Heart failure AHA

HEART FAILURE PATHOPHYSIOLOGYAND MANAGEMENT

MOCH. FATHONIDEPART. OF CARDIOLOGY

MEDICAL FACULTY, SEBELAS MARET UNIV.

1

2.1. Definition of Heart FailureHeart 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.

A PREVALENT CONDITIONPREVALENCE 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

A GROWING BURDEN

0

10000

20000

30000

40000

50000

1979 1985 1991 1997

HF

deat

hs

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

DEATHS FROM HF 1979-1997 (USA)

5

3

HEART FAILURE WAS VIEWED SOLELY AS HAEMODYNAMIC DISORDER

A major public healthA major public healthissueissue

6

4

NEURO-HORMONAL ACTIVATION

AS A SIGNIFICANT FACTOR AS A SIGNIFICANT FACTOR CONTRIBUTING TO PROGRESSIVE CONTRIBUTING TO PROGRESSIVE

SYSTOLIC DYSFUNCTION SYSTOLIC DYSFUNCTION ANDAND PROGRAMMED MYOCARDIAL PROGRAMMED MYOCARDIAL CELL DEATH, CELL DEATH, ALSO CALLEDALSO CALLED

APOPTOSISAPOPTOSIS

7

4

FACT AND PENDING FACT AND PENDING QUESTIONQUESTION

8

NEURO-HORMONAL ACTIVATION

NEURO-HORMONE SECRETION IN NEURO-HORMONE SECRETION IN RESPONSE TO HEART FAILURE 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

9


ENDOTHELINE CAUSED VASOCONSTRICTION AND MYOCYTE TOXICITY

ANTIDIURETIC HORMONE (VASOPRESSINE) CAUSED VASOCONSTRICTION AND WATER REABSORPTION

TUMOR NECROSIS FACTOR ALPHA(TNF α) CAUSED DIRECT MYOCITE TOXICITY

10


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

11

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 .

13

1. CORONARY ARTERY DISEASE : AMI2. HYPERTENSIVE HEART DISEASE3. VALVULAR HEART DISEASE ex. AS,MS4. CARDIOMYOPATHY : Restrictive, Dilated

Hyperthrophic5. PERICARDIAL DISEASE6. HIGH OUTPUT SYNDROME ex. ANEMIA,

HYPERTHYROIDIS7. AGE RELATED DIASTOLIC SYNDROME

14Common ETHYOLOGIES of HF in OLDER Patients

iI

1. RENAL DYSFUNCTION2. CHRONIC LUNG DISEASE3. COGNITIVE DYSFUNCTION:

DIETARY,MEDICATION ec4. DEPRESSION, SOSIAL ISOLATION5. URINARY INCONTINENCE6. NUTRITIONAL DISORDER7. POLYPHARMACY – DRUG INTERACTION

15Common Comorbidities in OLDER Patients

iI

DIAGNOSA KLINIK GAGAL JANTUNG

• RIWAYAT KLINIK

• PEMERIKSAAN FISIK

• PEMERIKSAAN EKG

• FOTO RONGEN TORAKS

• EKOKARDIOGRAM

• PEMERIKSAAN RADIONUKLIR

• PEMERIKSAAN INVASIF

16

RIWAYAT KLINIK

• PASCA INFARK MIOKARD

• ANGINA PEKTORIS

• HIPERTENSI

• KELAINAN KATUP/ DEMAM REMATIK

• PENYAKIT JANTUNG BAWAAN

• PALPITASI

17

CLASIFIED BY AN EJECTION FRACTION LESS THAN 40 % , IS CHARACTERIZED BY A REDUCED CARDIAC OUTPUT SECONDARY TO DEPRESSED MYOCARDIAL 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 D‘ EFFORT,PND.

, FATIGUE, AND ORTHOPNEA) AND FOURTH HEART SOUND.

SYSTOLIC HEART FAILURE DIASTOLIC HEART FAILURE

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.


• 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.


• 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.


• 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.


• 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.

http://www.medicinenet.com/script/main/art.asp?articlekey=100539



THE CLASSIC SYMPTOM OF CHF IS SHORTNESS 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.

iI

IF HISTORY AND PHYSICAL EXAMINATION CLEARLY INDICATE A NON CARDIAC CAUSE FOR THESE SYMPTOMS( EG. SEVERE PULMONARY DISEASE), THEN HEART FAILURE EVALUATION IS NOT NECESSARY.

Continued

1. DYSPNEA ON EXERTION

2. DYSPNEA AT REST3. ORTHOPNEA4. PAROXISMAL

NOCTURNAL DYSPNEA (PND)

5. FATIGUE6. ANKLE SWELLING

19

1. DYSPNEA ON EXERTION2. CONFUSION3. AGITATION4. DEPRESSION5. INSOMNIA6. WEAKNESS7. ANOREXIA OR NAUSEA8. COUGH

YOUNG ADULT PATIENTS ELDERLY PATIENTS

SYMPTOMS OF CHF

CLASIFIED BY AN EJECTION FRACTION LESS THAN 40 % , IS CHARACTERIZED BY A REDUCED CARDIAC OUTPUT SECONDARY TO DEPRESSED MYOCARDIAL 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 D‘ EFFORT,PND.

, FATIGUE, AND ORTHOPNEA) AND FOURTH HEART SOUND.

SYSTOLIC HEART FAILURE DIASTOLIC HEART FAILURE

PEMERIKSAAN PENUNJANG

1. PEMERIKSAAN EKG

2. FOTO RONGEN THORAKS

3. HEMOGLOBIN

4. FUNGSI TIROID

5. FUNGSI GINJAL

6. FUNGSI HATI

7. PEMERIKSAAN EKOKARDIOGRAFI

21

DISFUNGSI SISTOLIK• GAGAL JANTUNG YANG SERING

BERHUBUNGAN DENGAN KELAINAN FUNGSI SISTOLIK DIMANA MIOKARDIUM GAGAL BERKONTRAKSI 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

DISFUNGSI DIASTOLIK• GAGAL JANTUNG YANG

DISEBABKAN OLEH KELAINAN FUNGSI DIASTOLIK DIMANA COMPLIANCE/ KEMAMPUAN MIOKARDIUM MENURUN

• MASALAH INI SERING TERJADI PADA ORANG TUA



• TERAPI : MENGATASI PENYAKIT YANG MENDASARI/ MENGIKUTINYA SEPERTI HIPERTENSI HARUS DIBERIKAN OBAT UTK. MENGURANGI TENSI DAN MENCEGAH HIPERTROFI VENTRIKEL KIRI.

• TANDA-2 KONGESTI /BENDUNGAN DIKURANGI DENGAN DIURETIKA.


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.



• 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


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.



• 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


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.



• TERAPI : DISINI DIPERLUKAN PERBAIKAN NUTRISI, FAKTOR HORMONAL DAN METABOLIK YANG DAPAT MENYEMBUHKAN KELAINAN INI.


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


ATASI PENYEBAB DISFUNGSI VENTRIKEL KIRI.

• DISFUNGSI SISTOLIK• DISFUNGSI DIASTOLIK• KELAINAN KATUB• KELAINAN JANTUNG BAWAAN• KELAINAN METABOLIK• KELAINAN PERIKARDIUM/

ENDOKARDIUM.

30


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

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.





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.











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

12

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

22

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.






PEMERIKSAAN PENUNJANG

1. PEMERIKSAAN EKG

2. FOTO RONGEN THORAKS

3. HEMOGLOBIN

4. FUNGSI TIROID

5. FUNGSI GINJAL

6. FUNGSI HATI

7. PEMERIKSAAN EKOKARDIOGRAFI

21

2

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

3

HF: MORTALITY REMAINS HIGH

• ACEI RISK REDUCTION 35% (MORTALITY AND HOSPITALIZATIONS)1

BLOCKERS RISK REDUCTION 38% (MORTALITY AND HOSPITALIZATIONS)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) 2 Gibbs et al. BMJ 2000;320:495-498 (meta analysis: 18 trials, n=3023)

4

9

ANGIOTENSIN I

ANGIOTENSINOGEN(LIVER)

AT1 AT2

ANGIOTENSIN II

ACE INHIBITOR

VALSARTANAT1 RECEPTOR BLOCKER

RENIN INHIBITOR

BRADYKININ

PEPTIDES

CHYMASE

LOCAL ANG II SYNTHESIS IS INDEPENDENT OF ACE

BLOCKADE OF RAS 10

ROLE OF AT1 AND AT2 RECEPTORS

VASOCONSTRICTIONVASCULAR PROLIFERATION

ALDOSTERONE SECRETION

CARDIAC MYOCYTE PROLIFERATION

INCREASED SYMPATHETIC TONE

VASODILATION

ANTIPROLIFERATION

APOPTOSIS

AT1 AT2

ANGIOTENSIN II

11

22

25

Treatment Strategies for Heart Failure

ALDO PIETRO MAGGIOTTIDirector of the Reseach Center of the Italian Association

Of Hospital

Cardiologist (ANMCO), Pirenze, ITALY

25

ALDO PIETRO MAGGIOTTIDirector of the Reseach Center of the Italian Association

Of Hospital

Cardiologist (ANMCO), Pirenze, ITALY

26Which patients with HF are suitable 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 hypertension2. Heart rate > 90 beat/ mnt.

27

Which patients with HF are less likely to benefits ?

• 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 dysfunction4. Comorbidities (DM, COPD, renal disease,

peripheral vasculopathy)

28

Continued

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

29

Continued

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

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

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

31

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

32

NITRATES • 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

33

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

34

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

553535

CONCLUSIONS

• THE PHARMACOLOGICAL TREATMENT OF HF HAS BECOME COMBINED SYMPTOMATIC - PREVENTIVE MANAGEMENT STATEGY

• EARLY RECOGNATION AND PREVENTION THERAPIES COMBINED WITH LIFESTYLE MODIFICATION, ARE ESSENTIAL

36

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

38

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 heart to deliver adequate oxygen-rich blood.

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 diseasehigh blood pressure (hypertension) longstanding alcohol abusedisorders of the heart valvesunknown (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

PREVALENCE OF HF (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

A GROWING BURDEN

0

10000

20000

30000

40000

50000

1979 1985 1991 1997

HF

deat

hs

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

DEATHS FROM HF 1979-1997 (USA)

HF: MORTALITY REMAINS HIGH

• ACEI RISK REDUCTION 35% (MORTALITY AND HOSPITALIZATIONS)1

BLOCKERS RISK REDUCTION 38% (MORTALITY AND HOSPITALIZATIONS)2

• ORAL NITRATES AND HYDRALAZINEBENEFIT VS. PLACEBO; INFERIOR TO ENALAPRIL (MORTALITY)

HOWEVER: 4-YEAR MORTALITY REMAINS ~40%

1 Davies et al. BMJ 2000;320:428-431 (metanalysis: 32 trials, n=7105) 2 Gibbs et al. BMJ 2000;320:495-498 (metanalysis: 18 trials, n=3023)

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

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 dollars

SEKIANTERIMA KASIH

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Heart failure AHA