Cardiospecific sevoflurane treatment quenches inflammation but does not attenuate myocardial cell damage markers: a proof-of-concept study in patients undergoing mitral valve repair

Abstract

Nederlands Trial Register NTR2089.

Sevoflurane-enriched blood cardioplegia: the intramyocardial delivery of a volatile anesthetic

“…This can attenuate the systemic inflammation. 10 The observed comprehensive attenuation of systemic inflammation is in line with an earlier study of Nader and colleagues in patients undergoing coronary artery bypass grafting. 12,13 …”

“…In a previous proof-of-concept study, no beneficial effects on reducing postoperative markers of myocardial cell damage, plasma creatinine values, ventilation time or intensive care unit length of stay were observed. 10 Furthermore, we showed by controlling the pO 2 and pCO 2 levels within the normal range that the effect of adding sevoflurane to the cardioplegia solution is not the result of a higher oxygen concentration. …”

New therapy in cardioprotection

“…Although inflammatory markers were reduced in patients receiving intramyocardial sevoflurane, this did not extend to a reduction in markers of myocardial damage such as troponin T, creatinine kinase, and creatinine kinase-MB [34]. A comparison of sevoflurane, isoflurane, and desflurane found no significant difference in pediatric ventricular septal defect repairs, but all three were found to be superior to the placebo control group in reducing creatinine kinase-MB [33].…”

“…Anesthetic agents are known to have cardioprotective properties and their use in anesthetic preconditioning, has been widely studied in cardiac surgery [33,34].…”

Sevoflurane downregulates interleukin-6 and interleukin-8 levels in patients after cardiopulmonary bypass surgery: a meta-analysis

“…The results of this meta-analysis indicated that both IL-6 and IL-8 levels were decreased after CPB in sevoflurane-treated patients, confirming that inflammatory cytokines play important roles in myocardial ischemia reperfusion injury. One possible explanation might be that during CPB procedures, direct contact of blood with pipeline, ischemia/reperfusion, and other anesthesia and surgical factors might induce systemic inflammatory response at the surface-blood interface or during ischemic reperfusion, and lead to the production of inflammatory mediators (Xu et al, 2011;Kortekaas et al, 2014). The accumulation and activation of inflammatory mediators and neutrophils, in turn, play leading roles in increasing the pulmonary endothelial permeability; hence, damage to lung tissue structure is a critical event for initiating an pulmonary edema, atelectasis, or hypoxemia postoperatively (Grommes and Soehnlein, 2011;Muller-Redetzky et al, 2014).…”