Heart Failure Guidelines: Introduction to the New Agents

G. Blair Sarbacker, PharmD, BCACP; Alyson G. Wilder, PharmD, BCPS

Disclosures

US Pharmacist. 2018;43(2):22-26. 

In This Article

Abstract and Introduction

Abstract

Heart failure (HF) causes significant morbidity and mortality and imposes a large cost burden on the U.S. healthcare system. It has been estimated that the prevalence of HF will increase 46% by the year 2030. For these reasons, hospital readmissions are now being monitored by several agencies. In 2016, the American College of Cardiology, the American Heart Association, and the Heart Failure Society of America published a focused update on new pharmacologic therapy for HF, which was prompted by recent evidence and availability of the novel agents Entresto (sacubitril/valsartan) and Corlanor (ivabradine). Pharmacists are in a unique position to assist in HF care, as the use of specific medications has proven to decrease morbidity, mortality, and hospital readmissions.

Introduction

An estimated 6.5 million Americans aged 20 years and older are burdened with heart failure (HF). In 2014, HF was listed as the cause of one in every nine deaths. Approximately 50% of patients die 5 years after being diagnosed with HF. The direct medical costs for HF in 2012 were projected to be about $21 billion.[1] It has been estimated that the prevalence of HF will increase 46% by the year 2030.[2] This means that one in every 33 Americans—numbering more than 8 million people—will have HF. Cost projections for the healthcare system suggest that, in 2030, $53 billion and $70 billion will be attributed to direct medical costs and indirect costs of HF, respectively.[2] Roughly 45% of HF patients who are symptomatic have reduced ejection fraction (EF).[1] Because of the high rate of readmission for HF, the Centers for Medicare & Medicaid Services and the Hospital Quality Alliance currently require reporting of 30-day hospital readmissions for HF.[3] Medicare data from 2015 show that 16.4% of Medicare patients with HF experienced a potentially preventable readmission; this is a decline of 3.1% from 2010.[4]

HF occurs when the heart pumps an insufficient amount of blood to meet the body's metabolic demands. Risk factors for HF include atherosclerotic disease, diabetes, hypertension, metabolic syndrome, and smoking. Patients with HF often present with symptoms of dyspnea, edema, and fatigue.[5]

Left ventricular (LV) dysfunction is classified as impaired ventricular contraction and ejection (systolic dysfunction) and impaired relaxation and ventricular filling (diastolic dysfunction). This, in turn, causes decreased cardiac output, which leads to global hypoperfusion. Hypoperfusion activates compensatory mechanisms to aid in maintaining circulation. These compensatory mechanisms include neurohormonal activation, increased contractility, vasoconstriction, and ventricular hypertrophy and remodeling. Long-term activation of these mechanisms leads to the progression of HF.[6]

Neurohormonal activation promotes sodium and water retention, and the overstimulation of the sympathetic nervous system and the release of catecholamines increase heart rate and contractility. Activation of the renin-angiotensin-aldosterone system (RAAS) and the release of vasopressin increase vasoconstriction. The chronic hemodynamic stresses on the heart lead to remodeling. As the ventricle continues to enlarge and the myocardium hypertrophies, wall tension and fibrosis increase, further impairing contractility.[6]

Natriuretic peptides counteract vasoconstriction and are released upon atrial or ventricular stretch. Natriuretic peptides cause vasodilation, excretion of salt and water, and inhibition of renin, aldosterone, and vasopressin secretion. Additionally, endothelium-derived vasoactive substances, such as nitric oxide and bradykinin, act locally to promote vasodilation.[6] Natriuretic peptides and bradykinin are degraded by neprilysin, a neutral endopeptidase.[7]

HF with preserved EF (HFpEF), also referred to as diastolic dysfunction, is defined as clinical signs of HF with an EF of 50% or greater. HFpEF may be further classified as borderline (EF = 41%-49%) and improved (EF >40%). HF with reduced EF (HFrEF), also referred to as systolic dysfunction, is distinguished by an EF of 40% or less.[5] There is a paucity of efficacy data on the treatment of HFpEF. Treatment effectiveness has been demonstrated only in patients with HFrEF.

HF staging is broken down into structural and functional classifications. The American College of Cardiology Foundation (ACCF) and the American Heart Association (AHA) provide structural classification, and the New York Heart Association (NYHA) provides functional classification. Table 1 summarizes staging of HF.[5]

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