Transcript Primary Care Evaluation & Management of Outpatient Congestive

Heart Failure
Guidelines
Patrice M. Schneider RN BSN
Heart Failure Coordinator
South Jersey Heart Group
Lourdes Cardiology Services
Background

NHLBI estimates that @ any given time:
35% of pts with heart failure are NYHA I
 35% of pts with heart failure are NYHA II
 25% of pts with heart failure are NYHA III
 5% of pts with heart failure are NYHA IV
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
Therefore > 85% pf pts with heart failure are
treated primarily in the ambulatory setting
CONGESTIVE HEART FAILURE
Scope of the Problem in U.S.
 Prevalence
of CHF:
 Worldwide
 Incidence of
>
3,000,000
in U.S.
>15,000,000
CHF:
 Most
> 400,000/year
in U.S.
common hospital discharge diagnosis in
patients over 65 years old
 Mortality
 Cost
 All
of CHF:
of CHF:
Approx 200,000/yr in
U.S.
> $ 7 Billion/yr for
Hospital Care
of above are likely to increase with population aging
Etiology of Heart Failure
What causes heart failure?
 The loss of a critical quantity of functioning
myocardial cells after injury to the heart due
to:
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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
ACC/AHA
HF Stage
NYHA
Functional
Class
A
B
C
D
High risk of
developing HF
Structural
heart disease
but without
symptoms of
HF
Structural heart
disease with HF
symptoms,
either prior or
current
Refractory
HF requiring
specialized
interventions
I
II–III
IV
Asymptomatic
HF
Mild and
Moderate HF
Severe HF
No symptoms
Symptoms upon Symptoms
mild to moderate at rest
exertion
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
ACC/AHA
HF Stage
NYHA
Functional
Class
A
B
C
D
High risk of
developing HF
Structural
heart disease
but without
symptoms of
HF
Structural heart
disease with HF
symptoms,
either prior or
current
Refractory
HF requiring
specialized
interventions
I
II–III
IV
Asymptomatic
HF
Mild and
Moderate HF
Severe HF
No symptoms
Symptoms upon Symptoms
mild to moderate at rest
exertion
Stages of Heart Failure
Evaluation of The Patient With
Cardiomyopathy

Historical Data
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ECG Findings
Biochemical parameters
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Levels of various neurohormones
Measurement of effect of NH activation
Hemodynamic parameters
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Etiology
Duration of symptoms
Initial
After tailored therapy
Exercise Capacity
Trends
Risk of sudden deterioration
Etiology of Cardiomyopathy
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Abnormal loading conditions
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Valvular disease
Hypertention
Shunts
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Chemotherapeutics
Cobalt/heavy metal
Acohol
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familial
Muscular dystrophies
Mitochondrial disorders
Hypertrophic
ARVD
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Ischemia
Tachycardia
High PVC burden
Viral
Thyroid disease
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Peripartum
Idiopathic
HIV
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Toxins
Genetic
Insults
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Unclear etiology
Infiltrative
Hemachromatosis
 Sarcoidosis
 amyloid
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Historical Data & Prognosis
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Duration of illness
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Shorter duration of illness associated with a
greater likelihood of spontaneous improvement
Patients with recent onset (<6-7 months require
close clinical surveillance)
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But signs of hemodynamic instability
Or end organ underperfusion
Stevenson AM J Med 1987
Steimle JACC 1994
New York Heart Association
Functional 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
 NYHA II
 NYHA III
 NYHA IV

5%
3-25 %
10-45%
50-77%
Some overlap II/III likely related to differences in
classification from center to center, subjective
interpretation, II, predominantly better than III
Exercise Capacity
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6 minute walk test (6MWT)
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Assess day-to-day efforts at submax exertion
Measures distance an individual able to traverse
over 6 minute period
In moderate heart failure 6MWT has been shown
to be
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Inversely related to QOL score
Inversely related to NYHA
Predictive 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
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Cahalin Chest 1996
Prognosis and CMP
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Trends
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Serial determination
of LVEF may enhance
prognostic value
Mortality @ 1 year

<-5
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Survival based on change in EF
1.0
> 10
.50
<-5
29%
>10

13 % *
24
48
Months
V-HeFT I and II data
72
Prognosis and CMP

Trends
 Decrease
in EF
 Decrease in exercise capacity
 Increase in left ventricular diastolic
dimension
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Risk of sudden Deterioration
 Non-revascularizable
coronary lesion with a
high ischemic burden
 Increase in number of arrhythmic events
Treatment
Chronic Systolic Heart Failure
Vasodilator Therapy
Ace-inhibitors & H/I
B-Blockers
Aldosterone
Inhibitors
ARBs
CRT
OHT
DT
Reduction in Mortality with ACE-I
& B-Blocker therapy
SOLVD
II/III
16%
3 yr
CONSENSUS
IV
40 %
1 yr
ACE-I
MERIT HF
II/III
34 %
1 yr
US CARVEDILOL COPERNICUS
II/III
IIIB
65%
½ yr
B-Blocker
35%
10 mos
Which BB should we use?
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US CARVEDILOL Trial
Coreg
 Target 25 mg bid
 Caveats
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> 70 kg: 50 mg bid
 Able to decrease vasodilator to allow uptitration to maximal dose
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MERIT-HF Trial
Metoprolol Succinate
 Target: 150 mg daily
 Caveat
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Metoprolol Tartrate is inferior (however it was underdosed in the trial)
CIBIS II Trial
Bisoprolol
 Target: approximately 7.5 mg daily
 Asthmatics
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Carvedilol Dose-Response Trial (MOCHA):
Effect on Ejection Fraction and Morbidity
Changes in
LVEF
Cardiovascular hospitalizations

8
0.4

6

5
4
3
2
Mean number/subject
LVEF (EF units)
7
0.3
0.2
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0.1
1
0
Placebo
6.25 mg bid 12.5 mg bid
Carvedilol
25 mg bid
0
Placebo
6.25 mg bid 12.5 mg bid
25 mg bid
Carvedilol
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
Mortality
40
Sudden death
31.6
%
30
Pump Failure
6.1
22.5
20
4.5
12.3
19.4
8.9
11.9
10
13.2
6.1
0
ACEI-/BB-
ACEI+/BB-
Slide courtesy of J. Cohn
2.5
7.5
7.4
3.0
2.0
ACEI-/BB+
HF Therapy
11.9
ACEI+/BB+
ARBs
ELITE II
3152
NYHA III-IV
Val-HeFT
5010
NYHA II-IV
CHARM –added
2548
II-IV
Losartan 50 mg QD vs Capoten 50 mg TID
No difference in mortality, well tolerated
Pitt et al. Lancet 2000;355;1582-1587
Valsartan 160 mg BID vs placebo
No Death
difference in mortality
Significant
decrease
in morbidity & mortality
Hospitalizations
for CHF*
CohnCardiac
et al. NEJM
arrest2001;345:1667-75
Intravenous therapy
Triple therapy adverse effect on mortality
Candesartan 24 mg QD vs Placebo all on ACE-I
Significant decrease in CVd and HF admit
McMurray The LANCET 2003:362;767
Where Does
Hydralazine/Isosorbide Fit in?
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ACE-I or ARB intolerant
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ACE-I or ARB are supperior
But if intolerant due to
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Cough
Hyperkalemia, renal insufficiency
Angioedema
BIDIL (V-HeFT Trial)
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AA who still have NYHA II-IV HF despite
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ACE/ARB and BB
ON TOP of baseline therapy, not instead of
3 times a day
Aldosterone Inhibitors
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RALES Trial
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1663 NYHA III-IV
25 mg Aldactone vs
Placebo
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Progressive HF
SCD
35% reduction in
hospitalization
 Significant
improvement in NYHA
functional class
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Pitt et al. NEJM 1999;341:709
6632 pts 3-14 d after
AMI, EF < 40%
And sign of HF
 Or DM with or without
signs of HF
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30% reduction in
death*
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EPHESUS Trial
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50 mgQD Eplerenone vs
placebo
Significant reduction
in:
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Death 14 % v 17%
CVd/hosp 27% v 30%
SCD 4.9% vs 6%
Pitt NEJM 2003;348:1309
Ventricular Resynchronization
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Sinus
node
Ventricular dyssynchrony
30 - 50% CHF patients
with IVCD
 As QRS widens
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AV
node
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
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Conduction
block
Stimulation
therapy
Abraham WT and Hayes DL, Circulation 2003; 108:2596-2603
Chronic Heart Failure

NYHA I
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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
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NYHA IV
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ACE-I- CONSENSUS
B-Blocker- COPERNICUS
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Aldosterone Blocker – RALES
Resynchronization therapy (EF <35%, QRS > 130ms)
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ACE-I SAVE Trial
B-Blocker CAPRICORN Trial
Eplerenone EPHESUS Trial
NYHA III/IV
Post-AMI
Mechanism of Death in HF
SCD
64%
Other
24%
HF
12%
Other
15%
SCD
59%
NYHA II
HF
26%
NYHA III
HF = mortality secondary to worsening heart failure
SCD = sudden cardiac death
MERIT-HF Study Group. Lancet 1999
SCD
33%
Other
11%
HF
56%
NYHA IV
Ultimate Goal
Delay progression of heart failure or
death to the point where good quality
and quantity of life is achieved