DIAGNOSTIC ET TRAITEMENT DE L’INSUFFISANCE CARDIAQUE

Prof O. Gurné

UCL – Cliniques Univ St Luc

Heart Failure (HF) Definition

A complex clinical syndrome in which the heart is incapable of maintaining a cardiac output adequate to accommodate metabolic requirements and the venous return.

Etiology and Pathophysiology of Heart Failure

Etiology of Heart Failure

What causes heart failure?

The loss of a critical quantity of functioning myocardial cells after injury to the heart due to:

– Ischemic Heart Disease

– Hypertension

– Idiopathic Cardiomyopathy

– Infections (e.g., viral myocarditis)

– Toxins (e.g., alcohol or cytotoxic drugs)

– Valvular Disease

– Prolonged Arrhythmias

30%30%

70%70%

Diastolic DysfunctionDiastolic DysfunctionSystolic DysfunctionSystolic Dysfunction

(EF < 40%)(EF < 40%)(EF > 40 %)(EF > 40 %)

Left Ventricular Dysfunction

• Systolic: Impaired contractility/ejection– Approximately two-thirds of heart failure patients

have systolic dysfunction1

• Diastolic: Impaired filling/relaxation

1 Lilly, L. 1 Lilly, L. Pathophysiology of Heart DiseasePathophysiology of Heart Disease. Second Edition p 200. Second Edition p 200

PreventionPrevention

TherapyTherapy

NYHANYHAClassClass

II

IIII

IIIIII

IVIV

Ventricular dysfunctionVentricular dysfunction

Overt heart failureOvert heart failure

MildMild

ModerateModerate

SevereSevere

Progress of heart failure

Curry CW, et al. Mechanical dyssynchrony in dilated cardiomyopathy with intraventricular conduction Curry CW, et al. Mechanical dyssynchrony in dilated cardiomyopathy with intraventricular conduction delay as depicted by 3D tagged magnetic resonance imaging. Circulation 2000 Jan 4;101(1):E2. delay as depicted by 3D tagged magnetic resonance imaging. Circulation 2000 Jan 4;101(1):E2.

Compensatory MechanismsVentricular RemodelingAlterations in the heart’s size, shape, structure, and function brought about by the chronic hemodynamic stresses experienced by the failing heart.

Injury to heartInjury to heart

SympatheticSympathetic

Disease progressionDisease progression

Neurohormonal Neurohormonal activationactivation

Renin angiotensinRenin angiotensinaldosteronealdosterone

Neurohormonal activation in heart failure

Initially Adaptive, Deleterious if SustainedInitially Adaptive, Deleterious if Sustained

ResponseShort-Term Effects

Long-Term Effects

Salt and Water Retention Augments Preload Pulmonary Congestion, Anasarca

Vasoconstriction Maintains BP for perfusion of vital organs

Exacerbates pump dysfunction (excessive afterload), increases cardiac energy expenditure

Sympathetic Stimulation Increases HR and ejection

Increases energy expenditure

Neurohormonal Responses to ImpairedCardiac Performance

Jaski, B, MD: Jaski, B, MD: Basics of Heart Failure: A Problem Solving ApproachBasics of Heart Failure: A Problem Solving Approach

Diagnostic of Heart Failure

Left Ventricular DysfunctionSystolic and Diastolic

• Symptoms

– Dyspnea on Exertion

– Paroxysmal Nocturnal Dyspnea

– Tachycardia

– Cough

– Hemoptysis

• Physical Signs

– Basilar Rales

– Pulmonary Edema

– S3 Gallop

– Pleural Effusion

– Cheyne-Stokes Respiration

Right Ventricular FailureSystolic and Diastolic

• Symptoms

– Abdominal Pain

– Anorexia

– Nausea

– Bloating

– Swelling

• Physical Signs

– Peripheral Edema

– Jugular Venous Distention

– Abdominal-Jugular Reflux

– Hepatomegaly

Patient suspected to have LVDPatient suspected to have LVD

EchocardiogramEchocardiogram

ECGECGChest X-rayChest X-ray

Lung function testsLung function testsFull blood countFull blood count

Thyroid function testsThyroid function testsBiochemistryBiochemistry

Current diagnostic algorithm

Natriuretic Peptides: Origin and Stimulus of Release

Adapted from Burnett JC, J Hypertens 2000;17(Suppl 1):S37-S43

ANP = Atrial Natriuretic PeptideBNP = B-type Natriuretic PeptideCNP = C-type Natriuretic Peptide

Peptide Primary Origin Stimulus of Release

ANP Cardiac atria Atrial distension

BNP Ventricular myocardium Ventricular overload

CNP Endothelium Endothelial stress

BNP LEVELS IN PATIENTS WITN DYSPNEA

0

100

200

300

400

500

600

700

800

CHF LVD / NOCHF

PULMON OTHERCARD

OTHERS

Morrison et al, J Am Coll Cardiol 2002;39:202

100

200

300

400

500

0

600

Pulmponary Asthma COPD Pneumonia Acute Tbc Lung Pulmonary fibrosis bronchitis cancer Embolism n = 1 11 42 8 14 2 4 3

Types of Lung Disease

BNP (pg/ml)

Morrison et al, J Am Coll Cardiol 2002;39:202

ROC Curves for BNP and ED Diagnosis Using All 250 Patients

Dao, Q., Maisel, A. et al. J. American College of Cardiology, Vol 37, No. 2, 2001

0 10 20 30 40 50 60 70 80 90 100

0102030405060708090

100

1 - Specificity (%)

Se

ns

itiv

ity

(%

)

--- BNP --- ED diagnosisAUC 0.8840.9790

BNP in LV Dysfunction

30

567+/-113

391+/-89

1077+/-272

0

200

400

600

800

1000

1200

BN

P p

g/m

L

Normal Systolic Diastolic Systolic &Diastolic

N=105 N=53 N=42 N=14

Maisel, A., De Maria, A. et al. American Heart Journal, Vol. 141, No. 3, 2001

Patient suspected to have LVDPatient suspected to have LVD

EchocardiogramEchocardiogram

BNPBNP

IncreasedIncreased

Normal Normal LVD LVD unlikelyunlikely

Future diagnostic algorithm

Treatment of Heart Failure

General Measures

Lifestyle Modifications:

• Weight reduction

• Discontinue smoking

• Avoid alcohol and other cardiotoxic substances

• Exercise

Medical Considerations:

• Treat HTN, hyperlipidemia, diabetes, arrhythmias

• Coronary revascularization

• Anticoagulation

• Immunization

• Sodium restriction

• Daily weights

• Close outpatient monitoring

TRAITEMENT INSUFFISANCE CARDIAQUE

I II A IIB III IV

DIUR

ACE - INH

INH A II

B B

SPIRO

DIG

Digitalis and Inotropic Agents Compounds

Like the carrot placed in front of the donkey

Digoxine in heart failure

Digoxine better Digoxine better Placebo better Placebo better

DIG trial

– Overall death

– Hospitalization

0.99

0.82

NEJM 1997; 336 : 525-533NEJM 1997; 336 : 525-533

MORTALITY DIGOXIN PLACEBO RR PVALUE

WORSENING CHF

11.6 % 13.2 % 0.88 (0.77-1.01)

0.06

OTHER CARDIAC

15.0 % 13.0 % 1.14 (1.01-1.30)

0.04

BUTBUTBUTBUT

Diuretics, ACE Inhibitors

Reduce the number of sacks on the wagon

SOLVD Investigators N Engl J Med 1991;325:293-302

0

10

20

30

40

50

0 6 12 18 24 30 36 42 48

PlaceboEnalapril

Follow-up (months)

Mortality (%)

Risk reduction 16%p=0.0036

Studies of Left Ventricular Dysfunction – SOLVD (Treatment Study)

ACE INHIBITORS - IN WHOM AND WHEN?

Indications:• potentially all patients with heart failure• 1st line treatment (along with beta-blockers) in NYHA class I-IV heart failureContra-indications:• history of angioneurotic oedemaCautions:• significant renal dysfunction (creatinine > 2.5 mg/dL or 221 µmol/L) or hyperkalaemia (K+ > 5.0

mmol/L)• symptomatic or severe asymptomatic hypotension (SBP < 90 mmHg)Drug interactions to look out for:• K+ supplements/ K+ sparing diuretics (including spironolactone)• NSAIDs avoid unless essential • AT1-receptor blockers

ACE INHIBITORS - HOW TO USE

• start with a low dose • Increase dose progressively• aim for target dose or, failing that, the highest tolerated

dose• remember some ACE inhibitor is better than no ACE

inhibitor• monitor blood chemistry (urea, creatinine, K+) and blood

pressure

ACE INHIBITORS - PROBLEM SOLVING

Asymptomatic low blood pressure does not usually require any change in therapy

Symptomatic hypotension:• if dizziness, light-headedness and/or confusion and a low blood pressure

occurs, reconsider need for nitrates, calcium channel blockers** and other vasodilators

• if no signs/symptoms of congestion, consider reducing diuretic dose

**calcium channel blockers should be discontinued unless absolutely essential (eg. for angina or hypertension)

ACE INHIBITORS - PROBLEM SOLVING (cont.)

Cough:

• cough is common in patients with heart failure, many of whom have smoking-related lung disease

• cough is also a symptom of pulmonary oedema which should be excluded if a new or worsening cough develops

• ACE inhibitor-induced cough rarely requires treatment discontinuation: ± 5 – 10 % max

• if a very troublesome cough develops (eg. one stopping the patient sleeping) and can be proven to be due to ACE inhibition (ie. recurs after ACE inhibitor withdrawal and rechallenge) substitution with an AT1-receptor blocker can be considered

ACE INHIBITORS - PROBLEM SOLVING (cont.)

Worsening renal function:

• some increase in urea (blood urea nitrogen), creatinine and K+ is to be expected after initiation; if the increase is “small” and asymptomatic no action is necessary

• an increase in creatinine of up to 50% above baseline, or 3 mg/dL (266 µmol/L), whichever is the smaller, is acceptable

• an increase in K+ 6.0 mmol/L is acceptable

• if urea, creatinine or K+ rise excessively consider stopping concomitant nephrotoxic drugs (eg. NSAIDs), other K+ supplements/ K+ retaining agents (triamterene, amiloride) and, if no signs of congestion, reducing the dose of diuretic

• if greater rises in creatinine or K+ than those outlined above persist despite adjustment of concomitant medications, halve the dose of ACE inhibitor and recheck blood chemistry; if there is still an unsatisfactory response, check for renal artery stenosis

ACE INHIBITORS - PROBLEM SOLVING (cont.)

Worsening renal function (cont.):

• If K+ rises to > 6.0 mmol/L or creatinine increases by >100% or to above 4 mg/dL (354 µmol/L), the dose of ACE inhibitor should be stopped

• Blood chemistry should be monitored serially until K+ and creatinine have plateaued

NB: it is very rarely necessary to stop an ACE inhibitor and clinical deterioration is likely if treatment is withdrawn

Blockade of RAS

ANGIOTENSIN I

ANGIOTENSINOGEN(LIVER)

AT1 AT2

ANGIOTENSIN II

ACE INHIBITOR

AT1 RECEPTOR BLOCKER

RENIN INHIBITOR

BRADYKININ

PEPTIDES

CHYMASE

LOCAL ANG II SYNTHESIS IS INDEPENDENT OF ACE

A

Biollaz et al. J Cardiovasc Pharmacol 1982;4:966

NG II levels increase over time despite ACEI

HOSPITAL

0

4

8

12

16

20

24

PLACEBO 4H 24H 1 2 3 4 5 6 MONTHS

80

100

120

140

160

180

BLOODPRESSURE

mm Hg

PLASMAANG IIpg/mL

NYHA III* or IV heart failureNYHA III* or IV heart failure

LVEF LVEF 35%35%

ACE-I + loop diuretic ± digoxinACE-I + loop diuretic ± digoxin

NYHA III* or IV heart failureNYHA III* or IV heart failure

LVEF LVEF 35%35%

ACE-I + loop diuretic ± digoxinACE-I + loop diuretic ± digoxin

Spironolactone Spironolactone 25 mg/day 25 mg/day(n = 822)(n = 822)

Spironolactone Spironolactone 25 mg/day 25 mg/day(n = 822)(n = 822)

Primary EndpointPrimary Endpoint Total mortalityTotal mortality

Secondary EndpointSecondary Endpoint Cardiac mortalityCardiac mortality Cardiac hospitalizationCardiac hospitalization Cardiac mortality or cardiac hosptitalizationCardiac mortality or cardiac hosptitalization Changes from baseline in NYHA classificationChanges from baseline in NYHA classification

Primary EndpointPrimary Endpoint Total mortalityTotal mortality

Secondary EndpointSecondary Endpoint Cardiac mortalityCardiac mortality Cardiac hospitalizationCardiac hospitalization Cardiac mortality or cardiac hosptitalizationCardiac mortality or cardiac hosptitalization Changes from baseline in NYHA classificationChanges from baseline in NYHA classification

PlaceboPlacebo(n = 841)(n = 841)

PlaceboPlacebo(n = 841)(n = 841)

Pitt et al, N Engl J Med, 1999.Pitt et al, N Engl J Med, 1999. *History of NYHA IV within 6 months before first dose*History of NYHA IV within 6 months before first dose

3 years3 years

RALES: Study DesignRALES: Study Design

0.00

0.45

0.50

0.55

0.60

0.65

0.70

0.75

0.80

0.85

0.90

0.95

1.00

0 3 6 9 12 15 18 21 24 27 30 33 36

Spironolactone

Placebo

Probability of survival

Months

Randomized Aldactone Evaluation Study (RALES)

All causes mortality

Pitt B et al. N Engl J Med 1999;10:709-717

Risk reduction 30%

95% CI : 18-40 %p<0.001

SPIRONOLACTONE - IN WHOM AND WHEN?

Indications:

• potentially all patients with symptomatically moderately severe or severe heart failure

• 2nd line therapy (after ACE inhibitors and beta-blockers) in patients with NYHA class III-IV heart failure

Cautions:

• significant renal dysfunction (creatinine > 221 µmol/L or 2.5 mg/dL)• significant hyperkalaemia (K+ > 5.0 mmol/L)

SPIRONOLACTONE - HOW TO USE

• start at 25 mg once daily (12.5)• check blood chemistry at 1, 4, 8 and 12 weeks; 6, 9

and 12 months; 6 monthly thereafter• if K+ rises to between 5.5 and 6.0 mmol/L or

creatinine rises to 2.5 mg/dL (221 µmol/L) reduce dose to 25 mg on alternate days and monitor blood chemistry closely

• if K+ rises to > 6.0 mmol/L or creatinine to > 4.0 mg/dL (354 µmol/L), stop spironolactone

• Vasoconstriction

• Hypertrophy

• Inotrope +• Chronotrope +• Hypertrophy (HVG)• Fibrosis

• sodium and water retention• Vasoconstriction of afferent and efferent arterioles

• Aldosterone secretion• Catecholamines secretion

• Stimulation thirst center• Vasopressin release• sympathetic activation

AT1

ANGIOTENSINE II

Goodfriend et al. N Engl J Med 1996;334:1649-1654

Jackson and Garrisson. In: Hardman et al. eds. Goodman & Gilman ’s The Pharmacological Basis of Therapeutics 9th ed.

New York: McGraw Hill: 1996;733-758

Bauer and Reams Arch Intern Med 1995;155:1361-1368

Effects of Angiotensin II via AT1 receptors

Study DesignStudy DesignLosartan Heart Failure Survival StudyELITE II

60 yrs; NYHA II-IV; EF 40% ACE-I/AIIA naive or <7 days in 3 months prior to

entryStandard Rx (± Dig/Diuretics), ß-blocker

stratification

Captopril50 mg 3 times daily (N=1574)

Primary Endpoint: All-Cause MortalitySecondary Endpoint: Sudden Cardiac Death and/or Resuscitated

ArrestOther Endpoin: All-cause Mortality/Hospitalizations Safety and Tolerability

Event DrivenEvent Driven(Target 510 Deaths)(Target 510 Deaths)

~ 2 years~ 2 years

Losartan50 mg Daily

(N=1578)

Losartan Heart Failure Survival Study - ELITE II Primary Endpoint: All-Cause Mortality

0 100 200 300 400 500 600 700

Days of Follow-up

0.0

0.2

0.4

0.6

0.8

1.0

Pro

babi

lity

of S

urvi

val

Losartan Losartan (N=1578)(N=1578) 280 Events280 EventsCaptoprilCaptopril (N=1574) (N=1574) 250 Events250 Events

Captopril/Losartan Hazard Ratio (95% C.I.):Captopril/Losartan Hazard Ratio (95% C.I.):0.88 (0.75, 1.05) P=0.160.88 (0.75, 1.05) P=0.16

CHARM Added

CHARMPreserved

CHARM Programme

3 component trials comparing candesartan to placebo in patients with symptomatic heart failure

CHARMAlternative

n=2028

LVEF 40%ACE inhibitor

intolerant

n=2548

LVEF 40%ACE inhibitor

treated

n=3025

LVEF >40%ACE inhibitor

treated/not treated

Primary outcome for Overall Programme: All-cause death

Primary outcome for each trial: CV death or CHF hospitalisation

n=3025

LVEF >40% ACE inhibitor

treated/not treated

CHARM Added

CHARMPreserved

CHARMAlternative

n=2028

LVEF 40%ACE inhibitor

intolerant

n=2548

LVEF 40%ACE inhibitor

treated

Primary outcome:CV death or CHF hosp

CHARM Programme

3 component trials comparing candesartan to placebo in patients with symptomatic heart failure

CHARM-Alternative: Primary outcome CV death or CHF hospitalisation

0 1 2 3 years0

10

20

30

40

50

Placebo

Candesartan

%

HR 0.77 (95% CI 0.67-0.89), p=0.0004Adjusted HR 0.70, p<0.0001

Number at risk

Candesartan 1013 929 831 434 122

Placebo 1015 887 798 427 126

3.5

406 (40.0%)

334 (33.0%)

n=3025

LVEF >40%ACE inhibitor

treated/not treated

CHARM Added

CHARMPreserved

CHARMAlternative

n=2028

LVEF 40% ACE inhibitor

intolerant

n=2548

LVEF 40%ACE inhibitor

treated

Primary outcome:CV death or CHF hosp

CHARM Programme

3 component trials comparing candesartan to placebo in patients with symptomatic heart failure

CHARM-Added: Primary outcomeCV death or CHF hospitalisation

0 1 2 3 years0

10

20

30

40

50

Placebo

Candesartan

Number at risk

Candesartan 1276 1176 1063 948 457

Placebo 1272 1136 1013 906 422

3.5

HR 0.85 (95% CI 0.75-0.96), p=0.011Adjusted HR 0.85, p=0.010

483 (37.9%)538 (42.3%)

%

n=3025

LVEF >40%ACE inhibitor

treated/not treated

CHARM Added

CHARMPreserved

CHARMAlternative

n=2028

LVEF 40% ACE inhibitor

intolerant

n=2548

LVEF 40%ACE inhibitor

treated

Primary outcome:CV death or CHF hosp

CHARM Programme

3 component trials comparing candesartan to placebo in patients with symptomatic heart failure

CHARM-Preserved: Primary outcome CV death or CHF hospitalisation

0 1 2 3 yearsNumber at risk

Candesartan 1514 1458 1377 833 182

Placebo 1509 1441 1359 824 195

3.50

10

20

30Placebo

Candesartan

5

15

25

HR 0.89 (95% CI 0.77-1.03), p=0.118Adjusted HR 0.86, p=0.051

%

366 (24.3%)333 (22.0%)

ß-Blockers

Limit the donkey’s speed, thus saving energy

Carvedilol(n=696)

Placebo(n=398)

Survival

Days

0 50 100 150 200 250 300 350 400

1.0

0.9

0.8

0.7

0.6

0.5

Risk reduction = 65%Risk reduction = 65%p<0.001

Packer et al (1996)

Lancet (1999)0 200 400 600 800

1.0

0.8

0.6

0

Bisoprolol

Placebo

Time after inclusion (days)

p<0.0001

Survival

Risk reduction = 34%Risk reduction = 34%

The MERIT-HF Study Group (1999)

Months of follow-up

Mortality %

0 3 6 9 12 15 18 21

20

15

10

5

0

Placebo

Metoprolol CR/XL

p=0.0062

Risk reduction = 34%Risk reduction = 34%

US Carvedilol StudyUS Carvedilol Study

blockers in blockers in heart failure -heart failure -

all-cause mortalityall-cause mortality

CIBIS-IICIBIS-II MERIT-HFMERIT-HF

COPERNICUS

Patient Characteristics

• Symptoms of heart failure at rest or minimal exertion for at least 2 months

• LV ejection fraction <25%

• Receiving diuretics and an ACE inhibitor (+ digitalis) 2 months. Diuretics optimised to achieve euvolaemia

• No need for intensive care and no treatment with IV inotropic or IV vasodilator therapy within 4 days of screening

0000

% S

urv

ival

% S

urv

ival

33 66 99 1212 1515 1818 2121MonthsMonths

100100

9090

8080

6060

7070

pp=0.00013=0.0001335% risk reduction35% risk reduction

CarvedilolCarvedilol

PlaceboPlacebo

COPERNICUS

All-cause mortalityAll-cause mortality

RandomisedRandomised30293029

CarvedilolCarvedilol15111511

MetoprololMetoprolol15181518

Assigned to drug Assigned to drug and received at least one tabletand received at least one tablet

Withdrew consent 10Withdrew consent 10Lost to follow-up Lost to follow-up 3 3

Withdrew consent 18Withdrew consent 18Lost to follow-up Lost to follow-up 2 2

Flow chart of patients

Time (years)Time (years)

Mo

rtal

ity

(%)

Mo

rtal

ity

(%)

00

1010

2020

3030

4040

00 11 22 33 44 55

MetoprololMetoprolol

CarvedilolCarvedilol

hazard ratio 0.83, hazard ratio 0.83, 95% CI 0.74-0.93, P = 0.001795% CI 0.74-0.93, P = 0.0017

Number at riskNumber at risk

CarvedilolCarvedilol 15111511 13671367 12591259 1155 1155 10021002 383383MetoprololMetoprolol 15181518 13591359 12341234 1105 1105 933933 352352

Primary endpoint of mortality

BETA-BLOCKERS - IN WHOM AND WHEN?Indications: • potentially all patients with stable mild and moderate heart failure; patients with severe

heart failure should be referred for specialist advice• 1st line treatment (along with ACE inhibitors) in patients with stable NYHA class I-III

heart failure; start as early as possible Contra-indications:• asthmaCautions:• severe (NYHA Class IV) heart failure ( ! COPERNICUS)• current or recent (< 4 weeks) exacerbation of heart failure eg. hospital admission with

worsening heart failure • heart block or heart rate < 60 beats/min• persisting signs of congestion – raised jugular venous pressure, ascites, marked

peripheral oedema

BETA-BLOCKERS - IN WHOM AND WHEN? (cont.)

Drug interactions to look out for:• verapamil/diltiazem (should be discontinued)• amiodarone

BETA-BLOCKERS - WHERE?• in the community in stable patients (NYHA class IV/severe heart failure

patients should be referred for specialist advice)• not in unstable patients hospitalised with worsening heart failure• other exceptions – see CAUTIONS

BETA-BLOCKERS - HOW TO USE

• start with a low dose • double dose at not less than 2 weekly intervals• aim for target dose or, failing that, the highest tolerated dose• remember some beta-blocker is better than no beta-blocker• monitor HR, BP, clinical status (symptoms, signs – especially signs of

congestion) and body weight)• check blood chemistry 1-2 weeks after initiation and 1-2 weeks after final

dose titration • a specialist heart failure nurse may assist with patient education, follow-up

(in person/by telephone) and dose up-titration• when to down-titrate/stop up-titration – see PROBLEM SOLVING

BETA-BLOCKERS - ADVICE TO PATIENT

• explain expected benefits (see WHY?)• emphasise that treatment given as much to prevent

worsening of heart failure as to improve symptoms; beta-blockers also increase survival

• if symptomatic improvement occurs, this may develop slowly, 3 - 6 months or longer

• temporary symptomatic deterioration may occur (estimated 20 - 30% of cases) during initiation/up-titration phase

BETA-BLOCKERS - ADVICE TO PATIENT (cont.)

• advise patient to report deterioration (see PROBLEM SOLVING) and that deterioration (tiredness, fatigue, breathlessness) can usually be easily managed by adjustment of other medication; patients should be advised not to stop beta-blocker therapy without consulting their physician

• patients should be encouraged to weigh themselves daily (after waking, before dressing, after voiding, before eating) and to increase their diuretic dose should their weight increase, persistently (> 2 days), by >1.5 – 2.0 kg

BETA-BLOCKERS - PROBLEM SOLVING

Worsening symptoms/signs (eg. increasing dyspnoea, fatigue, oedema, weight gain):

• if increasing congestion, double dose of diuretic and/or halve dose of beta-blocker (if increasing diuretic does not work)

• if marked fatigue (and/or bradycardia – see below) halve dose of beta-blocker (rarely necessary)

• review patient in 1-2 weeks; if not improved seek specialist advice• if serious deterioration halve dose of beta-blocker or stop this

treatment (rarely necessary); seek specialist advice

BETA-BLOCKERS - PROBLEM SOLVING (cont.)

Low heart rate:

• if < 50 beats/min and worsening symptoms – halve dose beta-blocker or, if severe deterioration, stop beta-blocker (rarely necessary)

• review need for other heart rate slowing drugs eg. digoxin, amiodarone, diltiazem

• arrange ECG to exclude heart block

BETA-BLOCKERS - PROBLEM SOLVING (cont.)

Asymptomatic low blood pressure:• does not usually require any change in therapy

Symptomatic hypotension:• if dizziness, light-headedness and/or confusion and a low blood pressure occur,

reconsider need for nitrates, calcium channel blockers and other vasodilators• if no signs/symptoms of congestion, consider reducing diuretic dose

NOTE: Beta-blockers should not be stopped suddenly unless absolutely necessary (there is a risk of a “rebound” increase in myocardial ischaemia/infarction and arrhythmias) – ideally specialist advice should be sought before treatment discontinuation

How could we do better than better … perhaps one day ?

Treatment of Heart Failure

HEART FAILURE - TREATMENT

• MEDICAL THERAPY• TECHNICAL DEVICE

– Biventricular pacing

– Défibillateur implantable

– Assist devices

– Artificial heart• Bridge to transplant

• Permanent

• GENE / CELLULAR THERAPY

Cardiac Resynchronization Therapy

Increase the donkey’s (heart) efficiency

BIVENTRICULAR PACING in CHF BIVENTRICULAR PACING in CHF

“Conventional” target population

• High functional class (NYHA III or IV)

• Prolonged QRS ( > 150 ms)

• Dilated LV with EF <0.35

• PR interval > 150 ms

• Relative clinical stability

... % of CHF patients reflect these findings !

(4) Lancet 1998; 352 : SI15-SI18(4) Lancet 1998; 352 : SI15-SI18

Structure of heart failure clinicStructure of heart failure clinic

Effect of Multidisciplinary Intervention in Treatment of Heart Failure

In-hospital In-hospital patientpatient

CardiologistCardiologist

NursingNursing

DieticianDietician

PhysiotherapistPhysiotherapist

Out-Out-patientpatient

GPGP

Home Home nursingnursing

Social Social servicesservices

EXEMPLE :EDUCATION DU PATIENT

• DEBUTE A L’HOPITAL

• POURSUIVI A LA MAISON

• Connaissance de sa pathologie

• Relation avec sa médication

• Relation avec son hygiène de vie, son régime

• Connaissance des signes précoces de décompensation

Ex: prise du poids