Stage B, a Pre-cursor of Heart Failure, An Issue of Heart Failure Clinics

Gary S. Francis, Jay N. Cohn

Description

In the joint American College of Cardiology /American Heart Association classification system, Stage B heart failure refers to patients with structural heart disease but no symptoms of heart failure. Preventing progression of heart failure in Stage B patients is a central concern to heart failure specialists, so two issues have been devoted to this topic. Part I focuses on an understanding of structural heart disease and the factors that cause progression from risk of heart failure to development of structural changes.

Sujets

• Médecine
• Spécialités médicales
• Medical
• Cardiology

Informations

• Publié par: Saunders
• Date de parution: 28 janvier 2012
• Nombre de lectures: 0
• EAN13: 9781455742844
• Langue: English
• Poids de l'ouvrage: 2 Mo

Extrait

Heart Failure Clinics , Vol. 8, No. 1, January 2012
ISSN: 1551-7136
doi: 10.1016/S1551-7136(11)00112-7

Contributors
Heart Failure Clinics
Stage B, a Pre-cursor of Heart Failure, Part I
Jay N. Cohn, MD
University of Minnesota Medical School, Minneapolis, MN 55455, USA
Gary S. Francis, MD
University of Minnesota Medical School, Minneapolis, MN 55455, USA
ISSN  1551-7136
Volume 8 • Number 1 • January 2012

Contents

Contributors
Forthcoming Issues
Reducing the Burden of Stage B Heart Failure Will Require Connecting the Dots Between “Knowns” and “Known Unknowns”
Stage B, a Pre-cursor of Heart Failure
Myocyte Changes in Heart Failure
Changes in the Myocardial Interstitium and Contribution to the Progression of Heart Failure
Pressure Overload
Volume Overload
Ischemia/Infarction
Cardiomyopathies: Classification, Diagnosis, and Treatment
Role of Apoptosis in Adverse Ventricular Remodeling
Neurohumoral Stimulation
Role of Oxidative Stress in Disease Progression in Stage B, a Pre-cursor of Heart Failure
From Risk Factors to Structural Heart Disease: The Role of Inflammation
Diabetes and the Risk of Heart Failure
Arterial Stiffness/Elasticity in the Contribution to Progression of Heart Failure
Aging-Associated Cardiovascular Changes and Their Relationship to Heart Failure
Index
Heart Failure Clinics , Vol. 8, No. 1, January 2012
ISSN: 1551-7136
doi: 10.1016/S1551-7136(11)00114-0

Forthcoming Issues
Heart Failure Clinics , Vol. 8, No. 1, January 2012
ISSN: 1551-7136
doi: 10.1016/j.hfc.2011.10.001

Editorial
Reducing the Burden of Stage B Heart Failure Will Require Connecting the Dots Between “Knowns” and “Known Unknowns”

Ragavendra R. Baliga, MD, MBA
Division of Cardiovascular Medicine, Ohio State University Medical Center, Columbus, OH, USA
E-mail address: [e-mail]
E-mail address: [e-mail]

James B. Young, MD
Lerner College of Medicine, Endocrinology and Metabolism Institute, Cleveland Clinic, Cleveland, OH, USA
E-mail address: [e-mail]
E-mail address: [e-mail]


Ragavendra R. Baliga, MD, MBA, Consulting Editor

James B. Young, MD, Consulting Editor

There are known knowns; there are things we know we know.
We also know there are known unknowns; that is to say we know there are some things we do not know.
But there are also unknown unknowns—the ones we don’t know we don’t know.
—Former United States Secretary of Defense Donald Rumsfeld 1
The American College of Cardiology/American Heart Association heart failure guidelines define Stage B heart failure as patients with structural heart disease but no current or prior symptoms of heart failure 2 and include patients with prior myocardial infarction, left ventricular hypertrophy, valvular heart disease, regional wall-motion abnormality, left ventricular enlargement, and systolic and diastolic dysfunction. 3 Despite their lack of symptoms, these patients with systolic dysfunction have a nearly five-fold risk of developing heart failure 4 ( Fig. 1 ). The common causes of stage B heart failure include ischemic heart disease and hypertension 5 - 7 ( Box 1 ). It is estimated that the prevalence of stage B heart failure is four times as great as that of stages C and D heart failure patients put together. One recent population-based study estimates that 34% of individuals >45 years of age have stage B heart failure. 8 This burden is projected to increase as the prevalence of tobacco use, obesity, 9, 10 hypertension, 11 hyperglycemia, 12 dyslipidemia, 13 and consequently ischemic heart disease continues to increase worldwide. 14 Efforts to reduce this burden will require reducing risk at an individual level 3, 15, 16 and a population-based approach 17 ( Fig. 2 )—an integrated approach that has successfully achieved near global eradication of communicable diseases such as poliomyelitis.

Fig. 1 Kaplan–Meier curves for survival. Referent group consists of subjects with normal left ventricular systolic function (EF >50%) and no history of congestive heart failure. Mild ALVD indicates mild asymptomatic left ventricular systolic dysfunction (EF 40% to 50%); mod/sev ALVD, moderate-to-severe asymptomatic left ventricular systolic dysfunction (EF <40%); systolic CHF, congestive heart failure with EF ≤50%.
( From Wang TJ, Evans JC, Benjamin EJ, et al. Natural history of asymptomatic left ventricular systolic dysfunction in the community. Circulation 2003;108(8):977–82; with permission.)

Box 1 Causes of stage B heart failure

• Ischemic etiology
• Nonischemic cause
Hypertension
Valvular heart disease
Cardiotoxin exposure particularly chemotherapy 52
Post-viral infection/myocarditis
Familial idiopathic dilated cardiomyopathy

Fig. 2 At any given time, about 5%–10% of the population are at very high risk of developing cardiovascular events. A much larger segment of the population is at moderate risk. If no preventive action is taken, individuals at the tail end of the distribution will develop fatal and nonfatal cardiovascular events. Many more events will occur in the segment of the population with modest elevation of risk, as the number of individuals in this segment is larger.
( From Mendis S. Cardiovascular risk assessment and management in developing countries. Vasc Health Risk Manag 2005;1(1):15–8.)
It is estimated that about 5%-10% of the population are at very high risk of developing cardiovascular events ( Fig. 2 ), whereas a much larger proportion of the population is at moderate risk. 17 - 20 Individuals at the tail end of the distribution are more prone to fatal and nonfatal cardiovascular events, whereas more individuals with moderate risk will develop cardiovascular events because the whole burden of moderate risk individuals is much larger. 9, 11 - 13 Therefore, it is vital that population-based strategies be pursued to shift the risk distribution of the population as a whole to the left, using both lifestyle changes and pharmacotherapy. 17, 21 These include reduction of salt intake 22 and trans-fatty acids 23, 24 at a population level through, arguably, legislation 25 and with a focus on health education, 26, 27 using mass media with attention paid to blood pressure, cholesterol, and obesity 28, 29 control, which are known to be cost effective. 18 - 20 The benefits of preventive guidelines and continuing medical education are increasingly becoming apparent, as evidenced by recent declines in heart failure mortality and hospitalizations. 30, 31
Reducing risk at an individual level will clearly require lifestyle changes, adherence to pharmacotherapy, 32 - 34 and possibly mechanical cardiac resynchronization. 35 - 37 The lack of physical activity, increased caloric intake, and use of tobacco result in hypertension, 5, 11 dyslipidemia, 13, 38 and hyperglycemia, 12 which in turn have been attributed to 75% of the cardiovascular event risk factors. Other established risk factors for cardiovascular disease include age, gender, obesity, past history of cardiovascular disease, family history of cardiovascular disease, and socioeconomic position. 39 These, for obvious reasons, are much harder to address with a goal of improvising outcomes. Also, a recent study reported that dysfunction of non-cardiac organs—particularly the renal, pulmonary, and hematopoietic systems—was associated with a 30% increase in overall risk of heart failure and the risk increased proportionally if more than one organ was involved. 40, 41 In this study, the average age of the participants was 76 years and most were women with a history of hypertension; not many had diabetes or coronary artery disease. These investigators found that dysfunction of the non-cardiac organs was relatively “mild” as reflected by serum creatinine >1.05 mg/dL, hemoglobin <13 g/dL, or FEV1/FVC ratio <91% predicted. These findings support earlier data regarding the additive effects of cardio-renal-anemia syndrome 42 and the effect of impaired lung function on both systolic and diastolic cardiac performance. 43, 44 Therefore, it has been argued that reducing risk at the individual level will require attention to both traditional risk factors and non-cardiac organ dysfunction ( Fig. 3 ).

Fig. 3 Interaction of cardiac and noncardiac dysfunctions and progression to heart failure.
( From Klein L. Omnes Viae Romam Ducunt: asymptomatic cardiac and noncardiac organ system dysfunction leads to heart failure. Circulation 2011;124:4–6; with permission.)
Although there are established strategies to reduce individual risk 18 - 20 and population-based risk, there is no definitive method to identify patients with stage B heart failure ( Box 2 ). 45 Identification of the individual with stage B heart failure involves screening of populations and promising strategies include using biomarkers. 46 - 51 To discuss such challenges pertaining to the management of stage B heart failure, Drs Jay Cohn and Gary Francis have assembled an international panel of experts. These expert opinions provide ample food for thought on developing an effective strategy to manage stage B pre-cursor to heart failure. We hope that these insightful articles will allow “connecting the dots” between what we know and the “known unknowns” of stage B pre-cursor to heart failure.

Box 2 Summary of proposed research designs 45

1. Determine the incidence of asymptomatic LVSD in community-based cohorts.
2. Characterize the natural history of asymptomatic LVSD in the community:
a. Natural history in individuals with different degrees of LVSD
b. Natural history in individuals with LVSD without previous MI
3. Examine the natural history of subclinical left ventricular diastolic dysfunction.
4. Examine the cost-effectiveness of various screening strategies for identifying left ventricular dysfunction and develop better screening tools.
5. Address the role of medications other than ACE inhibitors