Sex Differences in Characteristics, Treatments, and In-hospital Outcomes of Patients Undergoing Coronary Angiography or Intervention.

Background: Whether women have a higher risk of adverse events compared with men following coronary angiography (CAG) and percutaneous coronary intervention (PCI) remains controversial. We aimed to investigate the sex differences in characteristics, treatments and outcomes among patients undergoing CAG and PCI in a large Chinese cohort. Methods: We analyzed patients undergoing CAG and/or PCI in this multi-center registry cohort study Cardiorenal ImprovemeNt II (CIN-II) in 5 Chinese tertiary hospitals from 2007 to 2020. Clinical characteristics, treatment (discharge medication and PCI) and in-hospital outcomes (mortality and major bleeding) were compared between women and men. Results: Totally 141,459 patients underwent CAG (44,362 [31.4%] women), of which 69,345 patients underwent PCI (15,376 [22.2%] women). Women were older (64.4 vs. 60.8 years), had more chronic comorbidities and lower PCI rate for stable coronary artery disease (CAD) than men (52.8 vs. 64.2%). Women received less CAG and PCI procedures. Among women undergoing PCI they received similar discharge medication treatment. In addition, women undergoing PCI had mildly lower rate of major bleeding (0.2 vs. 0.3%, P = 0.033) but higher in-hospital mortality (1.2 vs. 0.8%, P < 0.001). After adjustment, women had a higher risk in the major bleeding (adjusted odds ratio, 2.04 [95% CI: 1.07 to 3.62]), and the in-hospital mortality (adjusted odds ratio, 1.87 [95% CI: 1.36 to 2.56]). Conclusion: Among our Chinese cohort, women are older with more chronic comorbidities, receiving less PCI procedure and similar discharge medication treatment. Women have nearly 90% higher risk of in-hospital mortality and over 1-fold increased risk of major bleeding after PCI compared with men.

Honokiol Inhibits Atrial Metabolic Remodeling in Atrial Fibrillation Through Sirt3 Pathway.

Background and Purpose: Atrial metabolic remodeling plays a critical role in the pathogenesis of atrial fibrillation (AF). Sirtuin3 (Sirt3) plays an important role in energy homeostasis. However, the effect of Sirt3 agonist Honokiol (HL) on AF is unclear. Therefore, the aim of this study is to determine the effect of HL on atrial metabolic remodeling in AF and to explore possible mechanisms. Experimental Approach: irt3 and glycogen deposition in left atria of AF patients were examined. Twenty-one rabbits were divided into sham, P (pacing for 3 weeks), P + H treatment (honokiol injected with pacing for 3 weeks). The HL-1 cells were subjected to rapid pacing at 5 Hz for 24 h, in the presence or absence of HL and overexpression or siRNA of Sirt3 by transfection. Metabolic factors, circulating metabolites, atrial electrophysiology, ATP level, and glycogens deposition were detected. Acetylated protein and activity of its enzymes were detected. Key Results: Sirt3 was significantly down-regulated in AF patients and rabbit/HL-1cell model, resulting in the abnormal expression of its downstream metabolic key factors, which were significantly restored by HL. Meanwhile, AF induced an increase of the acetylation level in long-chain acyl-CoA dehydrogenase (LCAD), AceCS2 and GDH, following decreasing of activity of it enzymes, resulting in abnormal alterations of metabolites and reducing of ATP, which was inhibited by HL. The Sirt3 could regulate acetylated modification of key metabolic enzymes, and the increase of Sirt3 rescued AF induced atrial metabolic remodeling. Conclusion and Implications: HL inhibited atrial metabolic remodeling in AF via the Sirt3 pathway. The present study may provide a novel therapeutical strategy for AF.

[Acidic fibroblast growth factor promotes the growth of skeletal muscle satellite cells: experiment with rabbits].

OBJECTIVE: To explore if human recombinant acidic fibroblast growth factor (rhaFGF) can promote the proliferation of skeletal muscle satellite cells (MSCs). METHODS: MSCs were obtained from rabbits and cultured, and divided into 2 groups: rhaFGF group, treated with rhaFGF of the concentrations of 0, 5, 10, 20, 40, 60, and 80 microg/L, and rhaFGF + low molecular weight heparin (LMWH) group, treated with rhaFGF of different concentrations and LMWH of the terminal concentration of 10 mg/L. MTT method was used to observe the proliferation of the MSCs so as to determine the appropriate concentration to be used in the next experiment. Other MSCs were cultured and treated with the rhaFGF of the appropriate concentration and then LMWH of the terminal concentration of 10 mg/L was added to be co-cultured for 3 days. Flow cytometry was used to observe the cell cycle of the MSCs. RESULTS: rhaFGF of the concentrations 20 approximately 60 ng/ml promoted the proliferation of MSCs, and 40 ng/ml was selected as the best concentration to be used in the next experiment. Treated with the rhaFGF of the concentration of 40 ng/ml and LMWH for 3 days, the proportion of MSCs at the stage G(0)/G(1) was significantly lower and those at the stage S significantly higher in comparison with the control group (both P < 0.01), however, not significantly different from those of the rhaFGF group. CONCLUSION: rhaFGF promotes the proliferation of MSCs.

[Meta-analysis of association of deletion allele of angiotensin-converting enzyme gene with coronary heart disease in China].

OBJECTIVE: To qualitatively and quantitatively assess the evidence regarding the relation of ACE I/D polymorphism to coronary heart disease (CHD) risk. METHODS: Medline (January 1994 to February 2005) and China Hospital Knowledge Databases (January 1994 to May 2005) were retrieved for all publications relating to case-control studies reporting a link between CHD risk factors and the ACE I/D polymorphism. All 16 association studies were identified and a meta-analysis was conducted by using the RevMan 4.2 estimate for odds ratio (OR) to determine whether the DD genotype might predict the outcome in CHD. RESULTS: Sixteen out of 48 identified studies reporting data on 1345 CHD patients and 1286 matched controls fulfilled these inclusion criteria. The overall distribution of genotypes in the control subjects was 35.88% II, 40.86% ID, and 23.26% DD. The odds ratio for CHD for DD versus ID/II genotypes across all studies was 2.56 [95% CI, 2.09 - 3.13]. The relative CHD risk appeared to be increased with the D allele (chi(Trend)(2) = 97.12, P < 0.01). CONCLUSIONS: ACE gene I/D polymorphism should be associated with susceptivity of coronary heart disease in China. The CHD risk is increased significantly in individuals with DD genotypes. The ACE D allele should be a risk factor for CHD.

[The effects of 40 mg atorvastatin on serum lipids, inflammatory markers and clinical events in ACS patients post PCI].

OBJECTIVE: To assess the safety and effects of 40 mg atorvastatin on serum lipids, inflammatory markers and clinical events in ACS patients post PCI. METHODS: A total of 92 patients with ACS post successful PCI were randomly divided into atorvastatin 10 mg/d (group A) and atorvastatin 40 mg/d (group B) on top of the standard medical therapy. Blood were taken at baseline, 4, 12 and 24 weeks for serum alanine aminotransferase (ALT), lipids, high-sensitive C-reactive protein (hs-CRP) and matrix metalloprotease-9 (MMP-9) measurements. The major adverse cardiac events (MACE) were also observed. RESULTS: There was no significant difference in medication withdrawn (2 vs. 3 cases) due to increased ALT (3 times higher than normal) and incidence of MACE (5 vs. 7 cases) between the groups. TC and LDL were significantly reduced in both groups 4 weeks and thereafter post medication compared to pre-treatment (P < 0.05) and the reduction was more significant in group B than that in group A at 24 weeks post medication (P < 0.05) while TG and HDL remained unchanged. hs-CRP was significantly reduced at 12 and 24 weeks in both groups compared to baseline and the reduction was more significant in group B than that in group A at 24 weeks. MMP-9 was significantly reduced in both groups 4 weeks and thereafter post medication compared to pre-treatment (P < 0.05) and the reduction was more significant in group B than that in group A at 12 weeks post medication (P < 0.05). CONCLUSION: Both atorvastatin doses significantly reduced TC, LDL, hs-CRP and MMP-9 in ACS patients post PCI and the reduction was more significant in high dose atorvastatin group at 24 weeks while the MACE and drug withdraw rates were similar between the groups.