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How Well is Chronic Heart Failure Being Managed?

How Well is Chronic Heart Failure Being Managed?. Gregg C. Fonarow, MD Eliot Corday Professor of Cardiovascular Medicine and Science UCLA Division of Cardiology Director, Ahmanson-UCLA Cardiomyopathy Center Director, UCLA Cardiology Fellowship Training Program Los Angeles, California.

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How Well is Chronic Heart Failure Being Managed?

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  1. How Well is Chronic Heart Failure Being Managed? Gregg C. Fonarow, MD Eliot Corday Professor of Cardiovascular Medicine and ScienceUCLA Division of CardiologyDirector, Ahmanson-UCLA Cardiomyopathy CenterDirector, UCLA Cardiology Fellowship Training ProgramLos Angeles, California

  2. Chronic Heart Failure • Approximately 5 million Americans have Chronic HF • 550,000 new cases annually • Hospital discharges 1,100,000 (2003) • Accounts for 12 million office visits/year • One of the largest expenses for Medicare • Five-year mortality rate as high as 50% HF, heart failure. AHA. 2006 Heart and Stroke Statistical Update. 2

  3. Burdens of Heart Failure Congestive Symptoms Activity Limitation Dysrrhythmias Hospitalizations Reduced Survival 3

  4. Decompensated Heart Failure: The Major Contributor to Cost of Care Health CareProfessionals $2.0 Billion (7%) Nursing Home/ Home Health Care $6.3 Billion (21%) Hospitalization for Decompensation$15.4 Billion (52%) Indirect $2.8 Billion (9.5%) Drugs/Other Medical Durables $3.1 Billion (10.5%) Total 2006$29.6 Billion American Heart Association. 2006 Heart and Stroke Statistical Update. 4

  5. Heart Failure Hospitalizations The number of heart failure hospitalizations is increasing in both men and women 600,000 500,000 400,000 Discharges 300,000 200,000 Women Men 100,000 0 ‘99 '79 '81 '83 '85 '87 '89 '91 '93 '95 '97 2001 CDC/NCHS: Hospital discharges include patients both living and dead. AHA, 1998 Heart and Stroke Statistical Update. NCHS, National Center for Health Statistics.AHA, Heart Disease and Stroke Statistics -- 2005 Update. 5

  6. Hospital Admissions for HF Remain on the Increase Due to… • Inevitable progression of disease • Rising incidence of chronic heart failure (population aging, improved survival with AMI/revascularization) • Incomplete treatment during hospitalization • Poor application of chronic heart failure management • Noncompliance with diet and drugs • Difficulty in assessing volume status and closely monitoring patients AMI, acute myocardial infarction. Fonarow GC, et al. Rev Cardiovasc Med. 2000;1:25-33. 6

  7. 6-Month Readmission Rates Among 17,448 Survivors of Hospitalization for CHF 60 44 40 Patients (%) 16 20 0 Rehospitalized at least once Rehospitalized at least twice CHF, congestive heart failure. 17,448 Medicare patients who survived hospitalization for HF. Krumholtz HM. Arch Intern Med. 1997;157:99-104. 7

  8. Outcomes During and After HF Hospitalization • In-hospital • Length of stay (mean) 6.2 days • Mortality rate 4.1% • Hospital readmissions • 20% at 30 days • 50% at 6 months • Longer-term mortality • 11.6% at 30 days • 33.1% at 12 months Fonarow GC, et al. J Card Failure. 2003;9:S79. Jong P, et al. Arch Intern Med. 2002;162:1689-1694. 8

  9. Long-Term Trends in Mortality With Heart Failure Temporal Trends in Age-Adjusted Mortality After the Onset of Heart Failure* 30-Day Mortality, % (95% CI) 1-Year Mortality, % (95% CI) 5-Year Mortality, % (95% CI) Period Women Men Men Women Men Women 1950–1969 12 (4-19) 18 (7-27) 30 (18-40) 28 (16-39) 70 (57-79) 57 (43-67) 1970–1979 15 (7-23) 16 (6-24) 41 (29-51) 28 (17-38) 75 (65-83) 59 (45-69) 1980–1989 12 (5-18) 10 (4-16) 33 (23-42) 27 (17-35) 65 (54-73) 51 (39-60) 1990–1999 11 (4-17) 10 (3-15) 28 (18-36) 24 (14-33) 59 (47-68) 45 (33-55) *All values were adjusted for age (<55, 55-64, 65-74, 75-84, and ≥85 years). Levy D, et al. N Engl J Med. 2002;347:1397-1402. 9

  10. Evidence-Based Treatment For Stage C Heart Failure Reduce Mortality Control Volume Salt Restriction* Diuretics* ACEI or ARB Aldosterone Antagonist -Blocker Treat Residual Symptoms CRT  an ICD* ICD* Hyd/ISDN* Digoxin* Enhance Adherence Treat Comorbidities Education Disease Management Performance Improvement Systems Aspirin* Warfarin* Statin* *For select indicated patients. ACEI, angiotensin-converting enzyme inhibitor; ARB, angiotensin receptor blocker; ICD, implantable cardioverter defibrillator; CRT, cardiac resynchronization therapy; Hyd/ISDN, hydralazine and isosorbide dinitrate. 10

  11. Utilization of Evidence-Based Therapies in Heart Failure History of HF and LVEF Documented and 0.40* 100 90 80.8 80 70 57.4 60 50.8 Enrolled Discharges (%) 50 41 40 30 20 12.8 10 0 ACE Inhibitor ARB -Blocker Diuretic Digoxin *Excludes patients with documented contraindications. LVEF, left ventricular ejection fraction.2300/7883 patients hospitalized with HF; prior known dx of systolic dysfunction HF; outpatient medical regimen.ADHERE Registry Report Q1 2002 (4/01-3/02) of 180 US Hospitals.Presented by GC Fonarow at the Heart Failure Society of America Satellite Symposium, September 23, 2002. 11

  12. Utilization of Evidence-Based HF Therapies: IMPROVEMENT International Survey 100 90 80 70 60 60 Patients (%) 50 40 34 30 20 20 12 10 0 ACE Inhibitors(ACEI) -Blockers(BB) ACEI + BB Aldosterone Antagonists International survey: 15 countries, 1363 physicians, 11,062 patients: Year 2000. Outpatient regimen in patients with Stage C HF, documented systolic dysfunction. 12 Cleland JG, et al. Lancet. 2002;360:1631-1639.

  13. ADHERE Quality of Care Conformity to JCAHO HF Performance Indicators Lagging Centers Leading Centers 120% 97% 100% 88% 85% 80% 72% 70% Utilization (%) 58% 60% 40% 20% 8% 1% 0% Discharge Instructions LV Function Measurement ACEI use Smoking Cessation All P<0.0001.81 142 admissions between 6/2002-12/2003 at 223 hospitals Grouped by Leading (90th percentile) and Lagging (10th percentile). JCAHO, Joint Commission on Accreditation of Healthcare Organizations. Fonarow GC, et al. Arch Intern Med. 2005;165:1469-1477. 13

  14. “Failure” of Usual Care in Heart Failure • Failure to prescribe evidence-based medications • Failure to discontinue medication that may exacerbate HF • Failure to titrate medications to target doses • Failure to adequately address co-morbidities • Failure to adhere to prescribed medications • Failure to comply with dietary regimen • Failure to adequately assess congestion • Failure to seek early care with escalating symptoms • Failure of adequate discharge planning • Failure of adequate follow-up • Failure of adequate monitoring • Failure of patient social support systems • Failure to address patient and caregiver needs 14

  15. Congestion in Heart Failure • Congestion is the primary cause of heart failure symptoms, hospital admissions, and hospital readmissions • Congestion is an important predictor of mortality and morbidity • Clinical congestion often lags behind rising filling pressures (hemodynamic congestion) • Congestion is often difficult to recognize, delaying appropriate interventions 15

  16. Clinical Presentation of Patients Hospitalized with Heart Failure 150,000 Hospitalization Episodes in ADHERE Any dyspnea (%) 89 Dyspnea at rest (%) 34 Fatigue (%) 32 Rales (%) 68 Peripheral edema (%) 66 Pulmonary congestion (%) 75 SBP <90 mm Hg (%) 2 ADHERE, Acute Decompensated Heart Failure National Registry. Adapted from Fonarow GC. Rev Cardiovasc Med. 2003;4(Suppl 7):S21-S30. 16

  17. Congestion Often Does not Translate into Signs/Symptoms • Among patients with severe heart failure1 • PCWP 33 ± 6 mm Hg, CI 1.8 ± 0.5, LVEF 0.18 ± 0.06 • CXR: 27% no congestion, 41% minimal congestion • Among patients with moderate to severe heart failure2 • PCWP 30 ± 9 mm Hg, CI 2.1 ± 0.8, LVEF 0.18 ± 0.06 • No rales: 84%, No edema: 80%, No JVP 50%, No orthopnea: 22% • Hemodynamic congestion may not be recognized clinically (doesn’t translate into symptoms/signs until late) PCWP, pulmonary capillary wedge pressure; CI, cardiac index; CXR, chest X-ray; JVP, jugular venous pressure. 1. Mahdyoon H, et al. Am J Card. 2003;63:625-627. 2. Stevenson LW, et al. JAMA. 1989;261:884-888. 17

  18. Hemodynamic vs Clinical Congestion Normal filling pressures Elevated filling pressures only with stress or exercise Elevated filling pressures at supine rest Physical Signs of Congestion Obvious Congestive Symptoms 18 Stevenson LW, et al. Circulation. 2006;113:1020-1033.

  19. Congestion Precedes Hospitalization Pressure Change Hospitalization 40 30 20 Change (%) 10 RV Systolic Pressure Estimated PA Diastolic Pressure 0 Heart Rate -10 Baseline -7 -6 -5 -4 -3 -2 -1 Recovery Days Relative to the Event RV, right ventricular; PA, pulmonary artery. Adamson PB, et al. J Am Coll Cardiol. 2003;41:565-571. 19

  20. Importance of Recognizing Congestion • In chronic heart failure,  LV filling pressures(even severe) infrequently cause rales and acute pulmonary edema1,2 • Recognizing hemodynamic congestion is challenging • Identifying congestion early will lead to early treatment, and possibly prevent progression of heart failure and hospitalizations 1. Mahdyoon H, et al. Am J Card. 1989;63:625-627. 2. Stevenson LW, et al. JAMA. 1989;261:884-888. 20

  21. Signs Jugular venous distention/elevation Peripheral edema Pulmonary congestion/ rales Pleural effusions S3 gallop Symptoms Dyspnea on exertion Orthopnea Paroxysmal nocturnal dyspnea Fatigue Abdominal fullness Anorexia, nausea, vomiting Common Signs and Symptoms of Congestion 21

  22. Conventional Methods Used in the Assessment of Congestive in Patients with Heart Failure • Symptoms • Change in weight • Physical examination • Chest X-ray • Echocardiogram • Right heart catheterization (Swan-Ganz) • Left heart catheterization 22

  23. The Challenge of DiagnosingHeart Failure: Physical Examination • JVP on Physical Exam • Great if well seen • In OPTIMIZE-HF and ADHERE, in the majority of hospitalized HF patients, initial exammissed it • Obesity epidemic: good luck • S3 on physical exam • Great if heard • Missed 4/5 times OPTIMIZE-HF, Organized Program to Initiate Life-Saving Treatment in Hospitalized Patients with Heart Failure. 23

  24. How Good Is the Physical Examination for Estimating Hemodynamics? RAP, right atrial pressure. 366 patients with heart failure undergoing examination and right heart catheterization. Capomolla S, et al. Eur J Heart Fail. 2005;7:624-630. 24

  25. The Limited Reliability of the Physical Examination in Heart Failure • Prospectively compared physical signs with hemodynamic measurement in 50 hospitalized patients • Rales, edema, JVP elevation absent in 18 of 43 patients with PCWP >24 mm Hg • Sensitivity 58%, specificity 100% Stevenson LW, et al. JAMA. 1989;261:884-888. 25

  26. Phonocardiographic Analysis of S3 and S4 in Patients Undergoing Catheterization LVEDP, left ventricular end-diastolic pressure. Marcus GM, et al. JAMA. 2005;293:2238-2244. 26

  27. Chest X-Ray in Heart Failure 27

  28. How Good Is Chest X-ray in Diagnosing Heart Failure? • CXR blows • Misses 20% of echo- proven cardiomegaly • Detection of pleural effusion if supine • 67% sensitivity • 70% specificity • Even worse if done portable Kono T, et al. Jpn Circ J. 1992;56(4):359-365. Ruskin JA, et al. Am J Roentgenol. 1987;148(4):681-683. 28

  29. Hospitalizations for Heart Failure • Congestion is the primary reason for heart failure admissions • Low cardiac output and associated signs/symptoms are uncommon • Suboptimal weight reduction during hospitalization • Although appear improved clinically, many patients are discharged with signs and symptoms (related to pulmonary congestion that is not being identified clinically) 29

  30. More than 50% of Patients Have Little or No Weight Loss During Hospitalization 33% 35 30 24% 25 20 Patients (%) 13% 15 15% 10 7% 6% 3% 5 2% 0 (<-20) (-20 to -15) (-15 to -10) (-10 to -5) (-5 to 0) (0 to 5) (5 to 10) (>10) Change in Weight (lbs) Fonarow GC. Rev Cardiovasc Med. 2003;4(Suppl 7):S21-S30. 30

  31. Change in Heart Failure Signs and Symptoms (Admission to Discharge) PND, paroxysmal nocturnal dyspnea. Gattis WA, et al. J Am Coll Cardiol. 2004;43:1534-1541. 31

  32. Hospitalization Outcomes Adams KF, et al. Am Heart J. 2005;149:209-216. Fonarow GC, et al. J Am Coll Cardiol. 2004;844-4A. 32

  33. Outpatient Monitoring of Congestion • Signs and symptoms • Daily weights • Natriuretic peptides (BNP and NT-pro BNP) • Noninvasive bioimpedence monitors BNP, brain (B-type) natriuretic peptide; NT, N-terminal. 33

  34. Limited Reliability of Daily Weights Over Time • Daily weights are helpful but not always reliable predictors of heart failure status • Many patients have difficulty operating/reading scales or remember to weigh themselves • Weight gain may reflect normal fluctuations, variation in time/conditions of weights, or improved appetite with improved heart failure • Weight loss due to loss of muscle/fat (cachexia) may obscure increased fluid retention 34

  35. Interventions to Relieve Congestion • Increase dietary sodium restriction • Fluid restriction • Increase dose, frequency, or mode of administration of loop diuretics • Add/adjust dose of aldosterone antagonist • Thiazide diuretics • Metolazone • Vasopressin antagonists* • Ultrafiltration* *Still investigational. 35

  36. Key Therapeutic Goal in HF:Maintain Optivolemic State Hypervolemia: Increased symptoms, increased risk of hospitalization, increased risk of arrhythmias, increased mortality Optivolemia: Low risk Hypovolemia: Is over-diuresis a problem? 36

  37. Loop Diuretics and Heart Failure • There have been no outcome studies of diuretictherapy for the treatment of heart failure and, thus, it’s effects on morbidity and mortality are not known • Diuretic therapy administered as monotherapy results in all of the following: • Further activation of renin-angiotensin-aldosterone system • Further activation of sympathetic nervous system • Reflex vasoconstriction, increased afterload • Decrease in stroke volume and cardiac output • Substantial reduction in glomerular filtration rate (GFR) Ravnan SL, et al. Congest Heart Fail. 2002;8:80-85. Brater DC. Drugs. 1985;30:427-443. 37

  38. Marked Activation of the Renin- Angiotensin-Aldosterone System By IV Loop Diuretics 1000 50 Mean (95% CI) Mean (95% CI) 600 10 Plasma aldosterone (pmol/L) Plasma renin activity (ng/mL/h) 2.5 200 0.5 100 Before Diuretic (n=12) After Diuretic (n=11) Before Diuretic (n=12) After Diuretic (n=11) Bayliss J, et al. Br Heart J. 1987;57:17-22. 38

  39. Acute Vasoconstrictor Response to IV Furosemide in Congestive Heart Failure Hemodynamic Variable Baseline 20 mins after IV Furosemide 40 mg P Value PAWP (mm Hg) 33 ± 9 28 ± 7 <0.01 SVI (mL/min/m2) 27 ± 8 24 ± 7 <0.01 HR (bpm) 87 ± 13 91 ± 16 <0.01 BP (mm Hg) 90 ± 15 96 ± 15 <0.01 SVR (dyn-s-cm-5) 1454 ± 384 1676 ± 415 <0.01 PRA (ng/mL) 9.9 ± 8.5 17.8 ± 16 <0.05 PNE (pg/mL) 667 ± 390 839 ± 368 <0.01 SVI, stroke volume index; HR, heart rate; BP, blood pressure; SVR, systemic vascular resistance; PRA, plasma renin activity; PNE, plasma norepinephrine. Kubo SH, et al. Am J Cardiol. 1987;60:1322-1328. 39

  40. Furosemide Monotherapy Causes a Significant Decline in Renal Function 15 Placebo 10 5 0 -5 GFR (% change) IV Furosemide -10 -15 -20 -25 0 500 1000 1500 2000 2500 Urine Output (mL) 0 - 8 hours Change in GFR after furosemide 80 mg IV, Class III HF n=16 age 61, LVEF 0.28, CAD 63%, Gottlieb SS, et al. Circulation. 2002;105:1348-1353. 40

  41. Higher Doses of Loop Diuretic is Associated with Increased Mortality in Severe HF 1.0 Group Diuretic dose ACE inhibitor dose A High Low n=240 B High High n=160 C Low Low n=526 D Low High n=224 0.8 A 0.6 B C Total mortality 0.4 D 0.2 Chi-square=33.83 P=0.0001 0 0 6 12 18 24 30 36 Months from Randomization • Retrospective analysis of 1153 patients with advanced HF from PRAISE study • Loop diuretic above and below median compared • High diuretic use independent predictor of: • Total mortality (HR 1.37; P=0.018) • SCD (HR 1.39; P=0.042) • Pump failure death (HR 1.51; P=0.034) • Metolozone use also independent predictor of mortality PRAISE, Prospective Randomized Amlodipine Survival Evaluation; SCD, sudden cardiac death. Neuberg GW, et al. Am Heart J. 2002;144:31-38. 41

  42. Difficulty Assessing Volume Status • May contribute to over diuresis and higher dose than necessary loop diuretic use • Over diuresis contributes to adverse symptoms such as dizziness and headache • Over diuresis contributes to renal dysfunction and increased risk of acute renal failure • Excess diuretic use is associated with further neurohumoral activation • Excess diuretic use is associated with increased mortality 42

  43. Key Therapeutic Goal in HF:Maintain Optivolemic State Hypervolemia: Increased symptoms, increased risk of hospitalization, increased risk of arrhythmias, increased mortality Optivolemia: Low risk Hypovolemia: Increased symptoms, increased risk of hospitalization, increased risk of renal failure, increased mortality 43

  44. Conventional View: Pathophysiological Differentiation of Symptoms and Progression in Heart Failure • What produces heart failure symptoms? • Hemodynamic abnormalities (e.g., changes in cardiac function and peripheral hemodynamics) • What produces disease progression? • Neurohormonal abnormalities (e.g., activation of renin-angiotensin-aldosterone and sympathetic nervous systems)

  45. Time-Dependent Mortality Risk in Heart Failure Weekly Mortality Risk 5 HR=20 AHF Hospitalization Stage C Outpatient 4 4 3 HR=10 3 Mortality % 2 2 HR=4 2 1 1 1 1 0.8 0.8 0.8 0.8 0.8 0.5 0.5 0.5 0.5 0.5 0.4 0.4 0.4 0.4 0.4 0.4 0.4 0.2 0.2 0.2 0.2 0.2 0.2 0.2 0.2 0.2 0.2 0.2 0.2 0.2 0.2 0.2 0.2 0.2 0.2 0.2 0.2 0.2 0.2 0.2 0.2 0 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 Time (weeks) AHF, acute heart failure. 45

  46. Mechanisms by Which Elevated LV Filling Pressures Could Contribute to Mortality in HF • Stretch induced angiotensin II release • Mechanically induced myocardial structural remodeling • Progressive atrioventricular valvular regurgitation • Subendocardial ischemia/cell death by necrosis/apoptosis • Changes in extra cellular matrix structure and function • Myocardial stretch induced increase in intracellular cAMP and calcium • Desensitization of low pressure ventricular mechanoreceptors • What produces disease progression? • Neurohormonal abnormalities • Persistent elevation in ventricular filling pressures • Acute decompensation of heart failure

  47. Implantable Devices May Offer Unique Means to Monitor Fluid Status • Objectively track fluid accumulation and/or hemodynamics longitudinally over time • Multiple measurements per day are averaged to give a truer picture of that day’s trends • Acute changes are compared to the patient’s own expected baseline • Intrathoracic impedance is not affected by respiration or any complicating factors such as electrode placement that impact external systems • No compliance issues as with patient weights 47

  48. Information from Implanted Devices to Assist in HF Disease Management 48

  49. Congestion in Heart Failure: Conclusions • Congestion is the primary cause of heart failure symptoms, hospital admissions, and hospital readmissions • Congestion is an important predictor of mortality and morbidity • Congestion contributes to progression of heart failure • Clinical congestion often lags behind rising filling pressures • Congestion is often difficult to recognize, delaying appropriate interventions • Improved methods to monitoring congestion may improve clinical management and outcomes 49

  50. Optimal Care of Heart Failure: How to Improve Outcomes • Optimize survival enhancing oral medications (ACE inhibitors and/or ARB, beta-blockers, aldosterone antagonists) • Optimize survival-enhancing heart failure device therapies (ICD, CRT) • Optimize patient education and heart failure disease management • Maintain optimal volume status 50

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