developments in heart failure management and clinical practice in the uk

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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. - PowerPoint PPT Presentation

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Developments in heart failure Developments in heart failure management and clinical practice management and clinical practice

in the UKin the UK

Jamil MayetJamil Mayet

Department of CardiologyDepartment of Cardiology

St Mary’s HospitalSt Mary’s Hospital

Problems in heart failure Problems in heart failure managementmanagement

• Accurate diagnosisAccurate diagnosis

• Optimising drug therapyOptimising drug therapy

• Identification of patients who will benefit Identification of patients who will benefit from revascularisationfrom revascularisation

Heart failure therapy - rule of halves

Treatment - no CCF

CCF - inadequatetherapy

CCF -appropriatetherapy

Cardiac failure - diagnosisCardiac failure - diagnosis

ElectrocardiogramElectrocardiogram

If ECG normal very unlikely to be systolic dysfunctionIf ECG normal very unlikely to be systolic dysfunction

EchocardiographyEchocardiography

• Confirms / refutes diagnosis of systolic Confirms / refutes diagnosis of systolic dysfunctiondysfunction

• Can exclude significant valvular diseaseCan exclude significant valvular disease• Can suggest ischaemic aetiology if regional Can suggest ischaemic aetiology if regional

wall motion abnormalitywall motion abnormality• Can assess diastolic dysfunctionCan assess diastolic dysfunction

Easy access to investigationsEasy access to investigations

• GP educationGP education– Every patient with possible cardiac failure should Every patient with possible cardiac failure should

be considered for echocardiographybe 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”Mild MR; this is not clinically significant”– ““In the absence of clinical contra-indications…”In the absence of clinical contra-indications…”

Optimising drug therapyOptimising drug therapy

• ACE inhibitorsACE inhibitors– High doses used in clinical trialsHigh doses used in clinical trials– If cough AII antagonistsIf cough AII antagonists– If contra-indications hydralazine/nitratesIf contra-indications hydralazine/nitrates

• Beta blockersBeta blockers

• SpironolactoneSpironolactone

ACE inhibitor doses used in large ACE inhibitor doses used in large controlled trialscontrolled trials

• CONSENSUSCONSENSUS EnalaprilEnalapril 20mg*20mg*• V-HeFT IIV-HeFT II EnalaprilEnalapril 10mg*10mg*• SOLVDSOLVD EnalaprilEnalapril 10mg*10mg*• SAVESAVE CaptoprilCaptopril 50mg**50mg***twice daily*twice daily **three times a day**three times a day

• ATLAS study showed significant decrease in ATLAS study showed significant decrease in mortality+hospital admissions in high dose mortality+hospital admissions in high dose versus low dose lisinoprilversus low dose lisinopril

Treatment – AII antagonistsTreatment – AII antagonists• ELITE STUDYELITE STUDY

• 722 patients 722 patients 65 years with:65 years with:– CCF (NYHA class II-IV)CCF (NYHA class II-IV)– LVEF LVEF 40% 40%

• Captopril vs. losartanCaptopril vs. losartan• FU 1 yearFU 1 year• Mortality:Mortality:

– 4.8% losartan 4.8% losartan – 8.7% captopril (p=0.035)8.7% captopril (p=0.035)

• ELITE IIELITE IIEvaluation of Losartan in the Elderly. Lancet 1997;349:747-52Evaluation of Losartan in the Elderly. Lancet 1997;349:747-52

Treatment – beta Treatment – beta blockersblockers

Beta-blockers for CCFBeta-blockers for CCF

CIBIS-II: cardiac insufficiency bisoprolol study (II)CIBIS-II: cardiac insufficiency bisoprolol study (II)• >2500 patients>2500 patients

– EF EF 35% ; NYHA III-IV; 50% IHD 35% ; NYHA III-IV; 50% IHD– ~ all on ACE I & diuretics; 50% on digoxin~ all on ACE I & diuretics; 50% on digoxin

• Bisoprolol vs. placeboBisoprolol vs. placebo– Starting dose 1.25mg, gradually Starting dose 1.25mg, gradually to 10mg od over 4/52 to 10mg od over 4/52

• Study ended prematurely after 1.3 years:Study ended prematurely after 1.3 years:– Annual mortality: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; 353:9-13Lancet 1999 Jan 02; 353:9-13

Treatment – beta blockersTreatment – beta blockers

Patients were largely in NYHA class II-IIIPatients were largely in NYHA class II-III

Benefits are additive to those conferred by ACEI Benefits are additive to those conferred by ACEI

Treatment – beta blockersTreatment – beta blockers

Treatment – spironolactoneTreatment – spironolactone• 1663 patients with:1663 patients with:

– Stable CCF NYHA III-IVStable CCF NYHA III-IV

– LVEF LVEF 35%35%

– On ACE I and diureticsOn ACE I and diuretics

– Some also on digoxinSome also on digoxin

• SpironolactoneSpironolactone (25-50mg od) vs. (25-50mg od) vs. placeboplacebo• Primary endpoint:Primary endpoint: death from any cause death from any cause• Study stopped prematurely:Study stopped prematurely:

– 30% 30% mortality in spironolactone group mortality in spironolactone group

• Significant improvement in functional classSignificant improvement in functional class

Randomized Aldactone Evaluation Study. NEJM 1999;341:709-717Randomized Aldactone Evaluation Study. NEJM 1999;341:709-717

Diagnosing ischaemic heart Diagnosing ischaemic heart diseasedisease

• 75% of white males in SOLVD were related 75% of white males in SOLVD were related to ischaemic heart diseaseto ischaemic heart disease

• 50% of patients in Framingham had an 50% of patients in Framingham had an ischaemic aetiology to their heart failureischaemic aetiology to their heart failure

• Identification of patients who will benefit Identification of patients who will benefit from revascularisationfrom revascularisation

Hibernating myocardiumHibernating myocardium

• Chronic LV dysfunction does not Chronic LV dysfunction does not necessarily imply dead myocardiumnecessarily imply dead myocardium

• ““Hibernating myocardium” termed by Hibernating myocardium” termed by Rahimtoola in 1989Rahimtoola in 1989

• LV systolic function improved following LV systolic function improved following coronary revascularisationcoronary revascularisation

Rahimtoola. Am Heart J 1989;117:211-Rahimtoola. Am Heart J 1989;117:211-2121

Hibernating myocardiumHibernating myocardium

Prediction of functional recovery Prediction of functional recovery following revascularisationfollowing revascularisation

TechniqueTechnique SensitivitySensitivity SpecificitySpecificity Number ofNumber of

PatientsPatients

Number ofNumber of

StudiesStudies

Tc 99m MIBITc 99m MIBI

ScanningScanning

83%83% 69%69% 207207 1010

DobutamineDobutamine

Stress EchoStress Echo

84%84% 81%81% 448448 1616

Th 201 StressTh 201 Stress

RedistributionRedistribution

86%86% 47%47% 209209 77

1818F PETF PET 88%88% 73%73% 327327 1212

Th 201 RestTh 201 Rest

RedistributionRedistribution

90%90% 54%54% 145145 88

Wijns et al. N Engl J Med 1998;339:173-81Wijns et al. N Engl J Med 1998;339:173-81

Implications of viable Implications of viable myocardiummyocardium

• 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;33:1848-54Senior et al. J Am Coll Cardiol 1999;33:1848-54

MV - revascularisedMV - revascularised

MV – med PxMV – med PxNo MV – med PxNo MV – med PxNo MV - revascularisedNo MV - revascularised

Implications of viable myocardiumImplications of viable myocardium

Senior et al. J Am Coll Cardiol 1999;33:1848-54Senior et al. J Am Coll Cardiol 1999;33:1848-54

Cardiac failure – services Cardiac failure – services available at St Mary’savailable at St Mary’s

• Open access ECG / CXR / echocardiographyOpen access ECG / CXR / echocardiography

• Routine outpatients for specialist opinion and Routine outpatients for specialist opinion and invasive investigationinvasive 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

Specialist referralSpecialist referral

• Confirm diagnosisConfirm diagnosis

• Invasive assessment to diagnose underlying Invasive assessment to diagnose underlying ischaemic aetiologyischaemic aetiology

• Addition of beta-blockers and/or Addition of beta-blockers and/or spironolactonespironolactone

• Management of difficult / deteriorating Management of difficult / deteriorating casescases

Heart failure specialist nurseHeart failure specialist nurse

• Monitoring weight and blood testsMonitoring weight and blood tests

• Educating patient and familyEducating patient and family– Daily weighingDaily weighing– Self management of diureticsSelf management of diuretics– Regular exerciseRegular exercise

• Promoting long term compliancePromoting long term compliance

• Implementing treatment protocolsImplementing treatment protocols

Diastolic heart failureDiastolic heart failure

• Up to a third of patients have clinical heart Up to a third of patients have clinical heart failure with normal LV systolic functionfailure with normal LV systolic function

• Underlying pathophysiology relates to Underlying pathophysiology relates to diastolic dysfunctiondiastolic dysfunction

• Commonest underlying pathologies Commonest underlying pathologies – Normal ageingNormal ageing– HypertensionHypertension– Myocardial ischaemiaMyocardial ischaemia

Mechanisms of diastolic Mechanisms of diastolic dysfunctiondysfunction

• Impaired ventricular relaxationImpaired ventricular relaxation– Energy dependent processEnergy dependent process– Susceptible to myocardial ischaemiaSusceptible to myocardial ischaemia

• Decreased myocardial complianceDecreased myocardial compliance– Altered compliance mediated by collagenAltered compliance mediated by collagen– Fibrosis related to activation of RAASFibrosis 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 Treatment of diastolic heart failurefailure

• Treat underlying cause eg ischaemiaTreat underlying cause eg ischaemia

• Impaired relaxationImpaired relaxation– Theoretically rate-limiting agents effectiveTheoretically 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

Treatment of diastolic heart Treatment of diastolic heart failurefailure

• RestrictionRestriction– Drugs which reduce fibrosis and lower LA Drugs which reduce fibrosis and lower LA

pressure theoretically should be effectivepressure theoretically should be effective• ACEIACEI• AII blockersAII blockers• DiureticsDiuretics

– If LA pressure lowered too much cardiac output If LA pressure lowered too much cardiac output significantly worsenedsignificantly worsened

• Can cause significant morbidityCan cause significant morbidity

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