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Shear Stress

Abstract

Recommended Article

Low shear stress induces vascular eNOS uncoupling via autophagy-mediated eNOS phosphorylation Role of local coronary blood flow patterns and shear stress on the development of microvascular and epicardial endothelial dysfunction and coronary plaque Comparison Of High Shear Stress-Induced Thrombotic And Thrombolytic Effect Between Aspirin, Clopidogrel And Very Low Dose Rivaroxaban And Aspirin, Ticagrelor Treatments In Patients With Acute Coronary Syndrome Evolving insights into the role of local shear stress in late stent failure from neoatherosclerosis formation and plaque destabilization Low shear stress induces endothelial reactive oxygen species via the AT1R/eNOS/NO pathway Role of Low Endothelial Shear Stress and Plaque Characteristics in the Prediction of Nonculprit Major Adverse Cardiac Events: The PROSPECT Study Transcatheter Aortic Valve Implantation Represents an Anti-Inflammatory Therapy Via Reduction of Shear Stress-Induced, Piezo-1-Mediated Monocyte Activation Implications of the local hemodynamic forces on the formation and destabilization of neoatherosclerotic lesions
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Original Research

JOURNAL：Circulation. Article Link

ACC19 Late Breaking Science and Simultaneous Publications

CBSMD


AMI without Cardiogenic Shock

Study Design: multicenter, prospective, randomized exploratory safety and feasibility trial, 50 patients （1:1 randomization） with anterior STEMI to LV unloading by using the Impella CP followed by immediate reperfusion (U-IR) versus delayed reperfusion after 30 minutes of unloading (U-DR).

Study Endpoints: The primary safety outcome was a composite of major adverse cardiovascular and cerebrovascular events at 30 days. Efficacy parameters included the assessment of infarct size by using cardiac magnetic resonance imaging.

Editorial - “Percutaneous Support Devices for Percutaneous Coronary Intervention”


AMI without Cardiogenic Shock

Study Design: multicenter, randomized, open-label trial

Study Results: Follow-up was completed for 591 of 600 patients (98.5%). Mortality was not different between the IABP and the control group (66.3% versus 67.0%; relative risk, 0.99; 95% CI, 0.88–1.11; P=0.98). There were also no differences in recurrent myocardial infarction, stroke, repeat revascularization, or rehospitalization for cardiac reasons (all P>0.05). Survivors’ quality of life as assessed by the EuroQol 5D questionnaire and the New York Heart Association class did not differ between groups.

Editorial -














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