1

HEART FAILURE
PATHOPHYSIOLOGY
AND MANAGEMENT
MOCH. FATHONI
DEPART. OF CARDIOLOGY
MEDICAL FACULTY, SEBELAS MARET UNIV.
2.1. Definition of Heart Failure
Heart failure is a complex clinical syndrome
that can result from any structural or
functional cardiac disorder that impairs the
ability of the ventricle to fill with or eject
blood. The cardinal manifestations of HF are
dyspnea and fatigue, which may limit exercise
tolerance, and fluid retention, which may lead
to pulmonary congestion and peripheral
edema.
 4

A PREVALENT CONDITION
PREVALENCE OF HEART FAILURE
(PER 1000 POPULATION)

Age (years) Men Women

50-59 8 8

80-89 66 79

All ages 7.4 7.7

Framingham Heart Study: Ho et al. 1993 J Am Coll Cardiol;22:6-13

 5

A GROWING BURDEN
DEATHS FROM HF 1979-1997 (USA)
50000

40000
HF deaths

30000

20000

10000

0
1979 1985 1991 1997

Source: Vital Statistics of the United States, National Center for Health Statistics
 63
HEART FAILURE WAS VIEWED SOLELY AS
HAEMODYNAMIC DISORDER

A major public health

issue
 74

NEURO-HORMONAL ACTIVATION

AS A SIGNIFICANT FACTOR
CONTRIBUTING TO PROGRESSIVE
SYSTOLIC DYSFUNCTION AND
PROGRAMMED MYOCARDIAL CELL
DEATH, ALSO CALLED
APOPTOSIS
 84

NEURO-HORMONAL ACTIVATION

FACT AND PENDING

QUESTION
 NEURO-HORMONE SECRETION IN 9

RESPONSE TO HEART FAILURE

NOREPINEPHRINE CAUSED
VASOCONSTRICTION, INCREASED HEART RATE
AND MYOCYTE TOXICITY

ANGIOTENSIN II CAUSED VASOCONSTRICTION,

STIMULATES RELEASE OF ALDOSTERONE AND
ACTIVATES THE SYMPATHETIC NERVOUS
SYSTEM

ALDOSTERONE CAUSED SODIUM AND WATER

RETENTION
 NEURO-HORMONE SECRETION IN 10

RESPONSE TO HEART FAILURE

ENDOTHELINE CAUSED
VASOCONSTRICTION AND MYOCYTE
TOXICITY

ANTIDIURETIC HORMONE (VASOPRESSINE)

CAUSED VASOCONSTRICTION AND WATER
REABSORPTION

TUMOR NECROSIS FACTOR ALPHA(TNF α)

CAUSED DIRECT MYOCITE TOXICITY
NEURO-HORMONE SECRETION IN 11

RESPONSE TO HEART FAILURE

INTERLEUKIN I (IL-1) AND IL-6
CAUSED MYOCYTE TOXICITY
NEURO- HORMONE (ATRIAL
NATRIURETIC PEPTIDE AND
BRAIN NATRIURETIC PEPTIDE)
CAUSED VASODILATATION,
EXCRETION OF SODIUM AND
ANTIPROLIFERATIVE EFFECT ON
MYOCYTES
 13

ETHYOLOGY
• The most common cause of heart failure is left
ventricular (LV) systolic dysfunction (about 60%
of patients). In this category, most cases are a result
of end-stage coronary artery disease, either with a
history of myocardial infarction or with a
chronically underperfused, yet viable, myocardium.
In many patients, both processes are present
simultaneously . Other common causes of LV
systolic dysfunction include idiopathic dilated
cardiomyopathy, valvular heart disease,
hypertensive heart disease, toxin-induced
cardiomyopathies (alcohol), and congenital heart
disease .
 Common ETHYOLOGIES of HF 14
in OLDER Patients

1. CORONARY ARTERY DISEASE : AMI

2. HYPERTENSIVE HEART DISEASE
3. VALVULAR HEART DISEASE ex. AS,MS
4. CARDIOMYOPATHY : Restrictive, Dilated
Hyperthrophic
5. PERICARDIAL DISEASE
6. HIGH OUTPUT SYNDROME ex. ANEMIA,
i HYPERTHYROIDIS
I
7. AGE RELATED DIASTOLIC SYNDROME
 15
Common Comorbidities in OLDER Patients

1. RENAL DYSFUNCTION
2. CHRONIC LUNG DISEASE
3. COGNITIVE DYSFUNCTION:
DIETARY,MEDICATION ec
4. DEPRESSION, SOSIAL ISOLATION
5. URINARY INCONTINENCE
6. NUTRITIONAL DISORDER
7. POLYPHARMACY – DRUG INTERACTION
i
I
 16

DIAGNOSA KLINIK
GAGAL JANTUNG
• RIWAYAT KLINIK
• PEMERIKSAAN FISIK
• PEMERIKSAAN EKG
• FOTO RONGEN TORAKS
• EKOKARDIOGRAM
• PEMERIKSAAN
RADIONUKLIR
• PEMERIKSAAN INVASIF
 17

RIWAYAT KLINIK
• PASCA INFARK MIOKARD
• ANGINA PEKTORIS
• HIPERTENSI
• KELAINAN KATUP/ DEMAM REMATIK
• PENYAKIT JANTUNG BAWAAN
• PALPITASI
 20
PHYSICAL EXAMINATION

SYSTOLIC HEART FAILURE DIASTOLIC HEART FAILURE

CLASIFIED BY AN CLASSIFIED BY A
EJECTION FRACTION NORMAL EJECTION
LESS THAN 40 % , IS FRACTION ( GREATER
CHARACTERIZED BY THAN OR EQUAL TO 50 %,
A REDUCED CARDIAC IN THE PRESENCE OF
PULMONARY
OUTPUT SECONDARY CONGESTION AND OTHER
TO DEPRESSED HF SYMPTOMS ( FOR EX. .
MYOCARDIAL DYSPNEA D‘ EFFORT,PND ,
CONTRACTILITY. FATIGUE, AND
ORTHOPNEA) AND
FOURTH HEART SOUND.
 CLASSIFICATION OF HEART
FAILURE
• Class I there are no restrictions of physical
activity. Patients generally don’t complain of
being overly tired or of experiencing shortness
of breath. A patient is still able to control the
disease. Regular exercise, limiting alcohol
consumption, and eating healthy (with
moderate sodium intake), are all actions that
can be taken quite easily. High blood pressure
will need to be treated. Quitting smoking is
crucial.
 CLASSIFICATION OF HEART
FAILURE

• With Class II heart failure, patients will

feel slight restrictions with everyday
physical actions like bending over or
walking. They will be tired and shortness
of breath may occur. Non-invasive
surgical procedures like ACE-Inhibitors
or Beta Blockers (depending on the
patient), may be considered.
 CLASSIFICATION OF HEART
FAILURE
• Class III heart failure patients experience
definite limitations during physical
activity. They may remain comfortable at
rest, but most all physical activity will
cause undue fatigue. Under physician care,
their diet and exercise may be monitored.
Diuretics, to combat water retention, may
be prescribed.
 CLASSIFICATION OF HEART
FAILURE
• Patients in Class IV heart failure are
virtually unable to do any physical
activity without discomfort. There
may be significant signs of cardiac
problems even while resting. Surgical
options will be explored along with
the same attention given to treatments
in Classes I-III.
 CLASSIFICATION OF HEART
FAILURE
• The National Heart, Lung and Blood Institute
estimates that 35% of patients with Heart
Failure are in functional NYHA Class I, 35%
are in Class II, 25% are in Class III and 5%
are in Class IV. It has been estimated that
between 5 and 15 % of patients with Heart
Failure have persisting sever symptoms.
 PHYSICAL SIGNS
• There are a few physical signs that may
indicate Heart Failure. Fluid retention, which
causes weight gain and possible swelling of the
feet, ankles, or even abdomen, is associated
with the disease. Another physical sign is
bulging of the neck veins. When the pulmonary
veins aren’t functioning as they should, an
insufficient supply of blood is making it to the
heart, thus causing fluid to build up in the
arteries and body tissues (edema).
Congestive heart failure can affect many organs of the body. For
example:
The weakened heart muscles may not be able to supply enough blood to
the kidneys, which then begin to lose their normal ability to excrete salt
(sodium) and water. This diminished kidney function can cause the body
to retain more fluid.
The lungs may become congested with fluid (pulmonary edema) and the
person's ability to exercise is decreased.
Fluid may likewise accumulate in the liver, thereby impairing its ability
to rid the body of toxins and produce essential proteins.
The intestines may become less efficient in absorbing nutrients and
medicines.
Fluid also may accumulate in the extremities, resulting in edema
(swelling) of the ankles and feet.
Eventually, untreated, worsening congestive heart failure will affect
virtually every organ in the body.
 18
SYMPTOMS OF CHF

THE CLASSIC SYMPTOM OF CHF IS

SHORTNESS OF BREATH
SPECIFIC COMMON SYMPTOM INCLUDE :
1. PAROXYSMAL NOCTURNAL DYSPNEA
(AWAKENING FROM SLEEP WITH SHORTNESS
OF BREATH).
2. ORTHOPNEA.
3. OR NEW ONSET DYSPNEA ON EXERTION.
i
IF HISTORY AND PHYSICAL EXAMINATION CLEARLY
I INDICATE A NON CARDIAC CAUSE FOR THESE SYMPTOMS(
EG. SEVERE PULMONARY DISEASE), THEN HEART
FAILURE EVALUATION IS NOT NECESSARY.
Continued
 19
SYMPTOMS OF CHF

YOUNG ADULT PATIENTS ELDERLY PATIENTS

1. DYSPNEA ON 1. DYSPNEA ON EXERTION

EXERTION 2. CONFUSION
2. DYSPNEA AT REST 3. AGITATION
3. ORTHOPNEA 4. DEPRESSION
4. PAROXISMAL 5. INSOMNIA
NOCTURNAL 6. WEAKNESS
DYSPNEA (PND) 7. ANOREXIA OR NAUSEA
5. FATIGUE 8. COUGH
6. ANKLE SWELLING
 20
PHYSICAL EXAMINATION

SYSTOLIC HEART FAILURE DIASTOLIC HEART FAILURE

CLASIFIED BY AN CLASSIFIED BY A
EJECTION FRACTION NORMAL EJECTION
LESS THAN 40 % , IS FRACTION ( GREATER
CHARACTERIZED BY THAN OR EQUAL TO 50 %,
A REDUCED CARDIAC IN THE PRESENCE OF
PULMONARY
OUTPUT SECONDARY CONGESTION AND OTHER
TO DEPRESSED HF SYMPTOMS ( FOR EX. .
MYOCARDIAL DYSPNEA D‘ EFFORT,PND ,
CONTRACTILITY. FATIGUE, AND
ORTHOPNEA) AND
FOURTH HEART SOUND.
 21

PEMERIKSAAN PENUNJANG
1. PEMERIKSAAN EKG
2. FOTO RONGEN THORAKS
3. HEMOGLOBIN
4. FUNGSI TIROID
5. FUNGSI GINJAL
6. FUNGSI HATI
7. PEMERIKSAAN EKOKARDIOGRAFI
 JENIS GAGAL JANTUNG DAN 24
TERAPINYA

ETIOLOGI DAN PATOFISIOLOGI PENATALAKSANAAN

DISFUNGSI SISTOLIK
• GAGAL JANTUNG YANG SERING • PENTING UNTUK MENGENALI
BERHUBUNGAN DENGAN SECARA DINI PASIEN INI KARENA
KELAINAN FUNGSI SISTOLIK PROGNOSANYA DAPAT MEMBAIK.
DIMANA MIOKARDIUM GAGAL • TERAPI : BETA BLOCKER/
BERKONTRAKSI SECARA PENGHAMBAT BETA, ACE
NORMAL, MENGAKIBATKAN INHIBITOR/ PENGHAMBAT ACE,
DILATASI VENTRIKEL KIRI DIKOMBINASIKAN DENGAN
• PENYEBAB TERSERING ADALAH DIURETIKA, DIGITALIS ATAU
INFARK MIOKARD, HIPERTENSI VASODILATOR
DAN KARDIOMIOPATI
 JENIS GAGAL JANTUNG DAN 25
TERAPINYA

ETIOLOGI DAN PATOFISIOLOGI PENATALAKSANAAN

DISFUNGSI DIASTOLIK
• GAGAL JANTUNG YANG • PENTING UNTUK MENGENALI
DISEBABKAN OLEH KELAINAN SECARA DINI PASIEN INI KARENA
FUNGSI DIASTOLIK DIMANA PROGNOSANYA DAPAT MEMBAIK.
COMPLIANCE/ KEMAMPUAN • TERAPI : MENGATASI PENYAKIT
MIOKARDIUM MENURUN YANG MENDASARI/
• MASALAH INI SERING TERJADI MENGIKUTINYA SEPERTI
PADA ORANG TUA HIPERTENSI HARUS DIBERIKAN
OBAT UTK. MENGURANGI TENSI
DAN MENCEGAH HIPERTROFI
VENTRIKEL KIRI.
• TANDA-2 KONGESTI /BENDUNGAN
DIKURANGI DENGAN DIURETIKA.
 JENIS GAGAL JANTUNG DAN
TERAPINYA
ETIOLOGI DAN PATOFISIOLOGI
KELAINAN KATUB
• GAGAL JANTUNG YANG
DISEBABKAN OLEH KELAINAN
KATUB SERING DITEMUKAN PADA
GOL. SOSIAL EKONOMI RENDAH /
DIDAERAH DIMANA PENYAKIT
DEMAM REUMATIK BANYAK
DIJUMPAI.
• STENOSIS AORTA KARENA
KALSIFIKASI MERUPAKAN
MASALAH YANG SERING TERJADI
PADA ORANG TUA.
26
PENATALAKSANAAN
• PENTING UNTUK MENGENALI
SECARA DINI PASIEN INI KARENA
PROGNOSANYA DAPAT MEMBAIK.
• TERAPI : MENGATASI PENYAKIT
YANG MENDASARI. PEMBEDAHAN
DAN PROSEDUR INTERVANSI
SEPERTI VALVULOPLASTI
/VALVULOTOMI MEMBERIKAN
HASIL YANG BAIK.
• KELAINAN REGURGITASI KATUB
YANG TIDAK DAPAT DIOPERASI,
DAPAT DIBERIKAN DIURETIKA
DAN VASODILATOR
 JENIS GAGAL JANTUNG DAN 27
TERAPINYA

ETIOLOGI DAN PATOFISIOLOGI PENATALAKSANAAN

KELAINAN JANTUNG BAWAAN

• GAGAL JANTUNG YANG
DISEBABKAN OLEH KELAINAN
JANTUNG BAWAAN DAPAT
DITEMUKAN PADA MASA ANAK-
ANAK ATAU MASA DEWASA.
• BEBERAPA TIPE SEPERTI DEFECT
ATRIUM MUNGKIN TIDAK
TERLIHAT SECARA DINI, DAN
BARU DIKETAHUI SETELAH
TERJADI GAGAL JANTUNG.
• PENTING UNTUK MENGENALI
SECARA DINI PASIEN INI KARENA
PROGNOSANYA DAPAT MEMBAIK.
• TERAPI : MENGATASI PENYAKIT
YANG MENDASARI. PEMBEDAHAN
DAN PROSEDUR INTERVENSI
SEPERTI KOREKSI/PENUTUPAN
DEFECT MEMBERIKAN HASIL
YANG BAIK.
• KELAINAN BAWAAN YANG TIDAK
DAPAT DIOPERASI MIS. ASD +PH
DENGA MPA ≥ 70 mm HG, DAPAT
DIBERIKAN DIURETIKA DAN
VASODILATOR
 JENIS GAGAL JANTUNG DAN
TERAPINYA
ETIOLOGI DAN PATOFISIOLOGI
KELAINAN METABOLIK
• KELAINAN TIROID, DEFISIENSI
TIAMIN (BERI-BERI), KADAR BESI
YANG BERLEBIH
(HEMOSIDEROSIS DAN
HEMOKROMATOSIS) SERTA
ANEMIA, MERUPAKAN JENIS
GAGAL JANTUNG YANG
DISEBABKAN OLEH KELAINAN
METABOLIK YANG DAPAT
MERUSAK MIOKARDIUM.
28
PENATALAKSANAAN
• PENTING UNTUK MENGENALI
SECARA DINI PASIEN INI KARENA
PROGNOSANYA DAPAT MEMBAIK.
• TERAPI : DISINI DIPERLUKAN
PERBAIKAN NUTRISI, FAKTOR
HORMONAL DAN METABOLIK
YANG DAPAT MENYEMBUHKAN
KELAINAN INI.
 29

TATA LAKSANA GAGAL

JANTUNG

• TEGAKKAN DIAGNOSA GAGAL JANTUNG SERTA

SINGKIRKAN KEADAAN YANG MENYERUPAI
GAGAL JANTUNG
• CARI PENYEBAB DASAR UNTUK DIATASI
DIMANA MUNGKIN
• CARI FAKTOR PENCETUS UNTUK DIATASI
DIMANA MUNGKIN
• PAHAMI PATOFISIOLOGI
• BERIKAN PENGOBATAN / TINDAKAN YANG
SESUAI
 30

TATA LAKSANA GAGAL

JANTUNG

ATASI PENYEBAB DISFUNGSI VENTRIKEL

KIRI.
• DISFUNGSI SISTOLIK
• DISFUNGSI DIASTOLIK
• KELAINAN KATUB
• KELAINAN JANTUNG BAWAAN
• KELAINAN METABOLIK
• KELAINAN PERIKARDIUM/
ENDOKARDIUM.
 31

TATA LAKSANA GAGAL

JANTUNG
TERAPI NON FARMAKOLOGIK :
• DIET RENDAH GARAM
• MENGURANGI BERAT BADAN
• MENGHINDARI FAT YANG BERLEBIHAN
• MENGURANGI STRESS PSIKIS
• MENGHINDARI ROKOK
• OLAH RAGA TERATUR
• OPERATIF
TERAPI FARMAKOLOGIK
• DIURETIKA
• PENGHAMBAT ACE
• PENGHAMBAT BETA
• DIGITALIS
• VASODILATOR
diminished kidney function can
cause the body to retain more fluid.

The lungs may become congested

with fluid (pulmonary edema) and
the person's ability to exercise is
decreased.

Fluid may likewise accumulate in

the liver, thereby impairing its
ability to rid the body of toxins and
produce essential proteins.

The intestines may become less

efficient in absorbing nutrients and
medicines.
Less common causes include viral infections of the stiffening
of the heart muscle, thyroid disorders, disorders of the heart
rhythm, and many others.
It should also be noted that in patients with underlying heart
disease, taking certain medications can lead to the
development or worsening of congestive heart failure. This is
especially true for those drugs that can cause sodium retention
or affect the power of the heart muscle. Examples of such
medications are the commonly used nonsteroidal anti-
inflammatory drugs (NSAIDs), which include ibuprofen
(Motrin and others) and naproxen (Aleve and others) as well
as certain steroids, some medication for diabetes (such as
rosiglitazone [Avandia] or pioglitazone [Actos]), and some
calcium channel blockers.
 12

KLASIFIKASI FUNGSIONAL
GAGAL JANTUNG (NYHA)
1. TIMBUL GEJALA SESAK NAFAS ATAU
CAPAI PADA KEADAAN / AKTIFITAS
FISIK YANG BERAT
2. TIMBUL GEJALA PADA KEGIATAN
FISIK YANG SEDANG
3. TIMBUL GEJALA PADA KEGIATAN
FISIK YANG RINGAN
4. TIMBUL GEJALA PADA KEGIATAN
FISIK YANG SANGAT RINGAN DAN
PADA WAKTU ISTIRAHAT
 22

KRITERIA DIAGNOSIS
GAGAL JANTUNG
• KRITERIA UTAMA GAGAL
JANTUNG
1. DISPNEA NOKTURNAL
PAROKSISMAL (PND)
2. KARDIOMEGALI
3. GALLOP (S-3)
4. PENINGKATAN TEKANAN VENA
5. REFLEKS HEPATOJUGULAR
6. RONKI
The physical examination is focused
on detecting the presence of extra
fluid in the body (breath sounds, leg
swelling, or neck veins) as well as
carefully characterizing the
condition of the heart (pulse, heart
size, heart sounds, and murmurs).
Useful diagnostic tests include the
electrocardiogram (ECG) and chest X-ray
to detect previous heart attacks, arrhythmia,
heart enlargement, and fluid in and around
the lungs. Perhaps the single most useful
diagnostic test is the echocardiogram, in
which ultrasound is used to image the heart
muscle, valve structures, and blood flow
patterns. The echocardiogram is very
helpful in diagnosing heart muscle
weakness.
Useful diagnostic tests include the
electrocardiogram (ECG) and chest X-ray
to detect previous heart attacks, arrhythmia,
heart enlargement, and fluid in and around
the lungs. Perhaps the single most useful
diagnostic test is the echocardiogram, in
which ultrasound is used to image the heart
muscle, valve structures, and blood flow
patterns. The echocardiogram is very
helpful in diagnosing heart muscle
weakness.
 21

PEMERIKSAAN PENUNJANG
1. PEMERIKSAAN EKG
2. FOTO RONGEN THORAKS
3. HEMOGLOBIN
4. FUNGSI TIROID
5. FUNGSI GINJAL
6. FUNGSI HATI
7. PEMERIKSAAN EKOKARDIOGRAFI
 3

USUAL TREATMENT TODAY

AIMS OF HEART FAILURE MANAGEMENT
TO IMPROVE SYMPTOMS
• DIURETICS
• DIGOXIN
• ACE INHIBITORS
TO IMPROVE SURVIVAL
• ACE INHIBITORS
•  BLOCKERS
• ORAL NITRATES PLUS HYDRALAZINE
• SPIRONOLACTONE
vies et al. BMJ 2000;320:428-431
 4
HF: MORTALITY REMAINS
HIGH
• ACEI
RISK REDUCTION 35% (MORTALITY AND
HOSPITALIZATIONS)1

•  BLOCKERS
RISK REDUCTION 38% (MORTALITY AND
HOSPITALIZATIONS)2

• ORAL NITRATES AND HYDRALAZINE

BENEFIT VS. PLACEBO; INFERIOR TO
ENALAPRIL (MORTALITY)
1 Davies et al. BMJ 2000;320:428-431 (meta analysis: 32 trials, n=7105) 2 Gibbs et al. BMJ
2000;320:495-498 (meta analysis: 18 trials, n=3023)
9
 10
BLOCKADE OF RAS
LOCAL ANG II SYNTHESIS IS INDEPENDENT OF ACE

ANGIOTENSINOGEN
(LIVER)

RENIN CHYMA
INHIBITOR
ANGIOTENSIN I
BRADYKININ
ACE
PEPTIDES INHIBITOR
ANGIOTENSIN II
VALSARTAN
AT1 RECEPTOR BLOCKER

AT1 AT2
ROLE OF AT1 AND AT2 11

RECEPTORS

ANGIOTENSIN II

AT1 AT2

VASOCONSTRICTION VASODILATION
VASCULAR ANTIPROLIFER
PROLIFERATION ATION
ALDOSTERONE SECRETION APOPTOSIS
CARDIAC MYOCYTE
PROLIFERATION
INCREASED SYMPATHETIC
TONE
22
 25

Treatment Strategies for Heart Failure

ALDO PIETRO MAGGIOTTI

Director of the Reseach Center of the Italian Association
Of Hospital
Cardiologist (ANMCO), Pirenze, ITALY
 25

ALDO PIETRO MAGGIOTTI

Director of the Reseach Center of the Italian Association
Of Hospital
Cardiologist (ANMCO), Pirenze, ITALY
Which patients with HF are suitable 26

for β Blocker treatment ?

Patients with symptomatic HF of any cause, EF ≤ 40 %, in
NYHA class II/III, clinically stable, already on treatment
wite ACE inh., diuretic, and digitalis

Which patients with HF are more

likely to benefits ?
1. Patients with history of hypertension
2. Heart rate > 90 beat/ mnt.
 Which patients with HF are less likely to
benefits ? 27

• Patients with severe biventricular dysfunction

• SBP < 100 mmHg

Which patients with HF are

uncertainties still exist ?
1. NYHA class IV, elderly ptns (> 75 years)
2. Asymptomatic LV dysfunction
3. HF by valvular disease or diastolic dysfunction
4. Comorbidities (DM, COPD, renal disease,
peripheral vasculopathy)
 28

β Blocker summary

1. At one time contraindicated in the treatment of heart

failure
2. The increased activation of the adrenergic system
induced by heart failure, provides the rationale for the
use of β Blockers in heart failure
3. While the effect of β Blockers on exercise capacity,
quality of life, and the neurohormonal profile are still
controversial, the LV shape and function, and the need
for hospitalisation are improve by β Blockers in heart
failure

Continued
 29

β Blocker summary

4. On the basis of all available evidence, all patients with

chronic, stable, mild to moderate, symptomatic HF
(NYHA CLASS II/III), and with the depressed LV
function should be treated with β Blockers
5. The studies showed that β Blockers significantly reduce
total and sudden mortality in HF patients
6. β Blockers tretment should be started in stable patients with
a very low initial dosage and then uptitrated in the maximal
tolerated

Continued
 30

β Blocker summary

7. Despite the impressive results in term of morbidity and

martality reduction, and the increasing availability of β
Blockers, these data showing only a minority of patients
being treated At one time contraindicated in the
treatment of heart failure
 31

DIURETICS
• DIURETICS SHOULD BE USED FOR ALL PATIENTS
WITH SYMPTOMS WHO HAVE EVIDENCE FOR
FLUID RETENTION
• SHOUD NOT BE USED ALONE, EVEN IF THE
SYMPTOMS OF HF ARE WELL CONTROLLED.
• ALTHOUGH THEY PRODUCED RAPID
SYMPTOMATIC RELIEF, THEY CANNOT
MAINTAIN CLINICAL STABILITY IN LONG- TERM,
SO THEYFORE GENERALLY BE ADMINISTERED
WITH ACE – INH/ β BLOCKERS
 32

ANTIARRHYTMIC DRUG
• In addition to progressive pump dysfunction, 25
– 70 % of all deaths patients with HF, caused by
ventricel arrhytmia
• Of the available antiarrhytmia, amiodarone is
the only one which seem to be potentially
beneficial in patients with HF, suppressing atrial
and ventricular arrhytmia
 NITRATES 33

• The use of nitrates in HF is most commonly

,in patients who cannot tolerate ACE
inhibitors due to hypotension or renal
insufficiency .

Ca. antagonists
• Ca. Antagonists are not recommended for use
in HFdue to their association with an increased
risk of cardiovascular event
 34

THE OTHERS MANAGEMENT

• For the patients who have survived cardiac

arrest the preferred treatment may be
implantable- defibrillator (ICD)
• Sceletal myoblast transfer
• Education for managing lifestyle modification
and optimizing of medical therapy
 5 35
535

CYTOKINES
• CYTOKINES ARE BEING IMPLICATED
FOR PATHOGENIC ROLE IN HF
PROGRESSION
• Cytokines antagonist : IL-6 antagonist and
TNF α antagonist currently under
investigation for HF treatment
 36

CONCLUSIONS
• THE PHARMACOLOGICAL TREATMENT OF
HF HAS BECOME COMBINED SYMPTOMATIC
- PREVENTIVE MANAGEMENT STATEGY
• EARLY RECOGNATION AND PREVENTION
THERAPIES COMBINED WITH LIFESTYLE
MODIFICATION, ARE ESSENTIAL
 38

CONCLUSIONS
• APPLY THE GUIDELINES TO EVERY
PATIENTS AS INDIVIDUAL, ADJUSTING THE
TREATMENT REGIMEN AS INDICATED BY A
PATIENTS ‘S CONDITION AND WHAT THE
GROWING MEDICAL EVIDENCE BASE DEEMS
APPROPRIATE
• THERE ARE MANY APPROACHS WERE
DESCRIBED AS THE RECENT MANAGEMENT
THANK YOU
What is congestive heart failure?
Congestive heart failure (CHF) is a
condition in which the heart's function as a
pump is inadequate to deliver oxygen rich
blood to the body. Congestive heart failure
can be caused by:
diseases that weaken the heart muscle,
diseases that cause stiffening of the heart
muscles, or
diseases that increase oxygen demand by
the body tissue beyond the capability of the
What causes congestive heart failure?
Many disease processes can impair the pumping
efficiency of the heart to cause congestive heart
failure. In the United States, the most common
causes of congestive heart failure are:
coronary artery disease
high blood pressure (hypertension)
longstanding alcohol abuse
disorders of the heart valves
unknown (idiopathic) causes, such as after
recovery from myocarditis
Less common causes include viral infections of the stiffening
of the heart muscle, thyroid disorders, disorders of the heart
rhythm, and many others.
It should also be noted that in patients with underlying heart
disease, taking certain medications can lead to the
development or worsening of congestive heart failure. This is
especially true for those drugs that can cause sodium retention
or affect the power of the heart muscle. Examples of such
medications are the commonly used nonsteroidal anti-
inflammatory drugs (NSAIDs), which include ibuprofen
(Motrin and others) and naproxen (Aleve and others) as well
as certain steroids, some medication for diabetes (such as
rosiglitazone [Avandia] or pioglitazone [Actos]), and some
calcium channel blockers.
 A PREVALENT CONDITION
EVALENCE OF HF (PER 1000 POPULATION)

Age (years) Men Women

50-59 8 8

80-89 66 79

All ages 7.4 7.7

ham Heart Study: Ho et al. 1993 J Am Coll Cardiol;22:6-13

 A GROWING BURDEN
DEATHS FROM HF 1979-1997 (USA)
50000

40000
HF deaths

30000

20000

10000

0
1979 1985 1991 1997

ital Statistics of the United States, National Center for Health Statistics
 HF: MORTALITY REMAINS
HIGH
• ACEI
RISK REDUCTION 35% (MORTALITY AND
HOSPITALIZATIONS)1

•  BLOCKERS
RISK REDUCTION 38% (MORTALITY AND
HOSPITALIZATIONS)2

• ORAL NITRATES AND HYDRALAZINE

BENEFIT VS. PLACEBO; INFERIOR TO
ENALAPRIL (MORTALITY)
HOWEVER: 4-YEAR MORTALITY REMAINS ~40%

MJ 2000;320:428-431 (metanalysis: 32 trials, n=7105) 2 Gibbs et al. BMJ 2000;320:495-498 (metanalysis: 18 tria
USUAL TREATMENT TODAY
AIMS OF HEART FAILURE MANAGEMENT

TO IMPROVE SYMPTOMS
• DIURETICS
• DIGOXIN
• ACE INHIBITORS
TO IMPROVE SURVIVAL
• ACE INHIBITORS
•  BLOCKERS
• ORAL NITRATES PLUS HYDRALAZINE
• SPIRONOLACTONE
Davies et al. BMJ 2000;320:428-431
 AN ECONOMIC BURDEN
ANNUAL COST OF HF ESTIMATED TO BE
$22.5 BILLION (USA)

Healthcare
Drugs
Indirect Costs providers Home health/Other
medical durables
2.2 1.5 1.1 2.2

15.5

Hospital/Nursing home
Costs in billions of dollars

American Heart Association, 2000 Heart and Stroke Statistical Update

 SEKIAN
TERIMA KASIH