BackgroundCardiac surgery patients often experience several types of tachyarrhythmias after admission to the intensive care unit (ICU), which increases mortality and morbidity. Dexmedetomidine (DEX) is a popular medicine used for sedation in the ICU, and its other pharmacological characteristics are gradually being uncovered.PurposeTo determine whether DEX has an antiarrhythmic effect after cardiac surgery.MethodsThe three primary databases MEDLINE, Embase (OVID SP) and the Cochrane Central Register of Controlled Trials (CENTRAL) were searched, and all English-language and randomized control-designed clinical publications comparing DEX to control medicines for sedation after elective cardiac surgery were included. Two colleagues independently extracted the data and performed other quality assessments. A subgroup analysis was performed according to the different medicines used and whether cardiopulmonary bypass (CPB) was applied. All tachyarrhythmias that occurred in the atria and ventricles were analyzed.ResultsA total of 1295 patients in 9 studies met the selection criteria among 2587 studies that were screened. After quantitative synthesis, our results revealed that the DEX group was associated with a lower incidence of ventricular arrhythmia (VA, OR 0.24, 95% CI 0.09–0.64, I2 = 0%, P = 0.005) than the control group. Subgroup analysis did not reveal a significant difference between the DEX and propofol subgroups (OR 0.13, 95% CI 0.03–0.56, I2 = 0%, P = 0.007). Additionally, no difference in the incidence of atrial fibrillation (AF) was observed regardless of the different control medicines (OR 0.82, 95% CI 0.60–1.10, I2 = 25%, P = 0.19) or whether CPB was applied.ConclusionsThis meta-analysis revealed that DEX has an antiarrhythmic effect that decreases the incidence of VA compared to other drugs used for sedation following cardiac surgery. DEX may not have an effect on AF, but cautious interpretation should be exercised due to high heterogeneity.
PurposeCardiac surgery patients always present with atrial fibrillation (AF) after admission to the intensive care unit, leading to high mortality and lengthy hospitalization. Dexmedetomidine (DEX) is a popular medication used for sedation in the intensive care unit; however, whether it can reduce AF needs to be analyzed.Materials and methodsThree primary databases, Medline, Embase (Ovid SP) and the Cochrane Central Register of Controlled Trials (CENTRAL), were searched. All English language and randomized control designed clinical publications comparing DEX to control medicines for sedation after elective cardiac surgery were included. Two independent colleagues conducted the data extraction and quality assessments. The subgroup analysis was performed according to the medicine used, age, AF history, and whether previous beta-blocker premedication and cardiopulmonary bypass (CPB) were applied. The overall incidence of AF was analyzed.ResultsA total of 1,295 patients in nine studies met the selection criteria among 2,587 studies screened from the database. After quantitative synthesis, our results revealed that the DEX group was not associated with a decreased incidence of AF compared with the placebo (risk ratio [RR] 0.76, 95% CI 0.37, 1.55, P=0.44) and morphine groups (RR 0.86, 95% CI 0.56, 1.31, P=0.48). Subgroup analysis also indicated that the DEX vs propofol comparison exhibited no difference: 1) for patients of age >60 years (P=0.69) or ≤60 years (P=0.69); 2) under CPB surgery (P=0.45) or without CPB surgery (P=0.88); 3) with beta-blocker premedication (P=0.32) or without beta-blocker premedication (P=0.90); and 4) with AF history (RR 1.07, 95% CI 0.85, 1.36, P=0.57) or without AF history (P=0.30).ConclusionThis meta-analysis revealed that DEX could not reduce the incidence of AF compared to control medicines following cardiac surgery. DEX may have an increased influence on AF occurrence if patients had a history of AF. However, cautious interpretation should be made due to high clinical heterogeneity.
Background: Myocardial ischaemia-reperfusion injury (IRI) has been confirmed to induce endoplasmic reticulum stress (ERS) when myocardial cell function continues to deteriorate to a certain degree. The clinical applications of effective tested strategies are sometimes inconsistent with the applications evaluated in experiments, although reasonable mechanisms and diverse signalling pathways have been broadly explored. Dexmedetomidine (DEX) has been shown to attenuate IRI of the heart in animal studies. This study aimed to determine whether DEX can protect injured cardiomyocytes under hypoxia/reoxygenation (H/R) at the cellular level and whether the mechanism is related to ERS and the p38 MAPK pathway. Methods: H9c2 cells were subjected to H/R or thapsigargin (TG) to build a model. DEX or 4-PBA was added to the medium either 1 h or 24 h before modelling, respectively. Model parameters were determined by assessing cell viability and injury, which were measured by assessing cell counting kit-8 (CCK8), lactate dehydrogenase (LDH) release and flow cytometry results, and the expression of GRP78, CHOP and caspase-12. In addition, the protein expression of p38MAPK and p-p38MAPK was examined, and SB202190, a negative regulator, was also preincubated in medium. Results: Compared to that of cells in the control group, the activity of cells in the H/R and TG groups was decreased dramatically, and the LDH concentration and proportion of apoptotic cells were increased. DEX could correspondingly reverse the changes induced by H/R or TG. Additionally, DEX effectively attenuated ERS defined as increased expression of GRP78, CHOP and caspase-12. Additionally, DEX could obviously depress the P38 MAPK phosphorylation and high p-p38 MAPK expression in the TG group, indicating DEX has a function similar to that of SB202190. Conclusion: H/R injury in H9c2 cells can lead to abnormal ERS and apoptosis, as well as activation of the p38MAPK signalling pathway. DEX can protect cardiomyocytes by intervening in ERS, regulating p38MAPK and the downstream apoptotic signalling pathway.
Myocardial ischemia-reperfusion injury (MIRI) has been confirmed to induce endoplasmic reticulum stress (ERS) during downstream cascade reactions after the sufficient deterioration of cardiomyocyte function. However, clinically outcomes have been inconsistent with experimental findings because the mechanism has not been entirely elucidated. Dexmedetomidine (DEX), an α 2 adrenergic receptor agonist with anti-inflammatory and organ-protective activity, has been shown to attenuate IRI in the heart. The present study aimed to determine whether DEX is able to protect injured cardiomyocytes under in vitro hypoxia/reoxygenation (H/R) conditions and evaluate the conditions under which ERS is efficiently ameliorated. The cytotoxicity of DEX in H9c2 cells was evaluated 24 h after treatment with several different concentrations of DEX. The most appropriate H/R model parameters were determined by the assessment of cell viability and injury with Cell Counting Kit-8 and lactate dehydrogenase (LDH) release assays after incubation under hypoxic conditions for 3 h and reoxygenation conditions for 3, 6, 12 and 24 h. Additionally, the aforementioned methods were used to assess cardiomyocytes cultured with various concentrations of DEX under H/R conditions. Furthermore, the degree of apoptosis and the mRNA and protein expression levels of glucose-regulated protein 78 (GRP78), C/EBP homologous protein (CHOP) and caspase-12 were evaluated in all groups. The addition of 1, 5 and 10 µM DEX to the cell culture significantly increased the proliferation of H9c2 cells by >80% under normal culture conditions. In the H/R model assessment, following 3 h of anoxia exposure, H9c2 cell viability decreased to 62.67% with 3 h of reoxygenation and to 36% with 6 h of reoxygenation compared with the control. The viability of H9c2 cells subjected to hypoxia for 3 h and reoxygenation for 3 h increased by 61.3% when pretreated with 1 µM DEX, and the LDH concentration in the supernatant was effectively decreased by 13.7%. H/R significantly increased the percentage of apoptotic cells, as detected by flow cytometry, and increased the expression levels of GRP78, CHOP and caspase-12, while treatment with either DEX or 4-phenylbutyric acid (4-PBA) significantly attenuated these effects. Additionally, despite the protective effect of DEX against H/R injury, 4-PBA attenuated the changes induced by DEX and H/R. In conclusion, treatment with 1 µM DEX alleviated cell injury, apoptosis and the increases in GRP78, CHOP and caspase-12 expression levels in H9c2 cells induced by 3 h of hypoxia and 3 h of reoxygenation.
Objective This study was performed to determine the effect of dexmedetomidine (DEX) administration on myocardial damage in cardiac surgery with sevoflurane postconditioning. Methods We retrospectively examined all cardiac valve replacement surgeries from 1 April 2016 to 30 April 2017. Eligible patients were divided into two groups based on whether DEX was infused. DEX infusion was permitted only between intubation and the beginning of cardiopulmonary bypass (CPB). Sevoflurane was inhaled via the standard postconditioning procedure starting at aortic declamping. The cardiac troponin I (cTnI) level was measured at different time points. The postoperative outcomes and complications were also analyzed. Results One hundred patients were included in the study (DEX group, n = 53; non-DEX group, n = 47). Increased cTnI levels were significantly correlated with the New York Heart Association classification, CPB time, and DEX use. DEX use and the CPB time were potential independent factors contributing to changes in the cTnI level. The cTnI level at 6, 12, and 24 hours postoperatively was remarkably lower in the DEX than non-DEX group by 1.14, 7.83, and 5.86 ng/mL, respectively. Conclusions DEX decreased the cTnI level after CPB when sevoflurane postconditioning was used, especially at 6, 12, and 24 hours postoperatively.
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