Acute ischaemic stroke induces persistent innate immune memory through epigenetic changes in myeloid progenitors in the bone marrow, and this innate immune training contributes to cardiac remodelling and dysfunction in the long term. These findings, published in Cell, provide insights into the mechanisms underlying the observed high long-term risk of secondary complications after a stroke.

Previous studies had shown that stroke leads to persistent systemic inflammation and that this chronic inflammatory response can cause complications such as infections and exacerbation of vascular inflammation. “However, these studies mostly focused on the acute and subsequent phase after stroke, and very little was known so far about the systemic immune changes in the chronic phase,” says Liesz. “In addition, patients with stroke very commonly develop cardiac complications, but the exact mechanisms were largely unclear,” he adds. Therefore, Simats, Liesz and colleagues set out to explore whether the immune system is persistently compromised after stroke and the potential effects on the heart.