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Refined balloon pulmonary angioplasty for inoperable patients with chronic thromboembolic pulmonary hypertension Volumetric characterization of human coronary calcification by frequency-domain optical coherence tomography Active and Passive Vaccination for Pulmonary Arterial Hypertension: A Novel Therapeutic Paradigm The Relation Between Optical Coherence Tomography-Detected Layered Pattern and Acute Side Branch Occlusion After Provisional Stenting of Coronary Bifurcation Lesions Chronic thromboembolic pulmonary hypertension Intravascular Ultrasound Pulmonary Artery Denervation to Treat Pulmonary Arterial Hypertension (TROPHY1): Multicenter, Early Feasibility Study Asia Pacific Consensus Document on Coronary Bifurcation Interventions Histopathological validation of optical coherence tomography findings of the coronary arteries Long-term outcomes of routine versus provisional T-stenting for de novo coronary bifurcation lesions: five-year results of the Bifurcations Bad Krozingen I study Percutaneous Coronary Intervention Techniques for Bifurcation Disease: Network Meta-analysis Reveals Superiority of Double-Kissing Crush

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.