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Heart Failure. Susan Schayes, MD, MPH Program Director Emory Family Medicine Residency Program Adapted from Dr. Joel Felner and Dr. Eddie Needham. Objectives. Define Heart Failure Know the 5 year mortality rate for heart failure

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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 Needham


  • 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


  • Know indications for an ICD

  • Know percent of patients who have diastolic dysfunction

Pre lecture needs assessment
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?


  • 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.

Define heart failure
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.


1. Acute (pulmonary edema)

2. Chronic stable a. Systolic / Diastolic dysfunction

3. Right / Left ventricular failure

4. High output states

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

Heart failure

Pulmonary edema is caused by

(1) imbalance of the Starling forces in the lung (cardiogenic)(2) disruption in the alveolar capillary membrane (non-cardiogenic).

Heart failure



1 hydrostatic ape
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


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.

Heart failure

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

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

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

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%

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

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

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

High output failure non cardiac circulatory overload
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

Clinical evaluation hf

  • Risk factors for CAD

  • Symptoms -only weakly related to LV dysfunction

  • Fluid status: serum Na / weight / edema

  • Functional status: NYHA classification

Precipitating factors

  • Diet: xs Na / H2O; alcohol

  • Non-compliance with medications

  • Arrhythmia

  • Infection

  • Anemia

  • Stress

  • Metabolic: thyroid disease / renal failure

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)


  • 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

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

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

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

Ventricular remodeling

  • Definition -altered chamber geometry -disproportionate cavity to wall thickness

  • Pathophysiology-altered extracellular matrix myocfibrosis -up-regulates pro-inflam cytokines -myocyte hypertrophy/apoptosis; -inotropy -imbalance between production of O- / NO -rearranges myocardial fibers: alters length/width ratio

Heart failure




LV Press.

Left Ventricular volume

LV PRESSURE-VOLUME LOOPS: SYSTOLIC DYSFUNCTION: Contractility: ejection impaired DIASTOLIC DYSFUNCTION: Chamber stiffness: filling impaired

Heart failure


Normal LV

Review cardiac physiology to understand these curves





LV Failure







Heart failure

















cap press



























LA cavity

Epidemiology of heart failure
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.

Epidemiology of heart failure1
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): 2007-18, 2003.

3 Nohria A, et al, Medical Management of Advanced Heart Failure, JAMA, 287(5): 628-40, 2002.

Epidemiology of heart failure2
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): 466-71, 2002.

Diagnosing heart failure symptoms
Diagnosing Heart FailureSymptoms

  • Decreased exercise tolerance

  • Fluid retention

  • Fatigue

  • Incidentally noted left ventricular dysfunction in an asymptomatic patient

Diagnosing heart failure clinical signs
Diagnosing Heart FailureClinical Signs

  • Elevated jugular venous pressure

  • Pulmonary rales

  • S3

    • S3 – volume overload

    • S4 – pressure overload

  • Peripheral edema

Diagnosing heart failure clinical signs1
Diagnosing Heart FailureClinical Signs

Auscultatory findings
Auscultatory Findings

  • S3

  • S4

  • http://www.egeneralmedical.com/listohearmur.html

  • Rales

  • http://www.wilkes.med.ucla.edu/intro.html

Cxr findings in heart failure

CXR findings in Heart Failure

Diagnosing heart failure
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


  • 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.

Heart failure stages vs nyha classes
Heart Failure Stages vsNYHA Classes

Heart failure treatment options
Heart Failure Treatment Options

  • Angiotensin Converting Enzyme Inhibitors (ACEIs)

  • Beta-blockers

  • Diuretics

  • Digoxin

  • Angiotensin Receptor Blockers (ARBs)

  • Other medications


  • 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.


  • 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): 303-10, 1991

Aceis what dose
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): 2312-8, 1999

Aceis what dose1
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: 2090-5, 2000.


  • 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): 145-153, 2000

  • Consider in patients with Stage A Heart Failure

Beta blockers1

  • 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.

Beta blockers2

  • 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): 1349-55, 1996.

Beta blockers3

  • 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.

Beta blockers4

  • 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): 1295-1302, 2000.

Beta blockers5

  • 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): 1385-90, 2001.

Beta blockers6

  • 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.

Beta blockers7

  • 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


  • 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.


  • Furosemide (Lasix) usually the first line, although HCTZ could be used.

  • Only loop diuretics are effective when the CrCl drops below 30cc/min.

Diuretics and the neurohormonal basis of heart failure
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): 709-17, 1999.

Diuretics and the neurohormonal basis of heart failure1
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, 348:1309-21, 2003.


  • 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.


  • 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): 525-33, 1997.

Angiotensin receptor blockers arbs
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.

Heart failure

  • 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): 747-52, 1997

Heart failure

  • 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. 3152 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): 1582-7, 2000

Heart failure

  • 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): 995-1003, 2002.

Heart failure

  • Val-HeFT: A randomized trial of the angiotensin-receptor blocker valsartan in chronic heart failure. 5010 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): 1667-75, 2001

Heart failure

  • 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).

Heart failure

  • 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.

  • Cardiovascular and noncardiovascular mortality were reduced significantly in the candesartan group (ARR = 4%, RRR = 10%), as were hospitalizations.

Heart failure

  • 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.

  • Yusuf S, Lancet, 362: 777-81, 2003.

Heart failure

  • VALIANT trial – valsartan is as effective as captopril post-MI in patients with decreased EF.

    • Pfeffer MA et al, NEJM, 349: 1893-906, 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: 1727-34, 2003

Yes we re talking about icds

Yes, we’re talking about ICDs

Implantable cardioverter-defibrillator

Scd heft trial sudden cardiac death in heart failure trial investigators
SCD-HeFT trialSudden 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 225-237

Scd heft trial sudden cardiac death in heart failure trial investigators1
SCD-HeFT trialSudden 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?

Current indications for icd
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 809 - 818

Summary points
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

Summary points1
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

Summary points2
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

Heart failure

  • 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.


CONSENSUS: Enalapril added to vasodilator therapy decreased mortality by 27% in patients with severe (NYHA IV) heart failure.

Anon., NEJM, 316(23): 1429-35, 1987.


ACEIs mortality by 27% in patients with severe (NYHA IV) heart failure.

  • 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): 669-77, 1992

ACEIs mortality by 27% in patients with severe (NYHA IV) heart failure.

  • 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): 685-91, 1992.

Beta blockers8
Beta-blockers mortality by 27% in patients with severe (NYHA IV) heart failure.

  • 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): 546-51, 2000.

Trends in prevalence and outcome of heart failure with preserved ejection fraction
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 251-259

Take home points
Take home points Preserved Ejection Fraction

  • 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.

Outcome of heart failure with preserved ejection fraction in a population based study
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 260-269

Outcome of heart failure with preserved ejection fraction in a population based study1
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 260-269

Systolic blood pressure on admission and patient outcomes
Systolic blood pressure on admission and patient outcomes a Population-Based Study

  • 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 2217-26

Straw poll sys 120 outcome vs sys 150 outcome who does better

Straw poll… a Population-Based StudySys 120 = outcome?vs Sys 150 = outcome?Who does better?

Systolic blood pressure on admission and patient outcomes1
Systolic blood pressure on admission and patient outcomes a Population-Based Study









Systolic blood pressure at admission in mmHg

Heart failure

  • Interesting outcomes a Population-Based Study

  • 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

Systolic and diastolic heart failure in the community
Systolic and Diastolic Heart Failure in the Community a Population-Based Study

  • 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 2209-2216

Systolic and diastolic heart failure in the community1
Systolic and Diastolic Heart Failure in the Community a Population-Based Study

  • 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 2209-2216

Patient presentation
Patient Presentation a Population-Based Study

  • 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 - 1-2+ pitting edema.

  • Where do you go from here?