Ischemic stroke is one of the leading causes of death worldwide. In 10–20% of patients, severe cardiac complications, such as arrhythmias or heart attacks, occur in the first days following a stroke. These cardiac events, known as “Stroke-Heart Syndrome,” significantly worsen prognosis and increase mortality after a stroke. The mechanisms underlying these cardiac complications following ischemic stroke are not yet fully understood, and existing therapies do not effectively prevent these events. This project aims to investigate how dysregulation of central stress networks after ischemic stroke leads to cardiac damage in a mouse model. These central stress networks will be manipulated using cutting-edge techniques such as chemogenetics and optogenetics, and the resulting cardiac damage will be comprehensively assessed. By unraveling the mechanisms, we hope to identify new therapeutic targets for improved prevention and treatment of Stroke-Heart Syndrome.