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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 • • • • 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: – – – – 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 • • • • • 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 – – – – 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 • • • • 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