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Objective:To evaluate the effects of slow breathing training on hypertension. Methods:Articles about slow breathing training for hypertension were retrieved from CNKI, Wangfang Data, PubMed and Web of Science, until March, 2021. The authors, publishing time, subjects, interventions and courses, and outcome indexes and conclusion were extracted. Results:There were 924 articles returned, and 35 included, which published mainly from 2009 to 2020. The subjects were patients with hypertension, and the outcome index was blood pressure. Conclusion:Slow breathing training may work for hypertension, which associates to baroreflex sensitivity, heart rate variability, sympathetic nerve activity and cardiopulmonary diastolic receptors.
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Objective To investigate the relationship of galectin-3 (Gal-3)and matrix metalloproteinase-9 (MMP-9)with in-stent restenosis (ISR).Methods We consecutively recruited 434 patients who had undergone successful drug eluting stent (DES)implantation.Then we divided them into ISR group (n=41)and NO-ISR group (n=393)according to the results of coronary angiography review.Independent risk factors for ISR were found out by multivariate analysis and the two groups were matched for these factors except for Gal-3 and MMP-9 .After elim-ination of the influence of confounders,serum Gal-3 and MMP-9 were compared between the groups and their rela-tions with the severity of ISR were analyzed.Patients were grouped based on Gal-3 and MMP-9 concentrations and major adverse cardiac events (MACEs)were compared between the two groups.Results After elimination of the influence of confounders,the results showed that serum levels of Gal-3 and MMP-9 were significantly higher in ISR group than in NO-ISR group (P＜0.001).Serum levels of Gal-3 and MMP-9 increased with the increased grade of classification.Serum levels of Gal-3 and MMP-9 were obviously higher in classes Ⅲ and Ⅳ ISR than in class Ⅰ (P＜0.05).Patients with higher levels of Gal-3 and MMP-9 had a higher incidence of MACEs (P＜0.01).ISR group had a higher incidence of MACEs than NO-ISR group (P＜0.05).Conclusion Serum levels of Gal-3 and MMP-9 are correlated with ISR and its severity,and they are independent risk factors for ISR.The rate of MACEs during follow-up period was increased with the increased levels of Gal-3 and MMP-9 .
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Objective To investigate the predictive values of platelet to lymphocyte ratio (PLR) and neutrophil to lymphocyte ratio (NLR)before percutaneous coronary intervention (PCI)and a reexamination of coronary angiography (CAG)on the development of in-stent restenosis (ISR)in patients implanted with coronary drug eluting stent (DES).Methods For this study we enrolled 123 patients who had undergone successful drug eluting stent implantation (SI)and a further CAG reexamination.Another 45 patients with non-coronary heart disease (NC)served as controls.PLR and NLR were measured before DES implantation or CAG and compared between the groups.Patients in SI group were further divided into two subgroups based on the results of CAG reexamination:ISR group and no-ISR group.Hematologic data were reexamined before further CAG and compared between the subgroups.Receiver operator characteristic curve (ROC)was drawn to evaluate the predictive values of PLR and NLR for ISR.Results PLR and NLR before PCI or a further CAG were significantly higher in ISR group (34 patients)than in non-ISR group (89 patients,P＜0.05).Before PCI,the best cutoff value of PLR in screening restenosis was 107.20;the sensitivity and the specificity were 64.7% and 65.2%.The best cutoff value of NLR in screening restenosis was 2.72; the sensitivity and the specificity were 61.8% and 70.8%. Before CAG reexamination,the best cutoff value of PLR in screening restenosis was 160.08;the sensitivity and the specificity were 26.5% and 97.8%.The best cutoff value of NLR in screening restenosis was 2.08;the sensitivity and the specificity were 73.5% and 56.2%.Conclusion Both PLR and NLR before PCI or CAG reexamination can be predictors of ISR in patients implanted with DES.
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Objective To analyze the association of atherogenic index of plasma (AIP)and serum bilirubin with coronary in-stent restenosis after drug-eluting stent implantation.Methods For this research we recruited 268 patients who had undergone successful drug-eluting coronary stent implantation and then received coronary angiography.Both ends (from the edge of the supporting frame≤5 mm)or the vessel's diameter stenosis ≥50% were used as the definition of restenosis.According to the results of coronary angiography,the subjects were divided into restenosis group (42 cases)and non-restenosis group (226 cases).The total bilirubin,direct bilirubin,indirect bilirubin and AIP in the two groups were compared to explore the correlation of AIP and serum bilirubin with in-stent restenosis.Results AIP in restenosis group was significantly higher than that in non-restenosis group (P＜0.05).The level of total bilirubin was significantly lower in the former group than in the latter one (P＜0.05). Conclusion AIP is a risk factor for restenosis,and serum total bilirubin is a protective factor for coronary stent restenosis.
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Objective To investigate the relationship between ischemia-modified albumin (IMA) and coronary artery stenosis in patients without myocardial infarction.Methods For this study we consecutively enrolled 345 patients who received coronary angiography (CAG).According to the results,the subjects were divided into coronary stenosis group (232 cases)and control group (113 cases)to investigate the the relationship of IMA and IMA/albumin (IMAr)with coronary stenosis.Results ① The levels of IMA and IMAr in coronary stenosis group were higher than those in control group (P＜0.001).② The IMA and IMAr were higher in single-branch and multi-branch lesion groups than in control group (P＜0.05),whereas there was no significant difference between single-branch lesion group and multi-branch lesion group (P＞0.05).③ In receiver operating characteristics curve analysis,the sensitivity of IMA and IMAr was 64.4% and 78.0%,respectively (AUC:0.653,0.705,P＜0.001)in predicting coronary stenosis.④ Multivariate logistic regression analysis showed that IMAr was an independent risk factor for coronary stenosis in patients without myocardial infarction (OR=73.05,P＜0.001).Conclusion IMA and IMAr are closely correlated with coronary stenosis and have a value in predicting coronary artery stenosis in patients without myocardial infarction.
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<p><b>BACKGROUND</b>Urotensin II (UII) is a new vasoconstrictive peptide that may activate the adventitial fibroblasts. Transforming growth factor-β1 (TGF-β1) is an important factor that could induce the phenotypical transdifferentiation of adventitial fibroblasts. This study aimed to explore whether TGF-β1 is involved in UII-induced phenotypic differentiation of adventitial fibroblasts from rat aorta.</p><p><b>METHODS</b>Adventitial fibroblasts were prepared by the explant culture method. TGF-β1 protein secretion from the cells was determined by enzyme-linked immunosorbent assay (ELISA). The mRNA and protein expression of α-smooth nuscle actin (α-SM-actin), the marker of phenotypic differentiation from fibroblasts to myofibroblasts, were determined using real-time quantitative RT-PCR (real-time RT-PCR) and Western blotting, respectively.</p><p><b>RESULTS</b>UII stimulated the secretion of TGF-β1 in cultured adventitial fibroblasts in a time-dependent manner. The secretion reached a peak at 24 hours, was higher by 69.8% (P < 0.01), than the control group. This effect was also concentration dependent. Maximal stimulation was reached at 10(-8) mol/L of UII (P < 0.01), which was increased by 59.9%, compared with in the control group (P < 0.01). The secretion of TGF-β1 induced by UII was significantly blocked by SB-710411 (10(-7) mol/L), a specific antagonist of UII receptor. In addition, both UII (10(-8) mol/L) and TGF-β1 significantly stimulated α-SM-actin mRNA and protein expression. Moreover, the α-SM-actin induced by UII was inhibited by the specific neutralizing antibody (20 µg/ml) of TGF-β1, while the α-SM-actin expression stimulated by TGF-β1 (20 ng/ml) was inhibited by SB-710411 (10(-7) mol/L), the UII receptor antagonist.</p><p><b>CONCLUSION</b>This study suggests that UII could induce TGF-β1 secretion in adventitial fibroblasts via UT activation, and TGF-β1 might be involved in phenotypic differentiation from adventitial fibroblasts into myofibroblasts induced by UII, and TGF-β1 signaling might be one of the important pathways by which UII is involved in vascular fibrosis.</p>