Feasibility of Distal Radial Access for Coronary Angiography and Percutaneous Coronary Intervention: A Single Center Experience.

OBJECTIVE: Asymptomatic radial artery occlusion remains the most common complication in transradial coronary interventional procedure. To prevent radial artery occlusion, distal transradial access (dTRA) has been suggested recently. In this article, we aim to describe our experience and to assess feasibility and safety of this new access site for routine coronary angiography (CAG) and percutaneous coronary intervention (PCI). METHODS: We retrospective analyzed 1,063 consecutive patients who were assigned to undergo CAG or procedural PCI through dTRA between 1 January 2018 and 31 December 2019 at Affiliated Zhongshan Hospital of Dalian University. The size of radial sheath used was 5 or 6 French. The sheath was removed at procedure termination, and hemostasis was obtained by compression bandage with gauze. The success rate of dTRA access defined by successful radial artery cannulation on the first dTRA side attempted, the cause of access failure, the hemostasis duration, the incidence of post-catheterization radial artery occlusion, and the other access-related complications including hematoma of forearm and thumb numbness were assessed. RESULTS: Radial artery cannulation via dTRA was successful in 953 of 1,063 patients with a success rate of 89.7%. Mean age of successful cases was 64.6 ± 11.2 years (26-94 years) with 339 (35.6%) women. A total of 363 (38.1%) cases were PCI. Among them, 95 cases (10%) underwent urgent PCI, including primary PCI in 64 patients with ST-segment elevation myocardial infarction and immediate PCI (<2 h from hospital admission) in 31 patients with very high-risk non-ST-segment elevation acute coronary syndrome. A total of 269 (28.2%) cases were via left dTRA. The 6 French sheath was used in 602 (63.2%) cases. Hemostasis was obtained within 2 h in 853 (89.5%) patients. There were 110 (10.3%) procedural failures: 59 (5.6%) cases of artery puncture failure, 49 (4.9%) cases of guide wire insertion failure, and 2 (0.2%) cases of sheath insertion failure. Complications potentially related to distal radial access included radial artery occlusion at the access site (13 cases, 1.4%), forearm radial artery occlusion (4 cases, 0.4%), hematoma of forearm (5 cases, 0.5%), and transient thumb numbness (2 cases, 0.2%). CONCLUSION: dTRA is a feasible and safe access and can be used as a rational alternative to traditional radial access for routine coronary interventional procedure.

Pharmacological inhibition of EZH2 by GSK126 decreases atherosclerosis by modulating foam cell formation and monocyte adhesion in apolipoprotein E-deficient mice.

Histone modifications play an important role in the occurrence and development of atherosclerosis in human and atherosclerosis-prone mice. Histone methylation in macrophages, monocytes and endothelial cells markedly influence the progression of atherosclerosis. However, it remains unclear whether treatment with a histone methyltransferase enhancer of zeste homolog 2 (EZH2) inhibitor may suppress atherosclerosis. The present study aimed to determine the effects of the EZH2 inhibitor, GSK126, on the suppression and regression of atherosclerosis in apolipoprotein E-deficient mouse models. In vitro, it was found that pharmacological inhibition of EZH2 by GSK126 markedly reduced lipid transportation and monocyte adhesion during atherogenesis, predominantly through increasing the expression levels of ATP-binding cassette transporter A1 and suppressing vascular cell adhesion molecule 1 in human THP-1 cells. In vivo, it was found that atherosclerotic plaques in GSK126-treated mice were significantly decreased when comparing with the vehicle-treated animals. These results indicated that the GSK126 has the ability to attenuate the progression of atherosclerosis by reducing macrophage foam cell formation and monocyte adhesion in cell and mouse models. In conclusion, the present study provided new insights into the molecular mechanism behind the action of GSK126 and suggested its therapeutic potential for the treatment of atherosclerosis.

The Relationship Between Chronic Kidney Disease and the Severity and Long-Term Prognosis of Patients with Coronary Artery Disease After Drug-Eluting Stent Implantation.

OBJECTIVE: To investigate the relationship between chronic kidney disease (CKD) and the severity and long-term prognosis of patients with coronary artery disease (CAD) after drug-eluting stent (DES) implantation. METHODS: There were 814 patients, who consecutively received a DES implantation, selected for this study. They were divided into two groups, according to whether or not they suffered CKD. There were 254 cases in the CKD group (31.2%), while there were 560 cases (68.8%) in the control group. The clinical characteristics, coronary artery lesions, and major adverse cardiac and cerebrovascular events (MACCE) of the two groups were compared, and the relationship between risk factors and MACCEs was analyzed by multivariate logistic regression. RESULTS: Compared with the control group, the CKD group had more severe coronary artery stenosis, expressed as the more diseased arteries (2.15 ± 0.82 vs 1.87 ± 0.83, p = 0.001), a high incidence of three diseased arteries (42.0% vs 28.3%, p = 0.001), and a higher Gensini score [37 (18.6, 66) vs 27.5 (12, 52.5), p = 0.009]. The one-year post-implant incidence of MACCE was higher in the CKD group compared with the control group (17.6% vs 9.9%, p = 0.006). CONCLUSION: CKD appears to be an important predictor for the prognosis of CAD.

Beneficial effects of early administration of recombinant human B-type natriuretic peptide in ST-elevation myocardial infarction patients receiving percutaneous coronary intervention treatment.

INTRODUCTION: We aimed to evaluate the clinical performance of early administration of recombinant human B-type natriuretic peptide (rhBNP) to ST-elevation myocardial infarction (STEMI) patients receiving percutaneous coronary intervention (PCI) treatment. METHODS: In total, 185 patients diagnosed with STEMI were enrolled and randomised into either the placebo-treated (n = 88) or rhBNP-treated (n = 97) group. Patients were given either saline or rhBNP ten minutes before PCI and monitored with various cardiac parameters, including accelerated idioventricular rhythm, frequent ventricular premature beat (FVPB), ventricular tachycardia, systolic blood pressure, thrombolysis in myocardial infarction (TIMI) 3 gradation, corrected TIMI frame count (cTFC) and myocardial blush grade (MBG) 3 classification. RESULTS: Our results revealed no difference in accelerated idioventricular rhythm between the two groups. However, FVPB and ventricular tachycardia were significantly decreased in rhBNP-treated patients compared to placebo-treated patients (p < 0.05). Moreover, the occurrence ratio of reperfusion-associated low blood pressure in rhBNP-treated patients was lower than in placebo-treated patients (p = 0.03), while no difference was observed in infarction-related arteries TIMI 3 blood flow between the two groups (p = 0.23). Importantly, measurement of post-reperfusion blood flow velocity via cTFC suggested that rhBNP treatment could significantly increase blood circulation (p = 0.003). After stent implantation, the acquisition rate of MBG 3 was higher in rhBNP-treated patients compared to placebo-treated patients (p = 0.071), although the difference was not significant. CONCLUSION: We concluded that early administration of rhBNP can ameliorate the severity of reperfusion injury for STEMI patients receiving PCI treatment.

The influence of the intestinal microflora to the efficacy of Rosuvastatin.

BACKGROUND: Intestinal microflora has been shown to play essential roles in the clinical therapies of metabolic diseases. The present study is aiming to investigate the potential roles and mechanisms of how intestinal microflora mediates lipid-reduction efficacy of Rosuvastatin. METHODS: To investigate the correlation between the intestinal microflora and efficacy of Rosuvastatin, we analyzed the diversity of intestinal microflora using PCR-DGGE analysis and 16S rDNA sequencing approaches. Furthermore, we compared the blood lipid levels of rat models with dysbiosis of intestinal microflora and control rats upon the Rosuvastatin administration. RESULTS: The diversity of the intestinal flora was obviously decreased upon the antibiotic treatment, this effect could be maintained for 2 weeks after establishment of the models. Importantly, the results from 16S rDNA sequencing demonstrated that the abundance of Lactobacillus and Bifidobacterium was remarkably diminished upon the antibiotic treatment in antibiotic+Rosuvastatin-treated group compared to that of Rosuvastatin-treated group and control group. Correspondently, the lipid-reduction efficacy of Rosuvastatin was significantly compromised. However, the diversity of the intestinal flora was recovered 4 weeks after the antibiotic treatment. Subsequently, the lipid-reduction efficacy of Rosuvastatin was also recovered to level of the control rats treated with Rosuvastatin alone. CONCLUSION: Intestinal flora could play an essential role in mediating the lipid-reduction efficacy of Rosuvastatin.

CLI-095 decreases atherosclerosis by modulating foam cell formation in apolipoprotein E-deficient mice.

Toll-like receptor 4 (TLR4) is considered to have a critical role in the occurrence and development of atherosclerosis in atherosclerosis-prone mice; however, it remains uncertain whether treatment with a TLR4 inhibitor may attenuate atherosclerosis. The present study aimed to determine the vascular protective effects of the TLR4 inhibitor CLI-095 on apolipoprotein E­deficient (ApoE­/­) mice. ApoE­/­ mice were fed either chow or a high­fat diet, and were treated with or without CLI­095 for 10 weeks. The mean atherosclerotic plaque area in the aortic sections of CLI­095­treated mice was 54.3% smaller than in the vehicle­treated mice (P=0.0051). In vitro, murine peritoneal macrophages were treated with or without CLI­095, and were subsequently stimulated with oxidized low­density lipoprotein. Treatment with CLI­095 markedly reduced the expression levels of lectin­like oxidized low­density lipoprotein receptor­1 and acyl-coenzyme A:cholesterol acyltransferase­1, and significantly upregulated the expression levels of ATP­binding cassette transporter A1, predominantly via suppressing activation of the TLR4/nuclear factor­κB signaling pathway. The results of the present study indicated that the TLR4 inhibitor CLI­095 has the ability to suppress the progression of atherosclerosis in an in vivo model by reducing macrophage foam cell formation.

Effect of epicardial fat pad ablation on acute atrial electrical remodeling and inducibility of atrial fibrillation.

BACKGROUND: Atrial electrical remodeling (AER) is the underlying mechanism of atrial fibrillation (AF). The present study investigated the impact of epicardial fat pad (FP) ablation on acute AER (AAER) and inducibility of AF. METHODS AND RESULTS: AAER was performed in 28 mongrel dogs through 4-h rapid atrial pacing (RAP). Before RAP, 14 dogs (ablation group) underwent FP ablation, and the other 14 (control group) underwent a sham procedure. The atrial effective refractory period (ERP) and vulnerability window (VW) of AF were measured with and without bilateral cervical vagosympathetic nerve stimulation (VNS) at the high right atrium, ostium of the coronary sinus (CS) and distal CS before and after every hour of RAP. In the control group, ERP was markedly shortened in the first 2 h of RAP and then stabilized. AF was only slightly induced. After RAP, the time course of ERP with and without VNS was similar. VNS significantly shortened ERP and increased VW before and after RAP. In the ablation group, ERP was significantly prolonged after FP ablation. Moreover, neither VNS nor RAP shortened the ERP or increased the VW. AF could not be induced (VW=0). CONCLUSIONS: RAP resulted in AAER, which may be mediated and aggravated by autonomic activity. Epicardial FP ablation generated denervation, which not only abolishes AF inducibility but also prevents RAP-mediated AAER.