1. Developments in heart failure management and clinical practice in the UK Jamil Mayet Department of Cardiology St Mary’s Hospital

3. Problems in heart failure management Accurate diagnosisAccurate diagnosis Optimising drug therapyOptimising drug therapy Identification of patients who will benefit from revascularisationIdentification of patients who will benefit from revascularisation

5. Cardiac failure - diagnosis

6. Electrocardiogram If ECG normal very unlikely to be systolic dysfunction

7. Echocardiography Confirms / refutes diagnosis of systolic dysfunctionConfirms / refutes diagnosis of systolic dysfunction Can exclude significant valvular diseaseCan exclude significant valvular disease Can suggest ischaemic aetiology if regional wall motion abnormalityCan suggest ischaemic aetiology if regional wall motion abnormality Can assess diastolic dysfunctionCan assess diastolic dysfunction

8. Easy access to investigations GP educationGP education –Every patient with possible cardiac failure should be considered for echocardiography Open and rapid access to echocardiographyOpen and rapid access to echocardiography Clear user-friendly reportsClear user-friendly reports –“Mild MR; this is not clinically significant” –“In the absence of clinical contra-indications…”

9. Optimising drug therapy ACE inhibitorsACE inhibitors –High doses used in clinical trials –If cough AII antagonists –If contra-indications hydralazine/nitrates Beta blockersBeta blockers SpironolactoneSpironolactone

11. ACE inhibitor doses used in large controlled trials CONSENSUSEnalapril20mg*CONSENSUSEnalapril20mg* V-HeFT IIEnalapril10mg*V-HeFT IIEnalapril10mg* SOLVDEnalapril10mg*SOLVDEnalapril10mg* SAVECaptopril50mg**SAVECaptopril50mg** *twice daily**three times a day ATLAS study showed significant decrease in mortality+hospital admissions in high dose versus low dose lisinoprilATLAS study showed significant decrease in mortality+hospital admissions in high dose versus low dose lisinopril

12. Treatment – AII antagonists ELITE STUDYELITE STUDY 722 patients  65 years with:722 patients  65 years with: –CCF (NYHA class II-IV) –LVEF  40% Captopril vs. losartanCaptopril vs. losartan FU 1 yearFU 1 year Mortality:Mortality: –4.8% losartan –8.7% captopril (p=0.035) ELITE IIELITE II Evaluation of Losartan in the Elderly. Lancet 1997;349:747-52

14. Treatment – beta blockers

15. Beta-blockers for CCF CIBIS-II: cardiac insufficiency bisoprolol study (II) >2500 patients>2500 patients –EF  35% ; NYHA III-IV; 50% IHD –~ all on ACE I & diuretics; 50% on digoxin Bisoprolol vs. placeboBisoprolol vs. placebo –Starting dose 1.25mg, gradually  to 10mg od over 4/52 Study ended prematurely after 1.3 years:Study ended prematurely after 1.3 years: –Annual mortality: 8.8% bisoprolol; 13.2% placebo; Hazards Ratio 0.668.8% bisoprolol; 13.2% placebo; Hazards Ratio 0.66 Risk reduction greatest in patients with IHDRisk reduction greatest in patients with IHD Lancet 1999 Jan 02; 353:9-13

16. Treatment – beta blockers Patients were largely in NYHA class II-III Benefits are additive to those conferred by ACEI

17. Treatment – beta blockers

18. Treatment – spironolactone 1663 patients with:1663 patients with: –Stable CCF NYHA III-IV –LVEF  35% –On ACE I and diuretics –Some also on digoxin Spironolactone (25-50mg od) vs. placeboSpironolactone (25-50mg od) vs. placebo Primary endpoint: death from any causePrimary endpoint: death from any cause Study stopped prematurely:Study stopped prematurely: – 30%  mortality in spironolactone group Significant improvement in functional class Significant improvement in functional class Randomized Aldactone Evaluation Study. NEJM 1999;341:709-717

19. Diagnosing ischaemic heart disease 75% of white males in SOLVD were related to ischaemic heart disease75% of white males in SOLVD were related to ischaemic heart disease 50% of patients in Framingham had an ischaemic aetiology to their heart failure50% of patients in Framingham had an ischaemic aetiology to their heart failure Identification of patients who will benefit from revascularisationIdentification of patients who will benefit from revascularisation

20. Hibernating myocardium Chronic LV dysfunction does not necessarily imply dead myocardiumChronic LV dysfunction does not necessarily imply dead myocardium “Hibernating myocardium” termed by Rahimtoola in 1989“Hibernating myocardium” termed by Rahimtoola in 1989 LV systolic function improved following coronary revascularisationLV systolic function improved following coronary revascularisation Rahimtoola. Am Heart J 1989;117:211-21

21. Hibernating myocardium

22. Prediction of functional recovery following revascularisation TechniqueSensitivitySpecificity Number of Patients Studies Tc 99m MIBI Scanning83%69%20710 Dobutamine Stress Echo 84%81%44816 Th 201 Stress Redistribution86%47%2097 18 F PET 88%73%32712 Th 201 Rest Redistribution90%54%1458 Wijns et al. N Engl J Med 1998;339:173-81

23. Implications of viable myocardium 87 patients with ischaemic CHF, LVEF<0.3587 patients with ischaemic CHF, LVEF<0.35 Low dose stress echoLow dose stress echo 40+/-17 months follow up40+/-17 months follow up 37 patients received revascularisation37 patients received revascularisation 22 cardiac related deaths22 cardiac related deaths Senior et al. J Am Coll Cardiol 1999;33:1848-54

24. MV - revascularised MV – med Px No MV – med Px No MV - revascularised Implications of viable myocardium Senior et al. J Am Coll Cardiol 1999;33:1848-54

25. Cardiac failure – services available at St Mary’s Open access ECG / CXR / echocardiographyOpen access ECG / CXR / echocardiography Routine outpatients for specialist opinion and invasive investigationRoutine outpatients for specialist opinion and invasive investigation Emergency assessment in A+EEmergency assessment in A+E Specialist cardiac failure follow up clinicSpecialist cardiac failure follow up clinic Specialist heart failure nurseSpecialist heart failure nurse

26. Specialist referral Confirm diagnosisConfirm diagnosis Invasive assessment to diagnose underlying ischaemic aetiologyInvasive assessment to diagnose underlying ischaemic aetiology Addition of beta-blockers and/or spironolactoneAddition of beta-blockers and/or spironolactone Management of difficult / deteriorating casesManagement of difficult / deteriorating cases

27. Heart failure specialist nurse Monitoring weight and blood testsMonitoring weight and blood tests Educating patient and familyEducating patient and family –Daily weighing –Self management of diuretics –Regular exercise Promoting long term compliancePromoting long term compliance Implementing treatment protocolsImplementing treatment protocols

28. Diastolic heart failure Up to a third of patients have clinical heart failure with normal LV systolic functionUp to a third of patients have clinical heart failure with normal LV systolic function Underlying pathophysiology relates to diastolic dysfunctionUnderlying pathophysiology relates to diastolic dysfunction Commonest underlying pathologiesCommonest underlying pathologies –Normal ageing –Hypertension –Myocardial ischaemia

29. Mechanisms of diastolic dysfunction Impaired ventricular relaxationImpaired ventricular relaxation –Energy dependent process –Susceptible to myocardial ischaemia Decreased myocardial complianceDecreased myocardial compliance –Altered compliance mediated by collagen –Fibrosis related to activation of RAAS

31. Doppler patterns of diastolic dysfunction Impaired relaxation –Reduced E/A ratio –Increased EDT –Increased IVRT Restriction –LA pressure increases due to myocardial stiffness –High peak E wave velocity –Short EDT –Very short IVRT

33. Treatment of diastolic heart failure Treat underlying cause eg ischaemiaTreat underlying cause eg ischaemia Impaired relaxationImpaired relaxation –Theoretically rate-limiting agents effective Beta-blockers, verapamilBeta-blockers, verapamil Reduce HR and prolong diastoleReduce HR and prolong diastole Reduce myocardial oxygen demandReduce myocardial oxygen demand Lower BP and reduce LVHLower BP and reduce LVH

34. Treatment of diastolic heart failure RestrictionRestriction –Drugs which reduce fibrosis and lower LA pressure theoretically should be effective ACEIACEI AII blockersAII blockers DiureticsDiuretics –If LA pressure lowered too much cardiac output significantly worsened Can cause significant morbidityCan cause significant morbidity