Heart failure: Local solutions for a growing problem

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Heart failure: Local solutions for a growing problem Dr Andrew Hannah Consultant Cardiologist ARI

What is heart failure? A clinical syndrome comprising of dyspnoea, fatigue or fluid retention due to cardiac dysfunction, either at rest or on exertion, with accompanying neurohormonal activation. Braunwald E. heart failure is NOT a final diagnosis and the term should be qualified by the underlying structural abnormality and cause heart failure due to severe aortic stenosis heart failure due to LV systolic dysfunction... due to IHD or due to inherited dilated cardiomyopathy etc etc

The size of the problem Prevalence of heart failure 1 2% of adult population and asymptomatic LVSD 0.4 2% Prevalence and incidence increase with age mean age of HF patient 74years prevalence approx. 8 10% in over 75s have heart failure Approximately 80 000 cases in Scotland or 8000 in Grampian prevalence and incidence are increasing ageing pop, better survival post MI/CHF

Projected HF prevalence in Scotland

Prognosis: Heart Failure vs Cancer Mortality Pancreas Lung Oesophagus Stomach Leukaemia Kidney Ovarian Heart failure Colon NHL Prostate Bladder Uterus Breast Melanoma 0 20 40 60 80 100 One year survival rate (%) The one-year survival rate for heart failure is worse than that for cancer of the breast, uterus, prostate & bladder Coronary heart disease statistics: heart failure supplement., BHF 2002, http://www.heartstats.org, accessed 25.02.04. Based on Quinn M et al. ONS 2001 & Cowie MR et al. Heart 2000; 83: 505-510. NHL= Non-Hodgkins lymphoma

Heart failure: What are we trying to achieve? Improved quality and length of life for patients Reduced hospitalisations and re admissions

How might we achieve this? Make an accurate diagnosis in a timely fashion Perform appropriate investigations: to determine aetiology and prognosis Education: patients, relatives and healthcare professionals Evidence based drug therapy for all Appropriate selection for device therapy (CRT / ICD) or surgery or cardiac transplantation

Heart failure can be easy to diagnose

.but usually it is difficult to diagnose on clinical grounds alone Studies show diagnosis incorrect in approx. 40 50% of cases * Chest crepitations, oedema, tachycardia not specific S3, JVP, displaced apex insensitive, poor inter observer agreement Many patients have symptoms only dyspnoea, fatigue are non specific Therefore objective evidence of cardiac dysfunction mandatory...usually by echo initially But we cannot cope with the volume of echo referrals 600/month at ARI alone *Wheeldon et al QJMed 1993:86:17 24

Are screening tests the answer? 12 Lead ECG LVSD unlikely if ECG normal (85 90% sensitive) Problems with confidence of interpretation in primary care, must be entirely normal or else loses reliability. Low specificity May be normal in other causes of HF BNP (brain (B type) natriuretic peptide) Simple blood test no subjective interpretation difficulties (cw ECG) LVSD virtually excluded if normal / low Much better specificity than the ECG Real world cost approx. 20 per test

Grampian BNP pilot NT pro BNP: more stable than BNP with equally good evidence base Different (higher) normal range Pilot commencing in Grampian Dec 2011 linking the test with the open access echo service Future funding will be dependent on proving cost effectiveness and /or improved patient care

LV systolic dysfunction: not a final diagnosis IHD related LVSD: infarcted, stunned, hibernating?? Dilated cardiomyopathy (LVSD with normal coronary arteries) Inherited: dilated, hypertrophic, ARVC, isolated non compaction Toxins: drugs, alcohol, Infections: prior and acute Immune mediated: viral, peripartum, autoimmune Endocrine: thyroid, phaeochomocytoma Metabolic/infiltrative: amyloid, haemachromatosis, sarcoid, mitochondrial disease muscular dystrophy related Obesity related, diabetic, ESRF Tachycardia related cardiomyopathy: AF/flutter, ventricular ectopic related, PJRT type SVTs Valvular heart disease related LVSD

Improving prognosis in LVSD heart failure

Grading of heart failure

Pharmacological treatment of chronic heart failure (due to LV systolic dysfunction) ACE inhibitors: uptitrated to max tolerated dose Betablockers: bisoprolol or carvedilol.max tolerated dose Aldosterone receptor blockers: spironolactone, eplerenone ARBs: if ACE I inolerant. Candesartan/valsartan Stop agents that exacerbate HF: NSAIDs, verapamil, diltiazem, doxazosin, dronedarone, class I AADs, glitizones Loop diuretics: as low a dose as possible to achieve euvolaemia Warfarin if AF Ivabradine: for some patients in SR if HR>70 despite max tolerated BB Hydralazine / ISDN if ACEI/ARB intolerant Digoxin: sometimes in AF rarely in SR

Betablockers in Heart failure US carvedilol trials NYHA I III (IV) n=1094, 4 separate trials, 65% RRR in mortality CIBIS II bisoprolol NYHA II III n=2647, mortality 11.8% v 17.3% (p<0.0001) MERIT metoprolol CR/XL NYHA II III improved mortality, morbidity and LVEF Betablockers reduce ABSOLUTE annual mortality by 6 8%

Probability of event-free survival 1.00 0.95 0.90 0.85 0.80 0.75 0.70 0.65 0.60 Carvedilol reduces risk of death or cardiovascular hospitalisation 38% reduction in death or hospitalisation p<0.001 Carvedilol Placebo 0 50 100 150 200 250 300 350 Duration of therapy (days) 400 Packer et al, NEJM 1996

Aldosterone receptor blockade Spironolactone 25mg or eplerenone 25 50mg

Spironolactone in NYHA III IV RALES: All Cause Mortality Probability of survival 1.00 0.95 0.90 0.85 0.80 0.75 0.70 0.65 0.60 0.55 Placebo + ACE inhibitor + loop diuretic ± digitalis Risk reduction 30% 95% CI (18%-40%) p < 0.001 Aldosterone receptor antagonist + ACE inhibitor + loop diuretic ± digitalis 0.50 0.45 0 3 6 9 12 15 18 21 24 27 30 33 36 Months Pitt B et al, N Engl J Med 1999; 341: 709-717

EMPHASIS HF: Eplerenone in NYHA II heart failure NYHA II LVEF <30% (severe) LVEF 30 35% if QRS>130ms Outcome Eplerenone (%) Placebo (%) Adjusted hazard ratio (95% CI) p Cardiovascular death/heart-failure hospitalization 18.3 25.9 0.63 (0.54 0.74) <0.001 Cardiovascular death 10.8 13.5 0.76 (0.61 0.94) 0.01 Heart-failure hospitalization 12.0 18.4 0.58 (0.47 0.70) <0.001 Hospitalization for hyperkalemia 0.3 0.2 1.15 (0.25 5.31) 0.85

Safely prescribing spironolactone /eplerenone: avoiding hyperkalaemia Check renal function and potassium before starting Repeat U+Es after 1 week, then 1 month (2 weeks if renal dysfunction or K+>5) Check U+Es 3 monthly Reduce/withold if K+ >5.5, reintroduce at ½dose Advise patients to temporarily stop spiro/epler if intercurrent illness such as D+V / N+V / reduced fluid intake and inform GP/HFSN: must check U+Es

A well treated LVSD patient in 2011.in Grampian. Diuretic BFZ or loop: as low a dose as required ACE I NYHA I IV, max. tolerated dose BB NYHA I IV: carvedilol, bisoprolol stable, compensated HF, start low, go slow: aim for 25mg BD (50mgbd if >85kg) or 10mgOD respectively Spironolactone 25mg NYHA III IV, watch potassium/renal function Spironolactone or eplerenone NYHA II with severe LVSD esp if LBBB Candasartan/valsartan good alternatives to ACE I if ACE I intolerant. Hydralazine/nitrate if ACE I/ARB intolerant (usually renal failure) Ivabradine: if HR >70bpm despite max tolerated BB, and particularly consider in asthmatic patients

Beyond pharmacological therapy CRTs and ICDs

Cardiac resynchronisation therapy (CRT) the theory In patients with CHF and LBBB not only is there poor LV contraction but dyssynchronous contraction LBBB patients have a poorer prognosis: increased rate of HF and sudden arrhythmic deaths Cardiac resynchronisation therapy can improve these factors and increase cardiac performance Biventricular pacing +/ ICD

CRT (cardiac resynchronisation therapy): Biventricular pacemaker

CARE HF n=813, NYHA III IV LVSD and LBBB Death/hosp for MACE: 224 (55%) in medical and 159 (39%) in CRT (HR 0.63, 0.51 0.77 p<0.001) Death: 120 (30%) in medical and 82 (20%) in CRT (HR 0.64,0.48 0.85) Death and HF hosp: 191 (47%) in medical group vs 118 (29%) in CRT (HR 0.54, 0.43 0.68 p<0.01)

Which patients should be considered for CRT? NYHA III IV despite maximum (tolerated) medical therapy No major co morbidity likely to be fatal in next 6 12 months or likely to be major contributor to poor QOL/SOB Evidence of conduction abnormalities (ideally LBBB) Age is not a contraindication

Mechanisms of death in CHF

Implantable cardioverter defibrillators: ICDs Implanted as per a pacemaker: local anaesthesia and sedation RV lead has a shocking coil and generator has defibrillator capacity Once inserted VF induced and device tested Secondary prevention well established: what about primary prevention?

What does NICE recommend? Ischaemic cardiomyopathies, >4 weeks post MI, NYHA < IV LVEF <35 % and NSVT on holter and inducible VT on EP testing LVEF<30% and QRS>120ms

Reducing HF admissions: why and how?

Hospitalisation for decompensated HF: an important event c10% in hospital mortality Mean 12 14 days in hospital stay c30% readmission rate by 3 months c15% 3 month mortality

Healthcare Improvement Scotland (QIS) and SPSP recommendations for in patients with HF 1.Evidence based drug therapies 2.HF specialist nurse review 3.HF specialist review: treat acute decompensation/consider precipitating factors/ consider specialist investigation, drug therapy optimisation and consider CRT device if appropriate

HF Specialist Nurse Intervention Time to first event (death from any cause or hospital admission for heart failure) in usual care and nurse intervention groups Blue et al BMJ 2001; 323: 715 8

The role of the heart failure specialist nurse Patient education Compliance, fluid balance awareness, daily weights, exercise, reduced anxiety Optimisation of drug therapy Contact point for patients All these contribute to less decompensations and earlier presentation: results in fewer hospitalisations and shorter admissions

Scottish National HF Audit 2008: n=1235

Scottish National HF Audit 2008 Table 9 Age adjusted in hospital mortality rates by specialty Specialty N Mean age (years) Deaths (% dead) Odds ratio (95% CI) p value Cardiology 400 72.4 13.0% Reference Care of the elderly 51 84.4 19.6% 1.07 0.9 General 760 78.4 20.0% 1.36 0.08

Grampian strategy to reducing readmissions Starting point: 30% re admission rate for decompensated HF at 3 months 17.7% in hospital mortality rate (national audit) HFSN review during admission and early post discharge Inpatient review /management by cardiologist / HF specialist Avoid stopping important drugs during decompensations esp betablockers Accurate, informative (and legible) interim DC letters GP review early post discharge Good patient education: self management, daily weight Optimise drug therapy post discharge Early cardiology clinic review for most Consider CRT devices in timely fashion

Trial trends in 1 year mortality in NYHA III/IV CHF 70 60 50 40 30 placebo therapy 20 10 0 CONSENSUS RALES COPERNICUS 1987 1999 2001 2005 CARE-HF

HFSN referrals 2011 Patient Referrals 35 30 Number of individuals 25 20 15 10 5 0 Jan Feb Mar Apr May Jun 2011

Reasons for optimism in Grampian? Improved diagnostic pathway with BNP Fastrack HF clinic for those at high risk HFSN referrals are up dramatically, hopefully leading to improved early post discharge care and fewer re admissions Renewed focus on HF in primary care: QOF pathway for HF finalised yesterday Active CRT service in ARI: improving pathways of care will result in higher referral rates