Coronary Angiography Within 48 Hours Before Cardiac Surgery Increases the Risk of Postoperative Acute Kidney Injury.

BACKGROUND: Cardiac surgery and coronary examination, such as invasive coronary angiography (CAG), are both possibly associated with acute kidney injury (AKI). Preoperative CAG examination and cardiac surgery within a short interval may increase the incidence of AKI. METHODS: We retrospectively reviewed 1112 patients who underwent CAG examination within 30 days prior to the cardiac operation in this study. Postoperative AKI was defined, according to Kidney Disease Improving Global Outcomes Definition and Staging (KDIGO) criteria. RESULTS: The total incidence of AKI was 40.8% and cystatin C level was 1.260 (1.028, 1.672) mg/L. For patients who received CAG, age, body mass index, cardiopulmonary time, and the time interval between preoperative CAG examination and cardiac operation within 48h was shown to be independent predictors of postoperative AKI. The incidence of AKI in patients undergoing preoperative CAG within 48h was 11.2% higher than in those more than 48h (P < 0.001). Patients undergoing valve surgery with or without coronary artery bypass grafting (CABG) exhibited a higher AKI risk than those only accepting CABG. The in-hospital stay of patients who developed AKI was 2 days longer than those without AKI. However, undergoing CAG within 48h prior to cardiac operation did not prolong ICU length of stay or hospital length of stay, nor did it increase the risk of death or renal failure after an operation. CONCLUSION: Undergoing CAG within 48 hours before cardiac surgery increases the risk of postoperative AKI.

Surgical Treatment of Primary Cardiac Paragangliomas: A Single-Center Experience.

BACKGROUND: Cardiac paragangliomas are rare neuroendocrine tumors that will cause significant morbidity if left undiagnosed. Because of the paucity of cohort data, their rapid diagnosis and appropriate management still pose unique challenges to cardiac surgeons. We aimed to investigate the clinical features and surgical management of primary cardiac paragangliomas in our single center. METHODS: From May 2014 to October 2020, patients diagnosed with primary cardiac paragangliomas retrospectively were reviewed. Demographic data, clinical presentation, preoperative imaging methods, surgical resection, perioperative management, histological analysis, and outcomes were recorded. Postoperative follow up also was reviewed. RESULTS: With multiple imaging methods, including echocardiography, computed tomography, positron-emission tomographic-computed tomography, and biochemical tests, there were five cases of primary cardiac paraganglioma verified by postoperative immunohistochemical staining, two of which were hormonally active. There were no metastatic cardiac paragangliomas, according to positron-emission tomographic-computed tomography, and all patients accepted surgical treatment. Preoperative adrenoceptor blockade was given to hormonally active patients, accordingly. Complete resection of the tumor was accomplished under cardiopulmonary bypass in each case. Tumor distribution included two masses on the roof of the left atrium, two masses in the right atrioventricular groove, and one between the ascending aorta and main pulmonary artery. Immunohistochemical staining for chromogranin, neuron-specific enolase, synaptophysin, and S-100 were positive, which were typical of cardiac paraganglioma. There were no operative deaths. All the patients had an uneventful recovery except one patient who underwent low cardiac output syndrome. During follow up (mean 4.2 years, range 0.6-7.0 years), all patients were well with New York Heart Association class I or II. Only one patient developed thyroid carcinoma three years after surgery but with no paraganglioma recurrence during periodic computed tomography, and this patient recovered well after thyroidectomy. CONCLUSION: Although cardiac paragangliomas are rare and may present surgical challenges for clinicians, surgical resection remains the choice of treatment with favorable outcomes through a multidisciplinary heart team. Moreover, lifelong surveillance still is recommended to detect possible recurrence or associated nonchromaffin tumors in time.

The protective effects of L-carnitine on myocardial ischaemia-reperfusion injury in patients with rheumatic valvular heart disease undergoing CPB surgery are associated with the suppression of NF-κB pathway and the activation of Nrf2 pathway.

Myocardial ischaemia-reperfusion injury (MIRI) is a main pathophysiologic change following CPB surgery. L-carnitine, a natural amino acid, is able to transport fatty acids for generating energy and has a protective effect on MIRI. We aim to investigate the protective effect of L-carnitine on MIRI in patients with rheumatic valvular heart disease (RVHD) performed CPB surgical operation and the underlying mechanism. In this study, patients were randomized to three groups. L-carnitine was added to the crystalloid cardioplegic solution for experimental group 1 (6 g/L) and experimental group 2 (12 g/L), whereas no L-carnitine was used in the control group. Our results showed that L-carnitine significantly attenuated myocardial injury after surgery in these patients. L-carnitine decreased serum markers of myocardial injury including CK-MB, cTnI, hs-cTnT and IMA. L-carnitine increased left ventricular ejection fraction (LVEF) but reduced wall motion score index (WMSI) after operation. L-carnitine also inhibited myeloperoxidase (MPO) activity and inflammatory cytokines in the myocardium of patients after unclamping the aorta. Additionally, L-carnitine increased levels of superoxide dismutase (SOD) and catalase (CAT) while decreased levels of malondialdehyde (MDA) and protein carbonyl content in the myocardium of patients after unclamping the aorta. Moreover, L-carnitine suppressed the activation of nuclear factor kappa B (NF-κB) and activated nuclear factor erythroid 2-related factor 2 (Nrf2). There was also no significant difference in these indices between two experimental groups after unclamping the aorta. Taken together, L-carnitine had a protective effect against CPB-induced MIRI in patients with RVHD, which might be related to its modulation of NF-κB and Nrf2 activities.

CTRP9 Ameliorates Pulmonary Arterial Hypertension Through Attenuating Inflammation and Improving Endothelial Cell Survival and Function.

Endothelial dysfunction and inflammation are believed to be 2 primary instigators of pulmonary arterial hypertension (PH). C1q/TNF-related protein 9 (CTRP9) plays important roles in anti-inflammation and improvement of epithelial function. However, the role of CTRP9 in the progression of PH remains still unclear. In this study, the role and mechanism of CTRP9 in the PH progression were explored. First, serum CTRP9 contents and CTRP9 mRNA expression in the pulmonary artery epithelial cells from patients with PH were detected. Our data on enzyme-linked immunosorbent assay and real-time quantitative Polymerase Chain Reaction showed that CTRP9 mRNA and protein content were markedly downregulated in the patients with PH. Then the pcDNA-CTRP9 expression vector or CTRP9 siRNA was transfected into the primary pulmonary artery epithelial cells from the patients with PH in vitro. CTRP9 overexpression significantly improved endothelial NOS protein expression and reduced the secretion of endothelin-1 (ET-1) and matrix metalloproteinase-2 (MMP-2), whereas knockdown of CTRP9 sharply reduced eNOS protein expression and promoted the secretion of ET-1 and MMP-2 in the cultured human epithelial cells. Moreover, the levels of phosphatidylinositol 3-kinase (PI3K) and pAkt were reduced in the epithelial cells and CTRP9 overexpression activated the PI3K/Akt pathway. CTRP9 could inhibit cell apoptosis and eNOS expression reduction in the cells pretreated with the PI3K/Akt inhibitor LY294002 and resist LY294002-induced ET-1 and MMP-2 secretion. Finally, to verify the role of CTRP9 in the progression of PH in vivo, the pcDNA-CTRP9 expression vector or CTRP9 siRNA was intravenously injected into rats with PH. Pulmonary arterial pressures of the rats were notably reduced by the pcDNA-CTRP9 injection and elevated by the CTRP9 siRNA injection. In conclusion, CTRP9 ameliorated PH by attenuating inflammation and improving endothelial cell survival and function.

Myocardial Protective Effects of L-Carnitine on Ischemia-Reperfusion Injury in Patients With Rheumatic Valvular Heart Disease Undergoing Cardiac Surgery.

OBJECTIVES: The authors used L-carnitine as an ingredient in cardioplegic solution during valve replacement surgery to investigate the protective effect of L-carnitine on myocardial ischemia-reperfusion injury (MIRI) and its possible mechanism. DESIGN: Prospective, randomized study. SETTING: A tertiary-care hospital. PARTICIPANTS: The study comprised 90 patients undergoing valve replacement under cardiopulmonary bypass. INTERVENTIONS: Patients were divided randomly into 3 groups. L-carnitine was added to the crystalloid cardioplegic solution for experimental group 1 (3 g/L) and experimental group 2 (6 g/L), whereas no L-carnitine was used in the control group. The remainder of the treatment was identical for all 3 groups. MEASUREMENTS AND MAIN RESULTS: Serum was collected from each patient 1 hour before the surgery and at 2, 6, 24, and 72 hours after unclamping the aorta, and tissue samples were obtained before cardiac arrest and after unclamping the aorta. The postoperative levels of serum aspartate aminotransferase, creatine kinase, creatine kinase-MB isozyme, and lactic acid dehydrogenase and the apoptotic index were all lower in the 2 experimental groups than those in the control group. In addition, each of the aforementioned serum enzyme levels and the apoptotic index in all 3 groups significantly increased after unclamping the aorta compared with baseline levels taken before surgery. Bcl-2 expression was higher and Bax was lower in the 2 experimental groups compared with those of the control group after unclamping the aorta. However, there was no significant difference in all the postoperative indices between the 2 experimental groups. CONCLUSION: L-carnitine may reduce cardiopulmonary bypass-induced myocardial apoptosis through modulating the expressions of Bcl-2 and Bax, resulting in a protective effect from MIRI.

Association of biomarkers related to preoperative inflammatory and coagulation with postoperative in-hospital deaths in patients with type A acute aortic dissection.

The aim of this study was to analyze the role of blood biomarkers regarding preoperative inflammation and coagulation in predicting the postoperative in-hospital mortality of patients with type A acute aortic dissection (AAD). A total of 206 patients with type A AAD who had received surgical treatment were enrolled in this study. Patients were divided into two groups: the death group (28 patients who died during hospitalization) and the survival group (178 patients). Peripheral blood samples were collected before anesthesia induction. Preoperative levels of D-dimer, fibrinogen (FIB), platelet (PLT), white blood cells (WBC) and neutrophil (NEU) were compared between the two groups. Univariable and multivariable logistic regression analysis were utilized to identify the independent risk factors for postoperative in-hospital deaths of patients with type A AAD. Receiver operating characteristic (ROC) curve were used to analyze the predictive value of these indices in the postoperative in-hospital mortality of the patients. Univariable logistic regression analysis showed that the P values of the five parameters including D-dimer, FIB, PLT, WBC and NEU were all less than 0.1, which may be risk factors for postoperative in-hospital deaths of patients with type A AAD. Further multivariable logistic regression analysis indicated that higher preoperative D-dimer and WBC levels were independent risk factors for postoperative in-hospital mortality of patients with type A AAD. ROC curve analysis indicated that application of combining FIB and PLT could improve accuracy in prediction of postoperative in-hospital mortality in patients with type A AAD. Both preoperative D-dimer and WBC in patients with type A AAD may be used as independent risk factors for the postoperative in-hospital mortality of such patients. The combination of FIB and PLT may improve the accuracy of clinical prognostic assessment.

Tetrandrine suppresses metastatic phenotype of prostate cancer cells by regulating Akt/mTOR/MMP-9 signaling pathway.

Tetrandrine (TET), a bisbenzylisoquinoline alkaloid found in traditional Chinese medicines, exerts anticancer activity in vitro and in vivo. However, its potential role in the prostate cancer metastatic process has not yet been elucidated. Thus, we investigated the inhibition effect of tetrandrine on prostate cancer migration and invasion and the corresponding molecular basis underlying its anticancer activity. Cell migration and invasion were determined using the Transwell chamber model. The protein expression of Akt, phosphorylated Akt, the mammalian target of rapamycin (mTOR), phosphorylated mTOR and matrix metalloproteinases 9 (MMP-9) was detected by western blot in the presence or absence of tetrandrine or in the group tetrandrine combination with LY294002 (inhibitor of Akt) and rapamycin (inhibitor of mTOR). Our studies showed that excluding the effect of tetrandrine on cell proliferation, tetrandrine significantly inhibited cell migration and invasion in prostate cancer DU145 and PC3 cells. Furthermore, tetrandrine decreased the protein levels of p-Akt, p-mTOR, and MMP-9. While the inhibition of Akt or mTOR by the respective inhibitors could potentiate this effect of tetrandrine on prostate cancer cells, the studies indicate that tetrandrine inhibits the metastasis process by negatively regulating the Akt/mTOR/MMP-9 signaling pathway. These results suggest that tetrandrine might serve as a potential metastasis suppressor to treat cancer cells that have escaped surgical removal or that have disseminated widely.