation (AFIB)? Now a new study from The Ohio State University Wexner Medical Center provides some insight. Research shows that the sinoatrial node (SAN) - a small but powerful structure in the human heart that serves as a natural pacemaker and initiates every normal heartbeat - runs on different gene blueprints in men and women. The study found that women have genes that make their hearts beat faster, while men have gene networks that lead to heart problems...

Study sheds light on why women have faster heartbeats than men

Doctors and researchers have puzzled for decades about a fundamental rhythm mystery: Why do women tend to have faster heartbeats while men are more likely to develop irregular rhythms like atrial fibrillation (AFIB)? Now a new study from The Ohio State University Wexner Medical Center provides some insight.

Research shows that the sinoatrial node (SAN) - a small but powerful structure in the human heart that serves as a natural pacemaker and initiates every normal heartbeat - runs on different gene blueprints in men and women. The study found that women have genes that make their hearts beat faster, while men have gene networks that can lead to heart problems like AFIB. The research was recently published in theAmerican Heart Association Dissemination: Arrhythmia and Electrophysiology.

We discovered for the first time that the genes that control the way SAN works are influenced by sex. This helps explain why women generally have a faster heart rate and are more likely to experience inappropriate sinus tachycardia, while men are at higher risk for heart rate disorders such as conduction block and atrial fibrillation. “

Vadim Fedorov, PhD, professor of physiology and cell biology, Corrine Frick Research Chair in Heart Failure and Arrhythmias at The Ohio State University College of Medicine and senior author of the study

Researchers from Ohio State University's Dorothy M. Davis Heart and Lung Research Institute and the Corrine Frick Center for Heart Failure and Arrhythmias studied donated human hearts to unmask unique sets of genes in the Sancormazer cells that are responsible for generating and maintaining heart rate. They analyzed genes and pathways involved in pace, metabolism, inflammation and fibrotic remodeling and discovered different patterns associated with biological sex. The hearts were donated for research by organ donor families through the Ohio Lifeline.

“Women showed higher levels of TBX3 and HCN1, which are two important genes that help drive faster heart rhythms,” said Ning Li, MD, PhD, professor of research and co-author of the study. “In contrast, male hearts had more activity in gene networks related to inflammation and collagen production, which can affect electrical signaling and increase the risk of arrhythmias.”

The findings could help lay the foundation for more personalized, patient-specific approaches to treating cardiac arrhythmias, Fedorov said. The study builds on Ohio State's broader efforts to understand and prevent the most common heart rhythms, which can result in dangerously slow or fast heart rates and often require interventions such as medication or pacemaker implantation. According to the American Heart Association, more than 6 million Americans are currently living with heart failure and many also suffer from arrhythmias that stem from SAN.

This investigation was supported by the National Institutes of Health, the Leducq Foundation, and the Bob and Corrine Frick Center for Heart Failure and Arrhythmia, the first center in the country dedicated to treating patients with heart failure and arrhythmia.


Sources:

Journal reference:

Li, N.,et al.(2025). Heart Rate Mystery Unveiled: Sex Differences in Human Sinoatrial Node Genes and Female Tachycardia. Circulation Arrhythmia and Electrophysiology. doi.org/10.1161/circep.124.013534.