Which patients with coronary artery disease should include oral nitrates on their discharge medication list?

BACKGROUND: Which patients with coronary artery disease (CAD) should have oral nitrates on their discharge medication list after coronary angiography (CAG)? To assess the relationship between oral nitrates included in the discharge medication list and major adverse cardiovascular events (MACEs) among CAD patients, we designed this retrospective cohort study. METHODS: A total of 2979 CAD patients hospitalised in the Department of Cardiology, Affiliated Hospital of Jining Medical University from May 2013 to October 2015 were enrolled, grouped according to whether oral nitrates were included at discharge after CAG, and followed up for MACEs for a mean of 4.42 years after discharge. The primary endpoint was MACEs. Multivariate Cox proportional hazards models were used to analyses potential confounding factors. Stratified analysis was used to observe the relationship between oral nitrates and MACEs by different covariates. RESULTS: The median follow-up time was 4.61 years, and 296 (9.94%) patients experienced MACEs. Multivariate Cox proportional hazards model analysis showed no association between oral nitrates on the discharge medication list and the occurrence of MACEs among patients with CAD (p > 0.05) after adjusting for some covariates, such as SYNTAX score (hazard ratio (HR): 1.18, 95% confidence interval (CI): 0.90-1.55, p = 0.2420). Stratified analysis revealed a higher incidence of MACEs among hypertensive patients prescribed oral nitrates at discharge (HR: 1.67, 95% confidence CI: 1.13-2.46, p = 0.0046). However, prescribing nitrates at discharge for patients with low uric acid levels increased the incidence of MACEs, which showed a possible trend towards significance (HR: 1.44, 95% CI: 0.99-2.09, p = 0.0525). CONCLUSION: There was no association between oral nitrates included in the discharge medication list and the development of MACEs among patients with CAD after adjusting for some covariates, such as SYNTAX score. Oral nitrates after discharge for CAD patients combined with hypertension increased the occurrence of MACEs. Oral nitrates after discharge for CAD patients combined with low uric acid levels may increase theoccurrence of MACEs, and close monitoring for any adverse events is recommended.

Predictive value of preoperative inflammatory indexes for postoperative early recurrence of hepatitis B-related hepatocellular carcinoma.

Objective: To investigate the predictive value of preoperative neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), systemic inflammation response index (SIRI), and systemic immune inflammation index (SII) for early recurrence after liver resection in patients with hepatitis B-related hepatocellular carcinoma. Methods: A retrospective study was conducted on 162 patients who underwent hepatitis B-related hepatocellular carcinoma (HCC) resection between January 2013 and April 2016. The Youden index was utilized to calculate the optimal cut-off value. The Pearson Chi-square test was applied to analyze the relationship between inflammatory indexes and common clinical and pathological features. The Kaplan-Meier method and Log-Rank test were implemented to compare the recurrence-free survival rate within 2 years of the population. The Cox regression analysis was used to identify the risk factors for early postoperative recurrence. Results: The best cut-off values of SIRI, PLR, NLR and SII were 0.785, 86.421, 2.231 and 353.64, respectively. Tumor diameter, degree of tumor differentiation, vascular invasion, SIRI>0.785, PLR>86.421, NLR>2.231 and SII>353.64 were risk factors for early recurrence. Combining the above seven risk factors to construct a joint index, the AUC of the joint prediction model was 0.804. The areas under the ROC curves of SIRI, PLR, NLR, and SII were 0.659, 0.725, 0.680, and 0.723, respectively. There was no significant difference in the predictive ability between the single inflammatory index models, but the predictive performance of the joint prediction model was significantly higher than that of the single inflammatory index models. The patients with lower SIRI, PLR, NLR, SII and joint index value had longer recurrence-free survival within 2 years. Conclusion: The joint index CIP, constructed by combining preoperative SIRI, PLR, NLP and SII with pathological features, can better predict the early recurrence of HBV-related HCC patients after surgery, which is beneficial in identifying high-risk patients and assisting clinicians to make better clinical choices.

Effects of emodin on Ca2+ signal transduction of smooth muscle cells in multiple organ dysfunction syndrome.

We have made several reports on the signal transduction mechanism that emodin enhance the calcium concentrations of smooth muscle cells (SMCs) in the physiological condition by inositol [1, 4, 5]-friphosphate (IP3). The observation that IP3 concentrations in SMCs were decreased in multiple organ dysfunction syndrome (MODS) prompted us to ask whether emodin can activate SMCs to contract by way of elevating [Ca2+] and thus modulating the critical Ca2+ signal transduction pathways involved in the contraction of the SMCs in the pathological setting of MODS. To test this hypothesis, we used the rat model of MODS to explore the potential roles of emodin in Ca2+ signal transduction in the SMCs of colon in rats. ML-7 [an inhibitor of myosin light-chain kinase (MLCK)] and Calphostin C [an inhibitor of protein kinase C (PKC)] were used to observe the influence of emodin on the muscle strips and SMCs in rats after MODS. Nifedipine (an antagonist of voltage-gated Ca2+ channel), EGTA (removal of extracellular Ca2+), heparine (a specific IP3 receptor antagonist), and ryanodine were used to probe the potential mechanisms involved in emodin-mediated elevation of the global cytoplasmic Ca2+ in SMCs of colon in the rats after MODS. Our results show that emodin is capable of contract the smooth muscles of colon in rats after MODS by MLCK increasing [Ca2+] of SMCs, and by PKC enhancing the calcium sensitivity of SMCs. The mechanism by which emodin triggers elevated [Ca2+] of smooth muscles of colon in rats after MODS is likely to operate through IP3 and RyR receptors in the sarcoplasm. It is hoped that deeper insights into how emodin modulates the critical calcium signaling in SMCs might lead to the potential development of emodin in the treatment of MODS.