Relationship between the postoperative lactate dynamic levels, the acute gastrointestinal injury and the prognosis among patients who undergo surgical treatment for acute type A aortic dissection.

Introduction: This study aimed to determine the relationship between the postoperative lactate dynamic levels, the postoperative acute gastrointestinal injury (AGI), and the prognosis among the patients who underwent surgical treatment for an acute Stanford type-A aortic dissection (aTAAD). Methods: A total of 271 aTAAD patients were recruited and monitored. Of the 271 aTAAD patients, 29.2% developed an AGI and were designated as the AGI group (n = 79); the other patients (n = 192) were designated as the non-AGI group. According to the 2-year follow up, the aTAAD patients were also divided into the alive and death subgroups for further analysis. Results: Binary logistic regression analysis revealed that the postoperative 4-h lactate (P4L) level, time-to-return to the normal blood lactate level (TRNL), postoperative 16-h lactate (P16L) level, and neutrophil granulocyte (NEU) count had a good predictive value for an AGI after aTAAD. The 8-week and 2-year mortality rates were higher in the AGI group than the non-AGI group (P < 0.05). Basic data and clinical characteristics were significantly different between the alive and death groups (P < 0.05). A higher AGI rate and mortality occurred in the P4L level ≥10.15 mmol/L subgroup, TRNL ≥21-h subgroup, P16L level ≥2.95 mmol/L subgroup, NEU count ≥10.9 × 109/L subgroup, PaO2 < 77.7 mmHg subgroup, WBC count ≥9.58 × 109/L subgroup, and the operative time ≥427 min subgroup than the corresponding comparison subgroups (P < 0.05). The postoperative 0-h lactate (P0L) level, TRNL, postoperative 24-h lactate (P24L) level, D-dimer level, fibrinogen degradation products (FDP) level, duration of mechanical ventilation, and length of hospitalization were independent factors influencing the 30-day mortality rate in patients who underwent surgery for an aTAAD (P < 0.05). Cox regression multivariate analysis after univariate analysis of all-cause mortality showed the TRNL, postoperative 12-h lactate (P12L) level, P16L level, P24L level, D-dimer level, FDP level, and length of hospitalization were independently associated with the 2-year mortality rate in patients who underwent surgery for an aTAAD (P < 0.05). Conclusion: The postoperative lactate changes and TRNL effectively predicted postoperative AGI and the mortality rate in patients with who underwent surgery for an aTAAD. The TRNL and P24L level were independent risk factors for the 30-day and 2-year mortality rates in patients who underwent surgery for an aTAAD.

Serum CIRP increases the risk of acute kidney injury after cardiac surgery.

Introduction: Acute kidney injury (AKI) is a frequent perioperative complication. The underlying mechanisms of cardiac surgery-associated AKI are still not completely elucidated. Cold-induced RNA-binding protein (CIRP) has been subsequently found to be regulated by various stress conditions. During cardiac surgery and cardiopulmonary bypass (CPB), the host is subjected to hypothermia and inadequate organ perfusion, resulting in an upregulation of CIRP secretion. The aim of this study is to evaluate the role of elevated extracellular CIRP level as a contributing factor in the development of AKI. Methods: A total of 292 patients who underwent cardiac surgery were retrospectively enrolled and their serum samples were collected preoperative and postoperative. Demographic data, intraoperative data, in-hospital outcomes, and the occurrence of AKI were also collected for the patients. The correlation between CIRP and intraoperative procedures, as well as its association with postoperative outcomes were analyzed. Results: In multivariable analysis, higher ΔCIRP (p = 0.036) and body mass index (p = 0.015) were independent risk factors for postoperative AKI. Meanwhile, patients with postoperative AKI exhibited lower survival rate in 2-year follow-up (p = 0.008). Compared to off-pump coronary artery bypass grafting surgery, patients who underwent on-pump coronary artery bypass grafting, valve surgery, aortic dissection and other surgery showed higher ΔCIRP, measuring 1,093, 666, 914 and 258 pg/mL, respectively (p < 0.001). The levels of ΔCIRP were significantly higher in patients who underwent CPB compared to those who did not (793.0 ± 648.7 vs. 149.5 ± 289.1 pg/mL, p < 0.001). Correlation analysis revealed a positive correlation between ΔCIRP levels and the duration of CPB (r = 0.502, p < 0.001). Patients with higher CIRP levels are at greater risk of postoperative AKI (OR: 1.67, p = 0.032), especially the stage 2-3 AKI (OR: 2.11, p = 0.037). Conclusion: CIRP secretion increases with prolonged CPB time after cardiac surgery, and CIRP secretion is positively correlated with the duration of CPB. Cardiac surgeries with CPB exhibited significantly higher levels of CIRP compared to non-CPB surgeries. Elevation of CIRP level is an independent risk factor for the incidence of AKI, especially the severe AKI, and were associated with adverse in-hospital outcomes.

miR-197 Participates in Lipopolysaccharide-Induced Cardiomyocyte Injury by Modulating SIRT1.

Sepsis is a systemic inflammation and is capable of inducing myocarditis, which is a major leading cause of death in patients. Studies have found that miR-197 is correlated with the prognosis of patients with inflammatory heart disease, but its effect on sepsis-induced cardiomyocyte injury remains unclear. We treated H9c2 cells with lipopolysaccharide (LPS), then detected the cell viability via the cell counting kit-8 (CCK-8) assay and quantified miR-197 expression via quantitative real-time polymerase chain reaction (qRT-PCR). Then, we investigated the role of miR-197 in LPS-induced H9c2 cells by CCK-8 assay, flow cytometry, lactate dehydrogenase (LDH) measurement, enzyme-linked immunosorbent assay (ELISA), qRT-PCR, and western blot. Subsequently, silent information regulator 1 (SIRT1) was downregulated in H9c2 cells to explore its interaction with miR-197 under LPS induction. LPS induced miR-197 overexpression in H9c2 cells. LPS restrained viability, the expressions of B-cell lymphoma-2 (Bcl-2) and SIRT1, but promoted apoptosis, LDH release, and levels of interleukin-6 (IL-6), interleukin-1ß (IL-1ß), acetyl (AC)-p53, BCL2-associated X (Bax), and cleaved caspase-3 in H9c2 cells. miR-197 inhibition reversed the effects of LPS on H9c2 cells. The protective role of miR-197 downregulation in LPS-induced H9c2 cells was reversed by SIRT1 silencing. miR-197 contributed to LPS-induced cardiomyocyte injury by modulating SIRT1, which might be used as a molecular marker in the management of sepsis.

Serum Levels of lncRNA CCHE1 and TCF21 in Patients with Coronary Artery Disease and Their Clinical Significances.

OBJECTIVE: To detect serum level changes of CCHE1 and TCF21 in coronary artery disease (CAD) patients and to explore their clinical significances. Patients and Methods. A total of 150 CAD patients were divided into the mild lesion group (n = 52), moderate lesion group (n = 48), and severe lesion group (n = 50), respectively, according to the Gensini score. In addition, they were divided into single vessel lesion (n = 42), two vessel lesions (n = 49), and three vessel lesions group (n = 59), respectively. Serum levels of CCHE1 and TCF21 in CAD patients were detected by quantitative real-time polymerase chain reaction (qRT-PCR). Spearman's rank correlation was conducted to assess the relationship between levels of CCHE1 and TCF21 and severity and numbers of vessel lesions in CAD. Pearson's correlation test was used for analyzing the correlation between CCHE1 and TCF21 levels. A multivariable logistic regression test was performed to evaluate the influences of CCHE1 and TCF21 levels on CAD severity and the occurrence of cardiovascular events within 3 years of follow-up. RESULTS: Significant differences in incidences of diabetes and hypertension were identified in CAD patients divided according to CAD severity. In addition, significant differences in incidences of drinking, diabetes, and hypertension were identified in CAD patients divided according to numbers of vessel lesions. The serum level of CCHE1 was positively related to CAD severity and numbers of vessel lesions, while TCF21 displayed a negative relationship. During the 3-year follow-up, the incidence of cardiovascular events was 39.3% (59/150). CAD severity, numbers of vessel lesions, and serum levels of CCHE1 and TCF21 were independent factors influencing the occurrence of cardiovascular events in CAD patients. CONCLUSIONS: The increased serum level of CCHE1 and decreased TCF21 level are closely related to CAD severity, which are able to influence the prognosis in CAD patients.

RIP1/RIP3/MLKL Mediates Myocardial Function Through Necroptosis in Experimental Autoimmune Myocarditis.

Cardiomyopathy often leads to dilated cardiomyopathy (DCM) when caused by viral myocarditis. Apoptosis is long considered as the principal process of cell death in cardiomyocytes, but programmed necrosis or necroptosis is recently believed to play an important role in cardiomyocyte cell death. We investigated the role of necroptosis and its interdependency with other processes of cell death, autophagy, and apoptosis in a rat system of experimental autoimmune myocarditis (EAM). We successfully created a rat model system of EAM by injecting porcine cardiac myosin (PCM) and showed that in EAM, all three forms of cell death increase considerably, resulting in the deterioration of cardiac conditions with an increase in inflammatory infiltration in cardiomyocytes. To explore whether necroptosis occurs in EAM rats independent of autophagy, we treated EAM rats with a RIP1/RIP3/MLKL kinase-mediated necroptosis inhibitor, Necrostatin-1 (Nec-1). In Nec-1 treated rats, cell death proceeds through apoptosis but has no significant effect on autophagy. In contrast, autophagy inhibitor 3-Methyl Adenine (3-MA) increases necroptosis, implying that blockage of autophagy must be compensated through necroptosis. Caspase 8 inhibitor zVAD-fmk blocks apoptosis but increases both necroptosis and autophagy. However, all necroptosis, apoptosis, and autophagy inhibitors independently reduce inflammatory infiltration in cardiomyocytes and improve cardiac conditions. Since apoptosis or autophagy is involved in many important cellular aspects, instead of suppressing these two major cell death processes, Nec1 can be developed as a potential therapeutic target for inflammatory myocarditis.

Spontaneous rupture of hepatic epithelioid hemangioendothelioma: A case report.

Hepatic epithelioid hemangioendothelioma (HEH) is a rare tumor of vascular endothelial origin. Spontaneous rupture of HEH is a life-threatening complication and is extremely rare. HEH has variable malignant potential, and the clinical diagnosis remains challenging. Here we report a case of HEH with spontaneous rupture. A 44-year-old man presented with constant cutting pains over the right upper abdomen after eating. He had hemoptysis 11 d previously. Diagnostic abdominal puncture demonstrated active bleeding. Chest and abdominal computer tomography scan showed multiple ground-glass nodules over the lungs, multiple low-density intrahepatic nodules and massive hemorrhage. Transcatheter arterial embolization and exploratory laparotomy were performed and subsequent immunohistochemical examination confirmed a diagnosis of HEH.