Safety and efficacy of using Judkins left 3.5 guiding catheters for transradial right coronary artery intervention.

OBJECTIVE: There is limited data about the use of a Judkins left (JL) 3.5 guiding catheter for routine transradial right coronary artery (RCA) percutaneous coronary intervention (PCI). This study investigated the safety and efficacy of JL3.5 for RCA PCI. PATIENTS AND METHODS: Patients with acute coronary syndrome (ACS) who underwent transradial RCA PCI between November 2019 and November 2020 at the Second Hospital of Shandong University were included. The study retrospectively compared JL 3.5 vs. other routine guiding catheters (GCs), including Judkins right (JR) 4.0 and Amplatz (left). Logistic multivariable analysis was used to analyze the factors associated with transradial RCA PCI success rate, in-hospital complications, and extra support. RESULTS: The study included 311 patients: 136 in the routine GC group and 175 in the JL 3.5 group. There were no significant differences between the two groups regarding in-hospital complications, extra support technics, or success. The multivariable analyses showed that coronary chronic total occlusion (CTO) was negatively associated with intervention success (OR = 0.06, 95% CI: 0.016-0.248, p < 0.001) but positively with extra support (OR = 8.74, 95% CI: 1.518-50.293, p = 0.015). Tortuosity was associated with extra support (OR = 16.50, 95% CI: 3.324-81.589, p = 0.001). In the JL 3.5 group, the left ventricular ejection fraction (OR = 1.11, 95% CI: 1.03-1.20, p = 0.006), CTO (OR = 0.07, 95% CI: 0.008-0.515, p = 0.009), and tortuosity (OR = 0.17, 95% CI: 0.03-0.95, p = 0.043) were independently associated with intervention success. CONCLUSIONS: JL 3.5 appears to be as safe and effective as the JR 4.0 and Amplatz (left) catheters for RCA PCI. When using the JL 3.5 catheter for RCA PCI, heart function, CTO, and tortuosity should be considered.

Decreased serum SIRT6 as a novel predictor of coronary artery disease.

OBJECTIVE: SIRT6 is an NAD-dependent histone deacetylase known to regulate aging, inflammation and energy metabolism, and might play an important role in atherosclerosis. However, whether it also plays a role in coronary artery disease (CAD) remains unclear. PATIENTS AND METHODS: In this study, we detected the expression of SIRT6 in serum by Western blotting. The concentrations of SIRT6 in serum specimens from 69 patients with CAD [30 with stable angina (SA) and 39 with acute coronary syndrome (ACS)] and 16 controls were analysed using the enzyme-linked immunosorbent assay (ELISA) method. RESULTS: Western blotting analysis of the serum samples found that SIRT6 expression was decreased in the SA group (p=0.000) and ACS group (p=0.000) compared with the control group. Significantly lower levels of serum SIRT6 were observed in SA patients (18.80±9.14 ng/mL) and ACS patients (16.85±9.66 ng/mL) than in healthy controls (25.79±14.23 ng/mL). SIRT6 concentrations were positively correlated with other markers of CAD, such as high-density lipoprotein cholesterol (r=0.362, p<0.01) and age (r=0.265, p<0.05), and negatively correlated with blood glucose (r=-0.284, p<0.05). Multivariate logistic regression analysis demonstrated that lower SIRT6 levels were independently associated with the presence of CAD in men (OR=0.817, 95% CI 0.694-0.962, p=0.015). Receiver operating characteristic (ROC) curve analysis showed that lower serum SIRT6 could distinguish CAD patients (AUC, 0.726; 95% CI, 0.508-0.943; p=0.041) from controls. SIRT6 is found downregulated in blood vessels of atherosclerotic APOE-/- mice and human aorta arteries. CONCLUSIONS: We demonstrated that SA and ACS patients had lower serum concentrations of SIRT6. The decreased serum SIRT6 level was independently associated with the diagnosis of CAD. SIRT6 may play a cardioprotective role in CAD patients, and future research is required to address this issue.

Androgen receptor inhibition alleviated inflammation in experimental autoimmune myocarditis by increasing autophagy in macrophages.

OBJECTIVE: Experimental autoimmune myocarditis (EAM) is characterized by pronounced macrophage infiltration, cardiac necrosis, and cardiac fibrosis. Our previous studies have demonstrated that suppressed androgen receptor (AR) enables anti-inflammation to promote tissue repair by decreasing M1 macrophages and increasing M2 macrophages in an EAM model. Given that autophagy mediates inflammatory response in macrophages, we investigated whether AR inhibition executes its protective role in inflammation through the autophagy pathway in EAM. MATERIALS AND METHODS: To determine whether AR inhibition can perform its anti-inflammatory effects by upregulating autophagy, we pre-treated mice with 3-methyl adenine (3-MA), a pharmacological inhibitor of autophagy. Immunofluorescence assay and Western blot were used to detect autophagy levels and autophagy activity in five different groups. Immunofluorescence marked F4/80 and LC3 to illustrate the autophagy level in macrophages. TUNEL assays were used to detect the apoptosis level in heart tissue of five different groups. RESULTS: We demonstrated that AR inhibition resolves injury with sustained inhibition of inflammatory cytokines associated with enhanced autophagy, especially in macrophages. Increased LC3II/I expression corroborated complete autolysosome formation detected by electron microscopy and correlated with degradation of SQSTM1/p62 in the AR inhibition group by Western blot. These effects could be reversed within 3-MA, a pharmacological inhibitor of autophagy. Specifically, pharmacological inhibition of autophagy increased apoptosis and inflammation, which could be attenuated by AR inhibition. CONCLUSIONS: AR inhibition alleviates the inflammatory response and tissue apoptosis by enhancing autophagy, especially in macrophages.

Clinical significance of miR-492 in peripheral blood of acute myocardial infarction.

OBJECTIVE: To detect the potential of microRNA-492 (miR-492) as a diagnostic biomarker of acute myocardial infarction (AMI) in the acute phase. PATIENTS AND METHODS: A total of 100 AMI patients and 100 controls (non-AMI patients with chest pain) were retrospectively analyzed. Blood samples were collected at 0, 6, 12, and 24 h after admission, followed by detection of the serum miR-492 level. Serum levels of cTnI and creatine kinase-MB (CK-MB) in AMI patients were examined by enzyme-linked immunosorbent assay (ELISA). The potential relationship between miR-492 level with cTnI and CK-MB levels was analyzed by Pearson correlation test. Moreover, diagnostic value of miR-492 was assessed by depicting receiver operating characteristic (ROC) curves. RESULTS: Serum level of miR-492 achieved the peak at 6 h after admission, which was time-dependently reduced at 12 h and 24 h.  Serum levels of cTnI and CK-MB were higher in AMI patients than those of controls. However, miR-492 level achieved the peak before cTnI and CK-MB increased to the highest levels. MiR-492 level was positively correlated to cTnI and CK-MB levels. ROC curves verified the diagnostic value of miR-492 in AMI (AUC=0.8621, 95% CI=0.8129-0.9112, sensitivity=80%, specificity=75%). CONCLUSIONS: Serum level of miR-492 remarkably increases in the acute phase of AMI, which may be used as an effective biomarker for diagnosing AMI.