Intracoronary pressure gradient measurement in acute myocardial infarction patients with the no-reflow phenomenon during primary percutaneous coronary intervention.

BACKGROUND: Various experimental and clinical studies have reported on coronary microcirculatory dysfunction ("no-reflow" phenomenon). Nevertheless, pathogenesis and effective treatment are yet to be fully elucidated. This study aimed to measure the intracoronary pressure gradient in the no-reflow artery during emergent percutaneous coronary intervention and explore the potential mechanism of no-reflow. METHODS: From September 1st, 2018 to June 30th, 2019, intracoronary pressure in acute myocardial infarction patient was continuously measured by aspiration catheter from distal to proximal segment in the Department of Coronary Care Unit, Tianjin Chest Hospital, respectively in no-reflow arteries (no-reflow group) and arteries with thrombolysis in myocardial infarction-3 flow (control group). At least 12 cardiac cycles were consecutively recorded when the catheter was pulled back. The forward systolic pressure gradient was calculated as proximal systolic pressure minus distal systolic pressure. Comparison between groups was made using the Student t test, Mann-Whitney U-test or Chi-square test, as appropriate. RESULTS: Intracoronary pressure in 33 no-reflow group and 26 in control group were measured. The intracoronary forward systolic pressure gradient was -1.3 (-4.8, 0.7) and 3.8 (0.8, 8.8) mmHg in no-reflow group and control group (Z = -3.989, P < 0.001), respectively, while the forward diastolic pressure gradient was -1.0 (-3.2, 0) and 4.6 (0, 16.5) mmHg in respective groups (Z = -3.851, P < 0.001). Moreover, the intracoronary forward pressure gradient showed significant difference between that before and after nicorandil medication (Z = -3.668, P < 0.001 in systolic pressure gradient and Z = -3.530, P < 0.001 in diastolic pressure gradient). CONCLUSIONS: No reflow during emergent coronary revascularization is significantly associated with local hemodynamic abnormalities in the coronary arteries. Intracoronary nicorandil administration at the distal segment of a coronary artery with an aspiration catheter could improve the microcirculatory dysfunction and resume normal coronary pressure gradient. CLINICAL TRIAL REGISTRATION: www.ClinicalTrials.gov (No. NCT03600259).

[Influence of PCSK9 gene E670G polymorphism on the risk of atherosclerotic coronary heart disease and plasma lipid level].

OBJECTIVE: To explore the influence of PCSK9 gene E670G polymorphism on the risk of coronary heart disease (CHD) among Chinese patients from Tianjin, and to compare the effect of atorvastatin treatment on CHD patients with various PCSK9 E670G genotypes. METHODS: Seven hundred and seventy-eight patients undergoing coronary angiography (CAG) were classified into CHD group (n = 502) and control group (n = 276). Total cholesterol (TC) and triglyceride (TG) were determined for all patients. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method was used to determine the E670G genotype for each patient. For 231 CHD patients who had taken atorvastatin calcium for 12 weeks and completed the follow-up, the lipid profile was determined again. RESULTS: The distribution of PCSK9 E670G genotype between the CHD and control groups differed significantly (P< 0.01). The frequencies of G allele were 15.99% and 9.34% in the CHD and control group, respectively, which showed a statistical significance (P< 0.01). Carriers of G allele had a higher risk of CHD than those with A allele (OR=1.847, 95%CI: 1.301-2.622, P< 0.01). Among CHD patients, those carrying G allele had higher TC and TG levels than those with AA genotype, while patients with a GG genotype had higher level of low density lipoprotein cholesterol (LDL-C) than those with a AA genotype (P< 0.05). Logistic regression analysis indicated that high density lipoprotein cholesterol (HDL-C) is a protective factor of CHD (OR=0.203, 95%CI: 0.100-0.414, P< 0.05). After treatment with atorvastatin, LDL-C level decreased more significantly in those with an AA genotype compared with AG and GG genotypes (P< 0.05). CONCLUSION: The E670G polymorphism of the PCSK9 gene is associated with the lipid levels and risk for CHD.

Tormentic acid inhibits H2O2-induced oxidative stress and inflammation in rat vascular smooth muscle cells via inhibition of the NF-κB signaling pathway.

Tormentic acid (TA) is a triterpene isolated from the stem bark of the plant Vochysia divergens and has been reported to exhibit anticancer, anti­inflammatory and anti­atherogenic properties. However, the functions of TA in hydrogen peroxide (H2O2)­induced oxidative stress and inflammation in rat vascular smooth muscle cells (RVSMCs) remain unclear. Therefore, the present study aimed to investigate whether TA suppressed H2O2­induced oxidative stress and inflammation in RVSMCs, and to determine its molecular mechanisms. The present study demonstrated that TA inhibited reactive oxygen species (ROS) generation, induced H2O2 in RVSMCs, and inhibited H2O2-induced expression of inducible nitric oxide synthase (iNOS) and NADPH oxidase (NOX) in RVSMCs. In addition, TA significantly decreased the production of tumor necrosis factor­α (TNF­α), interleukin 6 (IL­6) and IL­1ß. Furthermore, TA pretreatment prevented nuclear factor­κB (NF­κB) subunit p65 phosphorylation and NF­κB inhibitor α (IκBα) degradation induced by H2O2 in RVSMCs. TA is, therefore, suggested to inhibit H2O2-induced oxidative stress and inflammation in RVSMCs via inhibition of the NF­κB signaling pathway. TA may have potential as a pharmacological agent in the prevention or treatment of atherosclerosis.

Association between mobilization of circulating endothelial progenitor cells and time or degree of injury from angioplasty in patients with exertional angina: A prospective study.

The aim of the present study was to investigate the effect of coronary artery angioplasty on the recruitment of circulating endothelial progenitor cells (EPCs) in patients with angina pectoris. A total of 66 patients treated by coronary stenting were enrolled in the PCI group and 17 patients that underwent angiography alone were enrolled in the control group. The EPC count in the blood was measured by flow cytometry prior to and at 1, 3, 5, 7 and 24 h following angioplasty in the percutaneous coronary intervention (PCI) group, and at three time-points following angiography in the control group. Differences between the two groups included the characteristics of the coronary artery lesions, the incidence of diabetes and family history of coronary heart disease. The mean surface area of the stent deployed was 335.59±234.99 mm2. No significant change in EPC count was measured in the control group. In the PCI group, a moderate and delayed increase in the number of cluster of differentiation (CD)34+/kinase domain receptor (KDR)+ EPCs occurred at 24 h post-balloon inflation compared with the baseline level. The CD133-/CD34+/KDR+ subpopulations showed undulating changes at 3, 7 and 24 h post-PCI (P=0.016, P=0.01 and P=0.032, respectively). An arch shape was displayed in CD133+/KDR+ cells; initially, a reduction occurred at 3 h and was maintained constantly until 7 h (P=0.003, P=0.013 and P=0.033 at 3, 5 and 7 h, respectively), after which a slight increase to the baseline level occurred at 24 h (P=0.084). The CD133+/CD34+ cells increased in stepwise manner until 24 h. The CD34+/KDR+ EPC change magnitude correlated significantly with a global damage index by partial correlation analysis (P<0.001). The results suggested that a time-dependent mobilization of EPCs may be initiated by PCI; the change magnitude of the CD34+/KDR+ cells was associated particularly with endothelial injury degree from the PCI procedure.

NT-ProBNP levels are moderately increased in acute high-altitude pulmonary edema.

The aim of the present study was to investigate the effect of B-type natriuretic peptides (BNPs) in acute high-altitude pulmonary edema (HAPE). The study enrolled 46 subjects from lowland Han, including 33 individuals who had acutely ascended to a high altitude (21 individuals with HAPE as the case group and 12 individuals without HAPE as the high-altitude control group) and 13 healthy normal residents as the plain control group. The serum concentrations of N-terminal probrain natriuretic peptide (NT-proBNP), erythropoietin (EPO), vascular endothelial growth factor (VEGF) and nitric oxide (NO) were measured. There were significant differences in the serum concentrations of NT-ProBNP, NO, VEGF and EPO among the three groups. The serum concentrations of NT-ProBNP, EPO and VEGF were significantly higher in the HAPE patients and high-altitude control individuals than those of the plain group. No significant differences were identified between the HAPE patients and the high-altitude control group. In contrast to these three parameters, the serum concentrations of NO in the high-altitude control group were significantly higher than those of the HAPE patients and the plain group, while there were no significant differences in the serum concentrations of NO between the HAPE patients and the plain group. Furthermore, serum concentrations of NT-ProBNP and EPO were significantly reduced following treatment in the HAPE patients, however, no significant changes were identified in VEGF or NO concentrations. BNPs are increased in HAPE with severe hypoxia and right ventricular overload, but are decreased subsequent to treatment. BNPs may therefore be a potential biomarker for the diagnosis and prognosis of HAPE.

[Level of tissue plasminogen activator protein in pulmonary artery in acute pulmonary thromboembolism in rabbit].

OBJECTIVE: To study the changes in tissue plasminogen activator(t-PA) protein in pulmonary artery and its clinical significance after acute pulmonary thromboembolism (PTE). METHODS: Thirty rabbits were randomly divided into four groups after replicating a model of acute PTE in rabbit by thrombi occlusion method. Specimens were obtained from both normal and morbid pulmonary artery 3, 8 and 24 hours after APE, and protein contents of t-PA were determined using immunohistochemical method. RESULTS: A few endothelial cells and smooth muscle cells of the normal pulmonary artery were positive for t-PA. After 3 hours of PTE, there was no significant changes in t-PA positive stain among embolismic, non-embolismic and normal pulmonary artery. After 8 and 24 hours of PTE, strong positive staining was found in the residual endothelial cells and a part of smooth muscle cells (all P<0.01). CONCLUSION: There is significantly strong positive staining for t-PA in the pulmonary artery wall after pulmonary embolism, implying that the local fibrinolysis activity was enhanced, and it might be helpful for lysis of the embolus.