SUSPECTED HEART FAILURE: EVALUATING THE PATIENT
From Heart Failure Society of America’s Primary Care Heart Failure Symposium
| CASE PRESENTATION I—Sandra D. Dunbar, RN, DSN, Atlanta, GA; Michelle L. Edwards, RN, MSN, ANCP, Houston,
TX; Gary S. Francis, MD, Cleveland OH; Barry H. Greenberg, MD, San Diego, CA; Frank W. Smart, MD, Houston TX
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| Initial presentation: 53-yr-old businessman seen for initial visit; moved from Midwest; has not seen doctor for years;
history of high blood pressure (BP) without treatment; shortness of breath with hurrying, which he relates to being out of
shape; sedentary lifestyle; wants to join health club; past medical history unremarkable; high-stress job, drinks socially,
does not smoke; family history—hypertension and diabetes on father’s side; maternal grandmother died at age 56 yr of
myocardial infarction (MI); 2 siblings, 1 of whom had MI and stented at age 51 yr; current medications—occasional antacid
and nonsteroidal anti-inflammatory drug (NSAID); examination—BP 153/96 mm Hg, pulse 78/min, weight 236 lb;
moderately obese black man in no acute distress; head, eyes, ears, nose, throat (HEENT) unremarkable; neck veins 4 cm
above clavicle at 90°; rales at both lung bases; apical impulse at anterior axillary line (forceful double impulse); fourth but
no third heart sound; grade 2/6 apical systolic murmur; benign abdomen; extremities warm, with mild edema mid shin on
both sides
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| Panel response: staging—stage A because of hypertension; possibly stage B if structural abnormalities found on diagnostic
studies, eg, left ventricular hypertrophy (LVH) on electrocardiography (ECG); if diagnostic tests reveal heart failure
(HF), would be stage C because patient symptomatic; patient has early symptoms of HF but not admitting it, eg,
distended neck veins, peripheral edema; however, all peripheral edema not due to HF; apical impulse—in black man
with hypertension, wonder about LVH; if LVH present, patient clearly at greater risk for HF and would already have
structural heart disease, moving him into different stage; blacks develop more severe LVH and have more complications
of hypertension; work-up—must control volume; atherosclerosis work-up for ischemic heart disease; determine ejection
fraction (EF) and whether LVH present; start with ECG; chemistry panel; consider prescribing angiotensin-converting
enzyme (ACE) inhibitor and diuretic; order electrolytes and renal function tests (should know creatinine and potassium
before prescribing medications); 24-hr urine specimen for sodium intake; echocardiography and chest x-ray; metabolic
panel; exercise and diet advice, but hold off on exercise until evaluation finished; counseling about disease and testing
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| Results of tests: serum urea nitrogen (BUN) and creatinine mildly elevated, with normal electrolytes; nonfasting glucose
157 mg/dL; liver function and thyroid tests normal; B-type natriuretic peptide (BNP) 657 pg/mL; ECG revealed LVH
with ST and T wave abnormalities
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| Panel response to test results: LVH with ST and T wave depression formidable predictor of HF; control hypertension;
extended follow-up
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| Treatment/testing/follow-up: furosemide (Lasix) 20 mg/day, enalapril titrated to 10 mg bid; abnormal fasting glucose
on retesting, so glipizide started; cholesterol 233 mg/dL, low-density lipoprotein (LDL) 147 mg/dL, high-density lipoprotein
(HDL) 26 mg/dL, triglycerides 300 mg/dL; statin started also; dietary counseling given; advised moderate
walking exercise, no strenuous exercise; next visit (2 wk later)—lost 13 lb, BP 138/86 mm Hg, pulse 78/min, jugular
venous pressure within normal limits and ankle edema resolved; echocardiography results—left ventricular diameters
6.4 cm at end diastole and 5.6 cm at end systole; EF 28%; mild mitral regurgitation (MR) and left atrial enlargement
present
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| Panel response about further testing/treatment: better control of BP; evaluate for ischemia; coronary angiography
suggested due to LVH; stress testing (radionuclide stress test or stress echocardiography) could be used; if negative,
would still want angiography
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| Further treatment/testing/follow-up: carvedilol started; no myocardial ischemia on thallium stress test; continued
diet and exercise over 6 mo; BP 126/83 mm Hg, pulse 65/min; lost 30 lb; persistent cardiomegaly; BNP reduced by 200
points; glycohemoglobin in mid-6% range, down from mid-7% range; creatinine reduced; LDL reduced to 90 mg/dL
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| Panel’s response to follow-up: HF nicely recovering; repeat echocardiography to determine whether EF improving,
so patient can resume vigorous lifestyle, or could base increased exercise on clinical symptomatology
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| CASE PRESENTATION II—Barry H. Greenberg, MD, San Diego CA; JoAnn Lindenfield, MD, Denver, CO; Mandeep
R. Mehra, MD, Baltimore, MD; Douglas L. Mann, MD, Houston, TX; Ilena L. Pina, MD, Cleveland OH, John R. Teerlink,
MD, San Francisco, CA
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| Initial presentation: 41-yr-old man; presumed nonischemic cardiomyopathy; left ventricular EF 35% (systolic HF);
left ventricular end-diastolic dimension 5.3 cm; moderate MR, LVH, and enlarged atria on echocardiography; left bundle
branch block (LBBB) on ECG; presented to emergency department (ED) with abdominal fullness, fatigue with minimal
exertion, and reduced urinary output despite doubling diuretics; treated for chronic HF for ≈18 mo; 18 mo ago, left ventricular
EF ≈50%; started on digoxin, 0.25 mg/day but discontinued due to bradycardia; furosemide 80 mg bid for symptom
control; could only tolerate lisinopril 10 mg/day; β-blocker not tried because of concern about heart block and
reaction to digoxin; BP 109/70 mm Hg, heart rate 78/min, elevated jugular venous pressure, holosystolic apical murmur
suggestive of MR, and S3 gallop; clear lungs, right upper quadrant tenderness, and 2+ lower extremity edema; laboratory
values—sodium 135 mEq/L, BUN 51 mg/dL, creatinine 2.6 mg/dL, troponin 1.1 ng/mL, and BNP 681 pg/mL
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| Panel response: assess legs (warm or cold); laboratory values indicate either comorbidities (eg, diabetic renal disease)
or severe HF requiring hospitalization; assess for concomitant pulmonary hypertension; this degree of MR in patient
with LVH could lead to ischemia and sudden death; patient needs hospitalization; view decompensated HF as acute
cardiac syndrome; patient’s age, BUN, and BP important factors in how well patient will do during hospitalization; uncertain
whether acting on these factors will beneficially affect outcome, but helps with risk stratification; rales—
possible problems with patient being triaged to Medicine service instead of Cardiology service because clear lungs
might give impression patient does not have HF; patients with long-standing elevations of pulmonary capillary wedge
pressures often present with clear lung fields; rales may be absent more frequently than anticipated; elevated wedge
pressure can be picked up with Swan-Ganz catheter (especially in diabetics); sodium—sodium 135 mEq/L after furosemide
concerning; dropping sodium is poor marker; troponin—abnormal troponin can point to important troponin
leaks, even in dilated cardiomyopathy; know that cells lost (due to cardiac necrosis or apoptosis) every time patient
decompensates; with each hospitalization, function decreases, then stabilizes; ischemia work-up indicated; troponin increase
in HF correlated with adverse prognosis, decreases with therapy, and occurs in dilated cardiomyopathies; in this
patient, troponin increase could be due to kidney, HF, or ischemia; BNP—moderate elevation could be due to obesity;
not determining factor in patient with HF; single BNP does not help in determining wedge pressure, more benefit with
long-term follow-up; insertion of Swan-Ganz catheter—should not become routine care; in this patient, would use
higher dose of diuretic, then vasodilators, then inotropes; if no response in 30 to 60 min, then would use Swan-Ganz
catheter; no standard guidelines for decompensated HF; “wet” patient—normally reach for diuretics, double oral dose
as intravenous (IV) dose; double therapy (double blockade) with loop diuretic and metolazone; in IV setting, use furosemide
infusion, instead of frequent boluses; in oral setting, furosemide’s bioavailability decreases with bowel edema
(early satiety common sign of gut edema in patient with HF); may want to use torsemide (oral agent with better bioavailability);
in decompensated HF with renal insufficiency, use IV bolus, followed by infusion; gastrointestinal (GI)
symptoms often seen in younger HF patients; since patient’s liver tender and engorged, go to torsemide infusion; patient
likely has cardiorenal syndrome, so diuretics may not be effective; recommend using Swan-Ganz catheter;
echocardiography—obtain to determine degree of MR without use of Swan-Ganz catheter; significant MR might
support decision to use vasodilator; if patient has had echocardiography 2 to 3 wk before hospitalization for decompensation,
repeat only if change in underlying process suspected; treat with IV diuretics, which should reduce creatinine; if
patient does not respond to diuretic within ≈1 hr, cardiorenal condition worsening and different therapy needed; can
use impedence cardiography; younger patients tend to be “warm” in profound HF with low cardiac output; nitroprusside
vasodilator of choice with MR; need to up-titrate dose for renal concerns (more difficult without Swan-Ganz cathe
ter); if concerned about toxicity with nitroprusside, can use IV nitroglycerin instead; other treatment
recommendations—address cause of decompensation; evaluate for myocardial ischemia; learn more about MR; try β-
blocker; after patient on optimal medical therapy, evaluate for cardiac resynchronization therapy (CRT); elective device
insertions should not be rescue therapy in hospital setting; right ventricular pacing may worsen LV dysfunction by
causing more dyssynchrony; if bradycardia occurs with β-blocker, may use biventricular pacing
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| More patient information: patient’s LV end diastolic diameter 5.3 cm, so heart not highly dilated, even though EF decreased
from 48% to 35% in 18 mo; lack of dilated LV makes patient not candidate for CRT and may indicate MR recent
and patient needs optimal medical therapy to prevent remodeling; if creatinine does not improve, Foley catheter indicated
before starting inotrope (patient could have intrinsic renal problem being mistaken for HF); renal function did not improve;
24-hr urine for creatinine clearance and protein showed patient spilling protein; biopsy revealed cardiac amyloidosis
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| Panel response: biopsy recommended when cause for decompensation not obvious, eg, patients with relatively well preserved
systolic function with evidence of hypertrophy and severe HF; genetic abnormalities in some patients cause myocardial
fibrosis
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| INTEGRATING DEVICE THERAPY IN MANAGEMENT OF HF PATIENTS— John R. Teerlink, MD, Associate Professor
of Medicine, and Director, Heart Failure Clinic and Clinical Echocardiography, University of California, San Francisco, School of
Medicine
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| Diagnostic devices in HF: biomarker assays— standard BNP assay and N-terminal BNP distinguish between dyspnea
due to HF and dyspnea from other causes; troponin has prognostic influence and may help determine aggressiveness
of treatment; phonocardiography—visual interpretation of sound waves from stethoscope; predicts outcomes in HF patients;
impedence cardiography—electrodes on thorax and carotids; provides measurements of cardiac performance;
predicts outcomes or risk for hospitalization
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| Devices to treat acute decompensation: left ventricular assist device; aortic flow augmentation—experimental;
recirculates blood through thoracic and abdominal aorta; ultrafiltration—filters salt water from blood, then returns
blood to body; removes large amount of fluid efficiently in diuretic-resistant or highly fluid-overloaded patients; can remove
≈ 20 lb in 2 days; reduces length of hospital stay
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| Devices to treat chronic HF: patients with intermediate HF have 50% chance of sudden death; proportion of deaths high
early in development of HF; pump failure predominates in later stages; implantable cardioverter defibrillators (ICDs)—
in trials, reduced arrhythmic deaths by ≈65%, produced ≈29% reduction in all-cause mortality; CRT—3 components of ventricular
dyssynchrony 1) electrical conduction delays (LBBB), 2) structural (disruption of myocardial collagen matrix), and 3)
mechanical (regional wall motion abnormality; increased workload and stress); CRT synchronizes heart contraction, improving
performance; patients with wider QRS have higher rate of mortality, ie, baseline QRS abnormalities worsen outcomes, independently
of other factors; improved quality of life measures and 6-min walk test; CRT plus ICD keep patients out of hospital
and improves mortality; CRT patients feel better, with marked reduction in hospitalizations and mortality; American Heart
Association (AHA)/ American College of Cardiology (ACC) guidelines—use ICDs for primary prevention in Class II or
III HF patients, ie, those with 1) low EF, 2) prior MI with low EF, or 3) prior MI, low EF, and inducible sustained ventricular
tachycardia or ventricular fibrillation; use CRT in Class III or IV HF patients who remain symptomatic with optimal stable drug
therapy and have low EF, and widened QRS; decision in context of comorbidities; can have combination of regular pacemakers,
ICDs, and CRTs
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| Device placement: transvenous approach; standard pacing lead in right atrium, pacing lead in right ventricle, and special
lead that goes into LV and comes out into lateral wall; technically challenging to insert; patient off warfarin; can be on clopidogrel
(Plavix) and aspirin; usually done in cardiac catheterization lab or operating room; prepare patient to be in cold place
on uncomfortable table for long time (1-4 hr or longer); success rate >95%; for testing ICD, patients placed in ventricular fibrillation
and shocked out of it; complications—similar to those of pacemaker, plus coronary sinus dissection, coronary sinus
or vein perforation, extracoronary stimulation (diaphragmatic [hiccups, problems with breathing] and chest wall
twitches [typically in thin patients and dilated hearts] can develop later on); followed by cardiologist with expertise in pacemakers;
follow congestive HF symptoms carefully (specifically dizziness, lightheadedness, palpitations); hiccups and muscle
twitches relate to extracardiac stimulation; ask about ICD discharges; have patients call with first discharge and monitor
them telephonically; 10% to 25% rate of inappropriate discharge; look for pocket erosions at insertion site; if skin thinning
over site, refer to surgeon immediately to salvage pacemaker; if device erodes through skin, all electrodes must be removed
and pacemaker reinserted; can perform ECGs and echocardiography
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Educational Objectives
| The goal of this activity is to discuss the clinical presentation associated with early and decompensated heart failure(HF)
and the devices used in management of HF. After hearing and assimilating this program, the clinician will be better able to:
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 | 1. Describe the clinical features of early HF.
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| 2. Evaluate and treat early HF.
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| 3. Discuss the presentation of decompensated HF.
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| 4. Describe the risks and treatment of decompensated HF.
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| 5. Review the rationale for cardiac resynchronization therapy (CRT) and implantable cardioverter defibrillator (ICD) use in
chronic HF.
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Discussed on this Program
Carvedilol [Coreg]
Clopidogrel bisulfate [Plavix]
Digoxin [Digitek, Lanoxicaps, Lanoxin]
Enalapril maleate [Enalaprilat, Vasotec]
Furosemide [Lasix]
Glipizide [Glipizide ER, Glipizide Extended-Release, Glucotrol, Glucotrol XL]
Lisinopril [Prinivil, Zestril]
Metolazone [Zaroxolyn, Mykrox]
Nitroglycerin [Nitrobid, Nitro-Bid IV, Nitrogard, Nitroglyn, Nitrol, Nitrolingual, Nitrong, NitroQuick, Nitrostat, Nitrotab,
Nitro-Time, Tridil]
Nitroprusside sodium [Nitropress, Sodium Nitroprusside]
Torsemide [Demadex]
Panel Discussion Participants
Sandra B. Dunbar, RN, DSN, Charles Howard Cardlen Professor, Neil Hodgson Woodruff School of Nursing, Emory
University, Atlanta, GA; Michelle L. Edwards, RN, MSN, NP, Cardiology Nurse Practitioner, St. Luke’s Episcopal
Hospital, Houston, TX; Gary S. Francis, MD, Professor of Medicine, Cleveland Clinic Lerner College of
Medicine at Case Western Reserve University, and Head, Clinical Cardiology Section, Cleveland Clinic Foundation,
Cleveland, OH; Barry H. Greenberg, MD, Professor of Medicine and Director, Heart Failure/Cardiac Transplantation
Program, University of California, San Diego, School of Medicine; JoAnn Lindenfeld, MD, Professor of Medicine
and Medical Director, Cardiac Transplant Program, University of Colorado Health Sciences Center, Denver; Douglas L
Mann,MD, Chief, Section of Cardiology, Baylor College of Medicine, St. Luke’s Episcopal Hospital /Texas Heart Institute,
Houston, TX; Mandeep R. Mehra, MD, Herbert Berger Professor of Medicine and Chief, Division of Cardiology,
University of Maryland, Baltimore; Ileana L. Piña, MD, Professor of Medicine, Department of Medicine, Division
of Cardiology, Case Western Reserve University, and Director, Section of Heart Failure and Cardiac Transplantation, University
Hospitals, Cleveland, OH; Frank W. Smart, MD, Director, Advanced Heart Failure and Cardiac Transplantation,
Baylor College of Medicine, St. Luke’s Episcopal Hospital/Texas Heart Institute, Houston, TX
Suggested Reading
| Aaronson KD, Sackner-Bernstein J: Risk of death associated with nesiritide in patients with acutely decompensated
heart failure. JAMA 296:1465, 2006; Bonow RO et al: ACC/AHA clinical performance measures for adults with
chronic heart failure: a report of the American College of Cardiology/American Heart Association Task Force on Performance
Measures (Writing Committee to Develop Heart Failure Clinical Performance Measures) endorsed by the Heart Failure
Society of America. J Am Coll Cardiol 46:1144, 2005; Radford MJ et al: ACC/AMA key data elements and
definitions for measuring the clinical management and outcomes of patients with chronic heart failure: a report of the
American College of Cardiology/American Heart Association Task Force on Clincal Data Standards (Writing Committee to
Develop Heart Failure Clincal Data Standards): developed in collaboration with the American College of Chest Physicians
and the International Society for Heart and Lung Transplantation: endorsed by the Heart Failure Society of America. Circulation
112:1888, 2005; Cleland JG et al: Clinical trials update from the American College of Cardiology: darbepoetin
alfa, ASTEROID, UNIVERSE, paediatric carvedilol, UNLOAD, and ICDLAND. Eur J Heart Fail 8:326, 2006; Cleland
JG et al: The effect of cardiac resynchronization on morbidity and mortality in heart failure. N Engl J Med 352:1539,
2005; The ESCAPE Investigators and ESCAPE Study Coordinator: Evaluation study of congestive heart
failure and pulmonary artery catheterization effectiveness. JAMA 294:1625, 2005; Jarcho JA: Biventricular pacing. N
Engl J Med 355:288, 2006; Shah MR et al: Testing new targets of therapy in advanced heart failure: the design and rationale
of the strategies for tailoring advanced heart failure regimens in the outpatient setting: brain natrluretic peptide versus
the clinical congestion score (STARBRITE) trial. Am Heart J 150:893, 2005; Solomon SD et al: Sudden death in
patients with myocardial infarction and left ventricular dysfunction, heart failure, or both. N Engl J Med 352:2581, 2005;
Yancy CW et al: Clinical presentation, management, and in-hospital outcomes of patients admitted with acute decompensated
heart failure with preserved systolic function: a report from the Acute Decompensated Heart Failure National Registry
(ADHERE) Database. J Am Coll Cardiol 47:76, 2006
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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. Drs. Mehra, Smart, Pina,
Mann, and Francis and Ms. Dunbar have no financial relationship to disclose. Dr Teerlink receives research support from
CHF Solutions and Cardio Dynamics. Dr. Havranek is a consultant for McKesson and CV Therapeutics. Dr. Greenberg is a
speaker for GlaxoSmithKline, AstraZeneca, Pfizer, Merck, and Novartis and is a consultant for GlaxoSmithKline and CHF
Solutions. Dr Lindenfield is a speaker and consultant for Merck, Novartis, Amgen, Pfizer, Medtronic, Guidant, St Jude, and
AstraZeneca. Dr Miller is a speaker for Pfizer, Astra Zeneca, GlaxoSmithKline, CV Therapeutics, Sanofi, NitroMed, Wyeth,
and MedTime and receives research assistance from Pfizer, NitroMed, Medtronic, AstraZeneca, GlaxoSmithKline, and
Myogen. Ms. Edwards is a speaker for Scios, Inc.
All presentations were recorded at the Heart Failure Society’s Primary Care Heart Failure Symposium in Houston, TX,
on February 11, 2006. The Audio-Digest Foundation thanks the speakers and sponsor for their cooperation in production of
this program.
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