Morphologies and composition changes in nonculprit subclinical atherosclerosis in diabetic versus nondiabetic patients with acute coronary syndrome who underwent long-term statin therapy.

Although patients are undergoing similar lipid-lowering therapy (LLT) with statins, the outcomes of coronary plaque in diabetic mellitus (DM) and non-DM patients are different. Clinical data of 239 patients in this observational study with acute coronary syndrome was from our previous randomized trial were analyzed at 3 years, and 114 of them underwent OCT detection at baseline and the 1-year follow-up were re-anlayzed by a novel artificial intelligence imaging software for nonculprit subclinical atherosclerosis (nCSA). Normalized total atheroma volume changes (ΔTAVn) of nCSA were the primary endpoint. Plaque progression (PP) was defined as any increase in ΔTAVn. DM patients showed more PP in nCSA (ΔTAVn; 7.41 (- 2.82, 11.85) mm3 vs. - 1.12 (- 10.67, 9.15) mm3, p = 0.009) with similar reduction of low-density lipoprotein cholesterol (LDL-C) from baseline to 1-year. The main reason is that the lipid component in nCSA increases in DM patients and non-significantly decreases in non-DM patients, which leads to a significantly higher lipid TAVn (24.26 (15.05, 40.12) mm3 vs. 16.03 (6.98, 26.54) mm3, p = 0.004) in the DM group than in the non-DM group at the 1-year follow-up. DM was an independent predictor of PP in multivariate logistic regression analysis (OR = 2.731, 95% CI 1.160-6.428, p = 0.021). Major adverse cardiac events (MACEs) related to nCSA at 3 years were higher in the DM group than in the non-DM group (9.5% vs. 1.7%, p = 0.027). Despite a comparable reduction in LDL-C levels after LLT, more PP with an increase in the lipid component of nCSA and a higher incidence of MACEs at the 3-year follow-up was observed in DM patients.Trial registration: ClinicalTrials.gov. identifier: NCT02140801.

The association of diabetes mellitus with neointimal formation following deployment of second-generation drug-eluting stents: an optical coherence tomographic study.

OBJECTIVES: The purpose of this study was to evaluate the association of diabetes mellitus (DM) with neointimal formation after implantation of second-generation drug-eluting stent (DES) visualized by optical coherence tomography (OCT). METHODS: Patients with single de novo coronary artery disease treated with second-generation DES between June 2014 and June 2017 in our department underwent OCT examination at 1-year follow-up and were enrolled in this retrospective study. The primary end point was in-stent mean neointimal thickness (MNT), and secondary end points included uncovered stent strut, minimal lumen area (MLA), neointimal burden, neointimal hyperplasia (NIH) patterns and stent thrombosis (ST) after 1 year of OCT follow-up. RESULTS: A total of 68 patents with DM (DM group) and 216 patients without DM (non-DM group) were enrolled. At 1-year follow-up, the DM group compared with the non-DM group, showed: MNT [160 (85-245) µm vs. 120 (60-220) µm, P = 0.038] and neointimal burden [21.4 (8.3-30.1)% vs. 14.0 (5.7-26.1)%, P = 0.023] to be significantly increased. Concurrently, MLA [4.60 (3.53-6.06) mm vs. 5.76 (4.28-7.20) mm2, P = 0. 0.002] was significantly reduced. Interestingly, the degree of uncovered struts (7.3 ± 7.1% vs. 7.7 ± 6.7%, P = 0.704), NIH patterns (P = 0.984), and ST (7.9% vs. 7.4%, P = 0.88) were comparable between the two groups. After propensity score matching, the MNT [160 (90-240) µm vs. 110 (60-220) µm, P = 0.048] and neointimal burden [21.4 (8.3-30.1)% vs. 15.4 (5.6-26.3)%, P = 0.044] remained significantly different in the DM compared to the non-DM group. CONCLUSION: DM leads to significant increase in MNT and neointimal burden even with second-generation DES, nevertheless stent strut coverage, ST and NIH characteristics remained comparable among the cohorts at 1-year.

Percutaneous pulmonary artery denervation completely abolishes experimental pulmonary arterial hypertension in vivo.

AIMS: The study sought to assess the effect of percutaneous pulmonary artery denervation (PADN) on balloon-occlusion-induced acute pulmonary arterial hypertension (PAH) in vivo. The PADN is a minimally invasive and endovascular catheter-based interventional therapy using radiofrequency ablation to abolish the pulmonary arterial baroreceptors to pressure response. METHODS AND RESULTS: To examine the efficacy of balloon-occlusion-induced PAH, twenty Mongolian dogs were randomly assigned to one of two groups: group 1 (left distal pulmonary basal trunk occlusion) and group 2 (left pulmonary interlobar artery occlusion). Afterwards, PADN treatment at the main pulmonary artery bifurcation level with left pulmonary interlobar artery occlusion in all 20 dogs was conducted. Haemodynamic parameters were measured at baseline and during balloon occlusion as well as the PADN treatment at different time points: one, two, three, five, and ten minutes. Before the PADN treatment, most haemodynamic parameters of the pulmonary artery remained unchanged in group 1 with distal pulmonary basal trunk occlusion. However, in group 2 with the occlusion of the left pulmonary interlobar artery, mean pulmonary arterial pressure, mean right ventricular pressure, and pulmonary vessel resistance gradually increased, and mean absolute difference reached peak at five minutes (Δ16.6 mmHg, Δ14.1 mmHg and Δ1,144 dye/s/cm5, respectively; each p<0.01). These haemodynamic parameters at five minutes induced by left pulmonary interlobar artery occlusion were completely abolished with the PADN treatment compared to baseline (Δ0.3 mmHg, Δ0.2 mmHg, and Δ34 dye/s/cm5, respectively). CONCLUSIONS: Balloon occlusion of the left pulmonary interlobar artery led to a significant increase of haemodynamic parameters of the pulmonary artery. The pressure responses were completely abolished by the PADN treatment at the main bifurcation area of the left pulmonary artery.

[Analysis of heterogeneity in exon 4 of Coxsackievirus and Adenovirus receptor gene in dilated cardiomyopathy].

OBJECTIVE: To investigate the genetic pathogenesis of dilated cardiomyopathy (DCM) by examining the heterogeneity of Coxsackievirus binding domain (exon 4) of Adenovirus receptor (CAR) in DCM patients and healthy adults, and to detect possible mutation site in exon 4. METHODS: Using polymerase chain reaction (PCR), we amplified exon 4 of CAR DNA extracted from blood samples obtained from 50 DCM patients and 40 healthy adults. The PCR products were screened with single-strand conformation polymorphism (SSCP) and then sequenced alternatively based on the SSCP results. RESULTS: The segment of CAR exon 4 was successfully amplified and there was no single strand conformational disparity in all samples examined by SSCP. Sequence analysis demonstrated that all amplified sequences of CAR exon 4 from samples of the two groups were identical and there was no genetic heterogeneity of CAR exon 4 between the two groups. CONCLUSION: The genetic heterogeneity of CAR exon 4 might not be responsible for the pathogenesis of DCM.

Role of coxsackievirus and adenovirus receptor in the pathogenesis of dilated cardiomyopathy and its influencing factor.

BACKGROUND: Although clinical treatment for heart failure and sudden death has been improved over the last few decades, the morbidity and mortality of dilated cardiomyopathy (DCM) have increased. So a better understanding of the underlying molecular events leading to DCM is urgent. Persistent viral infection (especially coxsackievirus group B3) of the myocardium in viral myocarditis and DCM has never been neglected by experts. Recent data indicate that the up-regulation of coxsackievirus and adenovirus receptor (CAR) in viral cardiomyopathy contributes to viral infection as a key factor in the pathogenesis of this disease. This study aimed to investigate the role and regulatory mechanism of CAR in DCM by the bioinformatic method. METHODS: We identified the clusters of genes co-expressed with CAR by clustering algorithm based on the public available microarray dataset of DCM (Kittleson, et al. 2005), and mapped these genes into the protein-protein interaction networks to investigate the interaction relationship to each other at the protein level after confirming that the samples are characterized by the cluster of genes in correctly partitioning. RESULTS: The gene cluster GENESET 11 containing 33 genes including CAR with similar expression pattern was identified by cluster algorithm, of which 19 genes were found to have interaction information of the protein encoded by them in the current human protein interaction database. Especially, 12 genes present as critical nodes (called HUB node) at the protein level are involved in energy metabolism, signal transduction, viral infection, immuno-response, cell apoptosis, cell proliferation, tissue repair, etc. CONCLUSIONS: The genes in GENESET 11 together with CAR may play a pathogenic role in the development of DCM, mainly involved in the mechanism of energy metabolism, signal transduction, viral infection, immuno-response, cell apoptosis and tissue repair.