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

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Presentation on theme: "Heart Failure Heart Failure Susan Schayes, MD, MPH Program Director Emory Family Medicine Residency Program Adapted from Dr. Joel Felner and Dr. Eddie."— Presentation transcript:

1 Heart Failure 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 Define Heart Failure Know the 5 year mortality rate for 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) 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 Review and become familiar with treatment options Know the three beta-blockers demonstrating benefit, and the two that are FDA approved Know the three beta-blockers demonstrating benefit, and the two that are FDA approved

3 Objectives Know indications for an ICD Know indications for an ICD Know percent of patients who have diastolic dysfunction 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 NYHA classes of HF? What are the four ACC stages of HF? What are the four ACC stages of HF? Which medication classes are routinely prescribed in heart failure? Which medication classes are routinely prescribed in heart failure? Which three beta-blockers are approved to treat HF? 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. 5

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

8 ACUTE PULMONARY EDEMA Definition: Sudden change: structure/function(  LVFP) Definition: Sudden change: structure/function(  LVFP) Etiology: 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 8

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 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. I 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 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 2. “  -permeability pulmonary edema” (acute lung injury)

14 APE with NORMAL HEART SIZE* CARDIAC CAUSES Acute MR (torn chordae / ruptured PM) Acute MR (torn chordae / ruptured PM) Acute AR (dissection / flail leaflet) Acute AR (dissection / flail leaflet) Mitral stenosis Mitral stenosis Ischemic HD: AMI / stunned myocardium Ischemic HD: AMI / stunned myocardium Malignant HTN Malignant HTN Acute rapid AF (WPW) 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 Lung injury damages alveolar-capillary membrane  “capillary leak syndrome” ie, transudation of fluid from pulmonary capillaries to alveoli  oncotic pressure (hypoalbuminemia)  oncotic pressure (hypoalbuminemia) Impaired lymphatic drainage Impaired lymphatic drainage

16 SYSTOLIC DYSFUNCTION Defect: -myofibrils cannot shorten against a load 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 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% Annual mortality - NYHA II-III: 15-20% / NYHA IV: 50% 16

17 DIASTOLIC DYSFUNCTION Pathophysiology: “stiff” ventricle LV: poorly compliant;  filling/relaxation -systolic function: normal or markedly  -evidence of HF: 35% Pathophysiology: “stiff” ventricle LV: poorly compliant;  filling/relaxation -systolic function: normal or markedly  -evidence of HF: 35% Etiology : -- ischemia/LVH/fibrosis/normal aging Etiology : -- ischemia/LVH/fibrosis/normal aging Symptoms: congestive (pul venous HTN) Symptoms: congestive (pul venous HTN) Signs: apex-normal/ sustained+S 4 Signs: apex-normal/ sustained+S 4 Hemodynamic abn: LVEDP / LAP Hemodynamic abn: LVEDP / LAP Prognosis: not as bad as systolic dysfn Prognosis: not as bad as systolic dysfn 17

18 COMPARISON of the TYPES of MYOCARDIAL DYSFUNCTION SYSTOLIC DIASTOLIC Chamber size  /  Ejection fraction  Presence of S Presence of S 4 + /

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

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

21 HIGH OUTPUT FAILURE Non-cardiac circulatory overload HIGH OUTPUT FAILURE Non-cardiac circulatory overload Etiology -fistula / anemia / pregnancy / hyperT4 Etiology -fistula / anemia / pregnancy / hyperT4 Pathophysiology -  SV:  preload (VR) +  PVR(vasodilate) -  CO at rest:  afterload /  preload -  blood volume due to xs Na/H 2 O Pathophysiology -  SV:  preload (VR) +  PVR(vasodilate) -  CO at rest:  afterload /  preload -  blood volume due to xs Na/H 2 O Symptoms: congestion (  PCWP) Symptoms: congestion (  PCWP) Signs:  HR /  SBP/  DBP / wide PP / S 3 Signs:  HR /  SBP/  DBP / wide PP / S 3 21

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

23 PRECIPITATING FACTORS Diet: xs Na / H 2 O; alcohol Diet: xs Na / H 2 O; alcohol Non-compliance with medications Non-compliance with medications Arrhythmia Arrhythmia Infection Infection Anemia Anemia Stress Stress Metabolic: thyroid disease / renal failure Metabolic: thyroid disease / renal failure 23

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

25 PATHOPHYSIOLOGY 1. Ventricular injury / myocyte loss a. Chronic: CAD / HTN / valvular disease b. Acute: AMI / myocarditis / MR / AR 2. Compensation a. Ventricular remodeling -initially adaptive and benficial -eventually maladaptive and harmfulb. Peripheral remodeling 3. Decompensation 25

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

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

28 COMPENSATORY MECHANISMS COUNTERACTS  SV and  CO 1. Starling effect:  preload -limited role 2.  muscle (LVH): vs myocyte loss -key 3.  neurohumoral action:  contractility-bad -SNS:  EPI / NE (  HR / PVR) -RAAS: Na/H 2 O retention;  K/Mg;  GFR-endothelin / vasopressin / prostacyclin 4. Brain natriuretic peptide (BNP) -diagnostic / prognostic 5. Dilatation / remodeling 28

29 VENTRICULAR REMODELING Definition -altered chamber geometry -disproportionate  cavity to wall thickness 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 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 29

30 NEUROHORMONAL RESPONSES TO CHF Initially adaptive  Chronically maladaptive  Preload (aldosterone); to counteract low CO Dyspnea and  Na / H 2 O 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 30

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

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

33 MYOCARDIAL DYSFUNCTION / FAILURE ENDOTHELIAL DYSFUNCTION SYSTOLIC DYSFUNCTION DIASTOLIC DYSFUNCTION  CO RESERVE  ARTERIAL BLOOD VOL  NO  ENDO- THELIN  RAA  VASO- PRESSIN  SNS (NE) Periph constrict Renal constrict Na/H 2 O retention  PLASMA VOLUME  ALDO- STERONE FATIGUE/ RENAL DYSFN  PVR  Vascular stiffness  LA cavity  ANF EDEMADYSPNEA CONGESTION PeripheralPulmonary  LVEDP  Periph cap press  PCP 33

34 Epidemiology of Heart Failure Approximately 5 million patients in the USA have HF, with a yearly incidence of close to 500,000. 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. 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. 80% of hospitalized patients with HF are > 65yo. Heart failure is the most common Medicare DRG. Heart failure is the most common Medicare DRG.

35 Epidemiology of Heart Failure “…one-year mortality of approximately 45 percent.” 2 “…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 “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): , 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 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! Heart failure kills people much more surely than most cancers! Coronary artery disease is the cause of two thirds of left ventricular systolic dysfunction 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 Decreased exercise tolerance Fluid retention Fluid retention Fatigue Fatigue Incidentally noted left ventricular dysfunction in an asymptomatic patient Incidentally noted left ventricular dysfunction in an asymptomatic patient

38 Elevated jugular venous pressure Elevated jugular venous pressure Pulmonary rales Pulmonary rales S 3 S 3 S 3 – volume overload S 3 – volume overload S 4 – pressure overload S 4 – pressure overload Peripheral edema Peripheral edema Diagnosing Heart Failure Clinical Signs

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41 Auscultatory Findings S 3 S 3 S 4 S 4 html html html html Rales Rales

42 Common EKG Findings

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47 CXR findings in Heart Failure

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

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

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54 Heart Failure Stages vs NYHA Classes Heart Failure Stages vs NYHA Classes ACC-AHA StageNYHA 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) Angiotensin Converting Enzyme Inhibitors (ACEIs) Beta-blockers Beta-blockers Diuretics Diuretics Digoxin Digoxin Angiotensin Receptor Blockers (ARBs) Angiotensin Receptor Blockers (ARBs) Other medications 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. 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. 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. 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 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. 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 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. 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. 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: , 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 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 HOPE investigators, NEJM, 342(3): , 2000 Consider in patients with Stage A Heart Failure Consider in patients with Stage A Heart Failure

64 Beta-blockers

65 Beta-blockers Beta-1 selective = metoprolol and bisoprolol Beta-1 selective = metoprolol and bisoprolol Alpha-1 and beta-nonselective = carvedilol. Alpha-1 and beta-nonselective = carvedilol. Beta-blockers reduce the risk of death and the hospitalization. All three have shown benefit. 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. 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): , 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. 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, 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. 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): , 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. CAPRICORN: Effect of carvedilol on outcome after myocardial infarction in patients with left-ventricular dysfunction: the CAPRICORN randomized trial 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 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): , 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. COPERNICUS: Effect of carvedilol on the morbidity of patients with severe chronic heart failure: results of the carvedilol prospective randomized cumulative survival study 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 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, 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. COMET: Comparison of carvedilol and metoprolol on clinical outcomes in patients with chronic heart failure in the Carvedilol Or Metoprolol European Trial 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 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 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) 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. 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. Furosemide (Lasix) usually the first line, although HCTZ could be used. Only loop diuretics are effective when the CrCl drops below 30cc/min. 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. 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): , 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%). 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: , 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. 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, 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. 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): , 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. 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). ARBs are frequently used in patients who cannot tolerate ACEIs (cough, h/o angioedema). They are expensive. They are expensive.

82 ARBs ELITE: Evaluation of losartan in the elderly. 722 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. ELITE: Evaluation of losartan in the elderly. 722 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 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. 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 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. 508 patients on losartan experienced the composite endpoint of death, MI, or stroke, compared with 588 patients on atenolol (RR = 0.87). LIFE trial: Hypertensive patients were treated with either losartan or atenolol. Patients were followed for at least four years. 508 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): , 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. 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 Cohn J, et al, NEJM, 345(23): , 2001

86 ARBs CHARM-Alternative Trial (Candesartan substituted for ACEI in ACEI intolerant patients). CHARM-Alternative Trial (Candesartan substituted for ACEI in ACEI intolerant patients) 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) 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 CHARM-Added Trial In this trial, 2548 patients taking ACEIs with a decreased EF<40% were randomized to receive candesartan or placebo in addition to the ACEI. In this trial, 2548 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. 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.) CHARM-Preserved Trial: Candasartan in Heart failure Assessment of Reduction in Mortality and morbidity study. (A trio of trials.) In this trial, 3023 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. In this trial, 3023 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: , Yusuf S, Lancet, 362: , 2003.

89 ARBs VALIANT trial – valsartan is as effective as captopril post-MI in patients with decreased EF. VALIANT trial – valsartan is as effective as captopril post-MI in patients with decreased EF. Pfeffer MA et al, NEJM, 349: , 2003 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. 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 McKelvie RS et al, Eur Heart J, 24: , 2003

90

91 Number Needed to Treat* for Different Drugs in CHF ACE inhibitors 14 6One death over one year in patients with NYHA class III and IV failure 100One death over one year in patients with NYHA class I or II failure Beta blockers 15 23One death over one year 13One hospitalization over one year Spironolactone 2 9One death over two years in patients with NYHA class IV failure Hydralazine and isosorbide dinitrate 13 14One death over one year Digoxin 16 9Emergency 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 with NYHA class II or III were randomized to placebo, amiodarone, or ICD. Pts were already receiving standard medical therapy Pts were already receiving standard medical therapy Deaths Deaths Placebo group = 244 (29%) Placebo group = 244 (29%) Amiodarone = 240 (28%) Amiodarone = 240 (28%) ICD = 182 (22%) 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%. The ICD group had a 23% relative risk reduction, or an absolute risk reduction of 7.2%. NNT for benefit = ? NNT for benefit = ? So, who should get an ICD? So, who should get an ICD?

96 Current Indications for ICD Patients at high risk for ventricular arrhythmias Patients at high risk for ventricular arrhythmias Patients with EF < 35% and NYHA class II or III heart failure Patients with EF < 35% and NYHA class II or III heart failure Patients with a history of MI and EF < 30% 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. 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: There is a new staging system to classify heart failure: Stage A – at risk but no structural heart disease (HD) Stage A – at risk but no structural heart disease (HD) Stage B – no symptoms but structural HD present Stage B – no symptoms but structural HD present Stage C – patient with symptomatic HF Stage C – patient with symptomatic HF Stage D – refractory heart failure Stage D – refractory heart failure

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

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

100 Thank you for your time

101 The End 101

102

103

104 Additional material

105 BNP The Breathing Not Properly study 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, Maisel A, et al, Rapid Measurement of B-Type Natriuretic Peptide in the Emergency Diagnosis of Heart Failure, NEJM, 347(3): 161-7, A number > 100 is suggestive of heart failure. 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. 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. CONSENSUS: Enalapril added to vasodilator therapy decreased mortality by 27% in patients with severe (NYHA IV) heart failure. Anon., NEJM, 316(23): , 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. 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 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 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 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. 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): , 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. 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). 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): , 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 patients admitted to Mayo Clinic Hospitals from 1987 to % had reduced ejection fraction 53% had reduced ejection fraction 47% had preserved ejection fraction 47% had preserved ejection fraction Survival was slightly better among those with preserved EF – adjusted hazard ration for death = 0.96, p = Survival was slightly better among those with preserved EF – adjusted hazard ration for death = 0.96, p = Trends in Prevalence and Outcome of Heart Failure with 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. 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. 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 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% 31% had ejection fraction (EF) > 50% More likely to be older, female, history of HTN, history of atrial fibrillation More likely to be older, female, history of HTN, history of atrial fibrillation Outcome of Heart Failure with Preserved Ejection Fraction in a 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 ( 50%) vs reduced EF (<40%) at 30 days 5% vs 7% respectively 5% vs 7% respectively At one year, the rates were 22% vs 26%, p=0.07, not significantly different. 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 Patients with preserved EF have similar rates for mortality and readmission for heart failure Outcome of Heart Failure with Preserved Ejection Fraction in a 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 ,267 patients admitted for heart failure to 259 hospitals between March 2003 – December Good numbers! Good numbers! 21,149 (51%) had preserved systolic function 21,149 (51%) had preserved systolic function Meaning, half the patients had diastolic dysfunction 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 Systolic blood pressure at admission in mmHg Percent mortality at discharge 7.2% 3.6% 2.5% 1.7%

117 Interesting outcomes Interesting outcomes Lower systolic at admission directly correlated with increased mortality Lower systolic at admission directly correlated with increased mortality Concept of the “J” curve in treatment of hypertension 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? 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 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, Inpatients and outpatients diagnosed with heart failure underwent echocardiographic testing between September 10, 2003 and October 27, study participants 556 study participants Preserved EF > 50 % present in 308 (55%) of patients Preserved EF > 50 % present in 308 (55%) of patients Associated with older age, female sex, no h/o MI 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 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%) EF < 50% in 248 patients (45%) Diastolic dysfunction present in 204 (83%) of these patients Diastolic dysfunction present in 204 (83%) of these patients Systolic and Diastolic Heart Failure in the Community, JAMA, Nov. 8, 2006, 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… 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. 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. 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. Many patients will have a mix of systolic dysfunction (depressed EF) and diastolic dysfunction. Systolic and Diastolic Heart Failure in the Community, JAMA, Nov. 8, 2006, 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. 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 VS – stable Lungs – CTA, normal work of breathing Lungs – CTA, normal work of breathing CV – RRR, nl S1 S2, no MRG heard CV – RRR, nl S1 S2, no MRG heard Extremities pitting edema. Extremities pitting edema. Where do you go from here? Where do you go from here?


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