When the heart doesn't get enough blood and then gets it back, it can cause harmful changes in a part of the brain that controls stress and blood pressure, leading to a specific kind of brain cell damage in animals.

What we've found so far suggests that when blood flow to the heart is blocked and then restored in animals, it may lead to harmful changes in a brain region involved in regulating stress and blood pressure—the hypothalamus. This process appears to be linked to a specific type of brain cell damage [1]. Our analysis of the available research shows that this heart-related injury can trigger effects beyond the heart itself, extending to the brain. In animal studies, the disruption of blood flow followed by its return (a condition sometimes called ischemia-reperfusion) is associated with damage to neurons in the hypothalamus [1]. While the exact mechanisms are not fully detailed in the evidence we’ve reviewed, the pattern we see leans toward a connection between cardiac injury and neurological impact in this area of the brain. We do not have enough evidence to say whether iron buildup is directly involved, nor do we have data confirming how this process unfolds over time or whether it leads to long-term functional changes. The current data we’ve analyzed comes from one line of research that aggregates findings across seven supporting observations, with no studies in our review refuting this link [1]. Because our analysis is based on a limited number of assertions, we remain cautious in interpreting the strength of this link. What we can say is that the evidence we've reviewed points toward a connection between heart injury from blocked and restored blood flow and damage to specific brain cells in the hypothalamus of animals. Practical takeaway: In animal models, heart stress involving loss and return of blood flow might affect brain health in areas controlling vital functions—but we don’t yet know if this happens in humans or how it could be prevented.