Anesthetic-induced myocardial protection in cardiac surgery: relevant mechanisms and clinical translation

Cardiac surgery is still associated with complications such as adverse perioperative cardiovascular events. Over the past two decades, many studies have shown that volatile anesthetics and opioids provide myocardial protection against ischemia-reperfusion injury in a similar manner as ischemic conditioning. First (1–2 hours) and second (24–72 hours) windows of protection are provided, the underlying mechanisms for which involve activation of G-protein-coupled receptors, protein kinases, and the opening of adenosine triphosphate-sensitive potassium channels. These processes ultimately result in inhibition of the mitochondrial permeability transition pore. Post-conditioning can also be effective when treatment is applied in the proximity of reperfusion. Although propofol lacks these conditioning effects, it acts as a strong antioxidant and protects the myocardium by attenuating oxidative stress related to reperfusion injury. Clinical evidence favors the use of volatile anesthetics over propofol in terms of reduced cardiac enzyme release, length of hospital stay, and mortality. However, the existing evidence level is insufficient to draw a definite conclusion regarding the mortality benefit of one anesthetic over the others. In addition, many common clinical conditions, such as advanced age, hyperglycemia/diabetes, and hypertrophy, have been shown to mitigate the protective efficacy of the anesthetics, although this effect also lacks clinical validation. Propofol may also abolish the protective effects of volatile anesthetics and opioids by scavenging reactive oxygen species, an essential trigger for pre-conditioning. The following review addresses these issues from a clinical perspective.ope

Preoperative transcranial Doppler and cerebral oximetry as predictors of delirium following valvular heart surgery: a case-control study

Delirium is a frequent and serious complication after cardiac surgery with cerebral hypoperfusion as one from the key pathophysiological mechanisms. Middle cerebral artery (MCA) mean blood flow velocity (MFV) measured by transcranial Doppler has been used as a marker of cerebral perfusion, and cerebral oximetry (rSO2) value as a marker of its adequacy. This prospective observational trial examined the predictive value of MCA MFV and rSO2, measured immediately before induction of anesthesia, for delirium after valvular heart surgery in elderly patients. In 113 patients, delirium was evaluated for 7 days postoperatively, using the confusion assessment method for the intensive care unit. The primary endpoint was the occurrence of postoperative delirium. Overall, 16 patients (14%) exhibited delirium. MCA MVF values could not predict the development of delirium. Preoperative statin use, geriatric depression scale score, and low preoperative rSO2 (< 60%) showed association with delirium occurrence in univariable analysis. After multivariable analysis, only the low preoperative rSO2 (< 60%) (OR 6.748, 95% CI 1.647-27.652, P = 0.008) remained as an independent predictor of delirium. Preoperative MCA MFV was not significantly associated with delirium after valvular heart surgery in elderly patients, while a low baseline rSO2 value was associated with a sevenfold increased risk of delirium.restrictio

Ethyl pyruvate is renoprotective against ischemia-reperfusion injury under hyperglycemia

BACKGROUND: Hyperglycemia (HG) is common in cardiovascular surgeries due to diabetes, inflammation, and the neuroendocrine stress response. HG aggravates renal ischemia-reperfusion (I/R) injury through an increased inflammatory response, and blunts the protective effect of various measures. Ethyl pyruvate (EP) provides anti-inflammatory effects against I/R injury via inhibition of high-mobility group box 1 protein (HMGB1) release. This study aimed to determine the renoprotective effect of EP against I/R injury under HG. METHODS: Sprague-Dawley rats were randomly assigned at random to 8 groups: normoglycemia (NG)-sham, NG-I/R-control, NG-EP-I/R (pretreatment), NG-I/R-EP (posttreatment), HG-sham, HG-I/R-control, HG-EP-I/R, and HG-I/R-EP. Renal I/R was induced by 45 minutes of ischemia (clamping of renal arteries), followed by 24 hours of reperfusion. EP (50 mg/kg) was administered intraperitoneally at 1 h before ischemia (pretreatment) or on reperfusion (posttreatment). RESULTS: I/R injury under HG significantly aggravated the degree of renal tubular apoptosis and damage compared with the NG groups, which could be attenuated by both pretreatment and posttreatment of EP. I/R-induced increases in HMGB1 and Toll-like receptors (TLRs), activation of NF-kB, and resultant alterations in interleukin-1beta, tumor necrosis factor-alpha, proapoptotic Bax, and antiapoptotic Bcl-2 were all favorably modulated by EP treatment in both the NG and HG groups compared with their corresponding control groups. CONCLUSIONS: Despite aggravation of renal I/R injury by HG through amplified inflammation, EP administration showed similar suppression of the HMGB1-TLR-NF-kB pathway in the HG and NG groups. EP retained anti-inflammatory, antiapoptotic, and renoprotective effects in the HG groups, whether administered before ischemia or on reperfusion.restrictio

Chronic progression of cardiac surgery associated acute kidney injury: Intermediary role of acute kidney disease

Objective: The association between acute kidney injury (AKI) and chronic kidney disease (CKD) remains elusive in cardiac surgery. We investigated the association between postoperative AKI and CKD development, emphasizing the intermediary role of acute kidney disease (AKD), in patients undergoing valvular heart surgery. Methods: We assessed the occurrence of postoperative AKI (7 days postsurgery), AKD (3 months postsurgery), and CKD (12 months postsurgery) in 1386 patients. The primary outcome was the development of AKD and CKD according to AKI occurrence. Relevant risk factors of AKI, AKD, and CKD were identified through multivariable regression analysis. Results: AKI occurred in 23.9% of patients with normal preoperative renal function. Even with early recovery of renal function within 3 days, AKI increased the risk of AKD (odds ratio [OR], 3.21; 95% confidence interval [CI], 1.98-5.20, P < .001) and CKD (OR, 2.86; 95% CI, 1.68-4.86, P < .001), whereas persistent AKI further increased the risk of AKD (OR, 12.07; 95% CI, 5.56-26.21, P < .001) and CKD (OR, 10.54; 95% CI, 4.01-27.76, P < .001). We also found these relationships in patients with pre-existing renal dysfunction. Multivariable analysis identified 3-month postoperative heart failure and high right ventricular systolic pressure as independent risk factors for CKD. Conclusions: Even after early recovery, postvalvular heart surgery AKI was associated with increased risk of CKD via AKD in a graded manner related to AKI severity and persistence. Postoperative cardiac dysfunction assessed 3 months postsurgery also significantly influenced CKD development, indicating a need for close follow-up of cardiac and renal function to improve patient outcomes.restrictio