Resolving inflammatory links between myocardial infarction and vascular dementia

Abstract

Myocardial infarction is associated with increased risk for vascular dementia. In both myocardial infarction and vascular dementia, there is evidence that elevated inflammatory biomarkers are associated with worsened clinical outcomes. Myocardial infarction leads to a systemic inflammatory response, which may contribute to recruitment or activation of myeloid cells, including monocytes, microglia, and perivascular macrophages, within the central nervous system. However, our understanding of the causative roles for these cells linking cardiac injury to the development and progression of dementia is incomplete. Herein, we provide an overview of inflammatory cellular and molecular links between myocardial infarction and vascular dementia and discuss strategies to resolve inflammation after myocardial infarction to limit neurovascular injury.

Keywords: Myocardial infarction; Vascular dementia.

Figure 1.. Proposed inflammatory links between MI and VaD.

Following MI, levels of inflammatory cytokines are increased in the peripheral blood. In the spleen and bone marrow, myeloid cells, such as neutrophils and monocytes, undergo epigenetic reprogramming and are released into the circulation. Within the CNS, MI leads to activation and proinflammatory cytokine production by microglia and perivascular macrophages. Combined increase of both local and systemic inflammation leads to disruption in the blood brain barrier and CNS infiltration of neutrophils and monocytes from the periphery. Sustained inflammation and disruption of the CNS vasculature leads to progressive loss of oligodendrocytes and neurons. This results in clinical VaD, characterized by white matter lesions and cognitive deterioration.