Identifying the Mechanistic Trigger of Vasovagal Syncope Using Combined LBNP and MRI

• Applicant: Dr. Fabian Möller
• Subject Area: Anatomy and Physiology
• Term: since 2026
• Project identifier: Deutsche Forschungsgemeinschaft (DFG) - Project number 577528060

Vasovagal syncope (VVS) is a common type of fainting caused by a sudden drop in heart rate and blood pressure, leading to temporary loss of consciousness. It often affects healthy individuals during prolonged standing but becomes more likely after long periods of bed rest or exposure to weightlessness during spaceflight. These conditions reduce the body’s normal gravitational stimulation, which helps regulate blood pressure. Despite its frequency and clinical importance, the exact physiological trigger that causes VVS remains unresolved. For decades, researchers have debated whether VVS is triggered by slowing of the heart due to vagal nerve activity or by a sudden drop in sympathetic nervous system activity that causes the blood vessels to relax and blood pressure to collapse. Both mechanisms lead to reduced blood pressure in the brain and can cause syncope. However, most previous studies have relied on indirect or unreliable methods that could not clearly determine the primary cause. I specifically aim to determine whether syncope is initiated by sympathetic withdrawal rather than by vagal cardiac inhibition. We have a critical need to resolve this question for improving diagnosis, prediction, and prevention for patients, the elderly, and astronauts. My rationale is to combine real-time magnetic resonance imaging (MRI) with lower body negative pressure (LBNP) to identify heart function and nervous system activity during the critical moments leading to VVS. LBNP simulates the effects of standing upright by moving blood away from the upper body in the supine position. Devices compatible with MRI were developed at the host institution. The combination of LBNP with MRI allows me to precisely measure heart chamber volumes, blood flow, and autonomic responses at the exact point of syncope onset. My specific objectives are to: • Identify the physiological trigger of vasovagal syncope by quantifying heart chamber volumes, venous return, and sympathetic nerve activity during graded orthostatic stress. • Characterize individual differences in stroke volume, vascular tone, and autonomic regulation in response to orthostatic loading. • Assess the feasibility of combined LBNP and MRI as a personalized diagnostic and research tool to evaluate orthostatic tolerance and guide countermeasure development. This project will be conducted at the German Aerospace Center (DLR), which offers world-leading expertise and equipment for cardiovascular imaging and autonomic testing. I will be mentored by Professor Jens Tank, a recognized expert in human cardiovascular regulation. By precisely defining when and how fainting occurs, this study will help develop better methods to predict and prevent syncope in people affected by deconditioning, age, or gravitational unloading. The findings will have direct applications in clinical care, rehabilitation, and astronaut countermeasures for spaceflight.

• DFG Programme: Position