Postoperative troponin increases after noncardiac surgery are associated with raised neurofilament light: a prospective observational cohort study

Influence of perioperative dexmedetomidine on the incidence of postoperative delirium in adult patients undergoing cardiac surgery

“…2 In the first, systemic inflammation leads to the release of cytokines that act on the blood brain barrier and suppress neuronal excitability and connectivity. 3 The second hypothesis focuses on the role of cerebral insufficiency, resulting from low cardiac output, hypotension, embolism, and impaired cerebral vascular autoregulation, and secondary cellular metabolic stress. 4 Moreover, delirium has been associated with concomitant cardiac and neuronal injury, indicating a potential similar mechanism of underlying metabolic insufficiency.…”

“…4 Moreover, delirium has been associated with concomitant cardiac and neuronal injury, indicating a potential similar mechanism of underlying metabolic insufficiency. 3 After cardiac surgery, delirium remains the most common neurocognitive complication with an incidence of 6e46%. 5 Patients who have cardiac surgery are at higher risk of postoperative delirium than those following noncardiac surgery because of a higher prevalence of risk factors, such as older age, cerebrovascular disease, diabetes mellitus, and renal disease 6,7 and receipt of cardiopulmonary bypass.…”

The use of dexmedetomidine to prevent delirium after major cardiac and non‐cardiac surgery

“…Recent research showing that delirium is associated with neuronal (and cardiac) injury [12] and covert stroke [13] supports this as well as further research into the changes in brain activity. The other major theory is the ‘neuro‐inflammation hypothesis of delirium’ [12], which may explain more generally how systemic inflammatory insults can induce metabolic failure of the brain. Ultimately, it appears likely that neuro‐inflammation and metabolic impairment are intrinsically related in their roles in inducing delirium (Fig.…”

“…The first is the 'cerebral metabolic insufficiency hypothesis', which suggests that metabolic failure of the brain is the critical pathogenic step in delirium [11]. Recent research showing that delirium is associated with neuronal (and cardiac) injury [12] and covert stroke [13] supports this as well as further research into the changes in brain activity.…”

Mechanisms of Post-critical Illness Cardiovascular Disease

“…Importantly, the induction of NLRP3 assembly and pro-IL-1β (and pro-IL-18) production is dependent on a priming signal which in modern times might originate from persistent low grade systemic inflammation as occurs in obesity or aging, or indeed following a first-hit acute inflammatory insult such as surgery/trauma or early infection. Secretion of the proinflammatory cytokine IL-1β (and its IL-1 superfamily member IL-18) is thus intricately linked to cellular stress and regulated, necrosis-like cell death (pyroptosis) which may be partly responsible for myocardial injuries that are seen post-surgically and in association with sepsis and other critical illnesses (197,198). Although this implicates this pathway in pyroptosis, other forms of regulated cell-death (e.g., necroptosis) also implicated in cardiomyocyte death share a high degrees of cross-talk with it and may also be up or down-regulated (199).…”