HEART FAILURE 2006: UPDATE FOR THE PRIMARY CARE PHYSICIAN
Supported by educational grants from the 2006 HFSA Heart Failure
Awareness Roundtable: Abbott Laboratories; GlaxoSmithKline; Guidant Foundation;
Medtronic, Inc; St. Jude Medical
Presented February 11, 2006, in Houston, and cosponsored by the
Heart Failure Society of America
| WHY HEART FAILURE IS THE ONLY CARDIOVASCULAR DISEASE
INCREASING IN PREVALENCE: IMPLICATIONS REGARDING PREVENTION
óBarry H. Greenberg, MD |
| Practical hint 1: 90% of heart failure (HF)
attributed to coronary disease, hypertension, and/or diabetes
|
| Chain of events leading to HF: presence of risk
factors (eg, hypertension, obesity, diabetes) leads to
development of atherosclerosis and/or left ventricular hypertrophy (LVH),
then to overt coronary artery disease (CAD); without aggressive treatment,
patients may develop coronary thrombosis, leading to myocardial infarction
(MI) and loss of functioning myocardium; remodeling process occurs in
response to injury, leading to dilated ventricle and subsequent
development of progressive HF |
| Post-MI remodeling: initially, damaged area of
myocardium undergoes thinning and bulging, with small increase in overall
chamber volume; over time, increase in overall chamber volume, muscle
mass, and amount of fibrous tissue in non- infarcted segments of
myocardium; configuration of left ventricle (LV) changes, becoming more
spherical; changes lead to abnormalities in systolic and diastolic
function, resulting in HF |
| Functional changes associated with LVH: ventricle
develops relaxation abnormalities and, over time, becomes less compliant;
in order to fill with enough blood to maintain stroke volume, LV
end-diastolic pressure increases, which gets transmitted to pulmonary
circuit, and patient develops signs and symptoms of pulmonary congestion
|
| HF with preserved systolic function (diastolic HF):
impaired compliance of LV with normal or near-normal ejection
fraction (EF); prevalenceóin men, >40% of HF cases; in women,
≈66% of HF cases |
| Practical hint 2: cardiac remodeling initiated by
process that injures heart or increases workload, eg,
hypertension, MI; remodeling leads to progressive deterioration in cardiac
function, systolic and diastolic abnormalities, and HF
|
| Neurohormonal activation: precipitated by reduction
in cardiac performance; immediate consequences may include propensity to
retain salt and water and peripheral vasoconstriction; leads to increase
in cardiac fibrosis, apoptosis of cardiac myocytes, and myocardial
hypertrophy; Studies of Left Ventricular Dysfunction (SOLVD)
trialópatients with asymptomatic LV dysfunction randomized to
angiotensin-converting enzyme (ACE) inhibitor or placebo; prophylactic
treatment with ACE inhibitor reduced risk for death, HF, or
hospitalization by ≈20% and development of HF by
≈40%; ACE inhibitor associated with inhibition of
remodeling as evidenced by reduction in LV mass |
| Practical hint 3: primary and secondary prevention of
HF highly effective ways of reducing morbidity and mortality; strategies
for preventing HF include control of blood pressure (BP), prevention of
CAD and MI, optimization of diabetes care, and neurohormonal blockade to
inhibit remodeling |
| HOW TO DETECT HEART FAILURE AND ASSESS ITS
SEVERITY óAlan B. Miller, MD |
| Symptoms of HF: dyspnea at rest or on exertion;
reduction in exercise capacity; orthopnea; paroxysmal nocturnal dyspnea or
nocturnal cough; edema, ascites, scrotal edema; fatigue; less specific
indicatorsóearly satiety; nonspecific gastrointestinal (GI)
complaints; wheezing; change in mental status |
| Physical signs: jugular venous pressure
(JVP)ówith patient on examination table at 35∞ to 40∞ elevation, look
at neck veins; if JVP elevated, patient likely volume overloaded;
hepatojugular refluxówith patient breathing normally, press over
abdomen to see if heart can handle quick volume load;
noteóimportant for patients with chronic HF to be euvolemic
before implementing certain therapies, particularly β-blockers;
S3
gallopófilling sound that indicates whether
heart dilated or presence of valvular regurgitation; rales and
ascitesónonspecific but can help when following patient;
displaced point of maximal impulse (PMI)óindicates dilated heart;
heart murmuróparticularly mitral regurgitation (MR) and tricuspid
regurgitation; MR is component of HF that increases symptomatology
|
| Patient evaluation: history and physical examination;
electrocardiography (ECG) helps determine whether patient has normal
rhythm, intraventricular conduction delay, and ischemic heart or coronary
disease; chest x-rays; routine laboratory tests; assess cardiac structure
and function to determine presence of systolic dysfunction or preserved EF
(important for directing therapy); not necessary to perform cardiac
catheterization in all patients; evaluate for life-threatening arrhythmias
|
| Differential diagnosis: pulmonary infection; chronic
obstructive pulmonary disease (COPD); reactive airway disease; acute
coronary syndromes; pulmonary emboli; pneumothorax, pleural effusion;
aortic dissection |
| Determining presence of systolic or diastolic HF
|
 |
Physical examination: indicators of
systolic dysfunctionódilated heart, S3
gallop, murmur, and MR; indicators of diastolic
dysfunctionóhypertension, S4
(indicates stiff heart), and LVH on ECG |
 |
Imaging techniques: 2-D
echocardiographyóinexpensive; reproducible; can be performed at
bedside; radionuclide ventriculographyóvery helpful; cardiac
catheterizationóinvasive, although knowing end-diastolic pressure
helpful; cardiac magnetic resonance imaging (MRI)ólikely to
become gold standard |
|
Definition of systolic dysfunction: generally,
EF <40% to 45% |
| B-type natriuretic peptide (BNP): released from
ventricles when pressure and stretch in ventricular chamber increases; BNP
assay can be used to aid diagnosis of HF; some correlation with New York
Heart Association (NYHA) functional classification; if BNP <100 pg/mL,
dyspnea likely not due to cardiac etiology; BNP >1000 pg/mL likely due
to HF |
| Anemia: hemoglobin <11 g/dL associated with higher
mortality; mortality decreases as hemoglobin increases; unknown whether
correction of anemia changes prognosis |
| Severe HF: generally, patients with EF <20% have
bad prognosis; cardiopulmonary stress test expensive and complicated;
6-min walk test easier to perform (<200 m, severe HF; >400 m, mild
HF) |
| THE AFRICAN-AMERICAN PATIENT WITH HEART FAILURE
óClyde W. Yancy, MD |
| Background: review of literature shows blacks more
likely to have nonischemic etiology and whites more likely to have
ischemic etiology for HF |
| Hypertension: higher incidence in blacks; end-organ
manifestations dramatic, eg, end-stage renal disease, stroke,
LVH; management of hypertension in blacks reduces disease burden
substantially |
| RAND Health analysis: analysis of published trials
involving β-blockers; for nonblacks, β-blockers associated with mortality
risk reduction of 31%; for blacks, risk reduction only 3%; bucindolol
associated with poorer outcomes in blacks; carvedilol associated with
similar outcomes in blacks and whites |
| Nitric oxide deficiency: nitric oxide originally
termed endothelial-derived relaxation factor; some people function in
nitric oxide-deficient environment; study of forearm blood flow in
response to physiologic stress suggests blacks function as if manufacture
of nitric oxide impaired at baseline; suggestion that deficiency due to
dysequilibrium between nitric oxide synthase and oxidase, leading to
accumulation of superoxide (reactive O2
species) and disruption of cell cycles; addition of nitrates
enriches production of nitric oxide; addition of hydralazine (vasodilator
and antioxidant) impedes development of superoxide, reducing oxidative
stress |
|
Oxidative stress: defined as increase in
reactive O2 species and reduction in
nitric oxide; disrupts cell functioning and may be contributor to HF
|
| African-American Heart Failure Trial (A-HeFT):
>1000 black patients randomized to
hydralazine plus isosorbide dinitrate or placebo; trial stopped early
because of survival advantage in group receiving combination therapy;
composite end point of death, quality of life, and time to first
hospitalization; patient populationówomen 40%; average weight
>90 kg; predominantly NYHA class III; ischemic heart disease 25%;
nonischemic etiology 75% (mainly hypertension); at study entry, patients
being treated with ACE inhibitors, β-blockers, angiotensin-receptor
blockers (ARBs), and aldosterone antagonists; resultsóin
combination therapy group, mortality rate reduced ≈40%, time to first hospitalization reduced ≈40%, and significant improvement in quality of life;
>85% of patients in combination therapy group alive at 2 yr (mortality
rate <10% per yr); side effects of combination
therapyóheadache; dizziness |
| American College of Cardiology (ACC) and American Heart
Association (AHA) guidelines: addition of hydralazine plus
isosorbide dinitrate reasonable in patients with reduced LVEF already
taking appropriate therapy for symptomatic HF and who have persistent
symptoms (race independent) |
| Conclusions: differences in disease presentation and
etiology (particularly hypertension) exist in special populations; in
general, management should be same for all patients, irrespective of race
and gender |
| HEART FAILURE IN THE VERY OLD PATIENT: A COMMON PROBLEM
IN THE OFFICE SETTING óGary S. Francis, MD
|
| Background: ≈10% of patients
>70 yr of age have HF; LVH plagues older patients, particularly women;
with same degree of aortic stenosis, women have much higher incidence of
LVH than men; 20% to 25% of patients with HF have atrial fibrillation
|
| Alterations that occur with aging:
vascularóarteries stiffen; pulse pressure, pulse wave
velocity, and systolic BP increase; LVH develops; reduced exercise
toleranceócardiovascular reserve, peak exercise heart rate, peak
VO2 , and skeletal muscle mass decrease;
othersómore adverse drug interactions; more comorbid conditions
|
| Problem therapies in elderly
|
|
Digoxin: speaker rarely starts therapy in
digoxin-naive patients; can be problematic if renal function impaired; do
not use loading dose; begin with ≤0.125 mg/day;
monitor serum levels; interacts with spironolactone (leading to increased
toxicity), amiodarone, and other drugs; speaker advocates avoiding digoxin
in elderly patients |
|
Spironolactone: do not use if baseline
creatinine >2.0 mg/dL; stop or avoid potassium supplements; avoid
nonsteroidal anti-inflammatory drugs (NSAIDs); slow onset and offset;
hyperkalemia problematic in patients with diabetes or taking NSAIDs
|
|
Vasodilators: predominantly α-blockers taken
by men for prostatism; symptomatic hypotension; hyperkalemia and renal
insufficiency seen with ACE inhibitors and ARBs (orthostatic hypotension
not major problem); edema with dihydropyridines (can be mistaken for HF)
|
|
Diuretics: contraction alkalosis; renal
insufficiency; hypotension; urinary incontinence; ototoxicity; possible
increased mortality; hypokalemia; hypomagnesemia |
|
Warfarin: bleeding problems; drug
interactions; expensive |
|
Psychotropic agents: try to avoid at all costs
|
|
NSAIDs: associated with many problems,
including additional heart problems |
| Recommendations for treating elderly patient with HF:
use minimalist approach; start only one drug at a time; consider starting
drug at lowest possible dose and titrate gradually; avoid having patient
take all drugs at once; monitor creatinine and potassium carefully;
frequent office visits, phone calls, and follow-ups with nurse; quality of
life often more important than quantity of life |
| THE 2006 HEART FAILURE GUIDELINES AND WHAT THEY SAY
ABOUT SPECIAL POPULATIONS óJoAnn Lindenfeld, MD
|
| HF in elderly: >50% of new diagnoses of HF in
patients >80 yr of age; mortality increases with age
|
|
Recommendation: elderly patients, particularly
those >80 yr of age, should be evaluated for HF when presenting with
symptoms of dyspnea and fatigue |
|
BNP: level increases with age (same true for
N-terminal pro-BNP), but increases more in women than men; usual standards
of <100 pg/mL for BNP and <450 pg/mL for N-terminal pro-BNP not
adequate for elderly women |
|
Recommendation: β-blockers and ACE inhibitors
recommended as standard therapy in all elderly patients with HF due to LV
systolic dysfunction; in absence of contraindications, β-blockers and ACE
inhibitors also recommended in very elderly patients |
| HF in women: women far more likely to have preserved
EF; women also more likely to have side effect of cough with ACE
inhibitors (particularly problematic for elderly women with incontinence)
|
|
Recommendation: β-blockers and ACE inhibitors
recommended for women with HF due to symptomatic or asymptomatic LV
systolic dysfunction |
|
Recommendation: β-blockers and ACE inhibitors
recommended as part of standard therapy for African-Americans with HF due
to symptomatic or asymptomatic LV systolic dysfunction
|
|
Recommendation: combination of hydralazine and
isosorbide dinitrate recommended as part of standard therapy in addition
to β-blockers and ACE inhibitors for African-Americans with LV systolic
dysfunction and NYHA II, III, or IV HF |
| Heart Failure Society of America (HFSA) 2006 Comprehensive HF
Practice Guideline: available at www.hfsa.org
|
Educational Objectives
| The goal of this activity is to update the listener on all aspects of
heart failure (HF) management. After hearing and assimilating this
program, the clinician will be better able to: |
|
1. Identify the reasons for the increase in HF
and implement preventive strategies. |
|
2. Recognize HF and assess its severity.
|
|
3. Outline treatment strategies for HF in
black patients. |
|
4. Discuss problematic therapies in elderly
patients with HF. |
|
5. Implement current guidelines on the
management of HF in special populations. |
Discussed on This Program
Bucindolol (investigational)
Carvedilol [Coreg]
Digoxin [Digitek, Lanoxicaps, Lanoxin]
Isosorbide dinitrate/hydralazine HCL [BiDil]
Metoprolol succinate [Lopressor, Metoprolol Tartrate, Toprol XL]
Nebivolol (investigational)
Spironolactone [Aldactone]
Warfarin sodium [Coumadin]
Speakers
Barry H.
Greenberg, MD, Professor of Medicine and Director, Heart
Failure/Cardiac Transplantation Program, University of California, San Diego,
School of Medicine; Alan B. Miller, MD, Professor of Medicine
and Director, Heart Failure Clinic, University of Florida College of Medicine,
Jacksonville; Clyde W. Yancy, MD, Professor of Medicine and
Cardiology, and Medical Director, Heart Failure/Transplantation, University of
Texas Southwestern Medical Center; Associate Dean of Clinical Affairs, St. Paul
University Hospital, Dallas; Gary S. Francis, MD, Professor of
Medicine, Ohio State University Medical Center; Director, Acute Cardiac Care,
Cleveland Clinic Foundation, Cleveland; JoAnn Lindenfeld, MD,
Professor of Medicine and Medical Director, Cardiac Transplant Program,
University of Colorado Health Sciences Center, Denver.
Suggested Reading
Bozkurt
B, Deswal A: Obesity as a prognostic factor in chronic symptomatic
heart failure. Am Heart J 150:1233, 2005; Brown DW et al:
Racial or ethnic differences in hospitalization for heart failure among
elderly adults: Medicare, 1990 to 2000. Am Heart J 150:448, 2005;
Carson P et al; Vasodilator-Heart Failure Trial Study Group:
Racial differences in response to therapy for heart failure: analysis
of the vasodilator-heart failure trials. J Card Fail 5:178, 1999;
Economides E, Stevenson LW: The jugular veins: knowing enough
to look. Am Heart J 136:6, 1998; Eimer MJ et al:
Elevated B-type natriuretic peptide in asymptomatic men with chronic aortic
regurgitation and preserved left ventricular systolic function. Am J
Cardiol 94:676, 2004; Elesber AA, Redfield MM: Approach to
patients with heart failure and normal ejection fraction. Mayo Clin
Proc 76:1047, 2001; Evangelista LS et al: Racial
differences in treatment-seeking delays among heart failure patients. J Card
Fail 8:381, 2002; Juurlink DN et al: Rates of hyperkalemia
after publication of the Randomized Aldactone Evaluation Study. N Engl J
Med 351:543, 2004; Mamdani M et al: Cyclo-oxygenase-2
inhibitors versus non- selective non-steroidal anti-inflammatory drugs and
congestive heart failure outcomes in elderly patients: a population- based
cohort study. Lancet 363:1751, 2004; Masley S et al:
Planning group visits for high-risk patients. Fam Pract Manag
7:33, 2000; McAlister FA et al: A systematic review of
randomized trials of disease management programs in heart failure. Am J
Med 110:378, 2001; McCullough PA et al: B-type natriuretic
peptide and clinical judgment in emergency diagnosis of heart failure: analysis
from Breathing Not Properly (BNP) Multinational Study. Circulation
106:416, 2002; Perloff JK: Importance of elevated jugular
venous pressure and a third heart sound in asymptomatic left ventricular
dysfunction. Am J Med 114:499, 2003; Perloff JK: The
jugular venous pulse and third heart sound in patients with heart failure. N
Engl J Med 345:612, 2001; Taylor AL et al: Combination of
isosorbide dinitrate and hydralazine in blacks with heart failure. N Engl J
Med 351:2049, 2004; Yancy CW: The prevention of heart
failure in minority communities and discrepancies in health care delivery
systems. Med Clin North Am 88:1347, 2004.
Faculty Disclosure
In adherence
to ACCME guidelines, the Audio-Digest Foundation requests all lecturers to
disclose any significant financial relationship with the manufacturer or
provider of any commercial product or service discussed. The following has been
disclosed: Dr. Greenberg is a consultant and member of the scientific advisory
board for GlaxoSmithKline and CHF Solutions, and is on the Speakersí Bureau for
GlaxoSmithKline, Merck, Pfizer, AstraZeneca, and Novartis. Dr. Miller has
received research support from AstraZeneca, GlaxoSmithKline, Pfizer,
Bristol-Myers Squibb, Medtronic, Myogen, and NitroMed, and is on the Speakersí
Bureau for AstraZeneca, GlaxoSmithKline, Pfizer, Bristol-Myers Squibb,
Medtronic, Sanofi, Wyeth, King, NitroMed, CV Therapeutics, Novartis, and Abbott.
Dr. Yancy is a consultant for Scios, GlaxoSmithKline, CHF Solutions, Medtronic,
and Nitromed, has received research support from Scios, GlaxoSmithKline,
Medtronic, and NitroMed, and is on the Speakersí Bureau for Scios,
GlaxoSmithKline, Medtronic, Novartis, and NitroMed. Dr. Francis is a consultant
for Otsuka, a member of the scientific advisory board for GlaxoSmithKline and
Merck, has received research support from Pfizer, is on the Speakersí Bureau for
Otsuka, and is a member of the Data Safety Monitoring Board for Scios and Merck.
Dr. Lindenfeld is a consultant for and has received research support from
Novartis and Pfizer, and is on the Speakersí Bureau for Novartis.
This program was recorded at Heart Failure 2006: Update for the Primary Care
Physician, held February 11, 2006, in Houston and jointly sponsored by the
Heart Failure Society of America. The Audio-Digest Foundation thanks the
speakers and the Heart Failure Society of America for their cooperation in the
production of this program.
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