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INTERMACS Profiles and Outcomes Among Non–Inotrope-Dependent Outpatients With Heart Failure and Reduced Ejection Fraction Canagliflozin and Renal Outcomes in Type 2 Diabetes and Nephropathy Anticoagulation in Concomitant Chronic Kidney Disease and Atrial Fibrillation: JACC Review Topic of the Week Coronary plaque redistribution after stent implantation is determined by lipid composition: A NIRS-IVUS analysis Percutaneous Coronary Intervention for Vulnerable Coronary Atherosclerotic Plaque Low-density lipoproteins cause atherosclerotic cardiovascular disease: pathophysiological, genetic, and therapeutic insights: a consensus statement from the European Atherosclerosis Society Consensus Panel Criteria for Iron Deficiency in Patients With Heart Failure The impact of intravascular ultrasound guidance during drug eluting stent implantation on angiographic outcomes Histopathologic validation of the intravascular ultrasound diagnosis of calcified coronary artery nodules Prior Pacemaker Implantation and Clinical Outcomes in Patients With Heart Failure and Preserved Ejection Fraction

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.