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.

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

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 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 RESPONSE TO HEART FAILURE ENDOTHELINE CAUSED VASOCONSTRICTION AND MYOCYTE TOXICITY

10

ANTIDIURETIC HORMONE (VASOPRESSINE) CAUSED VASOCONSTRICTION AND WATER REABSORPTION

TUMOR NECROSIS FACTOR ALPHA(TNF ) CAUSED DIRECT MYOCITE TOXICITY

NEURO-HORMONE SECRETION IN RESPONSE TO HEART FAILURE

11

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 in OLDER Patients

14

1. 2. 3. 4.

CORONARY ARTERY DISEASE : AMI HYPERTENSIVE HEART DISEASE VALVULAR HEART DISEASE ex. AS,MS CARDIOMYOPATHY : Restrictive, Dilated Hyperthrophic 5. PERICARDIAL DISEASE 6. HIGH OUTPUT SYNDROME ex. ANEMIA, HYPERTHYROIDIS 7. AGE RELATED DIASTOLIC SYNDROME
i I

Common Comorbidities in OLDER Patients

15

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

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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

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PHYSICAL EXAMINATION
SYSTOLIC HEART FAILURE DIASTOLIC HEART FAILURE

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

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.

DIAGNOSIS

In general, a definitive diagnosis can be made when the rate of ventricular relaxation is slowed; this physiological abnormality is characteristically assocated with the finding of an elevated LV filling pressure in a patient with normal LV volumes and contractility

CLASSIFICATION OF HEART FAILURE

Class I there are no restrictions of physical activity. Patients generally dont 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 arent 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).

SYMPTOMS OF CHF

18

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 I

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

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SYMPTOMS OF CHF
YOUNG ADULT PATIENTS ELDERLY PATIENTS

1. DYSPNEA ON EXERTION 2. DYSPNEA AT REST 3. ORTHOPNEA 4. PAROXISMAL NOCTURNAL DYSPNEA (PND) 5. FATIGUE 6. ANKLE SWELLING

1. 2. 3. 4. 5. 6. 7. 8.

DYSPNEA ON EXERTION CONFUSION AGITATION DEPRESSION INSOMNIA WEAKNESS ANOREXIA OR NAUSEA COUGH

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PHYSICAL EXAMINATION
SYSTOLIC HEART FAILURE DIASTOLIC HEART FAILURE

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

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.

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

JENIS GAGAL JANTUNG DAN TERAPINYA

ETIOLOGI DAN PATOFISIOLOGI
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

24

PENATALAKSANAAN

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

JENIS GAGAL JANTUNG DAN TERAPINYA

ETIOLOGI DAN PATOFISIOLOGI
DISFUNGSI DIASTOLIK GAGAL JANTUNG YANG DISEBABKAN OLEH KELAINAN FUNGSI DIASTOLIK DIMANA COMPLIANCE/ KEMAMPUAN MIOKARDIUM MENURUN MASALAH INI SERING TERJADI PADA ORANG TUA

25

PENATALAKSANAAN

PENTING UNTUK MENGENALI SECARA DINI PASIEN INI KARENA PROGNOSANYA DAPAT MEMBAIK. 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.

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 TERAPINYA

ETIOLOGI DAN PATOFISIOLOGI
KELAINAN JANTUNG BAWAAN GAGAL JANTUNG YANG DISEBABKAN OLEH KELAINAN JANTUNG BAWAAN DAPAT DITEMUKAN PADA MASA ANAKANAK ATAU MASA DEWASA. BEBERAPA TIPE SEPERTI DEFECT ATRIUM MUNGKIN TIDAK TERLIHAT SECARA DINI, DAN BARU DIKETAHUI SETELAH TERJADI GAGAL JANTUNG.

27

PENATALAKSANAAN

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.

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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

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TATA LAKSANA GAGAL JANTUNG

ATASI PENYEBAB DISFUNGSI VENTRIKEL KIRI. DISFUNGSI SISTOLIK DISFUNGSI DIASTOLIK KELAINAN KATUB KELAINAN JANTUNG BAWAAN KELAINAN METABOLIK KELAINAN PERIKARDIUM/ ENDOKARDIUM.

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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

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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

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KRITERIA DIAGNOSIS GAGAL JANTUNG

KRITERIA UTAMA GAGAL JANTUNG DISPNEA NOKTURNAL PAROKSISMAL (PND) KARDIOMEGALI GALLOP (S-3) PENINGKATAN TEKANAN VENA REFLEKS HEPATOJUGULAR RONKI

1.
2. 3. 4. 5. 6.

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

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

HF: MORTALITY REMAINS HIGH

ACEI
RISK REDUCTION 35%
HOSPITALIZATIONS)1
(MORTALITY AND

BLOCKERS
RISK REDUCTION 38%
HOSPITALIZATIONS)2 (MORTALITY AND

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

Gibbs et al. BMJ

BLOCKADE OF RAS

10

LOCAL ANG II SYNTHESIS IS INDEPENDENT OF ACE

ANGIOTENSINOGEN
(LIVER)

RENIN INHIBITOR

CHYMA
ANGIOTENSIN I

BRADYKININ
PEPTIDES

ACE INHIBITOR

ANGIOTENSIN II

VALSARTAN
AT1 RECEPTOR BLOCKER

AT1

AT2

ROLE OF AT1 AND AT2 RECEPTORS

ANGIOTENSIN II
AT1
VASOCONSTRICTION VASCULAR PROLIFERATION ALDOSTERONE SECRETION CARDIAC MYOCYTE PROLIFERATION INCREASED SYMPATHETIC TONE

11

AT2
VASODILATION ANTIPROLIFER ATION APOPTOSIS

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 for Blocker treatment ?

26

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 ?

Patients with severe biventricular dysfunction SBP < 100 mmHg

27

Which patients with HF are uncertainties still exist ?

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

28

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 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 heart failure
Continued

29

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 Blockers 5. The studies showed that Blockers significantly reduce total and sudden mortality in HF patients 6. Blockers tretment should be started in stable patients with a very low initial dosage and then uptitrated in the maximal tolerated

Continued

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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 the treatment of heart failure

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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/ BLOCKERS

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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
The use of nitrates in HF is most commonly ,in patients who cannot tolerate ACE inhibitors due to hypotension or renal insufficiency .

33

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 5 35 35

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

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

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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

A PREVALENT CONDITION

EVALENCE 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

A GROWING BURDEN
50000 40000
HF deaths

DEATHS FROM HF 1979-1997 (USA)

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%
HOSPITALIZATIONS)1
(MORTALITY AND

BLOCKERS
RISK REDUCTION 38%
HOSPITALIZATIONS)2 (MORTALITY AND

ORAL NITRATES AND HYDRALAZINE

HOWEVER: 4-YEAR MORTALITY REMAINS ~40%

2

BENEFIT VS. PLACEBO; INFERIOR TO ENALAPRIL (MORTALITY)

MJ 2000;320:428-431 (metanalysis: 32 trials, n=7105)

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

15.5

Hospital/Nursing home

Costs in billions of dollars

American Heart Association, 2000 Heart and Stroke Statistical Update

SEKIAN TERIMA KASIH