Management of Heart FailureManagement of Heart Failure Management of Heart FailureManagement of Heart Failure

Prof. Karen SliwaProf. Karen Sliwa Department of CardiologyDepartment of Cardiology

Chris Hani Baragwanath Hospital Chris Hani Baragwanath Hospital Johannesburg, South AfricaJohannesburg, South Africa

Prof. Karen SliwaProf. Karen Sliwa Department of CardiologyDepartment of Cardiology

Chris Hani Baragwanath Hospital Chris Hani Baragwanath Hospital Johannesburg, South AfricaJohannesburg, South Africa

Definition:

•Imbalance between volume of blood supplied and thetissue requirements

•Definition of heart failure: Criteria 1 and 2 should be fulfilled in all cases

1 Symptoms of heart failure (at rest or during exercise) like breathlessness, ankle swelling and fatigue

and 2 Objective evidence of cardiac dysfunction (at rest)

and (in cases where the diagnosis is in doubt)

3 Response to treatment directed towards heart failure

Guidelines from European Society of Cardiology Task ForceW.J. Remme and K. Swedberg, European Heart Journal 2001; 22:1528

How big is the Problem?

•2% of the total western population has heart failure

( no data available for SA population)

•Patients over 70 years, the prevalence is > 10 %

•Only 50 % of all patients survive 4 years

•Increasing prevalence due to ageing population and increasing survivors of MI

Major Causes

•Valvular heart disease

•CAD

•HT

•Cardiomyopathy

–Idiopathic

–Ethanol

–Viral

–Infiltrative

–Metabolic-hypothyroidism/DM

•Pericardial dx

•High output states

•Incessant tachyarrythmias

Evolution of Heart Failure

Stage A: At risk for HFBut no structural heart disease or signs /symptoms of HF

e.g HT,CAD, DM, Cardiotoxins

Stage B: Structural heart disease But no symptoms of HF

e.g LVH, prior MI, asymptomatic valve disease

Stage C: Structural ht disease with prior or current symptoms of HF

e.g SOB,fatigue due to LV systolic dysfunction

Stage D: Advanced heart disease and severe symptoms at rest despite max therapy.Refractory HF.

unable to safely discharge without specialized support e.g LVAD

Hunt SA et al J Am Coll Cardiol 2001;38:2101

Functional Classification

New York Heart Association (NYHA)

Early failure, no symptoms with regular exercise or restrictions

> 95%

Ordinary activity results in mild symptoms,but comfortable at rest

80 - 90%

Classes

Grade I

Grade II

Grade III

Grade IVSevere failure;patient has symptoms at rest

5 - 15%

Description1 year

Survival Rate

Advanced failure, comfortable only at rest;increased physical restrictions 55 - 65%

Heart failure is a chronic progressive disease

Assessment of the patient with heart failure

Objectives of initial evaluation of a patient with possible or definitive heart failure:

•Early diagnosis is important

•In symptomatic patients can be in:

1. Left heart failure

2. Right heart failure

3. Low cardiac output

4. High cardiac output

•Cause of heart failure

•Identification of precipitating factors and reversible causes

•Identify markers of prognosis: left ventricular function

Investigations

Electrocardiogram

•Most pts with CHF due to systolic dysfunction have a significant abnormality on ECG

•Normal ECG 98% neg. predictive value

•Evidence of

–Ischeamic heart dx

–LVH

–Arrythmias eg atrial fib

–DCMO – limb leads low voltage/precordial LVH, wide QRS, LBBB

InvestigationsCXR

•Diff HF from lung dx

•CTR>50%

•Upper lobe diversion

•Kerley-B

•Pleural effusions

Investigations

Routine blood tests:

• Full blood count- Anemia

• Blood urea nitrogen and creatinine- Renal Dysfunction

• Electrolytes-Hyponatraemia,hypokalemia,hyperkalemia

• Albumin-Hypoalbuminemia

• Blood glucose-Diabetis mellitus

• Thyroxine ( in patients with AF or who are >65 years and

the heart failure has no obvious etiology- Hyper

and Hypothyroidism

InvestigationsEchocardiography

•Essential in all newly diagnosed

•Detect

•LV size & EF

•Wall thickness / ‘texture’

•RWMA

•Valve dx

•Pericardial dx

•Septal shunts

•RV size, pressures & fn

•LV thrombus

•Expensive/Expertise

LV thrombus postpartum

Naturetic Peptides

Features ANP BNP CNP Urodilatin

Amino acids 28 32 22 or 53 32 (= ANP + 4)

Main source cardiac atria cardiac vascular kidney

ventricle endothelium

Hormone type endocrine endocrine autocrine paracrine

paracrine

Main function Regulation of homeostasis of salt Regulation of Regulation of

and water excretion and blood vascular tone water and sodium

pressure (natriuretic, vasodilatory, reabsorbtion in

renin-and aldosterone inhibitory collecting duct

properties)

Cardiac specific

Sensitivity and specificity of clinical signs in HF

100 patients presenting to casualty with signs or symptoms of congestive heart failure(eg, dyspnea,edema, wt gain)

Specificity Sensitivity

Jugular Venous Pressure 92% 34%

Third Heart sound 90% 26%

Rales

BNP (>100pg/ml)

81%

98%

57%

100%

Dao et al, 49th Annual Scientific Session ofthe American College of Cardiology

Summary-Assessment of Heart FailureHeart failure is a composite of clinical symptoms, physical signs, and abnormalities on the hemodynamic, neurohormonal, biochemical, anatomic and cellular levels It’s a large problem both in the developed and developing world

A thorough history is vital in identifying cause and precipitating factors

Combination of clinical examination and basic investigations will aid in diagnosis, assessing severity and prognosis

Echocardiography essential in newly diagnosed patients

TREATMENT OF HEART FAILURE

• Acute heart failure and shock ( not discussed within this lecture): clinical presentation is regardless of the cause, with hypotension, tachycardia,

tachypnea, oliguriacauses:

-acute MI ( 8% of all cases)-acute mitral regurgitation, eg. post MI-acute AR, eg. SBE, Aortic dissection,-Acute myocarditis-pericardial tamponade,

-pulmonary embolism

• Chronic heart failure

GOALS OF THERAPY IN CHRONIC HEART FAILURE

GOAL Examples

Prevention Blood pressure control

Symptom reduction

Increased activity tolerance

Diuretics, digoxin, exercise training

Prevent progression

(remodeling)

ACE-inhibitors, Beta-blockers

Prolong survival ACE-inhibitors, beta-blockers, spironolactone

Pharmacological Treatment-Diuretics

Diuretics:

•WHO ?

-Those with signs of Na and water retention

I.e. peripheral or pulmonary oedema,↑JVP

Pharmacological Treatment-Diuretics

Spironolactone:

•RALES TRIAL reduction in all cause mortality by

27% in NYHA III-IV heart failure on conventional

treatment, 17% reduction in hospitalisations

•WHO ?

-NYHA III-IV on diuretics/ACE/digoxin

Pharmacological Treatment-Digoxin

Digoxin:

•- DIG TRIAL: no net effect on mortality in CHF, does improve symptoms and reduce hospitalisations

•- WHO ?

-Those with CHF in AF who need rate control

-Those with moderate or severe symptoms

despite optimal treatment

Pharmacological Treatment-Neurohormonal antagonists

Angiotensin Converting Enzyme Inhibitors:

•Several randomised controlled clinical trials as CONSENSUS I, SOLVD, VHeFT II have shown that in patients with CHF they reduce-

-mortality

-hospitalisation

-improve symptoms and signs

-slow progression from mild to congestive cardiac

failure

Pharmacological Treatment-Neurohormonal antagonists

Angiotensin II Type I receptor antagonists:

• WHO?

- Those intolerant to ACE-inhibitors ( especially because of

cough)

Pharmacological Treatment-Beta-blockers

Beta-blockers:• Over 13,000 patients evaluated in placebo-

controlled clinical trials

• Consistent improvement in cardiac function, symptoms and clinical status

• Decrease in all-cause mortality by 30–35% (p<0.0001)

• Decrease in combined risk of death and hospitalisation by 25–30% (p<0.0001)

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%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%

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%

US Carvedilol Study

blockers in heart failure -

all-cause mortality

CIBIS-II MERIT-HF

blockers in heart failure

Consensus recommendations

All patients with stable class II or III heart failure

due to left ventricular systolic dysfunction should

receive a beta-blocker (in addition to an ACE

inhibitor) unless they have a contraindication to its

use or cannot tolerate treatment with the drug

Implications for public health

Lives saved by treating1000 patients for 1 year

HOPE (ramipril) <1

SOLVD Prevention (enalapril) 7

SOLVD Treatment (enalapril) 17

MERIT-HF (metoprolol) 38

CIBIS-II (bisoprolol) 42

RALES (spironolactone) 52

COPERNICUS (carvedilol) 70

Packer, AHA 2000

Management of acute exacerbation of chronic heart failure

Investigation and treatment of precipitating factors: infections, thiamine deficiency ( alcohol abuse), anaemia

Intermittent use of positive inotropic drugs:

• WHO?

- patients admitted to hospital with severely decompensated heart failure, particular those with ‘ cardiorenal syndrome’ in which sufficient diuresis cannot be obtained without progressive deterioration of renal function

New concepts in the treatment of heart failure

-Anti-inflammatory/cytokine therapy

-Modification of cardiac matrix

-Myocyte/Myoblast implant

-Biventricular pacing

-Anti-remodeling strategies

-Cardiac transplantation

Summary-Treatment of CHF

Heart failure is a composite of clinical symptoms, physical signs, and abnormalities on the hemodynamic, neurohormonal, biochemical, anatomic and cellular levels Therapy should aim:

-To improve symptoms

-Prevent progression of disease Early diagnosis is important! All patients should be on a beta-antagonists ( preferentially carvedilol