Heart Failure Guidelines

Patrice M. Schneider RN BSNHeart Failure CoordinatorSouth Jersey Heart Group

Lourdes Cardiology Services

Background

NHLBI estimates that @ any given time:35% of pts with heart failure are NYHA I35% of pts with heart failure are NYHA II25% of pts with heart failure are NYHA III5% of pts with heart failure are NYHA IV

Therefore > 85% pf pts with heart failure are treated primarily in the ambulatory setting

CONGESTIVE HEART FAILUREScope of the Problem in U.S.

Prevalence of CHF: > 3,000,000 in U.S.

Worldwide >15,000,000

Incidence of CHF: > 400,000/year in U.S.

Most common hospital discharge diagnosis in patients over 65 years old

Mortality of CHF: Approx 200,000/yr in

U.S.

Cost of CHF: > $ 7 Billion/yr for Hospital Care

All of above are likely to increase with population aging

Etiology of Heart FailureWhat causes heart failure?The loss of a critical quantity of

functioning myocardial cells after injury to the heart due to:

Ischemic Heart Disease Hypertension Infections (e.g., viral myocarditis, Chagas’ disease) Toxins (e.g., alcohol or cytotoxic drugs) Valvular Disease Prolonged Arrhythmias Peripartum Idiopathic Cardiomyopathy

Classification of HF: Comparison Between ACC/AHA HF Stage and NYHA Functional

Class

Severe HF

Symptomsat rest

Mild and Moderate HF

Symptoms upon mild to moderate exertion

Asymptomatic HF

No symptoms

IVII–IIII

Refractory HF requiring specialized interventions

Structural heart disease with HF symptoms, either prior or current

Structural heart disease but without symptoms of HF

High risk of developing HF

DCBA

ACC/AHAHF Stage

NYHAFunctionalClass

Challenging Tradition

NYHA class changes over time Increasing evidence that heart failure is a

cellular disease Despite symptomatic improvement

neurohormonal, cytokine and cellular changes continue to occur and allow heart failure to progress

Ejection Fraction (EF) does not correlate with functional capacity (NYHA class)

Classification of HF: Comparison Between ACC/AHA HF Stage and NYHA Functional

Class

Severe HF

Symptomsat rest

Mild and Moderate HF

Symptoms upon mild to moderate exertion

Asymptomatic HF

No symptoms

IVII–IIII

Refractory HF requiring specialized interventions

Structural heart disease with HF symptoms, either prior or current

Structural heart disease but without symptoms of HF

High risk of developing HF

DCBA

ACC/AHAHF Stage

NYHAFunctionalClass

Stages of Heart Failure

Evaluation of The Patient With Cardiomyopathy

Historical Data Etiology Duration of symptoms

ECG Findings Biochemical parameters

Levels of various neurohormones Measurement of effect of NH activation

Hemodynamic parameters Initial After tailored therapy

Exercise Capacity Trends Risk of sudden deterioration

Etiology of Cardiomyopathy Abnormal loading conditions

Valvular disease Hypertention Shunts

Toxins Chemotherapeutics Cobalt/heavy metal Acohol

Genetic familial Muscular dystrophies Mitochondrial disorders Hypertrophic ARVD

Insults Ischemia Tachycardia High PVC burden Viral Thyroid disease

Unclear etiology Peripartum Idiopathic HIV

Infiltrative Hemachromatosis Sarcoidosis amyloid

Historical Data & Prognosis

Duration of illnessShorter duration of illness associated with a

greater likelihood of spontaneous improvementPatients with recent onset (<6-7 months

require close clinical surveillance)But signs of hemodynamic instabilityOr end organ underperfusion

Stevenson AM J Med 1987Steimle JACC 1994

New York Heart AssociationFunctional Classification

I. No limitations of physical activity, no symptoms with ordinary activities

II. Mild/slight limitation, symptoms with ordinary activities

III. Moderate/marked limitation, symptoms with less than ordinary activities

IV. Severe limitation, symptoms of heart failure at rest

Symptoms: Dyspnea or fatigue

Adapted from Criteria Committee of the New York Heart Association, 1994.

Exercise Capacity

NYHA (Gradman Card Clinics 1994)Annual mortality

NYHA I 5%NYHA II 3-25 %NYHA III 10-45%NYHA IV 50-77%

Some overlap II/III likely related to differences in classification from center to center, subjective interpretation, II, predominantly better than III

Cahalin Chest 1996

Exercise Capacity 6 minute walk test (6MWT)

Assess day-to-day efforts at submax exertionMeasures distance an individual able to

traverse over 6 minute period In moderate heart failure 6MWT has been

shown to be Inversely related to QOL score Inversely related to NYHAPredictive or mortality in moderate HF

In Severe HF (< 300 meters) Correlate to Peak VO2 Predictive of 6 month event-free survival

But not long term (>6 month) survival

V-HeFT I and II data

Prognosis and CMP

TrendsSerial determination of LVEF may

enhance prognostic valueMortality @ 1 year

< - 5 29%

>1013 % *

< - 5

> 10

Survival based on change in EF

Months

24 48 72

.50

1.0

Prognosis and CMP

TrendsDecrease in EFDecrease in exercise capacityIncrease in left ventricular diastolic

dimensionRisk of sudden Deterioration

Non-revascularizable coronary lesion with a high ischemic burden

Increase in number of arrhythmic events

Treatment

Chronic Systolic Heart Failure

Vasodilator TherapyAce-inhibitors & H/I

B-Blockers

ARBs AldosteroneInhibitors

CRT OHT DT

Reduction in Mortality with ACE-I & B-Blocker therapy

65%½ yr

35%10 mos

SOLVDII/III

CONSENSUSIV

MERIT HFII/III

US CARVEDILOLII/III

COPERNICUSIIIB

16%3 yr

40 %1 yr 34 %

1 yr

ACE-I B-Blocker

Which BB should we use? US CARVEDILOL Trial

Coreg Target 25 mg bid Caveats

> 70 kg: 50 mg bid Able to decrease vasodilator to allow uptitration to maximal dose

MERIT-HF Trial Metoprolol Succinate Target: 150 mg daily Caveat

Metoprolol Tartrate is inferior (however it was underdosed in the trial)

CIBIS II Trial Bisoprolol Target: approximately 7.5 mg daily Asthmatics

Carvedilol Dose-Response Trial (MOCHA):Effect on Ejection Fraction and Morbidity

Carvedilol

Placebo 6.25 mg bid 12.5 mg bid 25 mg bid0

1

2

3

4

5

6

7

8

LV

EF (

EF u

nit

s)

Changes in LVEF

Carvedilol

Placebo 6.25 mg bid 12.5 mg bid 25 mg bid0

0.1

0.2

0.3

0.4

Mean

nu

mb

er/

su

bje

ct

Cardiovascular hospitalizations

P<.001 P=.01

Patients receiving diuretics, ACE inhibitors, ± digoxin; follow-up duration 6 months; placebo (n=84), carvedilol (n=261).Adapted from Bristow et al, 1996. P<.05 vs placebo

Mortality in the placebo arm of Val-HeFT by treatment group: 23-month mean follow-up

0

10

20

30

40

ACEI-/BB- ACEI+/BB- ACEI-/BB+ ACEI+/BB+

HF Therapy

%

Mortality

Sudden death

Pump Failure

7.4

2.5

2.0

11.9

6.1

4.5

7.5

8.9

3.013.2

12.3

6.1

11.9

22.519.4

31.6

Slide courtesy of J. Cohn

ARBs

ELITE II3152 NYHA III-IV

Losartan 50 mg QD vs Capoten 50 mg TIDNo difference in mortality, well toleratedPitt et al. Lancet 2000;355;1582-1587

Val-HeFT5010 NYHA II-IV

Valsartan 160 mg BID vs placeboNo difference in mortalitySignificant decrease in morbidity & mortalityCohn et al. NEJM 2001;345:1667-75

DeathHospitalizations for CHF*Cardiac arrestIntravenous therapyTriple therapy adverse effect on mortality

CHARM –added2548II-IV

Candesartan 24 mg QD vs Placebo all on ACE-ISignificant decrease in CVd and HF admitMcMurray The LANCET 2003:362;767

Where Does Hydralazine/Isosorbide Fit in?ACE-I or ARB intolerant

ACE-I or ARB are supperiorBut if intolerant due to

CoughHyperkalemia, renal insufficiencyAngioedema

BIDIL (V-HeFT Trial)AA who still have NYHA II-IV HF despite

ACE/ARB and BBON TOP of baseline therapy, not instead of3 times a day

Aldosterone Inhibitors RALES Trial

1663 NYHA III-IV 25 mg Aldactone vs

Placebo 30% reduction in

death* Progressive HF SCD

35% reduction in hospitalization

Significant improvement in NYHA functional class

Pitt et al. NEJM 1999;341:709

EPHESUS Trial 6632 pts 3-14 d after

AMI, EF < 40% And sign of HF Or DM with or

without signs of HF 50 mgQD Eplerenone

vs placebo Significant reduction

in: Death 14 % v 17% CVd/hosp 27% v 30% SCD 4.9% vs 6%

Pitt NEJM 2003;348:1309

Ventricular Resynchronization

Ventricular dyssynchrony 30 - 50% CHF patients

with IVCD As QRS widens

Mortality increases Electrical delay

translates to mechanical delay/dyssynchrony

Improved A-V synchrony Interventricular

synchrony Intraventricular

synchrony Positive remodeling Reduction in heart

failure and all-cause morbidity and mortality

Sinus node

AVnode

Stimulation therapy

Conduction block

Abraham WT and Hayes DL, Circulation 2003; 108:2596-2603

Chronic Heart Failure NYHA I

ACE-inhibitor- SOLVD Prevention Trial NYHA II/III

ACE-I – SOLVD, V-HeFT II Hydralazine/ISDN – V-HeFT B-Blocker – MERIT-HF, US Carvedilol, Angiotensin Receptor Blocker- Val-HeFT, CHARM

NYHA IV ACE-I- CONSENSUS B-Blocker- COPERNICUS

NYHA III/IV Aldosterone Blocker – RALES Resynchronization therapy (EF <35%, QRS > 130ms)

Post-AMI ACE-I SAVE Trial B-Blocker CAPRICORN Trial Eplerenone EPHESUS Trial

Mechanism of Death in HF

MERIT-HF Study Group. Lancet 1999

NYHA IV NYHA II NYHA III

HF = mortality secondary to worsening heart failure SCD = sudden cardiac death

SCD64%

SCD59%

SCD33%

HF12%

HF26% HF

56%

Other11%Other

24%

Other15%

Ultimate Goal

Delay progression of heart failure or death to the point where good quality and quantity of life is

achieved