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).

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.

[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.