The Neurocardiac Axis in Myocardial Infarction: Emerging Role of Brain-Heart Inflammatory Signaling

Myocardial infarctions (MI) can lead to post-MI cardiac and neurocognitive dysfunctions due to the complex interplay of the neurocardiac “brain and heart” axis. Imbalanced autonomic nervous system (ANS) synchronization within the neurocardiac axis leads to infarcted or damaged tissues. This may influence potential inflammatory signaling mechanisms in post-MI pathology and, by extension, the repercussions of acute and chronic MI outcomes. Here, previous in-vivo experimental rodent and porcine models with surgically induced MI/heart failure (HF) and in-vitro models report brain-heart association regions and pathologies. Furthermore, clinical meta-analyses were compiled to provide a broad overview of the varying impacts of post-MI pathologies on the brain and heart. Other supplemental perspectives postulate other relevant inflammatory mechanisms, such as neurohumoral imbalances, a weakened immune system, and genetic predispositions, which expand a more holistic view of post-MI mechanisms. By examining in closer detail the inflammatory cells (e.g., microglia and astrocytes) and the blood-brain barrier (BBB), cardiogenic trauma from MI incites chronic systemic inflammation and exacerbates the stress response. This further weakens the BBB, prolongs neuroinflammation, and damages sites responsible for cardiac regulation and repair. Neurocardiac axis dysregulation induced by MI. This general schematic shows how the proper functioning of the neurocardiac axis relies on the undisrupted cardio-regulatory regions in the brain innervating the heart. Disruption to this axis, exacerbated by the onset of MI and prolonged, unresolved inflammation, contributes to cardiac and brain pathological outcomes