Transcript Cardiac failure management in the UK

Developments in heart failure
management and clinical practice
in the UK
Jamil Mayet
Department of Cardiology
St Mary’s Hospital
Problems in heart failure
management
• Accurate diagnosis
• Optimising drug therapy
• Identification of patients who will benefit
from revascularisation
Heart failure therapy - rule of halves
Treatment no CCF
CCF inadequate
therapy
CCF appropriate
therapy
Cardiac failure - diagnosis
Electrocardiogram
If ECG normal very unlikely to be systolic dysfunction
Echocardiography
• Confirms / refutes diagnosis of systolic
dysfunction
• Can exclude significant valvular disease
• Can suggest ischaemic aetiology if regional
wall motion abnormality
• Can assess diastolic dysfunction
Easy access to investigations
• GP education
– Every patient with possible cardiac failure should
be considered for echocardiography
• Open and rapid access to echocardiography
• Clear user-friendly reports
– “Mild MR; this is not clinically significant”
– “In the absence of clinical contra-indications…”
Optimising drug therapy
• ACE inhibitors
– High doses used in clinical trials
– If cough AII antagonists
– If contra-indications hydralazine/nitrates
• Beta blockers
• Spironolactone
ACE inhibitor doses used in large
controlled trials
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CONSENSUS
V-HeFT II
SOLVD
SAVE
*twice daily
Enalapril
Enalapril
Enalapril
Captopril
20mg*
10mg*
10mg*
50mg**
**three times a day
• ATLAS study showed significant decrease in
mortality+hospital admissions in high dose
versus low dose lisinopril
Treatment – AII antagonists
• ELITE STUDY
• 722 patients 65 years with:
– CCF (NYHA class II-IV)
– LVEF  40%
• Captopril vs. losartan
• FU 1 year
• Mortality:
– 4.8% losartan
– 8.7% captopril (p=0.035)
• ELITE II
Evaluation of Losartan in the Elderly. Lancet 1997;349:747-52
Treatment – beta blockers
Beta-blockers for CCF
CIBIS-II: cardiac insufficiency bisoprolol study (II)
• >2500 patients
– EF  35% ; NYHA III-IV; 50% IHD
– ~ all on ACE I & diuretics; 50% on digoxin
• Bisoprolol vs. placebo
– Starting dose 1.25mg, gradually  to 10mg od over 4/52
• Study ended prematurely after 1.3 years:
– Annual mortality:
• 8.8% bisoprolol; 13.2% placebo; Hazards Ratio 0.66
• Risk reduction greatest in patients with IHD
Lancet 1999 Jan 02; 353:9-13
Treatment – beta blockers
Patients were largely in NYHA class II-III
Benefits are additive to those conferred by ACEI
Treatment – beta blockers
Treatment – spironolactone
• 1663 patients with:
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Stable CCF NYHA III-IV
LVEF 35%
On ACE I and diuretics
Some also on digoxin
• Spironolactone (25-50mg od) vs. placebo
• Primary endpoint: death from any cause
• Study stopped prematurely:
– 30%  mortality in spironolactone group
• Significant improvement in functional class
Randomized Aldactone Evaluation Study. NEJM 1999;341:709-717
Diagnosing ischaemic heart
disease
• 75% of white males in SOLVD were related
to ischaemic heart disease
• 50% of patients in Framingham had an
ischaemic aetiology to their heart failure
• Identification of patients who will benefit
from revascularisation
Hibernating myocardium
• Chronic LV dysfunction does not
necessarily imply dead myocardium
• “Hibernating myocardium” termed by
Rahimtoola in 1989
• LV systolic function improved following
coronary revascularisation
Rahimtoola. Am Heart J 1989;117:211-21
Hibernating myocardium
Prediction of functional recovery
following revascularisation
Technique
Sensitivity
Specificity
Number of
Patients
Number of
Studies
Tc 99m MIBI
Scanning
83%
69%
207
10
Dobutamine
Stress Echo
84%
81%
448
16
Th 201 Stress
Redistribution
86%
47%
209
7
18F
88%
73%
327
12
90%
54%
145
8
PET
Th 201 Rest
Redistribution
Wijns et al. N Engl J Med 1998;339:173-81
Implications of viable
myocardium
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87 patients with ischaemic CHF, LVEF<0.35
Low dose stress echo
40+/-17 months follow up
37 patients received revascularisation
22 cardiac related deaths
Senior et al. J Am Coll Cardiol 1999;33:1848-54
Implications of viable myocardium
MV - revascularised
MV – med Px
No MV – med Px
No MV - revascularised
Senior et al. J Am Coll Cardiol 1999;33:1848-54
Cardiac failure – services
available at St Mary’s
• Open access ECG / CXR / echocardiography
• Routine outpatients for specialist opinion and
invasive investigation
• Emergency assessment in A+E
• Specialist cardiac failure follow up clinic
• Specialist heart failure nurse
Specialist referral
• Confirm diagnosis
• Invasive assessment to diagnose underlying
ischaemic aetiology
• Addition of beta-blockers and/or
spironolactone
• Management of difficult / deteriorating
cases
Heart failure specialist nurse
• Monitoring weight and blood tests
• Educating patient and family
– Daily weighing
– Self management of diuretics
– Regular exercise
• Promoting long term compliance
• Implementing treatment protocols
Diastolic heart failure
• Up to a third of patients have clinical heart
failure with normal LV systolic function
• Underlying pathophysiology relates to
diastolic dysfunction
• Commonest underlying pathologies
– Normal ageing
– Hypertension
– Myocardial ischaemia
Mechanisms of diastolic
dysfunction
• Impaired ventricular relaxation
– Energy dependent process
– Susceptible to myocardial ischaemia
• Decreased myocardial compliance
– Altered compliance mediated by collagen
– Fibrosis related to activation of RAAS
Doppler patterns of diastolic
dysfunction
• Impaired relaxation
– Reduced E/A ratio
– Increased EDT
– Increased IVRT
• Restriction
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LA pressure increases due to myocardial stiffness
High peak E wave velocity
Short EDT
Very short IVRT
Treatment of diastolic heart
failure
• Treat underlying cause eg ischaemia
• Impaired relaxation
– Theoretically rate-limiting agents effective
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Beta-blockers, verapamil
Reduce HR and prolong diastole
Reduce myocardial oxygen demand
Lower BP and reduce LVH
Treatment of diastolic heart
failure
• Restriction
– Drugs which reduce fibrosis and lower LA
pressure theoretically should be effective
• ACEI
• AII blockers
• Diuretics
– If LA pressure lowered too much cardiac output
significantly worsened
• Can cause significant morbidity