Introduction: This prospective, multicenter, randomized study was designed to analyze the benefits of ticagrelor over clopidogrel in reducing subclinical stent thrombosis (ST) in patients with coronary artery disease who underwent implantation of a second-generation drug-eluting stent (DES). Methods: About 352 patients with single de novo coronary stenosis were randomly assigne`d to either clopidogrel group (aspirin plus clopidogrel) or ticagrelor group (aspirin plus ticagrelor) after DES implantation for 1 year. Baseline clinical characteristics, blood chemistry markers, coronary artery angiography (CAG), and optical coherence tomography (OCT) were obtained during the index procedure. Data about clinic, CAG and OCT were also collected after 1 year follow-up. Intention-to-treat (ITT), per protocol set (PPS), and sensitivity analysis of subclinical ST were performed. Major factors associated with subclinical ST were analyzed by multivariable and univariable logistic regression models. Results: The incidence of subclinical ST in ticagrelor group was significantly low as compared to clopidogrel group (P < .05) at 1-year follow-up. Ticagrelor use was an independent factor in reducing subclinical ST (P < .05). The percentage of endothelial coverage, neointimal hyperplasia, malapposition, and edge dissection about stents were not different between the two groups (P > .05). Bleeding ratio was not markedly altered after ticagrelor treatment (P > .05). Not any significant differences were detected with regard to baseline clinical characteristics, CAG results, and DES between ticagrelor and clopidogrel groups (P > .05). Conclusion: In patients who underwent a second-generation DES implantation, using aspirin plus ticagrelor was associated with a significant reduction in subclinical ST. (ClinicalTrials.gov. Number: NCT02140801)

Background: The study sought to investigate the clinical predictive value of quantitative flow ratio (QFR) for the long‐term outcome in patients with heavily calcified lesions who underwent percutaneous coronary intervention (PCI) following rotational atherectomy (RA).Methods: In this retrospective study, 393 consecutive patients from 2009 to 2017 were enrolled. The QFR of the entire target vessel (QFRv) and the QFR of the stent plus 5 mm proximally and distally (in‐segment) (QFRi) were measured. The primary endpoint was target lesion failure (TLF), including target lesion‐cardiac death (TL‐CD), target lesion‐myocardial infarction (TL‐MI), and clinically driven‐target lesion revascularization (CD‐TLR).Results: A total of 224 patients with 224 calcified lesions completed the clinical follow‐up, and 52 patients had TLF. There was no significant difference in QFRv post‐PCI between non‐TLF and TLF groups (p > .05). However, QFRi post PCI was significantly higher in the non‐TLF group than in the TLF group. Multivariate Cox regression showed that QFRi post‐PCI was an excellent predictor of TLF after a 3‐year follow‐up (HR 1.7E⁻⁸ [5.3E⁻¹¹–5.6E^‐6]; p < .01). Furthermore, receiver‐operating characteristic curve analysis demonstrated that the optimal cutoff value of QFRi for predicting the long‐term TLF was 0.94 (area under the curve: 0.826, 95% confidence interval: 0.756–0.895; sensitivity: 89.5%, specificity: 69.2%; p < .01). The QFRi ≤ 0.94 post‐PCI was negatively associated with TLF, including TL‐CD, TL‐MI, and CD‐TLR (p < .01).Conclusions: QFRi post‐PCI showed a high predictive value for TLF for during a 3‐year follow‐up in patients who underwent PCI following RA; specifically, lower QFRi values post‐PCI were associated with worse TLF.

The function of zfp91 is mainly studied in vitro, but there is no study in vivo. Accumulative data suggest that zfp91 may be an important gene to regulate all aspects of human response. However, there are no data to date about the function of zfp91 on cardiac homeostasis. Thus, we aimed to observe the role of zfp91 gene in mouse cardiomyocytes on myocardial homeostasis and related mechanisms under pressure overload. In the study, zfp91 mRNA and protein levels were significantly reduced in TAC‐operated WT mice as compared with controls. Genetic ablation of zfp91 dramatically led to pathological cardiac dysfunction and hypertrophy after transverse aortic constriction (TAC). Adenosine A1 receptor (Adora1) mRNA and protein expressions were significantly down‐regulated in the heart of zfp91‐deletion mice with TAC. Zfp91 overexpression reversed isoproterenol‐induced cardiomyocyte hypertrophy, which was abolished by selective Adora1 antagonist. Dual‐luciferase reporter and ChIP‐qPCR assays indicated that zfp91 acted on Adora1 promoter through its binding site. Last, Adora1 agonist rescued heart dysfunction and cardiac hypertrophy in zfp91 loss mice after TAC. Zfp91 may transcriptionally regulate Adora1 expression in the heart, which mainly maintained cardiac homeostasis under pressure overload status. It will provide a new approach to treat cardiac hypertrophy.