Myocardial infarction induces cerebral alterations, including neuroinflammation and neuronal apoptosis, through signaling mechanisms mediated by systemic inflammation, extracellular vesicles, and microRNAs.
This review highlights the molecular mechanisms of the heart-brain axis after myocardial infarction, suggesting that targeting systemic inflammation, extracellular vesicles, and microRNAs could mitigate post-MI neurological and psychiatric complications.
Myocardial infarction (MI) is the leading cause of death among ischemic heart diseases and is associated with several long-term cardiovascular complications, such as angina, re-infarction, arrhythmias, and heart failure. However, MI is frequently accompanied by non-cardiovascular multiple comorbidities, including brain disorders such as stroke, anxiety, depression, and cognitive impairment. Accumulating experimental and clinical evidence suggests a causal relationship between MI and stroke, but the precise underlying mechanisms have not yet been elucidated. Indeed, the risk of stroke remains a current challenge in patients with MI, in spite of the improvement of medical treatment among this patient population has reduced the risk of stroke. In this review, the effects of the signaling from the ischemic heart to the brain, such as neuroinflammation, neuronal apoptosis, and neurogenesis, and the possible actors mediating these effects, such as systemic inflammation, immunoresponse, extracellular vesicles, and microRNAs, are discussed.
Gelosa et al. (Thu,) conducted a review in Myocardial infarction and subsequent brain disorders. Myocardial infarction induces cerebral alterations, including neuroinflammation and neuronal apoptosis, through signaling mechanisms mediated by systemic inflammation, extracellular vesicles, and microRNAs.