Abstract
Cerebral-cardiac syndrome (CCS) refers to cardiac dysfunction following varying brain injuries. Ischemic stroke is strongly evidenced to induce CCS characterizing as arrhythmia, myocardial damage, and heart failure. CCS is attributed to be the second leading cause of death in the post-stroke stage; however, the responsible mechanisms are obscure. Studies indicated the possible mechanisms including insular cortex injury, autonomic imbalance, catecholamine surge, immune response, and systemic inflammation. Of note, the characteristics of the stroke population reveal a common comorbidity with diabetes. The close and causative correlation of diabetes and stroke directs the involvement of diabetes in CCS. Nevertheless, the role of diabetes and its corresponding molecular mechanisms in CCS have not been clarified. Here we conclude the features of CCS and the potential role of diabetes in CCS. Diabetes drives establish a “primed” inflammatory microenvironment and further induces severe systemic inflammation after stroke. The boosted inflammation is suspected to provoke cardiac pathological changes and hence exacerbate CCS. Importantly, as the key element of inflammation, NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome is indicated to play an important role in diabetes, stroke, and the sequential CCS. Overall, we characterize the corresponding role of diabetes in CCS and speculate a link of NLRP3 inflammasome between them.
Highlights
Cerebral-cardiac syndrome (CCS) is an interplay between the brain and the heart, which is known as neurocardiogenic syndrome
CCS refers to the cardiac damage after ischemic stroke (IS) that has various clinical manifestations, including arrhythmia, myocardial damage, and heart failure
We try to indicate the role of diabetes in CCS and the link of NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome between diabetes and CCS
Summary
Cerebral-cardiac syndrome (CCS) is an interplay between the brain and the heart, which is known as neurocardiogenic syndrome. Various brain injuries such as ischemic stroke (IS), intracerebral hemorrhage, subarachnoid hemorrhage, traumatic brain injury, and stress are evidenced to cause cardiac injuries or to exacerbate preexisting heart disease, which manifests as arrhythmia, various myocardial damages, heart failure, and myocardial infarction [1,2,3,4,5]. CCS can be found after brain injury even without primary heart disease [6]. We summarize the special role and explain the underlying molecular mechanisms of diabetes in CCS. We speculate a reasonable link of NLRP3 inflammasome between diabetes and CCS
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
