Intracoronary microcatheter indwelling for continuous pumping of low-dose thrombolytic drugs: A new approach to reperfusion in acute myocardial infarction.

Reperfusion therapy of acute myocardial infarction (AMI) refers to physical or chemical recanalization and restoration of blood flow to an occluded coronary artery, and current techniques for reperfusion therapy include intravenous thrombolysis, percutaneous coronary intervention (PCI) and coronary artery bypass grafting (CABG). The number of patients receiving emergency CABG in the real world is decreasing due to the disadvantages of CABG and the improvement in PCI procedures. Thrombolytic therapy has some disadvantages such as low recanalization rate, high risk of reocclusion and bleeding, and short time window. On the other hand, intracoronary interventional therapy may meet the requirements of "early, complete and persistent" patency of coronary arteries at different time points. However, in the emergency PCI, although thrombus aspiration via a catheter or balloon dilation is performed, residual thrombus with heavy or low TIMI (thrombolysis in myocardial infarction) myocardial perfusion grading is still observed in some patients, suggesting disordered microcirculation. Currently, the treatment of microcirculatory disturbance in emergency PCI mainly employed injection of tirofiban, adenosine, thrombolytic agent or other drugs into the local area via a microcatheter in a short time, all of which can significantly reduce the thrombus load and improve TIMI perfusion. Herein, we report that a microcatheter was indwelled in the coronary artery for continuous pumping of low-dose thrombolytic drugs as reperfusion therapy in 12 patients with acute and subacute MI.

Low-Shear Stress Promotes Atherosclerosis via Inducing Endothelial Cell Pyroptosis Mediated by IKKε/STAT1/NLRP3 Pathway.

Atherosclerosis is initiated by vascular endothelial dysfunction, and low-shear stress (LSS) of blood flow is a key factor leading to endothelial dysfunction. Growing evidence suggests that endothelial cell pyroptosis plays an important role in the development of atherosclerosis. Studies have shown that low-shear stress can induce endothelial cell pyroptosis, but the exact mechanism remains unclear. Our experiments demonstrated that low-shear stress induced endothelial cell pyroptosis and the phosphorylation of IκB kinase ε (IKKε). IKKε knockdown not only significantly attenuated atherosclerosis lesions of aortic arch areas in ApoE-/- mice fed with high cholesterol diets, but also markedly reduced endothelial cell pyroptosis and NLRP3 expression triggered by low-shear stress. Further mechanism studies showed that IKKε promoted the expression of NLRP3 via activating signal transducer and activator of transcription 1 (STAT1) and the subsequent binding of STAT1 to NLRP3 promoter region. These results suggest that low-shear stress plays a pro-atherosclerotic role by promoting endothelial cell pyroptosis through the IKKε/STAT1/NLRP3 pathway, which provides new insights into the formation of atherosclerosis.

Efficacy of one- vs. two-stent implantation for coronary bifurcation lesions in diabetic patients utilizing AIR2 as an endpoint.

OBJECTIVE: This study aimed to assess the long term outcomes (all-cause death, myocardial infarction, target vessel revascularization, and silent restenosis at 12 months) of one-stent vs. two-stent implantation due to coronary bifurcation lesionsin diabetic patients using AIR2 as a new endpoint. METHODS AND RESULTS: A total of 178 diabetic patients with true coronary bifurcation lesions underwent percutaneous coronary intervention in the DK-Crush trials. All patients were stratified based on the stent placement strategy: one-stent group (n=76) and two-stent group (n=102). Results showed the primary endpoint, AIR2, in one-stent group was twice that in two-stent group (32.9% vs. 16.7%, P=0.013). The incidence of silent restenosis at 12 months was also significantly higher in one-stent group (19.7% versus 4.9%, P=0.003). Moreover, Kaplan-Meier analysis revealed the cumulative AIR2-free survival rate after a 12-month follow-up was markedly lower in one-stent group than in two-stent group. Interestingly, MACEs, including death, myocardial infarction and repeat revascularization, were not comparable between 2 groups (13.2% vs. 12.7%, P=0.935). Likewise, the incidence of definite or probable ST in one-stent group was also similar to that in two-stent group (2.6% vs. 4.9%, P=0.761). CONCLUSION: Our study indicates that, in terms of the AIR2 as a combined clinical and angiographic endpoint, two-stent implantation is superior to one-stent implantation for the treatment of coronary bifurcation intervention in diabetic patients.

Acute renal injury after thoracic endovascular aortic repair of Stanford type B aortic dissection: incidence, risk factors, and prognosis.

BACKGROUND/PURPOSE: Acute kidney injury (AKI) significantly increases the risk of mortality in patients following cardiovascular intervention procedures. This study was carried out to investigate the incidence, predictors, and prognostic implications of AKI after thoracic endovascular aortic repair (TEVAR) of Stanford type B aortic dissection. METHODS: A total of 156 patients with Stanford type B aortic dissection who underwent TEVAR were retrospectively analyzed between February 1, 2004 and October 31, 2011. Multivariable regression was used to predict risk factors for AKI. Association between baseline characteristics, postoperative AKI, and mortality during follow up was evaluated. RESULTS: AKI was identified in 48 (30.8%) of 156 patients, with seven (14.5%) patients requiring continuous renal replacement therapy. The in-hospital mortality rate was 0% in patients without AKI and 12.5% in those with AKI (p = 0.001). Univariate analysis identified preoperative chronic kidney disease, acute dissection, complicated dissection, malperfusion complications with comprehensive complications, and postoperative minimum estimated glomerular filtration rate within 48 hours as associated with AKI. Malperfusion complications [odds ratio (OR) = 4.828; 95% confidence interval (CI) = 1.163-20.03] were the only independent predictor of AKI. Patients suffering from AKI had a 14-fold increased risk for 30-day mortality (OR = 14.3; 95% CI = 1.7-118.4; p = 0.014) and a 10-fold increased risk for 1-year mortality (OR = 9.5; 95% CI = 2.02-44.9; p = 0.004). CONCLUSION: A significant rate of AKI was observed following TEVAR and was associated with an increase in 30-day and 1-year mortality. Malperfusion complications were identified as an independent predictor of AKI.