Abstract
Stroke-heart syndrome describes the neurocardiogenic mechanisms that lead to the development of poststroke cardiovascular complications. We describe a 25-year-old man with Carvajal syndrome who developed advanced biventricular heart failure 2 months after a large territory ischemic stroke. His condition was managed with inotropic support initially and required biventricular assist devices as a bridge to possible heart transplantation. This case highlights the increased risk of cardiovascular complications after stroke through dysregulation of the brain-heart axis. Poststroke neuron death leads to systemic and local inflammation through noradrenaline, interleukin-1, and other proinflammatory cells. This cumulatively leads to endothelial dysfunction and cardiomyocyte fibrosis/necrosis within the heart.