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Shear Stress

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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 Prediction of progression of coronary artery disease and clinical outcomes using vascular profiling of endothelial shear stress and arterial plaque characteristics: the PREDICTION Study Role of endothelial dysfunction in determining angina after percutaneous coronary intervention: Learning from pathophysiology to optimize treatment
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Review ArticleVolume 74, Issue 5, August 2019

JOURNAL：J Am Coll Cardiol. Article Link

From ACE Inhibitors/ARBs to ARNIs in Coronary Artery Disease and Heart Failure (Part 2/5)

DP Leong, JJV McMurray, PG Joseph et al. Keywords: ACE-I; ARB; ARNI; coronary disease; heart failure

ABSTRACT

The pharmacological inhibition of the renin-angiotensin-aldosterone system as a therapeutic strategy is one of the most significant advances in the treatment and prevention of cardiovascular disease in heart failure with reduced ejection fraction and in coronary artery disease. Recently, the addition of neprilysin inhibition to angiotensin receptor blockade has been shown to be even more effective than angiotensin-converting enzyme inhibition alone in heart failure with reduced ejection fraction, marking an important new milestone in heart failure treatment. This review summarizes the major trials that have informed the clinical role of inhibition of the renin-angiotensin-aldosterone and neprilysin pathways, as well as the limitations of these strategies.

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