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2013 ACCF/AHA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines

The medical profession should play a central role in evaluating the evidence related to drugs, …

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2013 ACCF/AHA Guideline for the Management of Heart Failure: Executive Summary A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines

Heart failure (HF) is a major public health issue, with a prevalence of over 5.8 million in the USA, and over 23 million worldwide, and rising. The lifetime risk of developing HF is one in five. Although promising evidence shows that the age-adjusted incidence of HF may have plateaued, HF still carries substantial morbidity and mortality, with 5-year mortality that rival those of many cancers. HF represents a considerable burden to the health-care system, responsible for costs of more than $39 billion annually in the USA alone, and high rates of hospitalizations, readmissions, and outpatient visits. HF is not a single entity, but a clinical syndrome that may have different characteristics depending on age, sex, race or ethnicity, left ventricular ejection fraction (LVEF) status, and HF etiology. Furthermore, pathophysiological differences are observed among patients diagnosed with HF and reduced LVEF compared with HF and preserved LVEF, which are beginning to be better appreciated in epidemiological studies. A number of risk factors, such as ischemic heart disease, hypertension, smoking, obesity, and diabetes, among others, have been identified that both predict the incidence of HF as well as its severity. In this Review, we discuss key features of the epidemiology and risk profile of HF.

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Epidemiology and risk profile of heart failure

Objectives Platelet activation and aggregation play an important role in the pathogenesis of cardiovascular disease. We examined the association of a single nucleotide polymorphism (SNP) in the GPIIIa platelet glycoprotein (Leu33Pro) with carotid artery plaque morphology and with expression of platelet markers using data from the Atherosclerosis Risk in Communities (ARIC) Carotid MRI study. Methods The study sample consisted of 1202 Caucasian members of the ARIC study cohort recruited in 2004–2005 to participate in the Carotid MRI Substudy under stratified sampling based on maximum carotid artery wall thickness. The Leu33Pro polymorphism was identified as SNP rs5918 in the ITGB3 gene. Plaque visualization was accomplished with contrast enhanced MRI examination of the thickest segment of the carotid artery. Expression of platelet markers was measured using fasting whole blood flow cytometry. Results This cross-sectional analysis based on age and gender adjusted weighted linear regression models suggests that those homozygous for the Leu33Pro risk allele (C) have decreased mean and minimum fibrous cap thickness. We did not observe differences in plaque lipid volume or maximum carotid artery wall thickness across SNP rs5918 genotypes. Carriers of the Leu33Pro polymorphism, as compared to major allele homozygotes, had greater percent of platelets expressing P-selectin, a platelet glycoprotein indicating activation status. Prevalent coronary heart disease did not affect estimates of fibrous cap thickness or of platelet activation. Conclusion Our results suggest that individuals with Leu33Pro polymorphism of the GPIIIa glycoprotein may be predisposed to increased risk of atherosclerotic plaque rupture. © 2011 Elsevier Ireland Ltd. All rights reserved.

The Atherosclerosis Risk in Communities (ARIC) Study

Heart failure (HF) is a rapidly growing public health issue with an estimated prevalence of >37.7 million individuals globally. HF is a shared chronic phase of cardiac functional impairment secondary to many aetiologies, and patients with HF experience numerous symptoms that affect their quality of life, including dyspnoea, fatigue, poor exercise tolerance, and fluid retention. Although the underlying causes of HF vary according to sex, age, ethnicity, comorbidities, and environment, the majority of cases remain preventable. HF is associated with increased morbidity and mortality, and confers a substantial burden to the health-care system. HF is a leading cause of hospitalization among adults and the elderly. In the USA, the total medical costs for patients with HF are expected to rise from US$20.9 billion in 2012 to $53.1 billion by 2030. Improvements in the medical management of risk factors and HF have stabilized the incidence of this disease in many countries. In this Review, we provide an overview of the latest epidemiological data on HF, and propose future directions for reducing the ever-increasing HF burden.

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Epidemiology and aetiology of heart failure

HFSA 2010 Comprehensive Heart Failure Practice Guideline.

Patients with cirrhosis and heart failure (HF) share the pathophysiology of decreased effective arterial blood volume because of splanchnic vasodilatation in cirrhosis and decreased cardiac output in HF, with resultant stimulation of the renin-angiotensin-aldosterone system. Hyperaldosteronism plays a major role in the pathogenesis of ascites and contributes to resistance to loop diuretics. Therefore, the use of high doses of aldosterone antagonist (spironolactone up to 400 mg/day) is the main therapy to produce a negative sodium balance in cirrhotic patients with ascites. Hyperaldosteronism also has increasingly been recognized as a risk factor for myocardial and vascular fibrosis. Therefore, low-dose aldosterone antagonists are being used in patients with HF for cardioprotective action. However, the doses (25 to 50 mg/day) at which they are being used in cardiac patients as reported in the Randomized Aldactone Evaluation Study are not natriuretic. It is likely, therefore, that the mortality benefit relates primarily from their effect on cardiac and vascular fibrosis. Resistance to commonly used loop diuretics is frequently present in patients with advanced HF. In patients with decompensated HF with volume overload who are loop diuretic resistant, ultrafiltration may be the only available option. This is, however, an invasive procedure. For these patients, natriuretic doses of aldosterone antagonists (spironolactone 50 mg/day) may be a potential option. The competitive natriuretic response of aldosterone antagonists is related to activity of the renin-angiotensin-aldosterone system: the higher the renin-an- giotensin-aldosterone system activity, the higher the dose of aldosterone antagonist required to produce natriuresis. This article will discuss the potential use of natriuretic doses of aldosterone antagonists in patients with HF, including the potential side effect of hyperkalemia. (Circ Heart Fail. 2009;2:370-376.)

Advances in Heart Failure Sodium Retention in Heart Failure and Cirrhosis Potential Role of Natriuretic Doses of Mineralocorticoid Antagonist

Blood Urea Nitrogen: A Marker for Adverse Effects of Loop Diuretics?

Sex-related differences in clinical and laboratory characteristics, course and prognosis are well documented in patients with heart failure. However, most information regarding heart failure therapies has been obtained from studies conducted primarily in men. Reviewing the existing literature indicates that the recommendations regarding pharmacological and device therapies should apply similarly to men and women. One possible exception, however, is the possibility of more benefit derived from angiotensin receptor blockers in women, and from angiotensin converting enzyme inhibitors in men. Future clinical trials should be conducted either exclusively in women or have a larger representation of women to insure the adequate assessment of the potential benefit versus risk in women.

JoAnn Lindenfeld

Papers

HFSA 2010 Comprehensive Heart Failure Practice Guideline.

Advances in Heart Failure Sodium Retention in Heart Failure and Cirrhosis Potential Role of Natriuretic Doses of Mineralocorticoid Antagonist

Blood Urea Nitrogen: A Marker for Adverse Effects of Loop Diuretics?

Sex differences in response to chronic heart failure therapies.

Exploring the Potential Synergistic Action of Spironolactone on Nitric Oxide–Enhancing Therapy: Insights From the African-American Heart Failure Trial