ASSESSMENT AND MANAGEMENT OF HEART FAILURE: CASE PRESENTATIONS
From Heart Failure 2007: A Focus on Guideline-Driven Care for Heart Failure, presented by the Heart Failure
Society of America, and held February 10, 2007, in San Francisco, CA
| Faculty listing on page 3
|
| CASE PRESENTATION I: METABOLIC SYNDROME ----- Clyde W. Yancy, MD, (moderator); Michael B. Fowler, MD;
Barry H. Greenberg, MD; Sharon A. Hunt, MD; JoAnn Lindenfeld, MD
|
| Case 1: woman, 75 yr of age, with sedentary lifestyle, presents with weakness; examination—blood pressure (BP) 175/68
mm Hg; clear lungs; normal first and second heart sounds (S1 and S2 ); no evidence of congestion; laboratory findings—
creatinine, 1.4 mg/dL; B-type natriuretic peptide (BNP), 189 pg/mL
|
| Assessment: fatigue and isolated systolic hypertension common and nonspecific in older patients; patient at high risk of
developing cardiovascular end points; elevated creatinine may indicate depressed glomerular filtration rate (GFR); no evidence
of overt heart failure (HF), eg, orthopnea, paroxysmal nocturnal dyspnea (PND), distended neck veins
|
| Treatment: with no signs of volume overload or HF, BP becomes primary target; options—diuretic not recommended;
electrocardiography (ECG) indicated; echocardiography and cardiac catheterization not indicated; Systolic Hypertension
in the Elderly Program (SHEP) and Systolic Hypertension in Europe (Syst-Eur) trial show benefit of calcium channel
blockers; angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB) preferred for patients
with renal dysfunction; thiazide diuretics effective in patients with isolated systolic hypertension (consider other options in
patients with renal dysfunction); renal dysfunction—knowledge of body mass index (BMI) or weight necessary to assess
renal function (creatinine clearance); ACE inhibitor or ARB appropriate, even in patients with mild renal dysfunction; calcium
channel blocker appropriate unless patient has proteinuria; combination therapy often recommended
|
| Exacerbating factors: nonsteroidal anti-inflammatory drugs (NSAIDs)—regular use may precipitate hypertension
and mild renal insufficiency in some patients (strong association in patients with HF); alcohol—high intake may result
in hypertension; treatment implications—identifying and eliminating these factors may reduce need for medication
|
| Other tests: BNP—increases with age, especially in women (level within 2 standard deviations [SDs] of norm not diag-
nostic for HF); imaging—in absence of specific signs and symptoms, echocardiography unnecessary (unlikely to affect
treatment decisions); blood glucose—ACE inhibitor or ARB recommended for patients with hyperglycemia (prevent
progression of renal disease in diabetic patients with hypertension)
|
| Negotiating NSAID use: patients with overt HF should avoid NSAIDs because they cause fluid retention; patients with
less severe disease may use cautiously, once BP lowered (watch for increase in BP and gastrointestinal effects); patient
education important; consider quality of life and functionality
|
| Case 2: man, 59 yr of age, presents for executive physical; history—regular physical exercise (3 miles/day, 4 times/wk);
no chest pain; history of “tough cold” with residual chest soreness for 1 week; physical examination—BP 138/86 mm
Hg; BMI 29; clear lungs; normal S1 and S2 ; ECG shows nonspecific ST-T wave changes; echocardiography shows reduced
left ventricular (LV) function (50%) with akinesis of lateral wall
|
| Imaging: given evidence of past MI, exercise stress test with myocardial imaging indicated; provides information about
exercise capacity and possibility of symptoms at peak exercise (useful for counseling); reveals ischemic disease
|
| Medical therapy: patient meets criteria for metabolic syndrome; manage BP and cardiovascular risk—ACE inhibitor;
β-blocker (after stress test); dyslipidemia (presumed)—obtain fasting lipid panel and prescribe statin
|
 | Guidelines: Heart Failure Society of America (HFSA)—risk-factor management appropriate for patients with “pre-
heart failure” (eg, ACE inhibitor or β-blocker for BP); in absence of clear evidence of MI or significantly reduced ejection
fraction (EF), β-blockers not specifically indicated; American College of Cardiology/American Heart Association
(ACC/AHA)—ACE inhibitors and β-blockers indicated for all patients with history of MI (or definitive evidence
of damage to myocardium), regardless of symptoms or EF
|
| Assessment of coronary disease: noninvasive assessment of ischemia indicated before initiating exercise program;
rationale—high BMI, lateral wall abnormality, and nonspecific changes on ECG suggest atherosclerotic burden; alternative
view—functional capacity determines natural history of coronary artery disease (CAD); history suggests functional
class I; patient does not meet criteria for revascularization; medical therapy and lifestyle interventions sufficient at
this time
|
| Aspirin: begin if patient not already taking
|
| CASE PRESENTATION II: THE COMPLICATED PATIENT ----- Barry H. Greenberg, MD, (moderator); Kathleen A. Dracup,
RN, DNSc; Gregg C. Fonarow, MD; Mandeep R. Mehra, MD; Ileana L. Piña, MD
|
| Patient history: man, 65 yr of age, with history of inferior MI; treated with angioplasty and triple vessel bypass (1989)
and prescribed β-blocker and aspirin; exercise history included daily running (3 miles); symptoms of HF developed in
1999; angiography revealed patent grafts (except for occluded right coronary artery, but collateral flow good) and EF of
30%; BP 70 to 80 mm Hg, increased with 1 L of fluid (LV end diastolic pressure, 25 mm Hg); implantable cardioverter
defibrillator (ICD) placed for episodes of nonsustained ventricular tachycardia; medical therapy consisted of low-dose
ACE inhibitor, digoxin, spironolactone, and atorvastatin (Lipitor); β-blocker discontinued; progression—exercise reduced
to ≈1 mile/day at slow pace; episode of rapid atrial fibrillation caused ICD to fire; amiodarone added to medical
regimen; β-blocker begun, but discontinued due to intolerance; referral to HF clinic in 2001; complaints included fatigue,
light headedness, and exertional dyspnea; BP, 83/62 mm Hg; heart rate (HR), 60 beats/min; jugular venous pressure, 10
cm H2 O; lungs clear; apex sustained in anterior axillary line; grade 1/6 systolic ejection murmur; 1 to 2+ pitting edema,
but warm extremities; end-diastolic dimension, 6.8 cm; EF, 26%; mild mitral regurgitation and tricuspid insufficiency;
diuretic initiated; patient lost 6 lb, and exertional dyspnea resolved, but exercise tolerance remained low; no reports of
PND; BP increased to 76/61 mm Hg; HR remained at 60 beats/min; sinus rhythm present, with QRS in normal range;
ECG shows pacing by ICD
|
| Comments from panel: amiodarone—chronotropic effects may cause problems (some patients require higher HR to
maintain hemodynamic stability); volume—orthostatic vital signs do not suggest volume overload; diuretics may have
resulted in hypovolemia; other cardiac considerations—systolic ejection murmur may indicate tricuspid regurgitation
(depending on location); long history of vascular disease increases risk for pulmonary hypertension
|
| Laboratory results: sodium, 136 mmol/L; creatinine 1.3 mg/dL; BUN, low to mid 20s (mg/dL); no evidence of abnormal
thyroid function
|
| Peripheral circulation: patient inappropriately warm in periphery (vasoconstriction expected at given dose of ACE inhibitor);
history of aerobic exercise may decrease peripheral vascular resistance; psoriasis—may decrease systemic vascular
resistance; worsened by ACE inhibitors
|
| β-blocker therapy: reinitiation possible in some previously intolerant patients; low dose and close monitoring necessary;
other medications may require adjustment; when tolerated, therapy may result in reversal of remodeling and increased
BP; referral to expert center recommended, especially for patients with low BP; other considerations—
discontinue amiodarone (clinical data show signal of harm in patients with class III HF) before reinitiating β-blocker
|
| Serial echocardiography: initial assessment—class I recommendation; echocardiography recommended as part of
standard assessment for all patients in whom HF suspected; subsequent echocardiography—recent guidelines recommend
(class IIa) repeat assessment for patient whose condition has changed or when change in therapy may affect ventricular
function
|
| β-blocker trial: metoprolol begun at 25 mg; BP increased to 74/47 mm Hg; no signs of intolerance; extremities warm; no
edema; other considerations—low HR may be result of long-term aerobic exercise; amiodarone has β-blocking properties,
and should be discontinued before starting β-blocker; uptitration of β-blocker—know chronotropic status before increasing
dose; but, tolerance to initial dose (little change in HR or BP) encouraging; symptomatic bradycardia may occur
with uptitration (relatively low frequency); eliminating amiodarone reduces risk for dyssynchrony caused by right ventricular
(RV) pacing; diastolic pressure—decreased with initiation of β-blocker; further decreases may provoke myocardial
ischemia
|
| Adjustments to medical therapy: lisinopril (Zestril) dosing changed from 2.5 mg bid to 5 mg at night; metoprolol increased
to 50 mg/day; good response at 1 mo, so diuretic reduced to every other day; BP 85/69 mm Hg; no evidence of
volume overload; metoprolol increased to 75 mg/day for 2 wk, then to 100 mg/day; patient continued to improve, remained
euvolemic, with BP reaching 96/43 mm Hg, and resumed jogging; later, furosemide (Lasix) decreased to 20 mg,
twice weekly; symptoms resolved, and appearance improved significantly; lisinopril increased to 10 mg/day, then to 10
mg bid; patient continues to do well 5 yr later
|
| Implications for practice: referral to expert center appropriate for difficult patients; β-blockers commonly discontinued
because of low BP, but euvolemic relatively stable patients may tolerate; missed opportunities—progression preventable
with appropriate medical therapy after initial MI; β-blockers and BP—symptomatic context important; in
general, patients with systolic BP ≥80 mm Hg tolerate β-blockers well (also used in patients with lower BPs); low initial
dose increased at 2-wk intervals, generally well tolerated, even in older patients with comorbidities; monitoring and patient
education important; good physiologic and cognitive responses indicate tolerance to β-blocker; hypotension—
educate patients about function of β-blocker therapy and that hypotension (especially orthostatic hypotension) may occur;
instruct patients to stagger medications (even in morning) to reduce impact on BP
|
| CASE PRESENTATION III: HEART FAILURE IN WOMEN ----- John Chin, MD (moderator); Barry M. Massie, MD; Ileana
L. Piña, MD; John Teerlink, MD; Mark A. Winchester, MD
|
| Presenting case: Hispanic woman, 68 yr of age, admitted after 1 day of chest pain described as “pressure-like” and not related
to exertion; history—hypertensive for \>20 yr; no history of diabetes, MI, valvular heart disease, smoking, or alcohol
use; father died of stroke at 78 yr of age; presence of nocturnal orthopnea and PND; exercise capacity limited to walking 1
block or climbing 10 stairs; examination—BMI, 36; respiratory rate, 18 breaths/min; BP, 146/91 mm Hg; HR, 92 beats/
min and regular; estimated jugular venous pressure, 15 cm H2 O; 2+ leg edema; point of maximum impulse (PMI), forceful,
localized, and nondisplaced; cardiac findings—right ventricular (RV) heave; S4 gallop; grade 2/6 holosystolic murmur,
primarily along left lower sternal border; grade 2/6 diastolic murmur over aortic area; lungs clear; peripheral pulses diminished;
echocardiography shows normal size of LV chamber, preserved LVEF (62%), and some LV hypertrophy
(LVH); interventricular septum, ≈13 mm; posterior wall, ≈12 mm; other findings include reversal of E/A ratio, 2+ aortic
insufficiency, 3+ tricuspid regurgitation, and estimated right ventricular pressure, ≈60 mm Hg
|
| Initial assessment: patient meets definition of HF with preserved EF; questions remain about presence of ischemia and
degree of valvular disease; pulmonary hypertension and right-sided heart failure not typical of HF with preserved EF;
recommended treatment—diuretics; BP control; follow-up—work-up for ischemia; assess efficacy of treatment with
follow-up echocardiography before considering invasive procedure
|
| Additional patient information: ECG shows normal sinus rhythm with LVH; troponin negative; serum sodium, 140
mmol/L; serum potassium, 3.6 mmol/L; GFR, 50 mL/min; total cholesterol, 184 mg/dL; high-density lipoprotein (HDL),
41 mg/dL; low-density lipoprotein (LDL), 122 mg/dL; current medications—hydrochlorothiazide and benazepril
|
| Differential diagnosis: rheumatic heart disease—common in some countries; RV heave highly suggestive of mitral
stenosis or mitral regurgitation that has progressed to HF; sleep apnea—obesity increases risk
|
| Recommended actions: diuresis; exercise stress test with nuclear scanning (eg, sestamibi [MIBI]); avoid dipyridamole
(Persantine); BP control; vasodilation; alternative view—use adenosine stress test to screen for high-grade disease (patient
unlikely to complete standard exercise stress test); add hydralazine-nitrite combination to medical therapy
|
| Other considerations: chronic pulmonary emboli could explain right-sided heart failure and chest discomfort; collagen
vascular disease may cause pulmonary hypertension in women; rheumatoid arthritis may result in dilated aorta; work-up
should include antinuclear antibodies and lupus antibodies
|
| Additional patient information: cardiac catheterization findings—LV pressure, 182/26 mm Hg, pulmonary capillary
wedge pressure, 22 mm Hg, cardiac output, 3.8 L/min, and pulmonary artery (PA) pressure, 68/30 mm Hg; LV angiography
findings—LVEF, 65%; luminal irregularities in mid-left anterior descending (LAD) and right coronary
arteries; no obvious obstructive disease
|
| Diagnosis: HF—ventricles under pressure; minimal edema and pulmonary congestion; diagnosis of HF directs therapy
(treat reversible factors, eg, BP, and control symptoms with, eg, diuresis, antihypertensive agents); evaluation for sleep
apnea recommended (treatment reduces neurohormonal levels, BP, and risk for progression and stroke); coronary
disease—“lumpy, bumpy” coronary disease typical in women; symptoms often disproportionate to angiographic findings;
evaluation of ischemia with stress test recommended; other targets—statins for elevated LDL; staging—stage C;
patient should respond well to aggressive treatment
|
| Follow-up: tricuspid regurgitation should improve or resolve as pulmonary hypertension decreases (useful for assessing response
to therapy, especially if follow-up echocardiography not approved by insurance); PA pressure estimated based on
strength of pulmonary component of S2 heard at left sternal boarder (clearly audible pulmonic second sound indicates PA pressure
≥50 mm Hg); additional treatment recommendations—ACE inhibitor to lower PA pressure
|
Speakers
John Chin, MD, Associate Clinical Professor of Medicine, University of California, Davis, and Director, Cardiac Transplant
Service, Sutter Memorial Hospital, Sacramento, CA; Kathleen A. Dracup, RN, DNSc, Dean and Professor, School of
Nursing, University of California, San Francisco; Gregg C. Fonarow, MD, Professor of Medicine, and Director, Ahmanson-UCLA
Cardiomyopathy Center, University of California, Los Angeles; Michael B. Fowler, MD, Professor of Medicine,
and Director, Heart Failure Program, Stanford University, Stanford, CA; Barry H. Greenberg, MD, Professor of
Medicine, and Director, Advanced Heart Failure Treatment Program, University of California, San Diego; Sharon A. Hunt,
MD, Professor of Medicine, and Medical Director, Post-Transplant Program, Stanford University; JoAnn Lindenfeld,
MD, Professor of Medicine, and Medical Director, Cardiac Transplant, University of Colorado Health Sciences Center, Denver;
Barry M. Massie, MD, Professor of Medicine, University of California, San Francisco, and Chief, Cardiology Division, Department
of Veterans’ Affairs Medical Center, San Francisco; Mandeep Mehra, MD, Herbert Berger Professor of Medicine,
and Chief, Division of Cardiology, University of Maryland, Baltimore; Ileana L. Piña, MD, Professor of Medicine, Case
Western Reserve University, Cleveland, OH; John R. Teerlink, MD, Associate Professor of Medicine, University of California,
San Francisco, and Director, Heart Failure Clinic, Department of Veterans’ Affairs Medical Center, San Francisco; Mark
A. Winchester, MD, Medical Director, Sutter Medical Center Heart Failure Service, Sacramento; Clyde W. Yancy,
MD, Medical Director, Baylor Heart and Vascular Institute, Baylor University Medical Center, Dallas, TX.
Suggested Reading
Asselbergs FW, van Gilst WH: Angiotensin-converting enzyme inhibition in cardiovascular risk populations: a practical approach
to identify the patient who will benefit most. Curr Opin Cardiol 22:267, 2007; Colucci WS et al: metoprolol reverses
left ventricular remodeling in patients with asymptomatic systolic dysfunction: the Reversal of Ventricular Remodeling with Toprol-
XL (REVERT) trial. Circulation 116:49; Fonarow GC et al: Improving the use of evidence-based heart failure therapies in
the outpatient setting: the IMPROVE HF performance improvement registry. Am Heart J 154:12, 2007; Hennekens CH et al:
The CHARM program: study design leads to findings of clinical and public health importance. J Cardiovasc Pharmacol Ther
12:124, 2007; Kalidindi SR et al: Drug insight: aldosterone-receptor antagonists in heart failure – the journey continues. Nat
Clin Pract Cardiovasc Med 4:368, 2007; Lenzen MJ et al: management of patients with heart failure in clinical practice: differences
between men and women. Heart June, 2007 [Epub ahead of print]; Martin JH, Krum H: Statins and clinical outcomes
in heart failure. Clin Sci (Lond) 113:119, 2007; Martin M et al: Health-related quality of life of heart failure and
coronary artery disease patients improved during participation in disease management programs: a longitudinal observational study.
Dis Manag 10:164, 2007; Nagatomo Y et al: Effects of beta-blocker therapy on high sensitivity C-reactive protein, oxidative
stress, and cardiac function in patients with congestive heart failure. J Card Fail 13:365, 2007; Solomon SD et al: Effect of angiotensin
receptor blockade and antihypertensive drugs on diastolic function in patients with hypertension and diastolic dysfunction: a
randomised trial. Lancet 369:2079, 2007; Torp-Pedersen C et al: The safety of amiodarone in patients with heart failure. J
Card Fail 13:340, 2007.
Educational Objectives
| The goal of this program is to improve the medical management of patients with heart failure and pre-heart failure.
After hearing and assimilating this program, the clinician will be better able to:
|
| Treat risk factors to prevent the development of left ventricular dysfunction and heart failure (HF).
|
| Assess severity of HF and prevent its progression.
|
| Implement evidence-based medical therapy for patients with HF.
|
| Monitor treatment responses and adverse effects of medical therapy.
|
| Educate patients about lifestyle changes, therapeutic goals, and potential adverse effects of medical therapy.
|
Faculty Disclosure
In adherence to ACCME Standards for Commercial Support, Audio-Digest requires all faculty members to disclose relevant
financial relationships within the past 12 months that might create any personal conflicts of interest. Any identified conflicts
were resolved to ensure that this educational activity promotes quality in health care and not a proprietary business or commercial
interest. For this program, the faculty reported nothing to disclose.
Acknowledgements
All speakers were recorded at Heart Failure 2007: A Focus on Guideline-Driven Care for Heart Failure, Update for the
Primary Care Physician, presented by the Heart Failure Society of America and held February 10, 2007 in San Francisco. The
Audio-Digest Foundation thanks the speakers and the Heart Failure Society of America for their cooperation in the production of this
program.
|
