Observation of Bleeding and MACCE Events in Patients with Liver Cirrhosis Complicated with Acute Coronary Syndrome after Antiplatelet Therapy.

OBJECTIVE: To evaluate the efficacy and safety of dual antiplatelet therapy (DATP) in subjects with Child-pugh class A cirrhosis complicated with acute coronary syndrome (ACS) after coronary Drug-eluting stent (DES) implantation. STUDY DESIGN: Observational study. Place and Duration of the Study: Department of Cardiology, Beijing You 'an Hospital, Capital Medical University, China, from January to August 2021. METHODOLOGY: Cirrhotic patients with ACS after DES were divided into an early cirrhosis group (n=90) and a non-cirrhosis group (n=66). They underwent monthly follow-ups for 12 months, and DATP was administered with acetylsalicylic acid and clopidogrel in standard doses. The endpoints included efficacy endpoints (Major Adverse Cardiovascular and Cerebrovascular Events, MACCE) and safety endpoints (bleeding events). Endpoint events were calculated. Cox regression model and Kaplan-Meier survival curve were used to analyse the correlation between the two groups. RESULTS: The overall frequency of five indicators was higher in the early cirrhosis group, including increased heart rate (HR), abnormal renal function, abnormal liver function, thrombocytopenia, and coronary multivessel disease (84.5% vs. 51.6%, all p<0.05). Kaplan-Meier survival analysis showed no significant difference between early cirrhosis and non-cirrhosis groups (p=0.688 for MACCE, p=0.960 for bleeding events). Multivariate Cox regression analysis also showed no statistical difference between the early cirrhosis group and the non-cirrhosis group (p=0.642 for MACCE, p=0.720 for bleeding events). CONCLUSION: In patients of ACS with early cirrhosis, 12 months of DAPT may be effectively and safely reduced MACCE after implantation of DES. KEY WORDS: Acute coronary syndrome, Liver cirrhosis, Dual antiplatelet therapy, Major adverse cardiovascular and cerebrovascular events.

Vitexin suppresses renal cell carcinoma by regulating mTOR pathways.

BACKGROUND: Renal cell carcinoma (RCC) is one of the most common malignant tumors in the world. Vitexin (apigenin-8-C-D-glucopyranoside), a bioactive compound isolated from a variety of plants, has multiple protective effects on human health. The purpose of this study was to investigate the role of vitexin in RC and the related molecular mechanism. METHODS: Proliferation was tested with Cell Counting Kit-8 and Edu staining. Apoptosis was studied with flow cytometry. Immunofluorescent was applied to show LC3 spots. BALB/c nude mice bearing ACHN cells were established and immunohistochemical staining was applied to validate the in vivo effects of vitexin. All the effects and possible signaling pathways involved were validated with western blotting. RESULTS: Seventy micromole of vitexin started to show significant effect on the growth of normal renal tubular epithelial cells (HK-2), so 0, 10, 20 and 40 µM of vitexin were used in later experiments. Vitexin inhibited growth and induced apoptosis of ACHN and OS-RC-2 cells in a dose-dependent manner, and promoted excessive autophagy by reducing p62 levels and increasing Beclin1 and LC3II levels. Western blotting revealed that vitexin significantly increased the phosphorylation levels of Adenosine Monophosphate Activated Protein Kinase (AMPK) and c-Jun N-terminal kinase (JNK) in ACHN and OS-RC-2 cells, while decreasing the phosphorylation levels of phosphatidylinositol 3-kinase/activates protein kinase/mammalian target of rapamycin (PI3K/AKT/mTOR). In BALB/c nude mice bearing ACHN cells, vitexin inhibited tumor growth, reduced Ki67 and increased caspase-3 levels in the tumor tissues. CONCLUSIONS: The results indicated that the tumor suppressive role of vitexin in ACHN and OS-RC-2 cells involved AMPK/mTOR, PI3K/AKT/mTOR, and JNK pathways. Therefore, vitexin may be a promising drug for the treatment of RCC.

Uremia and thrombotic microangiopathy: conditions that may havethe same manifestation.

In this article, we present the case of a man with uremia. Laboratory testing revealed thrombocytopenia, erythrocyte fragmentation, elevated lactate dehydrogenase, and malignant hypertension, manifestations that are similar to thrombotic microangiopathy (TMA). Thromboasthenia, manifested as a decrease in the platelet aggregation rate, was also noted. Regular hemodialysis (3 times per week) improved the patient's thrombocytopenia and thromboasthenia. This case supports the conclusion that uremic toxin, which can be removed by hemodialysis, inhibits the quantity and quality of platelets. We believe that the platelet aggregation rate can be a useful tool in distinguishing uremia from TMA.