Acute myocardial infarction (AMI) remains a leading cause of death. Among patients admitted to hospital with an AMI, 10% develop acute ischemic heart failure (AIHF) and account for 50% of those who die within 30 days. The prognosis for patients with AIHF has not improved over the past decade, since neither currently available drugs nor assist devices reduce mortality; and despite considerable efforts, cardioprotective therapies to limit myocardial injury in AMI have not been successful. Myocardial stunning (MS) refers to the sudden but reversible loss of myocardial function that occurs alongside irreversible necrosis in AMI. MS is not limited to AMI but can also occur in other cardiac conditions, including takotsubo in which patients develop pronounced stunning without significant myocardial necrosis in response to stress.
MS is thought to be caused by myocardial injury, but I hypothesize that it is a means of preserving energy for vital processes by shutting down energy-demanding contractile functions in settings of oxygen deprivation. The overarching aim of my projects is to understand how MS can be manipulated to optimize cardiac function and survival in AMI and takotsubo. To achieve this goal, I am conducting studies in a cohort of Swedish patients with AMI or takotsubo and a rat model of myocardial stunning as well as via the extensive Swedish healthcare registries with patient records. My integrated research approach allows me to easier translate findings in animals to clinical research, and investigate interesting findings in humans more in-depth in the rat model. My research could change how researchers and clinicians approach the pathophysiology, prognosis, and treatment of AMI and takotsubo and help mitigate the sex gap in the evidence supporting the use and benefit of current treatments.
