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