1. Heart Failure- II prognosis And Management
Dr Hanan ALBackr
10/11/1429
(8/11/2008)

2. DEFINITION
Heart failure (HF) 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.

3. PATHOPHYSIOLOGY

4. Pathophysiology

5. Prevalence
Prevalence 0.4-2% overall, 3-5 % in over 65s, 10% of over 80s
Commonest medical reason for admission
Annual mortality of 60% over 80s
> 10% also have AF
Progressive condition - median survival 5 years after diagnosis
Common condition
Prevalence above – one new case per 1000 population per annum, up to 10 per 1000 in elderly
Readmission rates as high as 50% over 3 months
Loss of cardiac reserve with age and HF may often complicate the presence of other conditions in the elderly
If AF and HF - risk of thromboembolic complications esp. stroke - risk 2% in pts in SR but may > 10%/year in pts with AF, no anticoag + other risk factors
Mortality varies according to aetiology and severity - prognosis can often be predicted according to the severity of the disease - annual mortality rate 10%
Most deaths occur due to progressive pump failure, sudden cardiac death and recurrent MI

6. Rates of Sudden Cardiac Death

7. Typical Presentations Of Heart Failure
Syndrome of decrease exercise tolerance
Syndrome of fluid retention
No symptoms but incidental discovery of LV dysfunction

8. HISTORY
Underlying causes –CAD, valvular disease, hypertension, family history etc.
Aggravating factors –arrhythmias (AF), anaemia etc.
Co-morbidities/differential diagnoses –COPD, obesity, chronic venous insuff etc.

9. Examination Raised JVP, peripheral oedema, ascites
Signs of poor tissue perfusion
Pulse –tachycardia, irregular, thready, pulsus alternans
Added heart sounds, murmurs, bibasal inspiratory crackles

10. TESTS 12leadECG CXR •BNP •Echocardiogram
Low sensitivity and specificity

12. EKG

14. CXR

15. Echocardiogram

17. Classification of severity
Class I - symptoms of HF only at activity levels that would limit normal individuals
Class II - symptoms of HF with ordinary exertion
Class III - symptoms of HF with less than ordinary exertion
Class IV - symptoms of HF at rest

18. I No limitation of activities; They suffer no symptoms from ordinary activities
II Slight, mild limitation of activity; They are comfortable with rest or with mild exertion
III Marked limitation of activity; They are comfortable only at rest
IV Confined to bed or chair; Any physical activity brings on discomfort and symptoms occur at rest

19. Stages of HF 
Stage A — High risk for HF, without structural heart disease or symptoms
Stage B — Heart disease with asymptomatic left ventricular dysfunction
Stage C — Prior or current symptoms of HF
Stage D — Advanced heart disease and severely symptomatic or refractory HF

21. Etiology

22. The major causes of heart failure in the developed world are ischaemic heart disease and hypertension

23. Diagnostic Work-up In all cases History, exam, ekg Echo etiology
MR? LVEDD, RV fxn
Labs
TSH, ferritin, Na, Cr
Exercise testing
Prognosis, VO2Max
Assessment of CAD
One of few reversible causes
In selected cases
Labs
Metanephrines
Catheterization
CAD
Hemodynamics
Endomyocardial biopsy
If infiltrative disease considered

26. Therapy Aims for therapy Reduce symptoms & improve QOL
Reduce hospitalization
Reduce mortality
Pump failure
Sudden cardiac death

27. The Donkey Analogy
Ventricular dysfunction limits a patient's ability to
perform the routine activities of daily living…

28. Management of Heart Failure
Overview
Diagnosis and Evaluation
Therapies
Diuretics
ACE-Inhibitors
Digoxin
Beta Blockers
Recent non-Pharmacological Advances
Sudden Death & ICD’s
Contractile Dysynchrony and Biventricular Pacing
Diastolic Dysfunction

29. Diuretics in Heart Failure
Benefits
Improves symptoms of
congestion
Can improve cardiac
output
Improved neurohormonal milieu
No inherit nephrotoxicity
Limitations
Oral absorption
unpredictable
Excessive volume
depletion
Electrolyte disturbance
Unknown effects on
mortality
Ototoxicity

30. Diuretics, ACE Inhibitors
Reduce the number of sacks on the
wagon

31. ACE Inhibitors Reduce mortality, MI, Symptoms
Decrease preload and afterload
CONSENSUS 1987 – enalapril vs. placebo – 31% reduction mortality in enalapril group
Confirmed by SOLVD, AIRE, SAVE, TRACE
1995 meta-analysis showed 23% reduction total mortality, 35% in combined mortality/hosp admission
Should be considered in all
Consider in all including asymptomatic esp if EF < 40%. Generally well tolerated
Reduce preload and afterload there by inc. CO
Act on renin-angiotensin-aldosterone system and reduce afterload by reducing production of angiotensin II
Indirect effect on Na and water retention by inhibiting the release of aldosterone and vasopressin thereby reducing venous congestion and preload
Inc CO leads to inc renal perfusion which helps alleviate oedema
CONSENSUS (cooperative new scandinavian enalapril survival study – landmark study in 253 NYHA class IV patients – benefits seen in 1 yr – red mortality and improvement in NYHA class in TX group enal up to 40mg/day
SOLVD enalapril up to 20mg/day, AIRE ramipril, TRACE trandolapril
Extensively investigated in large numbers of pts and found to reduce morbidity and mortality, improve NYHA class. This extends to different pt groups eg elderly, women, pts with or without CAD, with differing degrees of functional impairment and history of use of diuretics and dig
In absence of clear CI the should be used as first line Rx in all with LVSD who do or do not have Sx – recommeded as 1st line by NICE, european society of cardiology, ACC/AHA

32. Practical ACEI prescribing
Test dose
Titrate to higher end of range
Continue indefinitely
Caution in impaired renal function
RAS / Aortic stenosis
May cause hypotension may produce hypotension - most pronounced after 1st dose and sometimes severe - pts on high doses of loops and those with low circulating blood volume may be at highest risk
options - short acting eg captopril test dosing
Give at night
May be lessened by longer acting agents associated with lower risk signif BP drops eg ram, perin
Important to ensure that dose is titrated upwards to target dose that represents clinical trial data or represents the maximum tolerated by the patient ? Double dose slowly at not less than 2 weekly intervals
In clinical practice many patients may be being treated with sub optimal doses hence outcomes may not be as good as expected. However, some is better than none
(ATLAS 1999 study lisinopril mg od vs 2.5-5mg od – fewer hosp admissions with higher doses
Potentially hazardous in pre-existing renal disease but mild to mod renal imp is not c/I - blockage of renin-angiotensin-aldosterone system may lead to reversible deterioration of renal function (renal perfusion lower in HF and glomerular filtration dependant upon angiotension mediated arterial vasoconstriction)
Most are cleared by the kidney so other forms of dose related toxicity are more likely in renal imp Generally small increases in creatinine are acceptable, monitor for progressive increase – european guidelines 2005 suggest specialist input when Cr > 266micromol/L or 50% above baseline (whichever is smaller)
ACEI C/I in RAS where activated R-A-A system maintains renal perfusion and in AS as use can dec CO due to decreased filling pressure in the LV
Tolerate systolic 90mmHg

33. Potential problems with ACEI
Hyperkalaemia
Hypotension
Cough
Hepatic and renal dysfunction
Angiodema
Hyperkalaemia due to red circulating aldosterone – care with K supplements / K sparing agents (25-50mg spironolactone generally well tolerated however)
Cough due to impairment in bradykinin breakdown - develops in approx 10% pts and more common in women - difficult to attribute to ACEI as CCF also causes dry cough
Encourage pts to tolerate if poss / change to different ACEI
Rashes, loss or disturbances in taste, mouth ulcers and proteinuria may occur
Many are prodrugs – monitor in hepatic dysfunction as this could reduce benefits
Most depend upon kidney for excretion
Can cause renal dys
Need to individualise Tx to gain max benefit with min adverse FX

34. ß-Blockers
Limit the donkey’s speed, thus saving energy

35. Beta-blockers US Carvedilol studies 1996
65% decrease mortality in carvedilol group
27% reduction in hospitalisations, reduction in progression of CCF
CIBIS-II – Bisoprolol vs. placebo
34% reduction mortality (42% reduction in sudden death
32% hospitalisations
Us carvedilol studies 1996 – 4 separate studies 1094 class II to IV pts
CIBIS-II 1999 (coronary insufficiency bisoprolol study) – 2,647 class III and IV
Sub group analysis suggested that benefits of bisoprolol higher in high risk groups eg diabetics, elderly, renal imp

36. Beta-blockers MERIT-HF - metoprolol COPERNICUS
NYHA class IV, EF < 25%
35% reduction in mortality with carvedilol
CAPRICORN - 23% reduction in mortality post MI
Merit HF 1999 showed similar results with metop CR in class II to IV
COPERNICUS 2001 carvedilol prospective randomised cumulative survival study safe and effective in severe HF with 74% pts achieving target dose
CAPRICORN 2001– carvedilol post infarct survival control in left ventricular dysfunction – ef <33% post MI – indicating safe and effective post MI

37. Practical Beta blocker prescribing
“Start low, go slow”
Bisoprolol 1.25mg od
Carvedilol 3.125mg bd
Not rescue therapy
Contra indicated in PVD, severe bradycardia
Cardioselective agents in mild to moderate reversible airways disease
Symptoms likely to worsen before improve - start on low doses and titrate upwards – not more than 2 weekly intervals as per BNF recommendations
Severe bradycardia - < 50bpm – consider also concurrent therapy e.g. antiarrythmics, diltiazem, digoxin
Cochrane review 2001– no strong evidence to support withholding cardioselective BB in pts with reversible airways disease – use cardioselective agent and careful monitoring of resp function

38. Digitalis Compounds
Like the carrot placed in front of the donkey

39. Implantable Cardioverter Defibrillator (ICD)
1-3 leads + pulse generator
Sudden onset criteria
Stability criteria
Treatment zones
Pacing
Cardioversion
Defibrillation
Combined CRT-D available

40. Biventricular pacemaker
Resynchronise ventricles by simultaneous pacing
NICE guidance published 2007

41. Recommendations
An ACE inhibitor should be given to all patients with heart failure unless there are contraindications. In patients intolerant of ACE inhibitors, ARBs are an alternative (level of evidence, A).
In symptomatic patients with heart failure, beta-blockers are recommended to reduce mortality rates (level of evidence, A).
Aldosterone antagonists are recommended to reduce mortality rates in certain patients with heart failure. These include patients with current or recent history of dyspnea at rest, and patients with recent myocardial infarction who have systolic dysfunction with either clinically significant signs of heart failure or with concomitant diabetes mellitus (level of evidence, B).

42. Recommendations
For persistently symptomatic black patients with heart failure, direct-acting vasodilators reduce overall mortality rates when added to background therapy with ACE inhibitors, beta-blockers, and diuretics (if needed). Direct-acting vasodilators are also an alternative for patients with heart failure who are intolerant of ACE inhibitors (level of evidence, B).
For patients with heart failure and volume overload, diuretics are recommended (level of evidence, B).

43. Heart Failure: More than just drugs.
Dietary counseling
Patient education
Physical activity
Medication compliance
Aggressive follow-up
Sudden death assessment

44. Treatment - general No added salt Treat / prevent BP, IHD, EtOH
Stop smoking
Exercise and wt control
Education
Focus of heart failure management has changed significantly over the past 2 decades shifting from symptom management and palliation to improving prognosis and functional status
NSF CHD lists general goals of treatment as - relieve Sx, delay progression of disease, reduce cardiac events reduce hopitalisation and mortality - effective Tx can considerable improve QOL and increase survival
Pts often elderly with co-morbidities, other complications such as renal imp, polypharmacy/concordance may exist
Careful monitoring reqd to detect ADRs, suboptimal Rx and poor concordance
IHD – ca channel blockers such as amlodipine shown to be safe as more selective action on vascular tissue and less pronounced action on cardiac contractility than others

45. Patient education
Understanding of need for treatment and it’s risks and benefits
Timing of doses – diuretics, nitrates
Side effects of medicines
Self management - monitor weight, oedema
Side effects – ACEI
Signs of digoxin toxicity

46. Role of HF team Initiate, monitor and individualise therapy
Education and support for pts and carers
Liaison with Consultant and GP
Encourage and facilitate self management
Close links with Community matrons
Telephone support
End of life care – involvement of palliative care teams

47. Take home message Heart failure is a clinical diagnosis
ACE- inhibitors should be titrated to highest doses tolerable
Beta blockers should be used universally but must be titrated slowly
Spironolactone should be used in III-IV patients but K+ needs to be monitored closely
Digoxin can be used to reduce morbidity
Role of ARB remains to be determined in patient tolerating BB & ACE-I
Preventive therapy & patient education is the key to reduction of burden