CHRONIC CONGESTIVE HEART

FAILURE
A Comprehensive Overview on Diagnosis and Treatment

Dr. Irwan, SpJP.

Faculty of Medicine of Riau University

Arifin Achmad Hospital,Pekanbaru
Introduction
Definition : Heart Failure
“The situation when the heart is incapable of
maintaining a cardiac output adequate to
accommodate metabolic requirements and the
venous return.“ E. Braunwald
“Pathophysiological state in which an
abnormality of cardiac function is responsible
for the failure of the heart to pump blood at a
rate commensurate with the requirements of
the metabolizing tissues.” Euro Heart J; 2001. 22: 1527-1560
DEFINITION OF HEART FAILURE.
Criteria 1 and 2 should be fulfilled in all cases

1. Symptoms of heart failure

(at rest or during exercise)
And
2. Objective evidence of cardiac dysfunction
(at rest)
And
(in cases where the diagnosis is in doubt)
3. Response to treatment directed towards heart
failure
Task Force Report. Guidelines for the diagnosis and treatment of chronic heart failure.
European Society of Cardiology.2001
 EPIDEMIOLOGY
Europe

The prevalence of symptomatic HF range from 0.4-2%.

10 million HF pts in 900 million total population
Guidelines for the diagnosis and treatment of chronic heart failure
European Heart Journal (2001) 22, 1527-1560

USA

nearly 5 million HF pts.

± 500,000 pts are D/ HF for the 1st time each year.
Last 10 years  number of hospitalizations has increased.
Nearly 300,000 patients die of HF each year.
ACC/AHA Guidelines for the
Evaluation and Management of Chronic Heart Failure in the Adult 2001
DESCRIPTIVE TERMS in HEART FAILURE

 Acute vs Chronic Heart Failure

 Systolic vs Diastolic Heart Failure
 Right vs Left Heart Failure
 Mild , Moderate, Severe Heart Failure

Guidelines for the diagnosis and treatment of chronic heart failure

European Heart Journal (2001) 22, 1528
 New York Heart Association (NYHA)
Classification of Heart Failure
No limitation : ordinary physical exercise does
Class – I not cause undue fatigue, dyspnoea or palpita-
tions.

Slight limitation of physical activity : comfor-

Class – II table at rest but ordinary activity results in
fatigue, dyspnoea, or palpitation.

Marked limitation of physical activity : comfor-

Class - III table at rest but less than ordinary activity
results in symptoms.
Unable to carry out any physical activity with-
out discomfort : symptoms of heart failure are
Class - IV present even at rest with increased discomfort
with any physical activity.
Guidelines for the diagnosis and treatment of chronic heart failure
European Heart Journal (2001) 22, 1531
(Adapted from Williams JF et al., Circulation. 1995; 92 : 2764-2784)
 ACC/AHA – A New Approach To The Classification of HF
Stage Descriptions Examples
A Patient who is at high risk for Hypertension; CAD; DM;
developing HF but has no rheumatic fever; cardiomyopathy.
structural disorder of the heart.

B Patient with a structural disorder LV hypertrophy or fibrosis;

of the heart but who has never LV dilatation; asymptomatic VHD;
developed symptoms of HF. MI.

C Patient with past or current Dyspnea or fatigue ec LV systolic

symptoms of HF associated with dysfunction; asymptomatic
underlying structural heart patients with HF.
disease.

D Patient with end-stage disease Frequently hospitalized pts ; pts

awaiting heart transplantation etc

ACC/AHA Guidelines for the

Evaluation and Management of Chronic Heart Failure in the Adult 2001
Stages in the evolution of HF and recommended therapy by stage

Stage A Stage B Stage C Stage D

Pts with : Pts with : Pts with : Pts who have

• Hypertension • Previous MI • Struct. HD marked symptoms
• CAD Struct. • LV systolic Develop Refract. at rest despite
• DM Heart dysfunction Symp.of • Shortness of Symp.of maximal medical
breath and fatigue,
• Cardiotoxins Disease • Asymptomatic HF HF at rest therapy.
reduce exercise
• FHx CM Valvular disease
tolerance

THERAPY THERAPY THERAPY THERAPY

• Treat Hypertension • All measures under • All measures under • All measures under
• Stop smoking stage A stage A stage A,B and C
• Treat lipid disorders • ACE inhibitor • Drugs for routine use: • Mechanical assist
• Encourage regular • Beta-blockers • diuretic device
exercise • ACE inhibitor • Heart transplantation
• Stop alcohol • Beta-blockers • Continuous IV
& drug use • digitalis inotrphic infusions for
• ACE inhibition palliation

ACC/AHA Guidelines for the

Evaluation and Management of Chronic Heart Failure in the Adult 2001
 EVOLUTION OF
CLINICAL STAGES
NORMAL
No symptoms
Normal exercise
Asymptomatic
Normal LV fxn LV Dysfunction
No symptoms
Normal exercise
Compensated
Abnormal LV fxn CHF
No symptoms Decompensated
Exercise
Abnormal LV fxn CHF
Symptoms
Exercise
Refractory
Abnormal LV fxn CHF
Symptoms not controlled
with treatment
Patophysiology of C H F
 PULMONARY VENOUS
PRESSURE

Input

Filling Emptying
Stroke
ED volume x EF effective = volume
LV Distensibility Contractility x
Relaxation Afterload Heart
Left atrium Preload
Mitral valve rate
Structure
Pericardium
Diastolic function Systolic function

Output

CARDIAC OUTPUT

Block diagram of left ventricular pump performance

(Little, 2001)
 DETERMINANTS OF
VENTRICULAR FUNCTION

CONTRACTILITY

PRELOAD AFTERLOAD

STROKE
VOLUME

- Synergistic LV contraction HEART

- LV wall integrity RATE
- Valvular competence

CARDIAC OUTPUT
Frank-Starling Law

Normal
Cardiac Output Compensated

Normal C.O.

CHF

LVEDP
The Pathophysiology of Heart Failure

Hurst. The Heart. Diagnosis and Management of Heart Failure.10th ed. 688
 Pathophysiological Sequence of
CHF

Heart Failure

Inadequate Cardiac Output

( ) O2 Delivery (rest and/or exercise)

Systemic Vasoconstriction

SAS (NE)) RAAS (A-II)

() Flow to Skin, Gut,
and Renal Circulations
Neurohormonal Activation

Activation of
RAS and ANS

Hurst. The Heart. Diagnosis and Management of Heart Failure.10th ed. 688
 SNS
Preload Afterload
Renin release

Angiotensin II
Growth ALDO
factors
Vasoconstriction
Hypertrophy Fluid
Apoptosis accumulation
Collagen
deposition
Myofibril
necrosis
Perfusion of Vital Organs

RBF

Na filtered

Renin release

Angiotensin II

Growth ALDO
factors
Vasoconstriction
Fluid accumulation
Hypertrophy
Apoptosis Collagen deposition
Afterload
Myofibril necrosis
 Sympathetic nervous system up-regulation

Increased
Norepinephrine levels

Activation of the Decreased Direct

RAA system Renal blood Myocardial toxicity
flow
Myocyte dysfunction
Increased
Angiotensin II & Increased HR, PVR & Myocyte
Aldosteron arteriolar vasoconstriction necrosis

Increased myocardial Intracellular

Na+ & water oxygen demand Ca2+ overload/
retention Energy depletion

Vasoconstriction Cardiac remodeling Apoptosis

Cesario et.al; Reviews in cardiovascular medicine, vol 3, no.1, 2002

 Causes of Heart Failure

Myocardial Damage or Disease

 Infarction (Acute) / Ischemia
 Myocarditis
 Hypertrophic Cardiomyopathy

Excess Load on Ventricle

 Volume/ Pressure Overload
Resistance to Flow into Ventricle
Cardiac Arrhythmias
MI-INDUCED HEART FAILURE
Myocardial Damage

Contractility

Pump Performance
() Systolic Work Load () SAS Drive
Vasoconstriction

RAAS SYSTEM
FLUID RETENTION
Diagnosis of C H F
IDENTIFICATIONS OF HF PATIENTS

 With a Syndrome of Decrease Exercise

Tolerance

 With a Syndrome of Fluid Retention

 With No Symptoms or Symptoms of

Another Cardiac or Non Cardiac
Disorder
(MI, Arrythmias, Pulmonary or
Systemic Thromboembolic Events)
 SYMPTOMS AND SIGN

 Breathlessness, Ankle Swelling, Fatique

→ Characteristic Symptoms

 Peripheral Oedema, JVP ↑, Hepatomegaly

→ Signs of Congestion of Systemic Veins

 S3  , Pulmonary Rales , Cardiac Murmur 

 ECG
 A low Predictive Value
 LAH and LVH May Be Associated wit LV Dysfunction
 Anterior Q-wave and LBBB a good predictors of EF ↓↓
 Detecting Arrhytmias as Causative of HF

CHEST X-RAY

 A Part of Initial Diagnosis of HF

→ Cardiomegaly, Pulmonary Congestion
 Relationship Between Radiological Signs and
Haemodynamic Findings may Depend on the Duration
and Severity HF
 HAEMATOLOGY & BIOCHEMISTRY
 A Part of Routine Diagnostic
 Hb, Leucocyte, Platelets
 Electrolytes, Creatinine, Glucose, Hepatic Enzyme,
Urinalysis
 TSH, C-RP, Uric Acid

ECHOCARDIOGRAPHY
 The Preferred Methods
 Helpful in Determining the Aetiology
 Follow Up of Patients Heart Failure
 INVASIVE INVESTIGATION

 Elucidating the Cause and Prognostic Informations

 Coronary Angiography :
in CAD’s Patients

 Haemodynamic Monitoring :
To Assess Diagnostic and Treatment of HF

 Endomyocardial Biopsy :
in Patients with Unexplained HF
 NATRIURETIC PEPTIDES

 Cardiac Function ↓↓ (LV Function ↓↓) →

↑↑ Plasma Natriuretic Peptide Concentration
(Diagnostic Blood Use for HF)
 Natriuretic Peptide ↑↑ :
Greatest Risk of CV Events
Natriuretic Peptide ↓↓ :
Improve Outcome in Patients with
Treatment

 Identify Pts. With Asymptomatic LV

Dysfunction (MI, CAD)
 ALGORITHM FOR THE DIAGNOSIS OF THE HF
(ESC, 2001)
Suspected Heart Failure Because
of symptoms and signs

If Normal
Assess Presence of Cardiac Disease by ECG, X-Ray Heart Failure
or NatriureticPeptides (Where Available) Unlikely

Tests Abnormal

Imaging by Echocardiography (Nuclear If Normal

Angiography or MRI Where Available) Heart Failure
Unlikely

Tests Abnormal

Assess Etiology, Degree, Precipitating

Factors and Type of Cardiac Dysfunction
Additional Diagnosis Tests
Where Appropriate (e.g.
Coronary Angiography)
Choose Therapy
Treatment of C H F
 Aims of Treatment

1. Prevention
a) Prevention and/or controlling of diseases leading
to cardiac dysfunction and heart failure
b) Prevention of progression to heart failure once
cardiac dysfunction is established
2. Morbidity
Maintenance or improvement in quality of life
3. Mortality
Increased duration of life

Guidelines for the diagnosis and treatment of chronic heart failure

European Heart Journal (2001) 22, 1527-1560
 Management Outline

Establish that the patient has HF.

Ascertain presenting features: pulmonary oedema, exertional
breathlessness, fatigue, peripheral oedema
Assess severity of symptoms
Determine aetiology of heart failure
Identify precipitating and exacerbating factors
Identify concomitant diseases
Estimate prognosis
Anticipate complications
Counsel patient and relatives
Choose appropriate management
Monitor progress and manage accordingly

Guidelines for the diagnosis and treatment of chronic heart failure

European Heart Journal (2001) 22, 1527-1560
 TREATMENT

Correction of aggravating factors

Pregnancy Endocarditis
Arrhythmias (AF) Obesity
Infections Hypertension
Hyperthyroidism Physical activity
Thromboembolism Dietary excess
MEDICATIONS
 Treatment options
Non-pharmacological management
General advice and measures
Exercise and exercise training
Pharmacological therapy
Angiotensin-converting enzyme (ACE) inhibitors
Diuretics
Beta-adrenoceptor antagonists
Aldosterone receptor antagonists
Angiotensin receptor antagonists
Cardiac glycosides
Vasodilator agents (nitrates/hydralazine)
Positive inotropic agents
Anticoagulation
Antiarrhythmic agents
Oxygen
Devices and surgery
Revascularization (catheter interventions and surgery), other forms of surgery
Pacemakers
Implantable cardioverter defibrillators (ICD)
Heart transplantation, ventricular assist devices, artificial heart
Ultrafiltration, haemodialysis
Guidelines for the diagnosis and treatment of chronic heart failure
European Heart Journal (2001) 22, 1527-1560
 ACC/AHA & EUROPE (ESC) 2001
GUIDELINES FOR THE MANAGEMENT
OF HEART FAILURE

 ACE-inhibitor
→ Use as first line therapy
→ Should be up titrated to the dosages shown in the large
clinical trial, and not titrated based on symptomatic
improvement
 DIURETIC → to control fluid overload
 Β-BLOCKER
→ For all patients with stable mild-severe HF on
standard treatment
 ACC/AHA & EUROPE (ESC) 2001
GUIDELINES FOR THE MANAGEMENT
OF HEART FAILURE

 Aldosteron Receptor Antagonis

→ in advance HF ( NYHA III-IV )
 DIGOXIN
→ in AF
→ May be added for symptom relief
 ARB
→ Considered in patients not tolerate ACE
inhibitors and not on β - blocker
 TREATMENT

Normal
Asymptomatic
LV dysfunction
EF <40%
Symptomatic CHF
ACEI NYHA II Symptomatic CHF
Diuretics mild NYHA - III
Neurohormonal Symptomatic CHF
inhibitors Loop
Diuretics NYHA - IV
Digoxin?
Inotropes
Specialized therapy
Transplant
Secondary prevention
Modification of physical activity
Pharmacological therapy
Stages in the evolution of HF and recommended therapy by stage

Stage A Stage B Stage C Stage D

Pts with : Pts with : Pts with : Pts who have

• Hypertension • Previous MI • Struct. HD marked symptoms
• CAD Struct. • LV systolic Develop Refract. at rest despite
• DM Heart dysfunction Symp.of • Shortness of Symp.of maximal medical
breath and fatigue,
• Cardiotoxins Disease • Asymptomatic HF HF at rest therapy.
reduce exercise
• FHx CM Valvular disease
tolerance

THERAPY THERAPY THERAPY THERAPY

• Treat Hypertension • All measures under • All measures under • All measures under
• Stop smoking stage A stage A stage A,B and C
• Treat lipid disorders • ACE inhibitor • Drugs for routine use: • Mechanical assist
• Encourage regular • Beta-blockers • diuretic device
exercise • ACE inhibitor • Heart transplantation
• Stop alcohol • Beta-blockers • Continuous IV
& drug use • digitalis inotrphic infusions for
• ACE inhibition palliation

ACC/AHA Guidelines for the

Evaluation and Management of Chronic Heart Failure in the Adult 2001
1. ACE INHIBITOR
Angiotensin-converting enzyme inhibitors

Recommended as first-line therapy.

Should be uptitrated to the dosages shown to be
effective in the large, controlled trials, and not
titrated based on symptomatic improvement.
Moderate renal insufficiency and a relatively low blood
pressure (serum creatinine  250 µmol.l-1 and systolic
BP  90 mmHg) are not contraindications.
Absolute contraindications: bilateral renal artery
stenosis and angioedema.

Guidelines for the diagnosis and treatment of chronic heart failure

European Heart Journal (2001) 22, 1527-1560
 ACEI

MECHANISM OF ACTION
VASOCONSTRICTION VASODILATATION
ALDOSTERONE PROSTAGLANDINS
VASOPRESSIN Kininogen tPA
SYMPATHETIC Kallikrein
Angiotensinogen
RENIN
Angiotensin I
BRADYKININ

A.C.E. Inhibitor Kininase II

ANGIOTENSIN II Inactive Fragments

 ACEI

UNDESIRABLE EFFECTS
Inherent in their mechanism of action
- Hypotension - Dry cough
- Hyperkalemia - Renal Insuff.
- Angioneurotic edema
Due to their chemical structure
- Cutaneous eruptions
- Neutropenia, - Dysgeusia
thrombocytopenia - Proteinuria
- Digestive upset
 ACEI

CONTRAINDICATIONS

Renal artery stenosis

Renal insufficiency
Hyperkalemia
Arterial hypotension
Intolerance (due to side effects)
ACE-Inhibitors in Asymptomatic Heart Failure

 Development of symptomatic HF

 Hospitalization of HF

SAVE & TRACE Study Guidelines for the diagnosis and treatment of chronic heart failure
European Heart Journal (2001) 22, 1527-1560
ACE-Inhibitors in Symptomatic Heart Failure

All patients symptomatic Heart Failure should receive ACE-I.

A) No fluid retention, ACE-I should be given first.

B) With fluid retention, ACE-I + Diuretic

ACE-I : A) improves survival and symptoms.

B) reduces hospitalization.

Guidelines for the diagnosis and treatment of chronic heart failure

European Heart Journal (2001) 22, 1527-1560
2. DIURETICS
Diuretics

Essential for symptomatic treatment when

fluid overload is present and manifest.

Always be administered in combination

with ACE inhibitors if possible.

Guidelines for the diagnosis and treatment of chronic heart failure

European Heart Journal (2001) 22, 1527-1560
 DIURETICS

Thiazides
Inhibit active exchange of Cl-Na
Cortex in the cortical diluting segment of the
ascending loop of Henle

K-sparing
Inhibit reabsorption of Na in the
distal convoluted and collecting tubule

Loop diuretics
Medulla Inhibit exchange of Cl-Na-K in
the thick segment of the ascending
loop of Henle

Loop of Henle
Collecting tubule
 THIAZIDES

MECHANISM OF ACTION
Excrete 5 - 10% of filtered Na+
Elimination of K
Inhibit carbonic anhydrase:
increase elimination of HCO3
Excretion of uric acid, Ca and Mg
No dose - effect relationship
 LOOP DIURETICS

MECHANISM OF ACTION
Excrete 15 - 20% of filtered Na+
Elimination of K+, Ca+ and Mg++
Resistance of afferent arterioles
- Cortical flow and GFR
- Release renal PGs
- NSAIDs may antagonize diuresis
K-SPARING DIURETICS

MECHANISM OF ACTION
Eliminate < 5% of filtered Na+

Inhibit exchange of Na+ for K+ or H+

Spironolactone = competitive
antagonist for the aldosterone receptor

Amiloride and triamterene block

Na+ channels controlled by aldosterone
3. ALDOSTERONE INHIBITORS
 ALDOSTERONE INHIBITORS

Spironolactone ALDOSTERONE
Competitive antagonist of the
aldosterone receptor
(myocardium, arterial walls, kidney)

Retention Na+ Collagen

Edema deposition
Retention H2O

Fibrosis
Excretion K+ Arrhythmias - myocardium
Excretion Mg2+ - vessels
ALDOSTERONE INHIBITORS

INDICATIONS
FOR DIURETIC EFFECT
• Pulmonary congestion (dyspnea)
• Systemic congestion (edema)
FOR ELECTROLYTE EFFECTS
• Hypo K+, Hypo Mg+
• Arrhythmias
• Better than K+ supplements
FOR NEUROHORMONAL EFFECTS
• Please see RALES results,
N Engl J Med 1999:341:709-717
Aldosterone receptor antagonists - spironolactone

Recommended in advanced HF (NYHA III-IV),

in addition to ACE inhibition and diuretics to
improve survival and morbidity

Guidelines for the diagnosis and treatment of chronic heart failure

European Heart Journal (2001) 22, 1527-1560
4. ß-Blockers
Start Low Go Slow
Activation and Blockade of Neurohumoral
System in CHF

RAA System SNS System

Angiotensin II Noradrenalin

ACE-I β-Blocker

Hypertrophy, apoptosis, ischaemia,

arrhytmia, remodeling, fibrosis
 ADRENERGIC ACTIVATION
↑ CNS Sympathetic
Outflow

↑ Cardiac ↑ Sympathetic
Sympathetic activity activity to kidneys
& blood vessels

β1-receptors β2-receptors 1-receptors

Mycocyte hypertrophy & death, Vasoconstriction

dilatation, ischaemia & arrhytmia’s Sodium Retention

Packer, AHA 2000

 Benefits of “Add-on” β-Blocker
Short-term :
1. Improvement of symptoms (LVEF ↑)
2. Improvement of NYHA class
3. Improvement of daily activities
4. Reduction of hospitalization rate & length of
hospital stay (financial & psychological burden)
Long-term :
1. Slowing the progression of CHF
2. Increase of survival rate
Beta-adrenoceptor antagonists

Recommended for the treatment of all pts

with stable, mild, moderate and severe heart
failure on standard treatment, unless there is
a contraindication.

Patients with LV systolic dysfunction, with or

without symptomatic HF, following an AMI
long-term betablockade is recommended
in addition to ACE inhibitor.
Guidelines for the diagnosis and treatment of chronic heart failure
European Heart Journal (2001) 22, 1527-1560
THE RECOMMENDED PROCEDURE FOR
STARTING β-BLOCKER

1. Patient should be on standard therapy

(ACE inhibitor +/- diuretic)
2. Patient in stable conditions
 No iv inotropic therapy
 Without signs of marked fluid retention
3. Start initial low doses and titrate to maintenance dose
(the dose may be doubled every 1 – 2 weeks)

(ESC.Guidelines for HF, 2001)

 DOSES OF β-BLOCKER

β BLOCKER FIRST DOSE TARGET DOSE TITRATION

PERIOD

Bisoprolol 1.25 mg 10 mg Weeks – Month

Metoprolol 5 mg 150 mg Weeks – Month

Tartrate

Metoprolol 12.5 mg 200 mg Weeks – Month

Succinate

Carvedilol 2 x 3.125 mg 2 x 25 mg Weeks – Month

(European Heart Journal, vol. 22, Sept. 2001)

 CONTRAINDICATIONS OF
β-BLOCKER IN PATIENT H F

 Asthma Bronchial
 Severe Bronchial Desease
 Symptomatic Bradycardia and
Hypotension
 INTOLERANCE OF β-BLOCKER

Symptomatic Worsening HF Hypotension

Bradycardia
5. Angiotensin II receptor
antagonists
 ANGIOTENSIN II INHIBITORS

MECHANISM OF ACTION
RENIN

Angiotensinogen Angiotensin I
ACE
Other paths ANGIOTENSIN II
AT1
RECEPTOR
BLOCKERS
AT1 RECEPTORS AT2

Vasoconstriction Proliferative Vasodilatation Antiproliferative

Action Action
AT1 RECEPTOR BLOCKERS

DRUGS

Losartan
Valsartan
Irbersartan
Candesartan
Competitive and selective
blocking of AT1 receptors
Angiotensin II receptor antagonists

ARBs could be considered in patients who do not

tolerate ACE inhibitors for symptomatic
treatment.

It is unclear whether ARBs are as effective as

ACE inhibitors for mortality reduction.

In combination with ACE inhibition, ARBs may

improve heart failure symptoms and reduce
hospitalizations for worsening heart failure.

Guidelines for the diagnosis and treatment of chronic heart failure

European Heart Journal (2001) 22, 1527-1560
6. Cardiac glycosides
 DIGOXIN
Na-K ATPase Na-Ca Exchange
Na+ K+ Na+ Ca++

Myofilaments Ca++
K+ Na+

CONTRACTILITY
 DIGOXIN
DIGITALIZATION STRATEGIES
Maintenance
Loading dose (mg) Dose

i.v oral 12-24 h oral 2-5 d (mg)

0.5 + 0.25 / 4 h 0.75 + 0.25 / 6 h 0.25 / 6-12 h 0.125-0.5 / d

ILD: 0.75-1 1.25-1.5 1.5-1.75 0.25 / d

ILD = average INITIAL dose required for

digoxin loading
 DIGOXIN

HEMODYNAMIC EFFECTS
Cardiac output
LV ejection fraction
LVEDP
Exercise tolerance
Natriuresis
Neurohormonal activation
 DIGOXIN

NEUROHORMONAL EFFECTS

Plasma Noradrenaline
Peripheral nervous system activity
RAAS activity
Vagal tone
Normalizes arterial baroreceptors
 DIGOXIN

CLINICAL USES

AF with rapid ventricular response

CHF refractory to other drugs
Other indications?
Can be combined with other drugs
 DIGOXIN

CONTRAINDICATIONS
ABSOLUTE:
- Digoxin toxicity

RELATIVE
- Advanced A-V block without pacemaker
- Bradycardia or sick sinus without PM
- PVC’s and TV
- Marked hypokalemia
- W-P-W with atrial fibrillation
 DIGOXIN TOXICITY
CARDIAC MANIFESTATIONS
ARRHYTHMIAS :
- Ventricular (PVCs, TV, VF)
- Supraventricular (PACs, SVT)

BLOCKS:
- S-A and A-V blocks

CHF EXACERBATION
DIGOXIN TOXICITY

EXTRACARDIAC MANIFESTATIONS
GASTROINTESTINAL:
- Nausea, vomiting, diarrhea
NERVOUS:
- Depression, disorientation, paresthesias
VISUAL:
- Blurred vision, scotomas and yellow-green
vision
HYPERESTROGENISM:
- Gynecomastia, galactorrhea
Cardiac glycosides

indicated in atrial fibrillation and any degree of

symptomatic heart failure.

A combination of digoxin and beta-blockade

appears superior than either agent alone.

In sinus rhythm, digoxin is recommended to

improve the clinical status of patients with
persisting heart failure despite ACE inhibitor and
diuretic treatment.

Guidelines for the diagnosis and treatment of chronic heart failure

European Heart Journal (2001) 22, 1527-1560
7. Vasodilator agents
Vasodilator agents in chronic heart failure
No specific role for vasodilators in the treatment of HF
Used as adjunctive therapy for angina or concomitant
hypertension.
In case of intolerance to ACE inhibitors ARBs are
preferred to the combination hydralazine–nitrates.

HYDRALAZINE-ISOSORBIDE DINITRATE

Hydralazine (up to 300 mg) in combination with ISDN (up to 160

mg) without ACE inhibition may have some beneficial effect on
mortality, but not on hospitalization for HF.

Nitrates may be used for the treatment of concomitant angina or

relief of acute dyspnoea.

Guidelines for the diagnosis and treatment of chronic heart failure

European Heart Journal (2001) 22, 1527-1560
8. Positive inotropic therapy
POSITIVE INOTROPES

CARDIAC GLYCOSIDES

SYMPATHOMIMETICS
Catecholamines
ß-adrenergic agonists

PHOSPHODIESTERASE INHIBITORS
Amrinone Milrinone
Enoximone Piroximone
Others
 DOPAMINE AND DOBUTAMINE

EFFECTS

DA (µg / Kg / min) Dobutamine

<2 2-5 >5
Receptors DA1 / DA2 ß1 ß1 +  ß1
Contractility ± ++ ++ ++
Heart Rate ± + ++ ±
Arterial Press. ± + ++ ++
Renal perfusion ++ + ± +
Arrhythmia - ± ++ ±
POSITIVE INOTROPES

CONCLUSIONS

May increase mortality

Safer in lower doses
Use only in refractory CHF
NOT for use as chronic therapy
 10. Anticoagulation
11. Antiplatelet Drugs
ANTICOAGULANTS

PREVIOUS EMBOLIC EPISODE

ATRIAL FIBRILLATION
Identified thrombus
LV Aneurysm (3-6 mo post MI)
Class III-IV in the presence of:
- EF < 30
- Aneurysm or very dilated LV
Phlebitis
Prolonged bed rest
Anticoagulation

Recommendation

1. All pts with HF and AF should be treated with

warfarin unless contraindicated.

2. Patients with LVEF 35% or less.

HFSA Guidelines for Management of Patients With Heart Failure Caused by Left
Ventricular Systolic Dysfunction - Pharmacological Approaches 2000
 Chronic heart failure — choice of
A pharmacological therapy

Aldosterone
LV systolic dysfunction ACE inhibitor Diuretic Beta-blocker
Antagonist

Asymptomatic LV
Indicated Not indicated Post MI Not indicated
dysfunction

Indicated if
Symptomatic HF (NYHA II) Indicated Indicated Not indicated
Fluid retention

Indicated Indicated
Worsening HF (NYHA III-IV) Indicated Indicated
comb. diuretic

Indicated Indicated
End-stage HF (NYHA IV) Indicated Indicated
comb. diuretic

Guidelines for the diagnosis and treatment of chronic heart failure

European Heart Journal (2001) 22, 1527-1560
 Chronic heart failure — choice of
B pharmacological therapy
Angiotensin Vasodilator
(hydralazine/ Potassium -sparing
LV systolic dysfunction II receptor Cardiac glycosides
isosorbide diuretic
antagonists dinitrate)
Asymptomatic LV
Not indicated With AF Not indicated Not indicated
dysfunction
(a) when AF If ACE inhibitors
If ACE inhibitors If persisting
and angiotensin
are not tolerated (b) when improved hypokalaemia
Symptomatic HF (NYHA II) from more severe II antagonists
and not on beta-
HF in sinus are not
blockade
rhythm tolerated
If ACE inhibitors
If ACE inhibitors If persisting
and angiotensin
are not tolerated hypokalaemia
Worsening HF (NYHA III-IV) indicated II antagonists
and not on beta-
are not
blockade
tolerated
If ACE inhibitors
If ACE inhibitors If persisting
End-stage HF (NYHA IV) and angiotensin
are not tolerated hypokalaemia
indicated II antagonists
and not on beta-
are not
blockade
tolerated

Guidelines for the diagnosis and treatment of chronic heart failure

European Heart Journal (2001) 22, 1527-1560
Intervention
 Surgical
Revascularization
Non Surgical
Pts with heart failure of ischaemic origin revascularization 
symtomatic improvement.
A strong negative correlation of operative mortality and LVEF,
a low LVEF (<25%) was associated with increased
operative mortality. Advance HF symptoms (NYHA IV)
resulted in a greater mortality rate.
Off pump coronary revascularization may lower the surgical
risk for HF.
Heart Transplantation is an accepted mode of treatment for
end-stage HF.
Guidelines for the diagnosis and treatment of chronic heart failure
European Heart Journal (2001) 22, 1527-1560
 Care and Follow-up
Recommended components of programs

use a team approach

vigilant follow-up, first follow-up within 10 days of
discharge
discharge planning
increased access to health care
optimizing medical therapy with guidelines
intense education and counselling inpatient and
outpatient
strategies address barriers to compliance
early attention to signs and symptoms
flexible diuretic regimen

Guidelines for the diagnosis and treatment of chronic heart failure

European Heart Journal (2001) 22, 1527-1560
 Future treatment
Neurohormonal modulation
1. Sympathetic nervous system
2. The RAA system
3. Atrial and brain natriuretic peptides
4. Arginin vasopressin
5. Endothelin
6. Growth hormone
7. Calcitonin gene related peptide
Cardiac reparation: fixing the heart
with cells, new vessels and genes (1)
Cell based
interventions
Aims: to repopulate fibrous scars with new
contractile cells
1. Multiplication of residual myocytes
(forcing the cells to enter mytotic cycle)
2. Transforming fibrablasts in the scar
3. Implanting exogenous contractiles cells
(foetal cardiomyocites, skeletal
myoblasts, stem cells)
Eur Heart J 2002;4: D73-81
 CON’T (2)

Angiogenesis
Aims: to provides new blood supply to
the diseased heart
1. Administration of angiogenic growth factors
VEGF, basic FGF
2. Problems: nature of compound , dose,
route, and adverse events (abnormal blood
vessels, proliferative retinopathy, etc)

Eur Heart J 2002;4: D73-81

 CON’T(3)

Gene therapy
Aims: to improve the function of the failing
heart
1. Gene manipulation of 3 majors areas: Ca
handling, beta-adenergic signalling and
apoptosis
2. Inducing expression of silent genes
Safety problems: control of targeted protein
expression, inflammation, autoimmunity
and oncogenesis (basically irreversible)
Eur Heart J 2002;4: D73-81
 Dual-chamber pacemakers are
beneficial
• Drug-resistant CHF
• Intact sinus rhythm
• Absence of chronic atrial dysrhythmias
• EF <20%
• Viable myocardium
• No or stable angina
• DMC and PR >, MR and TR, QRS >, QRS
PR + QRS > 350 ms.
• QRS >140 ms, MR > 450 ms, and LV filling
time <200 ms
• HOCM
 Resume
Pharmacological Treatment :
I. Asymptomatic Systolic LV dysfunction :
• ACE Inhibitor
• -Blocker (in CAD)
II. Symptomatic Systolic LV dysfunction
A. No fluid retention
ACE Inhibitor
-Blocker
If ischaemia (+)  nitrate / revascularization
B. Fluid retention
Diuretic
ACE Inhibitor (ARBs if not tolerated)
-Blocker
± Digitalis
 Resume
III. Worsening HF
Standard treatment : ACE Inhibitor, -Blocker
Diuretic : doses  + loop diuretic
Low dose spironolactone
Digitalis
Consider :
» Revascularization
» Valve surgery
» Heart transplant

IV. End-stage HF
Intermittent inotrophic support
Circulatory support (IABP, Ventr.Assist Devices)
Haemofiltration on dialysis
 briddging to heart transplantation
 Conclusion

Management of HF must be starting from

the earlier stage (AHA/ACC stage A).
Treatment at each stage can reduce
morbidity and mortality.

Before initiating therapy :

Established the correct diagnose.
Consider management outline.
 Conclusion
Non pharmacolgical intervention are helpfull in :
improving quality of life
reducing readmission
lowering cost.

Organize multi-disciplinary care :

HF clinic, HF nurse specialist, pts telemonitoring.
Health care system.

To optimize HF management
Treatment should be according to the Guidelines,
intensive education, and behavioral change efforts.
Thank YoU
DIASTOLIC HEART
FAILURE
 SCOPE OF THE PROBLEM
• Epidemiological studies of HF have
suggested that 30-50% of cases of HF
have preserved LV systolic function.
• DHF has mortality rate equal as
systolic heart failure
• No guideline yet regarding the
treatment of DHF

Greenberg & Hermann 2004

 Defining Diastolic Heart Failure

• Diastolic dysfunction refers to a condition in which

abnormalities in mechanical function are presenting
during diastole.
• Diastolic dysfunction is a condition in which higher
than normal LV filling pressure are needed to maintain
a normal cardiac output.
• Diastolic heart failure is a clinical syndrome
characterized by the symptoms and signs of heart
failure, a preserved EF and abnormal diastolic
function.
(Vasan & Levy 2000)
(Mandinov,Eberli,Seiler,Hess.Cardiosvasc Res 2000)
 Other Methods in diagnosing DHF

• Plasma Brain Natriuretic Peptide

• Doppler tissue imaging
• Magnetic resonance imaging
• Radionuclide angiography
• Cardiac catheterization

Greenberg & Hermann 2004

Treatment of Diastolic Heart Failure

The guidelines are based on :

• Clinical investigations in relatively small

groups of patients
• Clinical experience
• Concepts based on pathophysiology
mechanisms
Treatment of Diastolic Heart failure

• symptom targeted treatment

• disease / pathological targeted treatment
• the underlying mechanism targeted
treatment

( Zile & Brutsaert, 2002 )

Diastolic Heart Failure: Treatment

Symptom targeted treatment

Decrease pulmonary venous pressure
Reduce LV volume
Maintain atrial contraction
Prevent tachycardia
Improve exercise tolerance
Use positive inotropic agents with caution
( Zile & Brutsaert, 2002 )
 Diastolic Heart Failure: Treatment
Symptom targeted treatment

Nonpharmacological treatment
Restrict sodium to prevent volume overload
Restrict fluid to prevent volume overload
Perform moderate aerobic exercise to improve cardiovascular
conditioning, decrease heart rate and maintain skeletal muscle
function
Pharmacological treatment
Diuretics including loop diuretics thiazides, spironolactone
Long-acting nitrates, -Adrenergic blockers
Calcium channel blockers
Renin angiotensin-aldosterone antagonists including ACE
inhibitors, angiotensin II receptor blockers and aldosterone
antagonists ( Zile & Brutsaert, 2002 )
 Diastolic Heart Failure
Disease-targeted treatment

Prevent/treat myocardial ischemia

Prevent/regress ventricular hypertrophy

Mechanisms targeted treatment

Modify myocardial and extramyocardial mechanisms

Modify intracellular and extracellular mechanisms

An ideal therapeutic agent.

- Should target the underlying mechanisms

- Improve calcium homeostasis and energetics

- Blunt neurohumoral activation

- Prevent and regress fibrosis

( Zile & Brutsaert, 2002 )