Chronic spinal cord damage changes heart structure and function, which is linked to an increased risk of cardiovascular disease. We look at the acuteto-chronic cardiac effects of spinal cord injury, as well as the role of altered bulbospinal sympathetic regulation in the deterioration in heart performance after spinal cord injury. We show that spinal cord injury produces a rapid and continuous loss in left ventricular contractile performance that occurs before anatomical alterations by integrating experimental rat models with prospective clinical data. We show in rodents that the loss of bulbospinal sympathetic regulation is responsible for the reduction in left ventricular contractile performance after spinal cord damage. We discovered that activating sympathetic circuitry below the level of spinal cord injury generates an instantaneous rise in systolic function in people. Our findings emphasise the need of early management in preventing heart functional decline after spinal cord injury.
