HEART FAILURE: DEALING WITH DIFFICULT CASES
From Heart Failure 2005: Update for the Primary Care Physician, presented February 12, 2005, in Sacramento by the Heart Failure Society of America
| Faculty listing on page 3 |
| CASE PRESENTATION 1 —Mandeep R. Mehra, MD (moderator); John Chin, MD; Barry H. Greenberg, MD; Ilena L. Piña, MD; Patricia A. Uber, PharmD; Clyde W. Yancy, MD |
| Presenting patient: 54-yr-old man; remote smoker with hypertension; no diabetes; referred for management of heart failure (HF) and consideration for transplantation; diagnosed with HF 3 yr ago; current symptoms—rated as New York Heart Association (NYHA) class III; left ventricular (LV) dysfunction; ejection fraction (EF) 20%; enlarged end-diastolic dimension (EDD; LV dilated 6.7 cm); hyperlipidemia; 3-vessel coronary artery disease; history—in 1999, coronary angiography revealed proximally occluded left anterior descending coronary artery, midcircumflex artery stenosis of 60%, and proximal stenosis of 95% in nondominant right coronary artery; medications—digoxin 0.25 mg qd; furosemide 40 mg qd; aspirin 325 mg qd; captopril 6.25 mg tid; metoprolol tartrate immediate release 50 mg bid; pravastatin 20 mg qd; initial management—captopril titrated to 50 mg tid; 24-hr Holter monitor revealed nonsustained ventricular tachycardia (VT); dobutamine echocardiography indicated no ischemia or viability; cardiopulmonary stress test revealed peak ventilatory O2 (VO 2 ) uptake of 14 mL/kg per minute; anaerobic threshold (AT) not obtained; respiratory exchange ratio (RER) 1.2; no ST segment changes, angina, or VT noted during exercise effort |
| Evaluation: patient at high risk for sudden death, so likely to benefit from implantable cardiac defibrillator (ICD), regardless of presence or absence of nonsustained VT; data suggest ICD beneficial for patients with EF ≤35%; patient displayed good effort level (RER >1.1 indicates anaerobic effort, but represents only 49% of predicted) |
| Recommendations: alcohol—patient’s cardiomyopathy does not appear alcohol related, so acceptable for patient to consume limited amount of alcohol; alcohol potent cardiotoxin, so important to recognize patients consuming more than reported and advocate abstinence; exercise—study data suggest β-blockers affect VO 2 levels, so wait until β-blocker titrated up to stable dose before testing for baseline VO 2 ; to avoid further deconditioning, reinitiate exercise program soon after patient returns home from hospital (allow 2 wk for patient to begin walking and performing activities of daily living) |
| Viability testing: dobutamine stress echocardiography helpful; positron emission tomography (PET) useful for patients suspected of having hibernating myocardium; important to explore all conventional surgical approaches before recommending cardiac transplantation; in patient with ischemic heart disease and depressed ventricular function, positive viability study would suggest need for revascularization, but no clear data |
 | Digoxin: dose (0.25 mg qd) potentially too high; good idea to check level on first consultation; reduce dose if patient’s level >0.8 ng/mL; evidence supports biphasic effect of digoxin; at lower levels, appears to be neutral or protective; at higher levels, tends to have adverse consequences; low dose advisable because of concerns about alterations in renal function |
| Loop diuretics: all generic, but large variability in price; furosemide cheapest everywhere; torsemide favored because of longer half-life and quicker onset of action; twice-daily dosing better than once daily; small dose before dinner beneficial for patients on low-sodium diet who have nocturnal symptoms; choice of drug largely dependent on pharmacokinetic ease of use and price; study data show torsemide to have aldosterone-receptor antagonist effects, so important to monitor potassium when aldosterone antagonist added to torsemide regimen; because patient not grossly volume overloaded, choice of loop diuretic probably unimportant; as degree of right-sided HF increases, bioavailability and absorption of loop diuretics affected; to increase potency, drugs should be tried in order of increasing absorption, ie, furosemide, bumetanide, torsemide; note—loop diuretics turn on renin-angiotensin system; American College of Cardiology/American Heart Association guidelines emphasize importance of flexible diuretic regimen; inform patient of “3 pounds in 3 days” rule so they know when to take diuretic; diuretics taken intermittently work better than daily dosing; monitor magnesium levels and be aware of hypomagnesemia |
| β-blockers: important to use evidence-based drug, ie, metoprolol succinate extended release or carvedilol; as patient exposed previously to metoprolol tartrate, change to metoprolol succinate indicated; titrate to doses used in clinical trials; metoprolol tartrate immediate release performed less well than carvedilol in prospective, randomized, double- blind trial; data from Carvedilol Prospective Randomized Cumulative Survival (COPERNICUS) trial support use of carvedilol in patients with more advanced HF; choice of drug should depend on availability, patient tolerability, and price |
| Aldosterone antagonists: addition of aldosterone antagonist to angiotensin-converting enzyme (ACE) inhibitor can cause hyperkalemia; Candesartan in Heart failure: Assessment of Reduction in Mortality and morbidity (CHARM) trial data suggest addition of angiotensin II receptor blocker will benefit patients with NYHA class III; other data suggest addition of aldosterone antagonist to ACE inhibitor has palpable benefit (number needed to treat <20); aldosterone antagonist contraindicated if creatinine >2.0 mg/dL or potassium >4.5 mmol/L |
| Hydralazine and isosorbide dinitrate: patient may benefit from addition of hydralazine and isosorbide dinitrate because he fits profile of participants in African-American Heart Failure Trial (A-HeFT), in which addition of hydralazine and isosorbide dinitrate to ACE inhibitor yielded marked improvement in mortality; important to educate patients on compound contents, particularly nitrate portion, to prevent adverse interactions, eg, with sildenafil |
| Additional patient information: patient deferred from cardiac transplantation; β-blocker changed to metoprolol succinate extended release and titrated up to 100 mg qd; amiodarone 200 mg qd added; during follow-up, patient suffered heartburn and atypical chest pain; nuclear scan showed anterior scar; repeat angiography showed no significant progression of disease |
| Medical therapy recommendations: increase metoprolol succinate extended release by titration (target dose in Metoprolol Controlled Release/Extended Release Randomized Intervention Trial in Chronic Heart Failure [MERIT-HF] was 200 mg); be aware patient may be bradycardic due to amiodarone; improved β-blocker dose may eliminate nonsustained VT; discontinue amiodarone (data from Sudden Cardiac Death in Heart Failure Trial [SCD- HeFT] showed no benefit) |
| Additional patient information: amiodarone discontinued; metoprolol succinate extended release increased to 150 mg qd; digoxin dose reduced because of potential interaction; captopril continued; follow-up at 1 yr —no emergency department (ED) visits or hospitalizations; no angina, palpitations, or syncope; symptoms improved to NYHA class II; echocardiography showed enlarged LV cavity; EF 20%; peak VO 2 22 mL/kg per minute; RER 1.15; AT 14.6 mL/kg per minute; mild QRS widening; QRS interval 119 msec |
| Surgical therapies: patient will benefit from ICD therapy and probably should have been fitted much earlier; if rhythm dyssynchronous, implantation of biventricular (BiV) pacer along with ICD indicated; patient’s mitral regurgitation (MR) grade 3+, so consider mitral valve repair or replacement; resynchronization therapy can improve MR, so reevaluate after implantation of BiV pacer before recommending surgery |
| CASE PRESENTATION 2—Marc A. Silver, MD (moderator); Kathleen A. Dracup, RN, DNSc; Barry H. Greenberg, MD; John R. Teerlink, MD; Mark A. Winchester, MD |
| Presenting patient: 76-yr-old man; visited clinic in past week complaining of increased dyspnea with any activity, weight gain, bloating, and increased leg edema; loop diuretic dose doubled and metolazone added; patient deteriorated and slept in recliner for past 3 nights; received phone call from patient’s wife at 2 AM ; history—patient hospitalized 6 times in past year and does not want to reenter hospital (patient depressed at prospect of being readmitted); bypass surgery for ischemic cardiomyopathy performed 9 yr ago; patient recatheterized in past year and found to have patent grafts, moderate MR, and EF 25% to 30%; no angina; laboratory data—serum sodium 132 mmol/L; serum urea nitrogen (BUN) 54 mg/dL (35 mg/dL at last discharge); creatinine 2.6 mg/dL (2.1 mg/dL at last discharge); B-type natriuretic peptide (BNP) 840 pg/mL at last discharge; elevated hemoglobin A1c ; electrocardiography (ECG) revealed sinus rhythm of 78 bpm; QRS interval 121 msec; medications—ACE inhibitor; digoxin; loop diuretic; metolazone; β-blockers discontinued because patient became hypotensive (systolic blood pressure [BP] 94 mm Hg); office BP 94/60 mm Hg |
| Diagnosis: possible intractable heart failure; rising BUN and creatinine suggest low cardiac output caused by massive volume overload |
| Initial recommendations: advise patient to go to ED; discuss with family possibility of admitting patient for intravenous (IV) diuretic therapy and initiation of β-blockers (asking nurses not to take BP can facilitate β-blocker initiation); ED procedures—perform chest x-ray and ECG; check cardiac enzymes; administer O2 , morphine, and nitrates (IV or topical); administer continuous positive airway pressure (CPAP) to lower LV filling pressures; start with 80-mg dose of IV diuretic because patient almost in extremis; patients often can have diuretic resistance and do not respond to increasing doses of oral or IV diuretics |
| Patient education: time in ED represents important opportunity to educate patient and, particularly, caregiver(s) about disease progression and long-term therapies to prevent future hospitalizations |
| Further evaluation: coronary disease—absence of angina does not preclude presence of ischemia; perform nuclear scan; if scan positive, perform catheterization procedure to detect suitable substrate for revascularization; device therapy may be beneficial; MR—evidence that pharmacologic therapy can dramatically improve MR; patient’s MR may be functional MR related to substantial subendocardial ischemia; patient unlikely to benefit from specific mitral valve repair or replacement surgery, so medical therapy advised |
| β-blocker therapy: refrain from measuring BP and add β-blocker; start with low dose and ensure patient well diuresed to help protect against adverse effects; reduce or discontinue β-blocker if patient becomes symptomatic; important to inform patient of expected outcomes; emphasize that β-blockers life-saving drugs; prudent to titrate up slowly from small dose; COPERNICUS trial—in similar patients, β-blocker reduced mortality and hospitalization risk 35% |
| B-type natriuretic peptide: useful therapeutic guide; measure BNP midway through admission and toward end to see whether levels decrease; BNP <350 pg/mL indicates optimal diuresis achieved without high probability of readmission; BNP ≥900 pg/mL suggests patient not fully diuresed and likely very sick, so close follow-up required; if BNP unchanged after diuresis, aggressive treatment and further diuresis indicated |
| Aldosterone antagonist therapy: check creatinine after patient stabilized, as it will likely return to 2.1 mg/dL (acceptable level to initiate aldosterone antagonist therapy); especially important to monitor creatinine and potassium levels because patient has baseline renal insufficiency; check creatinine and potassium at 1 wk, 1 mo, and every 1 or 2 mo thereafter, depending on patient’s clinical condition |
| Treatment barriers: reluctance to enter hospital often sign that patient does not want to continue with treatment; important to discuss other options and likely outcomes of no treatment; patient often ready to discuss end-of-life care; consider depression (40% of patients with HF have clinical depression); no clear evidence on efficacy of selective serotonin reuptake inhibitors in this patient population; cognitive dysfunction may also need addressing; patients often reluctant to discuss palliative care for fear that cardiac medications will be withdrawn; however, palliative care involves addition of symptom management techniques to cardiac medications |
| Surgical therapies: final decisions about device therapy need not be made on initial hospitalization, as patient may be depressed and feeling that he may not symptomatically improve; discuss ICD therapy when patient feeling better; benefits of ICD therapy generally not seen for at least 1 yr, so preferable for patient to have survival likelihood ≥1 yr |
Educational Objectives
| The goal of this activity is to provide the listener with information on the evaluation and management of heart failure (HF). After hearing and assimilating this program, the clinician will be better able to: |
| 1. Recognize the clinical characteristics of HF. |
| 2. Advise patients on when to resume exercise after hospitalization for HF. |
| 3. Prescribe medical therapy for the long-term management of HF. |
| 4. Discuss the initial management of a patient with HF who presents to the emergency department. |
| 5. Distinguish patients at or near end of life and initiate appropriate dialogue. |
Discussed on This Program
Amiodarone HCl [Cordarone, Pacerone] Aspirin (acetylsalicylic acid; ASA) [several trade names] Bumetanide [Bumex] Candesartan cilexetil [Atacand] Captopril [Capoten] Digoxin [Digitek, Lanoxicaps, Lanoxin] Furosemide [Lasix] Metolazone [Mykrox, Zaroxolyn] Metoprolol succinate [Lopressor, Metoprolol Tartrate, Toprol XL] Pravastatin sodium [Pravachol] Torsemide [Demadex]
Speakers
John Chin, MD, Associate Clinical Professor of Medicine, University of California, Davis, School of Medicine, and Medical Director, Heart Transplant Service, Sutter Medical Center, Sacramento; Kathleen Dracup, RN, DNSc, Dean, School of Nursing, University of California, San Francisco; Barry H. Greenberg, MD, Professor of Medicine and Director, Heart Failure/Cardiac Transplantation Program, University of California, San Diego, School of Medicine; Mandeep R. Mehra, MD, Vice Chairman, Department of Cardiovascular Medicine, and Chief, Cardiomyopathy and Heart Transplantation Center, Ochsner Clinic Foundation, New Orleans; Ilena L. Piña, MD, Professor of Medicine, Case Western Reserve University School of Medicine, and Director, Heart Failure/Cardiac Transplantation, University Hospitals, Cleveland; Marc A. Silver, MD, Clinical Professor of Medicine, University of Illinois School of Medicine; Chairman, Department of Medicine and Director, Heart Failure Institute, Advocate Christ Medical Center, Oak Lawn, Illinois; John R. Teerlink, MD, Associate Professor of Medicine, University of California, San Francisco, School of Medicine, and Director, Heart Failure Clinic, San Francisco Veterans Affairs Medical Center; Patricia A. Uber, PharmD, Clinical Cardiovascular Specialist, Ochsner Cardiomyopathy and Heart Transplantation Center, New Orleans; Mark A. Winchester, MD, Medical Director, Heart Failure and Preventive Cardiology Programs, Sutter Medical Center, Sacramento; 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
Suggested Reading
Adler A, Greenberg BH: Use of Beta Blockers in Patients with Post-MI Left Ventricular Dysfunction. Curr Treat Options Cardiovasc Med 6(4):335, 2004; Braunwald E et al: Angiotensin-converting-enzyme inhibition in stable coronary artery disease. N Engl J Med 351(20):2058, 2004; Croom KF, Keating GM: Valsartan: a review of its use in patients with heart failure and/or left ventricular systolic dysfunction after myocardial infarction. Am J Cardiovasc Drugs 4(6):395, 2004; Davis KL, Nappi JM: The cardiovascular effects of eplerenone, a selective aldosterone-receptor antagonist. Clin Ther 25(11):2647, 2003; Deedwania PC et al: Efficacy, safety and tolerability of metoprolol CR/XL in patients with diabetes and chronic heart failure: experiences from MERIT-HF. Am Heart J 149(1):159, 2005; Fonarow GC et al: Risk stratification for in-hospital mortality in acutely decompensated heart failure: classification and regression tree analysis. JAMA 293(5):572, 2005; Goodlin SJ et al: Consensus statement: Palliative and supportive care in advanced heart failure. J Card Fail 10(3):200, 2004; Gring CN, Francis GS: A hard look at angiotensin receptor blockers in heart failure. J Am Coll Cardiol 44(9):1841, 2004; Maisel AS et al: Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure. N Engl J Med 347(3):161, 2002; McMurray JJ et al: Which inhibitor of the renin-angiotensin system should be used in chronic heart failure and acute myocardial infarction? Circulation 110(20):3281, 2004; Mehra MR et al: Heart failure therapy at a crossroad: are there limits to the neurohormonal model? J Am Coll Cardiol 41(9):1606, 2003; Munger MA, Carter O: Epidemiology and practice patterns of acute decompensated heart failure. Am J Health Syst Pharm 60 Suppl 4:S3, 2003; Pantilat SZ, Steimle AE: Palliative care for patients with heart failure. JAMA 291(20):2476, 2004; Vasan RS, Levy D: Defining diastolic heart failure: a call for standardized diagnostic criteria. Circulation 101(17):2118, 2000; Yusuf S et al: Effects of candesartan in patients with chronic heart failure and preserved left-ventricular ejection fraction: the CHARM-Preserved Trial. Lancet 362(9386):777, 2003; Zile MR et al: Diastolic heart failure--abnormalities in active relaxation and passive stiffness of the left ventricle. N Engl J Med 350(19):1953, 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 for AstraZeneca, GlaxoSmithKline, and Pfizer, and has received honoraria from AstraZeneca GlaxoSmithKline, and Merck; Dr. Mehra is a consultant for AstraZeneca, GlaxoSmithKline, Guidant, and Medtronic; Dr. Piña is a consultant for AstraZeneca, Cardiovascular Clinical Studies LLC, Center for Medicare and Medicaid Services, Food and Drug Administration (FDA), and GlaxoSmithKline, and has received grants from Biosite and Cardiovascular Clinical Studies LLC; Dr. Teerlink is a consultant for Abbott, Actelion, Cytokinetics, and Geron, a stockholder in Cytokinetics, and has received honoraria from Actelion, GlaxoSmithKline, and Pfizer; Ms. Uber has received honoraria from Scios; Dr. Winchester is a consultant for Amgen, GlaxoSmithKline, Pfizer, and Scios, and has received honoraria from Amgen, GlaxoSmithKline, Medtronic, Pfizer, and Scios; Dr. Yancy is a consultant for GlaxoSmithKline, Scios, Nitromed, and Medtronic, and has received grants from GlaxoSmithKline, Scios, Nitromed, and Medtronic; Drs. Chin and Silver and Ms. Dracup have no relationships to disclose.
This program was recorded at Heart Failure 2005: Update for the Primary Care Physician, held February 12, 2005, in Sacramento and 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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