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Background: Currently, there is no optimal treatment strategy for ostial left anterior descending (LAD) or ostial left circumflex artery (LCx) lesions. This study explored effectiveness and safety of drug-coated balloons (DCB) in individuals presenting with ostial LAD or LCx lesions. Methods: A total of 137 patients with de novo ostial LAD or LCx lesions scheduled for DCB treatment were prospectively recruited into the study. After mandatory lesion preparation, DCB-only or hybrid strategy [DCB + drug-eluting stent (DES)] were performed on 120 patients (87.59%). The primary endpoint was the rate of 2-year target lesion revascularization (TLR). Rates of major adverse cardiovascular events (MACE), cardiac death, target vessel myocardial infarction (TVMI), and vessel thrombosis were explored as the secondary outcomes. Quantitative coronary angiography software was used to analyze coronary angiograms. Results: Of the participants, 58 were treated with DCB-only and 62 with hybrid strategy. Relative to the DCB-only group, patients in the hybrid group had longer target lesions (15.47 ± 10.08 vs. 36.85 ± 9.46 mm, P 0.05). Treatment strategy (DCB-only or hybrid) was not a significant risk factor for TLR. Patients who underwent DCB-only exhibited less late lumen loss compared with the patients who underwent hybrid strategy (-0.26 ± 0.59 vs. 0.42 ± 0.47 mm, P

IntroductionProvisional stenting using drug-eluting stent is effective for simple coronary bifurcation lesions. Kissing balloon inflation using conventional non-compliant balloon is the primary treatment of side branch (SB) after main vessel (MV) stenting. Drug-coating balloon (DCB) is reported to be associated with less frequent clinical events in in-stent restenosis and small vessel disease. The importance of DCB in bifurcation treatment is understudied. Accordingly, this trial is designed to investigate the superiority of DCB to non-compliant balloon angioplasty for SB after provisional stenting in patients with true coronary bifurcation lesions.Methods and analysisThe DCB-BIF trial is a prospective, multicentre, randomised, superiority trial including 784 patients with true coronary bifurcation lesions. Patients will be randomised in a 1:1 fashion to receive either DCB or non-compliant balloon angioplasty if SB diameter stenosis >70% after MV stenting. The primary endpoint is the composite of major adverse cardiac event at the 1-year follow-up, including cardiac death, myocardial infarction (MI) or clinically driven target lesion revascularisation. The major secondary endpoints include all-cause death, periprocedural MI, spontaneous MI, clinically driven target vessel revascularisation, in-stent restenosis, stroke and individual component of the primary endpoint. The safety endpoint is the risk of stent thrombosis.Ethics and disseminationThe study protocol and informed consent have been reviewed and approved by the Institutional Review Board of all participating centres. The written informed consent for participation in the trial will be obtained from all participants. The results of this study will be published in a peer-reviewed journal and disseminated at conferences.Trial registration numberNCT04242134.

This study investigated the interaction among valsartan (VAL), TGF-β pathways, and long non-coding RNA (lncRNA) cardiac hypertrophy-related factor (CHRF) in doxorubicin (DOX)-induced heart failure (HF), and explored their roles in DOX-induced HF progression. HF mice models in vivo were constructed by DOX induction. The expression of CHRF and TGF-β1 in hearts was detected, along with cardiac function, caspase-3 activity, and cell apoptosis. Primary myocardial cells were pretreated with VAL, followed by DOX induction in vitro for functional studies, including the detection of cell apoptosis with terminal deoxynucleotidyl transferase dUTP nick-end labeling and the expression of proteins associated with TGF-β1 pathways. HF models were established in vivo and in vitro. Expression of CHRF and TGF-β1 was up-regulated, and cell apoptosis and caspase-3 activity were increased in the hearts and cells of the HF models. VAL supplementation alleviated the cardiac dysfunction and injury in the HF process. Moreover, overexpressed CHRF up-regulated TGF-β1, promoted myocardial cell apoptosis, and reversed VAL’s cardiac protective effect, while interference of CHRF (si-CHRF) did the opposite. Down-regulation of CHRF reversed the increased expression of TGF-β1 and the downstream proteins induced by pcDNA-TGF-β1 in HL-1 cells, while overexpression of CHRF reversed the VAL’s cardiac protective effect in vivo. In conclusion, VAL regulates TGF-β pathways through lncRNA CHRF to improve DOX-induced HF.

With the development of molecular biological technology, the association between genes and diseases has drawn increasing attention of researchers; the endothelial nitric oxide synthase (eNOS) gene has been reported to be a candidate gene for cardiovascular disease (CHD). The present study aimed to investigate the association between a polymorphism of eNOS and the risk of CHD in young people (≤40 years old), in addition to the underlying mechanism. A total of 234 cases of CHD in young individuals were collected as the CHD group and 228 cases of healthy individuals as the control group. Peripheral blood was collected and the genotype of the eNOS G894T polymorphism was identified by polymerase chain reaction-restriction fragment length polymorphism, the gene frequency was calculated and the distributions of genotype and allele frequency between the two groups were compared. Bioinformatics tools were employed to analyze the differences in the local protein structures of the eNOS G894T polymorphism and the biological mechanism was preliminary discussed. The results demonstrated that there were significant differences in the distribution of genotype frequency and allele frequency of the eNOS G894T gene polymorphism between the CHD group and control group (P

Several epidemiological studies investigating the association between dietary vitamin E intake and the risk of lung cancer have demonstrated inconsistent results. Hence, a meta-analysis was conducted to summarise evidence of the association of dietary vitamin E intake with the risk of lung cancer.In this meta-analysis, a systematic literature search of PubMed and Web of Science was conducted to identify relevant studies published from 1955 to April 2015. If p0.05 or I250%, a random effect model was used to estimate overall relative risks (RRs) and 95% confidence intervals (CIs). Otherwise, a fixed effect model was applied. Publication bias was estimated using the funnel plot and Egger's test. The doseresponse relationship was assessed using the method of restricted cubic splines with 4 knots at percentiles 5, 35, 65, and 95 of the distribution.The pooled RR of lung cancer for the highest versus lowest categories of dietary vitamin E intake was 0.84 (95% CI=0.76-0.93). With every 2 mg/d increase in dietary vitamin E intake, the risk of lung cancer statistically decreased by 5% (RR=0.95, 95% CI =0.91-0.99, plinearity=0.0237).Our analysis suggests that higher dietary vitamin E intake exerts a protective effect against lung cancer.

Since its discovery by Tambe et al in 1972, exact mechanism or pathogenesis of delayed distal opacification of angiographically normal coronary artery or slow coronary flow phenomenon is still unknown. Although its long term prognosis is good, it can even lead to sudden cardiac death and can occur up to 25% incidence. It was thought to be due to small vessel disease, endothelial dysfunction, inflammation, hyperviscosity, hemoconcentration, increased Plaque & Platelet activity, systolic & diastolic dysfunction, anatomic factors or diffuse atherosclerosis until now. We like to report the results of our recent randomized controlled trial about finding the most influential mechanism(s) of this phenomenon. From October 2012 to April 2013, this approved and consented randomized trial was conducted at our cath labs of First Affiliated Hospital of Zhengzhou University by analyzing the theories mentioned before in one randomized controlled retrospective study. Among the approximately 2000 patients who had consecutively done coronary angiogram, 100 patients (81 male, 19 female; mean age 57 ± 10 years) were randomized and enrolled as SCF group from 212 patientswith slow coronary flowwithout significant lesion and another 100 patients (45male, 55 female;mean age 58 ±10 years) with neither slow coronary flow nor significant lesion were also randomized and enrolled as Control group. Patients with previous MI/PCI, renal dysfunction, connective tissue disease, obstructive coronary artery disease, coronary vasospasm, coronary ectasia or aneurysm were excluded. Slow coronary flow was diagnosed by standard TIMI Frame Counts and confirmed by other two cardiologists. Tortuosity status, patient demographic parameters and investigations (UA, RDW, MPV, Platelet Count, Fibrinogen, Gamma GT, Hb, HCT, Calculated Osmolarity, Lipid Profile, BNP, Troponin, CKMB, EF, LVEDD, EDV) were retrospectively recorded and compared within two groups. Calculated Osmolarity was calculated by the equation: Osmolarity = 2Na + Glucose + BUN. Tortuosity was defined whenever there was less than 125 degree angled three or more turns in slow coronary flow affected artery or two or more normal coronary arteries. Patient gender, HDL, hemoglobin, hematocrit and Uric Acid had strongest strength of correlation (all p = 0.000 and r N 0.31)with SCF group [Table 1]. But, only Uric Acid (p = 0.000, CI = 2.266–13.242), Tortuosity (p = 0.000, CI = 2.373–14.655), End Diastolic Volume (p = 0.041, CI = 1.061–15.231) and Calculated Osmolarity (p = 0.003, CI = 0.131–0.658) were left as independent determinant factors for slow coronary flow after multivariable logistic regression [Table 1]. After ROC curve analysis Uric Acid got the highest area under curve (AUC = 0.720) with the best cut off point of 286 μmol/L (Sensitivity = 69%, Specificity = 69%) [Fig. 1A, C] followed by Tortuosity, End Diastolic Volume and Calculated Osmolarity [Fig. 1B]. Whenwe analyzed our data, only Uric Acid and Tortuosity were the top determinant factors. Among them, confidence interval of Uric Acid was much less than that of Tortuosity although odds ratio of Uric Acid and Tortuosity were very similar [Table 1]. Moreover, Uric Acid had stronger strength of correlationwith slowcoronary flow thanTortuosity [Table 1]. Furthermore, after ROC curve analysis, Uric Acid got the highest area under curve [Fig. 1A]. Therefore we concluded that Uric Acid was the most determinant factor for slow coronary flow phenomenon in our study. Uric Acid (UA) is the inevitable by-product of cellular degradation which is converted from xanthine by xanthine oxidase (XO). It plays a role in inflammation. It is detectable in almost all inflammatory diseases. Moreover, the higher the Uric Acid, the more other inflammatory markers are increased. Serum UA is associated positively with IL-6, CRP and TNF-α and negatively with IL-1β, particularly in women [1]. It also plays a role in endothelial dysfunction although there are still controversies [2,3]. Uric Acid lowering drug, a xanthine oxidase inhibitor, allopurinol can improve endothelial dysfunction. We can also hypothesize that Uric Acid induces endothelial dysfunction because there is an inverse circadian relationship between serum UA levels and NO in healthy persons [4]. It should be noted that hyperuricemia itself is not a risk factor but a risk marker for presence of risk for the development of severe clinical complications. Most damages found with hyperuricemia are not directly caused byUA but by superoxide free radical produced by the enzyme XO [5]. Integrating above discussion with our results, we found that inflammation and endothelial dysfunction may be the most influential mechanism of slow coronary flow phenomenon according to our study. Although we didn't have a chance to record hsCRP, hCYand IL6 because of lack of consent, this study is the first study analyzing all the previously reported theories to find the most influential mechanism of slow coronary flow phenomenon in our knowledge. With better understanding about etiopathogenesis of slow coronary flow phenomenon, patients will be beneficial with newer therapies and implications.

To observe the expression and clinical implication of plasma miR-328 in patients with atrial fibrillation (AF).Fifty-eight patients with AF (AF group: 17 paroxysmal AF, 21 persistent AF, and 20 permanent AF) and 15 healthy volunteers (Control group) were included. General clinical data and related biochemical parameters were collected. Plasma miR-328 levels were detected with quantitative real-time polymerase chain reaction (qRT-PCR) analysis. The correlation between plasma miR-328 and AF risk factors was analyzed.(1) Compared with the control group, the expression level of plasma miR-328 was significantly elevated in AF group (fold 7.72 ± 9.32) (P0.05). (2) In AF group, the expression of plasma miR-328 was significantly different in different type of AF[paroxysmal AF with (1.98 ± 0.81), persistent AF with (6.57 ± 5.82) and permanent AF with (13.47 ± 12.29)] (P0.05), and which was increased in proportion to the duration of AF. (3) There was a positive correlation between plasma miR-328 level and left atrial diameter in the AF group (r = 0.310, P0.05).miR-328 expression is significantly increased in patients with AF, which may be involved in the atrial remodeling process of AF.

To assess left ventricular systolic synchronicity by quantitative tissue velocity imaging (QTVI) in patients with left ventricular noncompaction (LVNC).Eighteen LVNC patients and 30 healthy controls were included. Two-dimensional echocardiography, QTVI was applied on parasternal long axis view, apical two-chamber and four-chamber view. Tissue velocity curve was obtained from the middle and basal segments of left ventricular posterior, lateral, septal, anterior, inferior and anteroseptal walls. Time interval from the beginning of QRS complex to the peak systolic velocity (Q-Ts) and the maximal difference in Ts among all 12 LV segments (Max-DeltaTs) was calculated.Q-Ts from basal and middle segments of left ventricular inferior, lateral and posterior walls was significantly prolonged in LVNC patients compared to controls (P0.001). Max-DeltaTs was also significantly increased in LVNC patients [(161.9 +/- 93.2) ms] than that in controls [(61.2 +/- 27.4) ms, P0.001].There was significant left ventricular asynchronies in patients with LVNC and delayed systolic contraction occurred mostly in the basal and middle segments of left ventricular inferior, posterior and lateral walls.

To screen the mutations of RET proto-oncogene in sporadic patients with pheochromocytoma.Forty-two cases of sporadic pheochromocytoma were tested for mutations of RET gene. Of these 42 DNA samples, 12 were extracted from peripheral blood cells and 30 from paraffin-embedded pheochromocytoma specimens. The PCR product of exon 10 and exon 11 was used to molecular analysis of the RET proto-oncogene.Among 42 patients, 2 were found to have RET gene mutations. One of mutations located at codon 634 (TGCTAC) in exon 11 of RET proto-oncogene. Another one located at codon 632 (GAGAAG).Some patients with apparently sporadic pheochromacytoma were carrier of mutations, a routine genetic analysis for mutations of RET gene is indicated for these patients.

Slow flow of contrast without significant lesion in coronary arteries can manifest up to life threatening arrhythmia and sudden death. But, its responsible mechanism is still unknown. We here want to find the most influential mechanism of slow coronary flow by analyzing previously proposed theories