heart failure - aha

5/21/2018 Heart Failure - Aha

1/73

HEART FAILURE

PATHOPHYSIOLOGY

AND MANAGEMENT

MOCH. FATHONI

DEPART. OF CARDIOLOGY

MEDICAL FACULTY, SEBELAS MARET UNIV.

1


2/73

2.1. Definition of Heart Failure

Heart failure is a complex clinical syndromethat can result from any structural or

functional cardiac disorder that impairs the

ability of the ventricle to fill with or ejectblood. The cardinal manifestations of HF are

dyspnea and fatigue, which may limit exercise

tolerance, and fluid retention, which may lead

to pulmonary congestion and peripheraledema.


3/73

A PREVALENT CONDITION

PREVALENCE OF HEART FAILURE(PER 1000 POPULATION)

Age (years)

50-59

80-89

All ages

Men

8

66

7.4

Women

8

79

7.7

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

4


4/73

A GROWING BURDEN

0

10000

20000

30000

40000

50000

1979 1985 1991 1997

HF

deaths

Source: Vital Statistics of the United States, National Center for Health Statistics

DEATHS FROM HF 1979-1997 (USA)

5


5/73

3

HEART FAILURE WAS VIEWED SOLELY AS

HAEMODYNAMIC DISORDER

A major public health

issue

6


6/73

4

NEURO-HORMONAL ACTIVATION

AS A SIGNIFICANT FACTORCONTRIBUTING TO PROGRESSIVE

SYSTOLIC DYSFUNCTION ANDPROGRAMMED MYOCARDIAL CELL

DEATH, ALSO CALLED

APOPTOSIS

7


7/73

4

FACT AND PENDING

QUESTION

8

NEURO-HORMONAL ACTIVATION


8/73

NEURO-HORMONE SECRETION IN

RESPONSE TO HEART FAILURE

NOREPINEPHRINE CAUSEDVASOCONSTRICTION,INCREASED HEART RATEAND MYOCYTE TOXICITY

ANGIOTENSIN II CAUSED VASOCONSTRICTION,STIMULATES RELEASE OF ALDOSTERONE ANDACTIVATES THE SYMPATHETIC NERVOUS

SYSTEM

ALDOSTERONECAUSEDSODIUM AND WATERRETENTION

9


9/73



ENDOTHELINECAUSED

VASOCONSTRICTION AND MYOCYTE

TOXICITY

ANTIDIURETIC HORMONE (VASOPRESSINE)

CAUSED VASOCONSTRICTION AND WATER

REABSORPTION

TUMOR NECROSIS FACTOR ALPHA(TNF )

CAUSEDDIRECT MYOCITE TOXICITY

10


10/73



INTERLEUKIN I (IL-1) AND IL-6CAUSEDMYOCYTE TOXICITY

NEURO- HORMONE (ATRIAL

NATRIURETIC PEPTIDE ANDBRAIN NATRIURETIC PEPTIDE)

CAUSED VASODILATATION,

EXCRETION OF SODIUMANDANTIPROLIFERATIVE EFFECT ON

MYOCYTES

11


11/73

ETHYOLOGY

The most common cause of heart failure is leftventricular (LV) systolic dysfunction (about 60%of patients).In this category, most cases are a resultof end-stage coronary artery disease, either with ahistory of myocardial infarction or with achronically underperfused,yet viable, myocardium.In many patients, both processes are presentsimultaneously . Other common causes of LV

systolic dysfunction include idiopathic dilatedcardiomyopathy, valvular heart disease,hypertensive heart disease, toxin-inducedcardiomyopathies (alcohol), and congenital heartdisease .

13


12/73

1. CORONARY ARTERY DISEASE : AMI2. HYPERTENSIVE HEART DISEASE

3. VALVULAR HEART DISEASE ex. AS,MS

4. CARDIOMYOPATHY : Restrictive, DilatedHyperthrophic

5. PERICARDIAL DISEASE

6. HIGH OUTPUT SYNDROME ex. ANEMIA,

HYPERTHYROIDIS

7. AGE RELATED DIASTOLIC SYNDROME

14Common ETHYOLOGIES of HF

in OLDER Patients

i

I


13/73

1. RENAL DYSFUNCTION2. CHRONIC LUNG DISEASE

3. COGNITIVE DYSFUNCTION:

DIETARY,MEDICATION ec4. DEPRESSION, SOSIAL ISOLATION

5. URINARY INCONTINENCE

6. NUTRITIONAL DISORDER

7. POLYPHARMACYDRUG INTERACTION

15Common Comorbidities in OLDER Patients

i

I


14/73

DIAGNOSA KLINIK

GAGAL JANTUNG RIWAYAT KLINIK

PEMERIKSAAN FISIK

PEMERIKSAAN EKG

FOTO RONGEN TORAKS

EKOKARDIOGRAM PEMERIKSAAN

RADIONUKLIR

PEMERIKSAAN INVASIF

16


15/73

RIWAYAT KLINIK

PASCA INFARK MIOKARD

ANGINA PEKTORIS

HIPERTENSI

KELAINAN KATUP/ DEMAM REMATIK

PENYAKIT JANTUNG BAWAAN PALPITASI

17


16/73

CLASIFIED BY AN

EJECTION FRACTION

LESS THAN 40 % , IS

CHARACTERIZED BY

A REDUCED CARDIAC

OUTPUT SECONDARY

TO DEPRESSEDMYOCARDIAL

CONTRACTILITY.

20

PHYSICAL EXAMINATION

CLASSIFIED BY A

NORMAL EJECTION

FRACTION ( GREATER

THAN OR EQUAL TO 50 %,

IN THE PRESENCE OF

PULMONARY

CONGESTION AND OTHER

HF SYMPTOMS( FOR EX.DYSPNEA DEFFORT,PND

.

,

FATIGUE, AND

ORTHOPNEA) AND

FOURTH HEART SOUND.

SYSTOLIC HEART FAILURE DIASTOLIC HEART FAILURE


17/73

In general, a definitive diagnosis can

be made when the rate of ventricular

relaxation is slowed; thisphysiological abnormality is

characteristically assocated with the

finding of an elevated LV fillingpressure in a patient with normal LV

volumes and contractility

DIAGNOSIS


18/73

CLASSIFICATION OF HEART

FAILURE

Class I there are no restrictions of physicalactivity. Patients generally dont complain of

being overly tired or of experiencing shortnessof breath. A patient is still able to control thedisease. Regular exercise, limiting alcohol

consumption, and eating healthy (withmoderate sodium intake), are all actions thatcan be taken quite easily. High blood pressurewill need to be treated. Quitting smoking iscrucial.


19/73


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.


20/73


FAILURE

Class III heart failure patients experience

definite limitations during physical

activity. They may remain comfortable atrest, 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.


21/73


FAILURE

Patients in Class IV heart failure are

virtually unable to do any physical

activity without discomfort. Theremay 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.


22/73


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 HeartFailure have persisting sever symptoms.


23/73

PHYSICAL SIGNS

There are a few physical signs that mayindicate Heart Failure. Fluid retention, whichcauses weight gain and possibleswelling of thefeet, ankles, or even abdomen, is associatedwith the disease. Another physical sign isbulging of the neck veins.When the pulmonaryveins arent functioning as they should, an

insufficient supply of blood is making it to theheart, thus causing fluid to build up in thearteries and body tissues (edema).


24/73

THE CLASSIC SYMPTOM OF CHF ISSHORTNESS OF BREATH

SPECIFIC COMMON SYMPTOM INCLUDE :

18SYMPTOMS OF CHF

1. PAROXYSMAL NOCTURNAL DYSPNEA

(AWAKENING FROM SLEEP WITH SHORTNESS

OF BREATH).

2. ORTHOPNEA.

3. OR NEW ONSET DYSPNEA ON EXERTION.

i

I

IF HISTORY AND PHYSICAL EXAMINATION CLEARLYINDICATE A NON CARDIAC CAUSE FOR THESE SYMPTOMS(

EG. SEVERE PULMONARY DISEASE),THEN HEART

FAILURE EVALUATION IS NOT NECESSARY.

Continued


25/73

1. DYSPNEA ON

EXERTION

2. DYSPNEA AT REST

3. ORTHOPNEA

4. PAROXISMAL

NOCTURNAL

DYSPNEA (PND)5. FATIGUE

6. ANKLE SWELLING

19

1. DYSPNEA ON EXERTION

2. CONFUSION

3. AGITATION

4. DEPRESSION

5. INSOMNIA

6. WEAKNESS

7. ANOREXIA OR NAUSEA8. COUGH

YOUNG ADULT PATIENTS ELDERLY PATIENTS

SYMPTOMS OF CHF


26/73

CLASIFIED BY AN

EJECTION FRACTION

LESS THAN 40 % , IS

CHARACTERIZED BY

A REDUCED CARDIAC

OUTPUT SECONDARY

TO DEPRESSEDMYOCARDIAL

CONTRACTILITY.

20

PHYSICAL EXAMINATION

CLASSIFIED BY A

NORMAL EJECTION

FRACTION ( GREATER

THAN OR EQUAL TO 50 %,

IN THE PRESENCE OF

PULMONARY

CONGESTION AND OTHER

HF SYMPTOMS( FOR EX.DYSPNEA DEFFORT,PND

.

,

FATIGUE, AND

ORTHOPNEA) AND

FOURTH HEART SOUND.

SYSTOLIC HEART FAILURE DIASTOLIC HEART FAILURE


27/73

PEMERIKSAAN PENUNJANG

1. PEMERIKSAAN EKG

2. FOTO RONGEN THORAKS

3. HEMOGLOBIN

4. FUNGSI TIROID

5. FUNGSI GINJAL

6. FUNGSI HATI

7. PEMERIKSAAN EKOKARDIOGRAFI

21


28/73

DISFUNGSI SISTOLIK

GAGAL JANTUNG YANG SERING

BERHUBUNGAN DENGAN

KELAINAN FUNGSI SISTOLIK

DIMANA MIOKARDIUM GAGALBERKONTRAKSI SECARA

NORMAL, MENGAKIBATKAN

DILATASI VENTRIKEL KIRI

PENYEBAB TERSERING ADALAH

INFARK MIOKARD, HIPERTENSI

DAN KARDIOMIOPATI

24JENIS GAGAL JANTUNG DAN

TERAPINYA

PENTING UNTUK MENGENALI

SECARA DINI PASIEN INI KARENA

PROGNOSANYA DAPAT MEMBAIK.

TERAPI : BETA BLOCKER/PENGHAMBAT BETA, ACE

INHIBITOR/ PENGHAMBAT ACE,

DIKOMBINASIKAN DENGAN

DIURETIKA, DIGITALIS ATAU

VASODILATOR

ETIOLOGI DAN PATOFISIOLOGI PENATALAKSANAAN


29/73

DISFUNGSI DIASTOLIK

GAGAL JANTUNG YANG

DISEBABKAN OLEH KELAINAN

FUNGSI DIASTOLIK DIMANA

COMPLIANCE/ KEMAMPUANMIOKARDIUM MENURUN

MASALAH INI SERING TERJADI

PADA ORANG TUA


TERAPINYA




TERAPI : MENGATASI PENYAKITYANG MENDASARI/

MENGIKUTINYA SEPERTI

HIPERTENSI HARUS DIBERIKAN

OBAT UTK. MENGURANGI TENSI

DAN MENCEGAH HIPERTROFI

VENTRIKEL KIRI. TANDA-2 KONGESTI /BENDUNGAN

DIKURANGI DENGAN DIURETIKA.



30/73

KELAINAN KATUB

GAGAL JANTUNG YANG


KATUB SERING DITEMUKAN PADA

GOL. SOSIAL EKONOMI RENDAH /DIDAERAH DIMANA PENYAKIT

DEMAM REUMATIK BANYAK

DIJUMPAI.

STENOSIS AORTA KARENA

KALSIFIKASI MERUPAKAN

MASALAH YANG SERING TERJADIPADA ORANG TUA.


TERAPINYA




TERAPI : MENGATASI PENYAKITYANG MENDASARI. PEMBEDAHAN

DAN PROSEDUR INTERVANSI

SEPERTI VALVULOPLASTI

/VALVULOTOMI MEMBERIKAN

HASIL YANG BAIK.

KELAINAN REGURGITASI KATUBYANG TIDAK DAPAT DIOPERASI,

DAPAT DIBERIKAN DIURETIKA

DAN VASODILATOR



31/73

KELAINAN JANTUNG BAWAAN

GAGAL JANTUNG YANG


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.


TERAPINYA




TERAPI : MENGATASI PENYAKIT

YANG MENDASARI. PEMBEDAHAN

DAN PROSEDUR INTERVENSI

SEPERTI KOREKSI/PENUTUPAN

DEFECT MEMBERIKAN HASIL

YANG BAIK.

KELAINAN BAWAAN YANG TIDAKDAPAT DIOPERASI MIS. ASD +PH

DENGA MPA 70 mm HG, DAPAT

DIBERIKAN DIURETIKA DAN

VASODILATOR



32/73

KELAINAN METABOLIK

KELAINAN TIROID, DEFISIENSI

TIAMIN (BERI-BERI), KADAR BESI

YANG BERLEBIH

(HEMOSIDEROSIS DAN

HEMOKROMATOSIS) SERTA

ANEMIA, MERUPAKAN JENIS

GAGAL JANTUNG YANG


METABOLIK YANG DAPAT

MERUSAK MIOKARDIUM.


TERAPINYA




TERAPI : DISINI DIPERLUKAN

PERBAIKAN NUTRISI, FAKTOR

HORMONAL DAN METABOLIK

YANG DAPAT MENYEMBUHKAN

KELAINAN INI.



33/73

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

29


34/73

TATA LAKSANA GAGAL

JANTUNG

ATASI PENYEBAB DISFUNGSI VENTRIKELKIRI.

DISFUNGSI SISTOLIK

DISFUNGSI DIASTOLIK

KELAINAN KATUB

KELAINAN JANTUNG BAWAAN

KELAINAN METABOLIK KELAINAN PERIKARDIUM/

ENDOKARDIUM.

30


35/73

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

31


36/73


37/73


38/73


39/73

KLASIFIKASI FUNGSIONAL

GAGAL JANTUNG (NYHA)1. TIMBUL GEJALA SESAK NAFAS ATAU

CAPAI PADA KEADAAN / AKTIFITAS

FISIK YANG BERAT2. TIMBUL GEJALA PADA KEGIATAN

FISIK YANG SEDANG

3. TIMBUL GEJALA PADA KEGIATAN

FISIK YANGRINGAN

4. TIMBUL GEJALA PADAKEGIATAN

FISIK YANG SANGAT RINGAN DAN

PADA WAKTU ISTIRAHAT

12


40/73

KRITERIA DIAGNOSIS

GAGALJANTUNG

KRITERIA UTAMA GAGAL

JANTUNG

1. DISPNEA NOKTURNAL

PAROKSISMAL (PND)

2. KARDIOMEGALI

3. GALLOP (S-3)

4. PENINGKATAN TEKANAN VENA

5. REFLEKS HEPATOJUGULAR

6. RONKI

22


41/73


42/73

PEMERIKSAAN PENUNJANG

1. PEMERIKSAAN EKG

2. FOTO RONGEN THORAKS

3. HEMOGLOBIN

4. FUNGSI TIROID

5. FUNGSI GINJAL

6. FUNGSI HATI

7. PEMERIKSAAN EKOKARDIOGRAFI

21


43/73

3


44/73

USUALTREATMENT TODAY

TO IMPROVE SYMPTOMS

DIURETICS

DIGOXIN ACE INHIBITORS

TO IMPROVE SURVIVAL

ACE INHIBITORS BLOCKERS

ORAL NITRATES PLUS HYDRALAZINE

SPIRONOLACTONE

AIMS OF HEART FAILURE MANAGEMENT

vies et al. BMJ 2000;320:428-431

3

4


45/73

HF: MORTALITY REMAINS

HIGH

ACEIRISK REDUCTION 35% (MORTALITY ANDHOSPITALIZATIONS)1

BLOCKERSRISK REDUCTION 38% (MORTALITY ANDHOSPITALIZATIONS)2

ORAL NITRATES AND HYDRALAZINEBENEFIT VS. PLACEBO; INFERIOR TO

ENALAPRIL (MORTALITY)

1 Davies et al. BMJ 2000;320:428-431 (meta analysis: 32 trials, n=7105) 2Gibbs et al. BMJ

2000;320:495-498 (meta analysis: 18 trials, n=3023)

4


46/73

9


47/73

ANGIOTENSINI

ANGIOTENSINOGEN(LIVER)

AT1 AT2

ANGIOTENSIN II

ACE

INHIBITOR

VALSARTANAT1RECEPTOR BLOCKER

RENININHIBITOR

BRADYKININ

PEPTIDES

CHYM

LOCAL ANG II SYNTHESIS IS INDEPENDENT OF ACE

BLOCKADE OF RAS10

O O A A A


48/73

ROLE OF AT1AND AT2

RECEPTORS

VASOCONSTRICTION

VASCULARPROLIFERATION

ALDOSTERONE SECRETIONCARDIAC MYOCYTE

PROLIFERATIONINCREASED SYMPATHETIC

TONE

VASODILATION

ANTIPROLIFERATION

APOPTOSIS

AT1 AT2

ANGIOTENSIN II

11


49/73

22

25


50/73

25

Treatment Strategies for Heart Failure

ALDO PIETRO MAGGIOTTI

Director of the Reseach Center of the Italian AssociationOf Hospital

Cardiologist (ANMCO), Pirenze, ITALY

25


51/73

25

ALDO PIETRO MAGGIOTTIDirector of the Reseach Center of the Italian Association

Of Hospital

Cardiologist (ANMCO), Pirenze, ITALY

26Which patients with HF are suitable


52/73

26Which patients with HF are suitable

for Blocker treatment ?

Patients with symptomatic HF of any cause, EF 40 %, inNYHA 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 hypertension2. Heart rate > 90 beat/ mnt.

27benefits ?


53/73

27benefits ?

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 dysfunction3. HF by valvular disease or diastolic dysfunction

4. Comorbidities (DM, COPD, renal disease,

peripheral vasculopathy)

28


54/73

28

Continued

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 theuse of Blockers in heart failure

3. While the effect of 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 Blockers in heartfailure

29


55/73

29

Continued

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 Blockers5. The studies showed that Blockerssignificantly reduce

total and sudden mortality inHF patients

6. Blockerstretment should be started in stable patients with

a very low initial dosage and then uptitrated in the maximal

tolerated

30


56/73

30

Blocker summary

7. Despite the impressive results in term of morbidity and

martality reduction, and the increasing availability of

Blockers, these data showing only a minority of patients

being treated At one time contraindicated in thetreatment of heart failure


57/73

DIURETICS

DIURETICS SHOULD BE USED FOR ALL PATIENTSWITH SYMPTOMS WHO HAVE EVIDENCE FORFLUID RETENTION

SHOUDNOT BE USED ALONE, EVEN IF THESYMPTOMS OF HF ARE WELL CONTROLLED.

ALTHOUGH THEY PRODUCED RAPIDSYMPTOMATIC RELIEF, THEY CANNOTMAINTAIN CLINICAL STABILITY IN LONG- TERM,

SO THEYFORE GENERALLY BE ADMINISTEREDWITH ACEINH/ BLOCKERS

31


58/73

ANTIARRHYTMIC DRUG

In addition to progressive pump dysfunction, 25

70 % of all deaths patients with HF, caused by

ventricel arrhytmia Of the available antiarrhytmia, amiodaroneis

the only one which seem to be potentially

beneficial in patients with HF, suppressing atrialand ventricular arrhytmia

32

NITRATES 33


59/73

NITRATES

The use ofnitratesin HF is most commonly

,in patients who cannot tolerate ACEinhibitors due to hypotension or renal

insufficiency .

Ca. antagonists

Ca. Antagonists are not recommended for use

inHFdue to their association with an increased

risk of cardiovascular event

33

34


60/73

THE OTHERS MANAGEMENT

For the patients who have survived cardiac

arrestthe preferred treatment may be

implantable- defibrillator (ICD) Sceletal myoblast transfer

Educationfor managing lifestyle modification

and optimizing of medical therapy

34

5535

35


61/73

CYTOKINES

CYTOKINES ARE BEING IMPLICATEDFOR PATHOGENIC ROLE IN HF

PROGRESSION Cytokines antagonist : IL-6 antagonist andTNF antagonist currently underinvestigation for HF treatment

553535

36


62/73

CONCLUSIONS

THE PHARMACOLOGICAL TREATMENT OF

HF HAS BECOME COMBINED SYMPTOMATIC

- PREVENTIVE MANAGEMENT STATEGY EARLY RECOGNATION AND PREVENTION

THERAPIESCOMBINED WITH LIFESTYLE

MODIFICATION, ARE ESSENTIAL

36

38


63/73

CONCLUSIONS

APPLY THE GUIDELINES TO EVERY

PATIENTS AS INDIVIDUAL, ADJUSTING THE

TREATMENT REGIMEN AS INDICATED BY A

PATIENTS S CONDITIONAND WHAT THE

GROWING MEDICAL EVIDENCE BASE DEEMS

APPROPRIATE

THERE ARE MANY APPROACHS WEREDESCRIBED AS THE RECENT MANAGEMENT

38

THANK YOU


64/73

THANK YOU


65/73


66/73


67/73


68/73

A PREVALENT CONDITION

VALENCE OF HF (PER 1000 POPULATION)

Age (years)

50-59

80-89

All ages

Men

8

66

7.4

Women

8

79

7.7

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


69/73

A GROWING BURDEN

0

10000

20000

30000

40000

50000

1979 1985 1991 1997

HF

deaths

tal Statistics of the United States, National Center for Health Statistics

EATHS FROM HF 1979-1997 (USA)



70/73


HIGH

ACEIRISK REDUCTION 35% (MORTALITY ANDHOSPITALIZATIONS)1

BLOCKERSRISK REDUCTION 38% (MORTALITY ANDHOSPITALIZATIONS)2

ORAL NITRATES AND HYDRALAZINEBENEFIT VS. PLACEBO; INFERIOR TO

ENALAPRIL (MORTALITY)HOWEVER: 4-YEAR MORTALITY REMAINS ~40%

J 2000;320:428-431 (metanalysis: 32 trials, n=7105) 2Gibbs et al. BMJ 2000;320:495-498 (metanalysis: 18 tri


71/73

USUAL TREATMENT TODAY

TO IMPROVE SYMPTOMS

DIURETICS

DIGOXIN ACE INHIBITORS

TO IMPROVE SURVIVAL

ACE INHIBITORS

BLOCKERS

ORAL NITRATES PLUS HYDRALAZINE

SPIRONOLACTONE

AIMS OF HEART FAILURE MANAGEMENT

Davies et al. BMJ 2000;320:428-431


72/73

AN ECONOMIC BURDEN

American Heart Association, 2000 Heart and Stroke Statistical Update

Hospital/Nursing home

HealthcareprovidersIndirect Costs Home health/Other

medical durables

Drugs

15.5

2.2 1.5 1.1 2.2

ANNUAL COST OF HF ESTIMATED TO BE$22.5 BILLION (USA)

Costs in billions of dollar


73/73

SEKIANTERIMA KASIH

heart failure - aha

Documents

usa55212018 heart failure

heart failureinterleukin

common cause of heart

valvular heart disease

hypertensive heart disease3

framingham heart study

neurohormonal activationas

significant factorcontributing