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Heart Failure Susan Schayes, MD, MPH Program Director

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1 Heart Failure Susan Schayes, MD, MPH Program Director
Emory Family Medicine Residency Program Adapted from Dr. Joel Felner and Dr. Eddie Needham

2 Objectives Define Heart Failure
Know the 5 year mortality rate for heart failure Distinguish between New York Heart Association classes (I – IV) and the new American College of Cardiology stages (A – D) Review and become familiar with treatment options Know the three beta-blockers demonstrating benefit, and the two that are FDA approved

3 Objectives Know indications for an ICD
Know percent of patients who have diastolic dysfunction

4 Pre-lecture Needs Assessment
What are the four NYHA classes of HF? What are the four ACC stages of HF? Which medication classes are routinely prescribed in heart failure? Which three beta-blockers are approved to treat HF?

5 DEFINITION Clinical syndrome Inability of the heart to produce sufficient cardiac output to meet the metabolic demands of the peripheral tissues while operating at normal filling pressure.

6 Define Heart Failure “Heart failure is a complex syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood.” 1 The cardinal symptoms are dyspnea and fatigue, while the predominant clinical sign is fluid retention (rales, elevated jugular venous pulsations, and pedal edema). Given that not all patients are volume overloaded at the time of diagnosis (diastolic dysfunction), the term “heart failure” is now preferred over “congestive heart failure.” 1Hunt S, et al, ACC/AHA Guidelines for the Evaluation and Management of Chronic Heart Failure in the Adult: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Revise the 1995 Guidelines for the Evaluation and Management of Heart Failure). 2001, ACC web site, accessed November 12, 2004.

7 CLASSIFICATION 2. Chronic stable a. Systolic / Diastolic dysfunction
1. Acute (pulmonary edema) 2. Chronic stable a. Systolic / Diastolic dysfunction 3. Right / Left ventricular failure 4. High output states

8 ACUTE PULMONARY EDEMA Definition: Sudden change: structure/function(LVFP) Etiology: Cardiac myocardial (ischemia / infarction) mechanical (acute regurg; HTN urgency) -electrical (tachycardia: AF/VT) Non-cardiac high altitude pulmonary edema (HAPE) heroin overdose; chlorine,etc

9 Pulmonary edema is caused by
(1) imbalance of the Starling forces in the lung (cardiogenic) (2) disruption in the alveolar capillary membrane (non-cardiogenic).

10 CARDIOGENIC PULMONARY EDEMA
NON-CARDIOGENIC PULMONARY EDEMA

11 1. “hydrostatic APE” Acute cardiogenic or volume-overload pulmonary edema sudden  in pulmonary venous pressure  pulmonary interstitial and alveolar fluid -pulmonary and lymphatic drainage can’t compensate acutely to remove the fluid

12 continued Hallmark: rapid increase in hydrostatic pressure in the pulmonary capillaries causing increased transvascular fluid filtration. It is usually due to  pulmonary venous pressure from LVEDP/ LAP As LAP rises above 25 mmHg fluid breaks thru the lung epithelium flooding the alveoli with protein poor fluid.

13 2. “-permeability pulmonary edema” (acute lung injury)
Non-cardiogenic pulmonary edema Lymphatic drainage cannot compensate for the  lung water caused by the disrupted alveolar capillary membrane Caused by  vascular permeability of the lung   flux of fluid into the interstitium and air spaces

14 APE with NORMAL HEART SIZE* CARDIAC CAUSES
Acute MR (torn chordae / ruptured PM) Acute AR (dissection / flail leaflet) Mitral stenosis Ischemic HD: AMI / stunned myocardium Malignant HTN Acute rapid AF (WPW) *Enlarged heart: Exacerbation of chronic HF; Myocarditis

15 APE: NON-CARDIAC CAUSES PATHOPHYSIOLOGY
Lung injury damages alveolar-capillary membrane  “capillary leak syndrome” ie, transudation of fluid from pulmonary capillaries to alveoli  oncotic pressure (hypoalbuminemia) Impaired lymphatic drainage

16 SYSTOLIC DYSFUNCTION Defect: -myofibrils cannot shorten against a load
Various clinical presentations asymptomatic, w/ ejection fraction -evidence of CO: fatigue/confused/BUN -evidence of congestion: DOE/leg edema -dilated LV chamber on chest x-ray Annual mortality NYHA II-III: 15-20% / NYHA IV: 50% 20% of pts with low EF did not have clinical criteria for CHF; 51% with normal EF had evidence of CHF

17 DIASTOLIC DYSFUNCTION
Pathophysiology: “stiff” ventricle LV: poorly compliant;  filling/relaxation -systolic function: normal or markedly  -evidence of HF: 35% Etiology: ischemia/LVH/fibrosis/normal aging Symptoms: congestive (pul venous HTN) Signs: apex-normal/ sustained+S4 Hemodynamic abn: LVEDP / LAP Prognosis: not as bad as systolic dysfn More common in elderly pts (age-related) -ischemia/hypertension/atrial fibrillation Cause: CAD/HTN/HOCM/AS

18 COMPARISON of the TYPES of MYOCARDIAL DYSFUNCTION
SYSTOLIC DIASTOLIC Chamber size  /  Ejection fraction Presence of S3 + - Presence of S4 + / -

19 LEFT HEART FAILURE Etiology -CAD / HTN / Valvular HD / etc
Symptoms fatigue/congestion (SOB / DOE) Signs narrow pulse pressure -hypokinetic carotid pulse -inferolaterally displaced apex -S3/S4 gallops; murmurs of MR/TR

20 RIGHT HEART FAILURE Etiology lung disease: parenchymal / vascular congenital: ASD / Ebstein’s anomaly Symptoms fatigue / syncope / girth / edema Signs hypotension / parasternal lift distended neck veins / + HJ reflux -right-sided S3 / S4; murmur of TR hepatomegaly / ascites / peripheral edema

21 HIGH OUTPUT FAILURE Non-cardiac circulatory overload
Etiology fistula / anemia / pregnancy / hyperT4 Pathophysiology SV: preload (VR) + PVR(vasodilate) -CO at rest:  afterload / preload blood volume due to xs Na/H2O Symptoms: congestion (PCWP) Signs: HR / SBP/DBP / wide PP / S3 ANEMIA: HGB <7 Chronic intravascular circulatory congestion + LVEDP/Pul ven presstransudation of fluid from capillaries to interstitial spaces. APE: rate of transudation > lymph drainage

22 CLINICAL EVALUATION- HF
Risk factors for CAD Symptoms only weakly related to LV dysfunction Fluid status: serum Na / weight / edema Functional status: NYHA classification

23 PRECIPITATING FACTORS
Diet: xs Na / H2O; alcohol Non-compliance with medications Arrhythmia Infection Anemia Stress Metabolic: thyroid disease / renal failure

24 LABORATORY EVALUATION 2-D ECHO / DOPPLER
Most useful test Determines primary abnormality Derives Ejection Fraction (EF) -most important single measurement -but, poor correlation with symptoms Distinguishes systolic / diastolic dysfn Guide to prognosis (EF and ESV) Assesses disease progression (remodels) REMODELING: LV cavity/thickness/regional wall motion

25 PATHOPHYSIOLOGY Ventricular injury / myocyte loss a. Chronic: CAD / HTN / valvular disease b. Acute: AMI / myocarditis / MR / AR Compensation a. Ventricular remodeling initially adaptive and benficial eventually maladaptive and harmful b. Peripheral remodeling Decompensation

26 PATHOPHYSIOLOGY: THEORIES
OLD: hemodynamic disorder  ejection (EF) sx (fatigue / dyspnea) -Rx: contractility: inotropes unload periphery: dilators / diuretics CURRENT: uncontrolled LV remodeling -chamber dilates (spherical); hypertrophy -mechanism: neurohormonal system -Rx: counteract RAAS / SNS FUTURE: genetic abn / xs cytokines

27 PATHOPHYSIOLOGY: EVENTS
Primary response: SNS activation (/NE) -initiates vicious circle: afterload Secondary response: hormone constriction -RAAS: periph perfusion (Na retained) -Vasopressin: non-osmotic release Vascular endothelial dysfunction (NO) Result of neurohormonal compensation -adaptive / beneficial: maintains perfusion -long term: maladaptive / deleterious

28 COMPENSATORY MECHANISMS COUNTERACTS SV and CO
Starling effect: preload -limited role muscle (LVH): vs myocyte loss -key neurohumoral action:contractility-bad -SNS: EPI / NE (HR / PVR) RAAS: Na/H2O retention;K/Mg;GFR endothelin / vasopressin / prostacyclin Brain natriuretic peptide (BNP) diagnostic / prognostic Dilatation / remodeling

29 VENTRICULAR REMODELING
Definition altered chamber geometry disproportionate cavity to wall thickness Pathophysiology altered extracellular matrix myoc fibrosis -up-regulates pro-inflam cytokines myocyte hypertrophy/apoptosis; inotropy imbalance between production of O- / NO rearranges myocardial fibers: alters length/width ratio

30 NEUROHORMONAL RESPONSES TO CHF
Initially adaptive  Chronically maladaptive Preload (aldosterone); to counteract low CO Dyspnea and Na / H2O retention Vasoconstriction: Angiotensin II; to maintain BP Hypertrophy / LV cavity, i.e., remodeling; CO SNS (NEPI / EPI); to maintain forward CO Down-regulation adrenergic receptors; myocyte toxicity

31 DIASTOLIC DYSFUNCTION NORMAL
SYSTOLIC DYSFUNCTION DIASTOLIC DYSFUNCTION NORMAL LV Press. Left Ventricular volume LV PRESSURE-VOLUME LOOPS: SYSTOLIC DYSFUNCTION: Contractility: ejection impaired DIASTOLIC DYSFUNCTION: Chamber stiffness: filling impaired

32 Review cardiac physiology to understand these curves
FRANK-STARLING LV FUNCTION CURVES Normal LV Review cardiac physiology to understand these curves Stroke Volume Low CO LV Failure Congestion 10 15 20 LVEDP THE RELATIONSHIP BETWEEN SV and LVEDP

33 MYOCARDIAL DYSFUNCTION / FAILURE
DIASTOLIC DYSFUNCTION SYSTOLIC DYSFUNCTION ENDOTHELIAL DYSFUNCTION LVEDP ARTERIAL BLOOD VOL CO RESERVE NO ENDO- THELIN Periph cap press PCP SNS (NE) VASO- PRESSIN RAA FATIGUE/ RENAL DYSFN Periph constrict Renal constrict ALDO- STERONE PVR ANF CONGESTION Na/H2O retention Vascular stiffness Peripheral Pulmonary EDEMA DYSPNEA PLASMA VOLUME LA cavity

34 Epidemiology of Heart Failure
Approximately 5 million patients in the USA have HF, with a yearly incidence of close to 500,000. It is primarily a disease of the elderly, with 6-10% patients over 65 years old being diagnosed with HF. 80% of hospitalized patients with HF are > 65yo. Heart failure is the most common Medicare DRG.

35 Epidemiology of Heart Failure
“…one-year mortality of approximately 45 percent.” 2 “Survival ranges from 80% at 2 years for patients rendered free of congestion to less than 50% at 6 months for patients with refractory symptoms.” 3 2 Jessup M, Brozena S, Medical Progress: Heart Failure, NEJM, 348(20): , 2003. 3 Nohria A, et al, Medical Management of Advanced Heart Failure, JAMA, 287(5): , 2002.

36 Epidemiology of Heart Failure
“Heart failure admission rates are rising, and the prognosis of heart failure has been compared with that of malignancy, with a 6-year mortality rate of 84% in men and 77% in women.” 4 Heart failure kills people much more surely than most cancers! Coronary artery disease is the cause of two thirds of left ventricular systolic dysfunction 4 Mair F, et al, Evaluation of suspected left ventricular systolic dysfunction, JFP, 51(5): , 2002.

37 Diagnosing Heart Failure Symptoms
Decreased exercise tolerance Fluid retention Fatigue Incidentally noted left ventricular dysfunction in an asymptomatic patient

38 Diagnosing Heart Failure Clinical Signs
Elevated jugular venous pressure Pulmonary rales S3 S3 – volume overload S4 – pressure overload Peripheral edema

39 Diagnosing Heart Failure Clinical Signs

40

41 Auscultatory Findings
Rales

42 Common EKG Findings

43

44

45

46

47 CXR findings in Heart Failure

48

49

50 Diagnosing Heart Failure
Many different terms: Left vs right-sided failure Backward vs forward failure Volume vs pressure overload Systolic vs diastolic dysfunction – there is a lot of overlap as many patients have aspects of both entities

51

52 Echocardiography A generally accepted definition of depressed systolic function is an ejection fraction < 40%, from the ACC guideline on the use of echocardiography. Note that this is not a useful definition in diastolic dysfunction as the EF may actually be increased in diastolic dysfunction.

53

54 Heart Failure Stages vs NYHA Classes
ACC-AHA Stage NYHA Functional Classification A: At high risk for HF but without structural heart disease or symptoms of HF (Eg, patients with HTN or CAD) None B: Structural heart disease but without symptoms of HF I: Asymptomatic C: Structural heart disease with prior or current symptoms of HF II: Symptomatic with moderate exertion III: Symptomatic with minimal exertion D: Refractory HF requiring specialized interventions IV: Symptomatic at rest (cardiac cripple)

55 Stages of Heart Failure

56 Heart Failure Treatment Options
Angiotensin Converting Enzyme Inhibitors (ACEIs) Beta-blockers Diuretics Digoxin Angiotensin Receptor Blockers (ARBs) Other medications

57 Site of Action of Medications

58 ACEIs

59 ACEIs They are the most studied class with years of experience and large patient numbers in RCTs. Proven benefit to decrease mortality and hospitalization for HF.

60 ACEIs A comparison of enalapril with hydralazine-isosirbide dinitrate in the treatment of chronic congestive heart failure. 804 men on digoxin and diuretics were randomized to receive enalapril or hydralazine and isosorbide dinitrate. The enalapril arm demonstrated an 18% mortality rate at 2 years compared with 25% for the hydralazine and isosorbide dinitrate arm. Cohn JN, NEJM, 325(5): , 1991

61 ACEIs – what dose? ATLAS: Patients with NYHA class II to IV with and EF< or = 30% were assigned to either low dose (2.5 – 5.0mg) or high dose (32.5 – 35mg) of lisinopril for up to five years. Patients on the higher dose had a nonsignificant decrease in mortality of 8% with a significant 12% decrease in death or hospitalization for any reason, as well as 24% fewer hospitalizations for heart failure. Packer M, Circulation, 100(23): , 1999

62 ACEIs – what dose? Outcome of patients with congestive heart failure treated with standard versus high doses of enalapril: a multicenter study. There were no differences in mortality or hospitalizations between patients treated with up to 20 mg or those treated with up to 60 mg of enalapril. Nanas J, JACC, 36: , 2000.

63 ACEIs HOPE Trial: The use of ramipril in patients with multiple cardiac risk factors without known CHF or left ventricular dysfunction reduces the risk of death from any cause, MI, stroke, and heart failure. HOPE investigators, NEJM, 342(3): , 2000 Consider in patients with Stage A Heart Failure

64 Beta-blockers

65 Beta-blockers Beta-1 selective = metoprolol and bisoprolol
Alpha-1 and beta-nonselective = carvedilol. Beta-blockers reduce the risk of death and the hospitalization. All three have shown benefit.

66 Beta-blockers US Carvedilol Heart Failure Study Group: Carvedilol was added to background therapy of ACEI, diuretics, and digoxin. Patients receiving carvedilol experienced a 65% decrease in mortality, a 27% decrease in hospitalizations, and a 38% decrease in the combination of the two. Packer M, NEJM, 334(21): , 1996.

67 Beta-blockers CIBIS-II: Bisoprolol was added to standard therapy (diuretics and ACEIs) in patients with NYHA III or IV with EF < 35%. Study was stopped early because of the benefit. The hazard ratio of death was 0.56 vs placebo. Anon., Lancet, 353(9146): 9-13, 1999.

68 Beta-blockers MERIT-HF: Patients had NYHA class II to IV, an EF<40%, and were stabilized with optimum medical therapy. Patients were randomized to receive the beta-1 blocker metoprolol CR/XL. Patients in therapy experienced a 19% decrease in mortality or all-cause hospitalizations and a 31% decrease in HF hospitalizations. Hjalmarson A, JAMA, 283(10): , 2000.

69 Beta-blockers CAPRICORN: Effect of carvedilol on outcome after myocardial infarction in patients with left-ventricular dysfunction: the CAPRICORN randomized trial. 1959 patients post MI with EF<40% were randomized to carvedilol or placebo. All-cause (ARR 3%) and cardiovascular mortality, as well as non-fatal MI were reduced in patients on carvedilol. Dargie H, Lancet, 357(9266): , 2001.

70 Beta-blockers COPERNICUS: Effect of carvedilol on the morbidity of patients with severe chronic heart failure: results of the carvedilol prospective randomized cumulative survival study. 2289 patients with severe heart failure (EF<25%) were randomized to receive carvedilol or placebo for an average of ten months. Mortality from cardiovascular causes and heart failure mortality or hospitalization were both decreased by 27% and 31% respectively. In euvolemic patients with symptoms at rest or on minimal exertion, the addition of carvedilol to conventional therapy ameliorates the severity of heart failure and reduces the risk of clinical deterioration, hospitalization, and other serious adverse clinical events. Packer M, Circulation, 106(17):2194-9, 2002.

71 Beta-blockers COMET: Comparison of carvedilol and metoprolol on clinical outcomes in patients with chronic heart failure in the Carvedilol Or Metoprolol European Trial. 1511 patients on standard HF therapy with EF<35% were randomized to receive carvedilol or metoprolol. After 5 years, all cause mortality was 34% with carvedilol and 40% with metoprolol. The composite endpoint of all-cause mortality and hospitalization was the same in both groups. Poole-Wilson P, Lancet, 362(9377):7-13, 2003

72 Diuretics

73 Diuretics No dedicated RCTs to evaluate the use of loop diuretics. (Perhaps unethical now that their use is standard of care) Diuretics are added when patients experience symptoms or signs of volume overload.

74 Diuretics Furosemide (Lasix) usually the first line, although HCTZ could be used. Only loop diuretics are effective when the CrCl drops below 30cc/min.

75 Diuretics and the neurohormonal basis of heart failure
RALES Trial: Spironolactone was added to therapy in patients with severe heart failure and an EF<35% being treated with ACEIs, diuretics, and (in most cases) digoxin. The study was stopped early after demonstrating an absolute decrease in mortality of 11% (RR = 0.70) and an relative decrease in hospitalization of 35% (RR = 0.65). 10% of males had gynecomastia or mastalgia. Minimal hyperkalemia was reported. Pitt B, NEJM, 341(10): , 1999.

76 Diuretics and the neurohormonal basis of heart failure
Ephesus trial - The use of eplerenone in patients post-MI who had an EF<40% and clinical signs of heart failure showed benefit. Patients on the medication experienced and absolute risk reduction in mortality of 2.3% (RRR = 14%). Pitt B, et al. Eplerenone, a selective aldosterone blocker, in patients with left ventricular dysfunction after myocardial infarction. N Engl J Med, 348: , 2003.

77 Digoxin

78 Digoxin RADIANCE Study: Patients on a stable regimen of digoxin, ACEI, and diuretic were randomized to removal of digoxin or maintenance of therapy. Those patients off digoxin experienced a significant increase in worsening heart failure and decreased measures of functional capacity. Packer M, NEJM, 329(1): 1-7, 1993.

79 Digoxin Digitalis Intervention Group: Patients on ACEI and diuretics were randomized to receive digoxin or placebo. Overall mortality was similar in both groups. However, digoxin did decrease the risk of worsening heart failure and hospitalization. Rekha G, NEJM, 336(8): , 1997.

80 ARBs

81 Angiotensin Receptor Blockers (ARBs)
The ARBs – studies have shown that they have efficacy close to that of ACEIs. ARBs are frequently used in patients who cannot tolerate ACEIs (cough, h/o angioedema). They are expensive.

82 ARBs ELITE: Evaluation of losartan in the elderly patients older than 65 with EF<40% and ACEI naïve were randomized to losartan or captopril, in addition to standard therapies (ACEIs, diuretics, digoxin, nitrates and hydralazine). Patients on losartan has less side effects, a nonsignificant decrease in death and/or hospital admission for heart failure, and a significant decrease in all-cause mortality (risk reduction = 46%). Admissions for heart failure were the same in both groups. Pitt B, Lancet, 349(9054): , 1997

83 ARBs ELITE-II: Effect of losartan compared with captoril on mortality in patients with symptomatic heart failure: a randomized trial – the Losartan Heart Failure Survival Study patients 60 years or older with NYHA class II to IV heart failure and EF<40% were randomized to losartan or captopril. The mortality and rates of sudden death or resuscitated arrests were the same in both groups. Pitt B, Lancet, 355(9215): , 2000

84 ARBs LIFE trial: Hypertensive patients were treated with either losartan or atenolol. Patients were followed for at least four years patients on losartan experienced the composite endpoint of death, MI, or stroke, compared with 588 patients on atenolol (RR = 0.87). Dahlof B, Lancet, 359(9311): , 2002.

85 ARBs Val-HeFT: A randomized trial of the angiotensin-receptor blocker valsartan in chronic heart failure patients with NYHA class II to IV HF were randomized to receive valsartan or placebo in addition to standard therapy. Overall mortality was the same. Hospitalizations were 4.4% less. Treatment with valsartan improved NYHA class, EF, signs and symptoms of HF, and quality of life. Post hoc analysis showed the valsartan had a favorable outlook in patients receiving ACEI or beta-blockade but an adverse effect in patients receiving both. Cohn J, et al, NEJM, 345(23): , 2001

86 ARBs CHARM-Alternative Trial (Candesartan substituted for ACEI in ACEI intolerant patients). 2028 patients with symptomatic heart failure and EF<40% were randomized to candesartan or placebo, in addition to standard therapy. After 3 years, cardiovascular mortality and hospital admissions for CHF were both less (3% and 8% absolute risk reduction).

87 ARBs CHARM-Added Trial
In this trial, patients taking ACEIs with a decreased EF<40% were randomized to receive candesartan or placebo in addition to the ACEI. Cardiovascular and noncardiovascular mortality were reduced significantly in the candesartan group (ARR = 4%, RRR = 10%), as were hospitalizations.

88 ARBs CHARM-Preserved Trial: Candasartan in Heart failure Assessment of Reduction in Mortality and morbidity study. (A trio of trials.) In this trial, patients with a preserved EF>40% were randomized to receive candesartan or placebo. Cardiovascular and noncardiovascular mortality were the same in both groups, while hospitalizations were modestly decreased. Yusuf S, Lancet, 362: , 2003.

89 ARBs VALIANT trial – valsartan is as effective as captopril post-MI in patients with decreased EF. Pfeffer MA et al, NEJM, 349: , 2003 RESOLVD trial – candesartan with enalapril and ER metoprolol demonstrated the most improvement in EF from baseline. No clinical outcomes. McKelvie RS et al, Eur Heart J, 24: , 2003

90

91 Number Needed to Treat* for Different Drugs in CHF
ACE inhibitors14 6 One death over one year in patients with NYHA class III and IV failure 100 One death over one year in patients with NYHA class I or II failure Beta blockers15 23 One death over one year 13 One hospitalization over one year Spironolactone2 9 One death over two years in patients with NYHA class IV failure Hydralazine and isosorbide dinitrate13 14 Digoxin16 Emergency department visits or hospitalizations *--Number needed to treat (NNT) is the number of patients who need to be treated to prevent one outcome from occurring. NNT=100/absolute risk reduction.

92 Now, let’s have some shocking news…

93 Yes, we’re talking about ICDs
Implantable cardioverter-defibrillator

94 SCD-HeFT trial Sudden Cardiac Death in Heart Failure Trial Investigators
2521 pts with NYHA class II or III were randomized to placebo, amiodarone, or ICD. Pts were already receiving standard medical therapy Deaths Placebo group = 244 (29%) Amiodarone = 240 (28%) ICD = 182 (22%) Bardy, G, et al, SCD-HeFT, NEJM, January 20, 2005; 352: 3, pp

95 SCD-HeFT trial Sudden Cardiac Death in Heart Failure Trial Investigators
The ICD group had a 23% relative risk reduction, or an absolute risk reduction of 7.2%. NNT for benefit = ? So, who should get an ICD?

96 Current Indications for ICD
Patients at high risk for ventricular arrhythmias Patients with EF < 35% and NYHA class II or III heart failure Patients with a history of MI and EF < 30% Goldberger, Z, Implantable Cardioverter-Defibrillators, JAMA, February 15, 2006; 295:7, pp

97 Summary Points Heart failure has a prognosis similar to that of cancer. As such, treat it aggressively. There is a new staging system to classify heart failure: Stage A – at risk but no structural heart disease (HD) Stage B – no symptoms but structural HD present Stage C – patient with symptomatic HF Stage D – refractory heart failure

98 Summary Points Standard medication classes for HF include:
ACEIs Beta blockers Diuretics if volume overloaded Consider digoxin, spironolactone Consider ARBs, especially in ACEI intolerant patient Beta-blockers continue to look good for HF

99 Summary Points Preserved EF is about as common as depressed EF in heart failure. Many patients have diastolic dysfunction. Remember to also care for the patient as a person, not just a disease. A gentle touch and a kind smile might feel better than a lasix-induced diuresis 

100 Thank you for your time

101 The End

102

103

104 Additional material

105 BNP The Breathing Not Properly study
Maisel A, et al, Rapid Measurement of B-Type Natriuretic Peptide in the Emergency Diagnosis of Heart Failure, NEJM, 347(3): 161-7, 2002. A number > 100 is suggestive of heart failure. Some thought to using this prospectively to screen for heart failure, stage B. No RCTs to date.

106 ACEIs CONSENSUS: Enalapril added to vasodilator therapy decreased mortality by 27% in patients with severe (NYHA IV) heart failure. Anon., NEJM, 316(23): , 1987.

107 ACEIs SAVE Trial: Effect of captopril on mortality and morbidity in patients with left ventricular dysfunction after myocardial infaction. Results of the Survival And Ventricular Enlargement trial. 2231 patients with an EF<40% who survived an MI were randomized to receive captopril and followed for 42 months. Risks for mortality (5% absolute risk reduction), fatal and nonfatal major cardiovascular events, development of severe heart failure, and recurrent MI were all reduced. Pfeffer MA, NEJM, 327(10): , 1992

108 ACEIs SOLVD Trial: Enalapril therapy in patients with an EF< 35% not being treated for CHF demonstrated a statistically significant decrease in the combined endpoint of development of clinical CHF and death. Of note, when studying the end point of mortality, there was no statistical difference between enalapril and placebo. Anon., NEJM, 327(10): , 1992.

109 Beta-blockers Differential effects of beta-blockers in patients with heart failure: A prospective, randomized double-blind comparison of the long-term effects of metoprolol versus carvedilol. 150 patients with EF <35% were randomized to metoprolol or carvedilol. After 2 years, patients in the carvedilol showed a 3.7% increase in EF, greater stroke volume and decreased PCWP compared with metoprolol. Conversely, metoprolol showed a greater increase in exercise capacity. Mortality was similar (small study). Metra M, Circulation, 102(5): , 2000.

110 Trends in Prevalence and Outcome of Heart Failure with Preserved Ejection Fraction
4596 patients admitted to Mayo Clinic Hospitals from 1987 to 2001. 53% had reduced ejection fraction 47% had preserved ejection fraction Survival was slightly better among those with preserved EF – adjusted hazard ration for death = 0.96, p = 0.01. Owan, TE, et al, Trends in Prevalence and Outcome of Heart Failure with Preserved Ejection Fraction, NEJM, 355:3, July 20, 2006, pp

111 Take home points Starting with an ACEI is still standard of care.
However, future studies with FDA approved drugs for heart failure in the USA may confirm that beta-blockers are equally efficacious (noninferior) to ACEIs for the initial treatment of HF.

112 Outcome of Heart Failure with Preserved Ejection Fraction in a Population-Based Study
2802 patients admitted to 103 Canadian hospitals from April 1999 to March 2001 with a discharge diagnosis of heart failure. 31% had ejection fraction (EF) > 50% More likely to be older, female, history of HTN, history of atrial fibrillation Bhatia, RS, et al, Outcome of Heart Failure with Preserved Ejection Fraction in a Population-Based Study, NEJM, 355:3, July 20, 2006, pg

113 Outcome of Heart Failure with Preserved Ejection Fraction in a Population-Based Study
Mortality rate of preserved EF (>50%) vs reduced EF (<40%) at 30 days 5% vs 7% respectively At one year, the rates were 22% vs 26%, p=0.07, not significantly different. Patients with preserved EF have similar rates for mortality and readmission for heart failure Bhatia, RS, et al, Outcome of Heart Failure with Preserved Ejection Fraction in a Population-Based Study, NEJM, 355:3, July 20, 2006, pg

114 Systolic blood pressure on admission and patient outcomes
41,267 patients admitted for heart failure to 259 hospitals between March 2003 – December 2004. Good numbers! 21,149 (51%) had preserved systolic function Meaning, half the patients had diastolic dysfunction Gheorghiade, M, et al, Systolic Blood Pressure at Admission, Clinical Characteristics, and Outcomes in Patients Hospitalized With Acute Heart Failure, JAMA, Nov. 8, 2006, Vol. 296, No. 18, pp

115 Straw poll… Sys 120 = outcome? vs Sys 150 = outcome? Who does better?

116 Systolic blood pressure on admission and patient outcomes
7.2% Percent mortality at discharge 3.6% 2.5% 1.7% Systolic blood pressure at admission in mmHg

117 Interesting outcomes Lower systolic at admission directly correlated with increased mortality Concept of the “J” curve in treatment of hypertension So, what systolic blood pressure do we shoot for in patients with stable heart failure in the clinic? Still use national guidelines but stay tuned

118 Systolic and Diastolic Heart Failure in the Community
Inpatients and outpatients diagnosed with heart failure underwent echocardiographic testing between September 10, 2003 and October 27, 2005. 556 study participants Preserved EF > 50 % present in 308 (55%) of patients Associated with older age, female sex, no h/o MI Isolated diastolic dysfunction present in 242 of patients of these patients – 44% of total number (556) and 78% of patients with preserved EF EF < 50% in 248 patients (45%) Diastolic dysfunction present in 204 (83%) of these patients Bursi, F, Systolic and Diastolic Heart Failure in the Community, JAMA, Nov. 8, 2006, 296:18, pp

119 Systolic and Diastolic Heart Failure in the Community
Needham’s take on this data… A little more than half (55%) of patients had preserved EF at the time of diagnosis of heart failure. Almost 80% of all patients with heart failure have diastolic dysfunction, whether they have depressed or preserved EF. Many patients will have a mix of systolic dysfunction (depressed EF) and diastolic dysfunction. Bursi, F, Systolic and Diastolic Heart Failure in the Community, JAMA, Nov. 8, 2006, 296:18, pp

120 Patient Presentation Mr. Smith is a 67 yo male with a history of hypertension and diabetes who now presents to your clinic with mild dyspnea at the end of his 1 mile walk. No chest pain. He has occasional pedal edema. VS – stable Lungs – CTA, normal work of breathing CV – RRR, nl S1 S2, no MRG heard Extremities pitting edema. Where do you go from here?


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