The Beating Heart

Doctoral student Limor Arbel-Ganon of the Technion has won the first place in the poster competition at the Israeli Society of Physiology and Pharmacology (ISPP). The conference was held in Jerusalem on February 14, 2019.

Limor Arbel-Ganon

Limor Arbel-Ganon

Limor’s research is focused on how mechanical overload can modulate sinoatrial node function. The sinoatrial node is the heart’s primary heart pacemaker, and it controls heart rate and rhythm. Sinoatrial node failure is associated with increased mortality in heart failure patients and in patients suffering from other cardiovascular diseases, where rhythm disturbance is associated with over 40% of sudden deaths. To date, the mechanisms that lead to sinoatrial node failure remain unclear. Increased venous return, which for example has been documented in heart failure patients, affects right atrial filling, distending the atrial wall where the sinoatrial node is located. Thus, it is possible that stretch is involved in sinoatrial node dysfunction in heart failure. In line with this hypothesis, a preoperative analysis of right atrial pressure and sinoatrial node function in children scheduled to undergo a Fontan operation showed that sinoatrial node dysfunction was absent in patients presenting normal right atrial pressure, but present in those with elevated right atrial pressure.

Limor has developed a system to stretch mouse sinoatrial node tissue and measure in parallel the beating rate using advanced imaging techniques. The system was tested on tissue dissected from control mice at different stretch levels. She found that stretching the SAN tissue from healthy mice led to an increase in the beating rate and a decrease in its variability around the mean. To understand the internal mechanisms that connect between the mechanical load and pacemaker function, we simulated the effect of stretch on sinoatrial tissue from a heart disease patient. The research showed that changes in calcium and phosphate signaling are responsible for the rhythm disturbance in unhealthy sinoatrial node tissue and for the increase in beating rate in healthy sinoatrial node tissue.