The Failing Heart - RCP London

Dr Alex SimmsConsultant Cardiologist @LTHT

Specialist interest in Heart Failure, Devices, Inherited Cardiovascular Conditions and Pregnancy & heart disease

The Failing Heart

Outline

• Definition

• Why important

• What you need to know

What is heart failure?

A clinical syndrome with typical symptoms/signs caused by structural and/or functional cardiac abnormality,

resulting in a reduced cardiac output or elevated intracardiac pressures at rest/stress

ESC HF guidelines. EHJ 2016; 37:2129


HF reduced EF HF mildly reduced EF HF preserved EF

EF≤40% EF>40-49%+ ↑BNP

+ LVH, LAE or diastolic dysfunction

EF>50%+ ↑BNP

+ LVH, LAE or diastolic dysfunction

Limited evidence base for treatment

Exclude other causes

ESC HF guidelines. EHJ 2016; 37:2129


Reduced EF Preserved EF

Diastolic HFSystolic HF

Burden of heart failure

~1 million have HF in

UK

Cost ~£2.3 billion/year

Leading cause

admission >65 years

5% all hospital

admissions

£4K per admission

~2% have HF [WHO]

2% all NHS bed-days

70% costs due to

hospital admission


1. Conrad N et al. Lancet 2018;391:572;2. NICE: Chronic heart failure in adults:

management. CG108. 2010

↑12% HF incidence 2002-20141

Incidence HF = combined total 4 commonest cancers2

HF admissions ↑ ~50% in next 25 years2


Adapted from Gheorghiade M, et al. Am J Cardiol. 2005;96(6A):11G-17G.

Disease Progression

Cardiac Function

Chronic decline

Hospitalisation for acutedecompensation episodes

Conrad N et al. Lancet 2018;391:572–580

Outcomes in heart failure

Acute admission with HF

NICOR National Heart Failure Audit 2015/2016 Annual Report

18.7% 1-year mortality

70.5%

48.5%

10-year mortality

5-year mortality

In Primary Care (CHF)Taylor CJ et al. Family Practice 2017;34:161.


0 20 40 60 80 100

Prostate

Bladder

HF

Colorectal

Lung

5-year survival (%)

Men

0 20 40 60 80 100

Breast

Colorectal

HF

Ovarian

Lung

5-year survival (%)

Women

Mamas MA et al. Eur J Heart Fail 2017;19:1095–1104.

5-year survival


Mamas MA et al. Eur J Heart Fail 2017;19:1095–1104.

Heart failure

Sudden death

Other CV death

Other non-CV death


Hobbs F, et al. EHJ 2002;23:1867

Calvert MJ et al. Eur J Heart Fail 2005;7:243

Causes of heart failure

Ischaemic heart diseaseValvular heart diseaseHypertension

Idiopathic/Inherited (familial) DCMMyocarditisChemotherapy relatedAlcohol abusePeripartum cardiomyopathyTachycardiomyopathyInfiltrative (e.g. Sarcoid/amyloid)HIVEndocrine (DM)Muscle disorders

Reduced EF

Decreasing frequency

Preserved EF

Diabetes Mellitus

Pathophysiology of heart failure

Injury to myocardium

e.g: myocardial infarction

↑ myocyte stretch

↑ force contraction

↑ LV end diastolic pressure and volume

↓ Stroke Volume (↓Cardiac output)

Ventricular remodelling

Neurohormonal response in heart failure

↓Cardiac output

↓organ perfusion pressure

Baroceptors

Release Renin (Angiotensin II) – RAAS system activatedRelease ADH

Release Norepinephrine – SNS activated


RAAS activation

Activation Angiotensin IIRelease Aldosterone

Release ADH

Fluid and salt retentionVasoconstriction

SNS activation

Release Adrenaline & Noradrenaline

↑ sympathetic tone

↑heart rateVasoconstriction


Response Short term effects Longer term consequences

Salt and water retention

Augments preload Pulmonary congestion, fluid overload

Vasoconstriction Maintains BP for perfusion of organs

Exacerbates pump failure (excessive afterload), increases cardiac energy expenditure

Sympathetic stimulation

Increases HR and initially ejection fraction

Increases energy expenditureand risk of dysrhythmia and sudden cardiac death

Pressure overload

Left ventricular hypertrophy

Fibrosis

Longitudinal function reduction

Reduction in LV compliance

Volume overload

Left ventricular dilatation

Mitral annulus dilatation

Sarcomeric stretch

Reduction in LVEF

Ventricular remodelling

Vasoconstriction

Increased afterload

Salt and water retention

Cycle of contractility


Mechanical stretch of cardiac chambers

Release of natriuretic peptides

Vasodilatation Wedge pressure RAP SVR

Natriuresis and Diuresis Renal function Diuresis

Cellular effects Hypertrophy Fibrosis

Pathophysiology and drugs

↓ perfusion pressure in HF

Renin

Angiotensinogen Angiotensin I

Angiotensin II

ACE

Vasoconstriction

↑ Aldosterone

↑ ADH

RAAS activation

SNS activation

Natriuretic peptides

↑ Cardio-stretch

Neprilysin

Β-blockers

ACEi

ARB

MRA

Sacubitril/Valsartan

Pathophysiology of HFpEF

Increased “stiffness” myocardiumDecreased relaxation time

↑ filling pressures

↑LA pressures and dilatation

↑pulmonary & RH pressures

Restrictive Cardiomyopathy

Problem with HFpEF

The Medical Registrar

What you need to know about HF

Diagnosing Heart

Failure

Clinical features Sensitivity (%)

Specificity (%)

PPV (%)

Dyspnoea 66 52 23

Orthopnoea 21 81 2

PND 33 76 26

Oedema 23 80 22

Tachycardia 7 99 6

Chest Crackles 13 91 27

Oedema 10 93 3

Gallop (S3) 31 95 61

Elevated JVP 10 97 2

Cardiomegaly CXR 62 67 32

NTproBNP >400ng/L 99 43NPV PPV

98 64

Watson et al. BMJ 2000;320:236-239.

Ludman et al. BMJ 2015;350:h910.

Fatigue

“new” Suspected

AHFECG - abnormal

CXR – congestion/PO

NT pro BNP

FBC, U&Es, TFTs, Calcium, LFTS, CRP

Echocardiogram

AHF Likely Not sure

<300ng/L>300ng/L

HF not likely

Suspected “new” AHF

NICE Quality Standards for AHF 2015

1. Adults PC new suspected acute heart failure have a single measurement of NT pro BNP.

2. Adults suspected acute heart failure and NT pro BNP have ECHO <48 hours of admission.

3. Adults with AHF have input <24 hours of admission from a dedicated specialist heart failure team.

AHF for the Medical Reg

Acute HF Decompensated HFLook sick, rapid onset More time

Congested (pulmonary oedema) Congested (peripheral oedema)

Hypoperfused (cold) Perfused (warm)

Hypotensive Normotensive/hypotensive

Cardiogenic shock

Managing Cardiogenic shock

Buying time to recover

Managing Cardiogenic Shock

IV Diuretics – stat 50-100mg Frusemide

IV morphine

Avoid IV GTN unless high BP

Early Cardiology/ITU involvement


NIV or intubation/ventilation

N Engl J Med 2008; 359:142-151


Inotropes +/- Vasopressors

Dobutamine, dopamine, milrinone, noradrenalin, Levosimendan

JACC 2003; 41: 997-1003


IABP

N Engl J Med 2012; 367:1287-1296


Mechanical circulatory supportECMO/BIVAD

Advanced Heart FailureLong term LVAD/Cardiac Tx

Buying time to recovery

Managing Cardiogenic ShockHeartMate III = 77%

Managing Decompensated HF

Most patients ~90%

Treatment Goals

1. Improve symptoms and QoL2. Avoid hospitalisations and decompensations3. Improve prognosis/outcomes

Managing Decompensated HF

Decongest (diuretics)

Optimise treatments

Appropriate care

Diuresis in Decompensated HF

• Loop diuretic, Bumetamide>frusemide

• Start low and increase (naïve)

• Double dose (prior use)

• IV – if oedema above knee or no response to PO 24hrs

• Aim loss 1Kg/24h – daily weights imperative

Diuresis: Bolus vs Infusion?

DOSE trial. NEJM 2011;364:797

DRAIN Trial

Infusion Bolus P value

Free from Congestion

48% 25% 0.04

UO/72h 10,020ml 8,612ml 0.04

DRAIN trial. Clin Res Cardiol 2019

Diuresis in Decompensated HF

• Convert IV to PO – oedema below knees/weight ↓

• Give higher PO than IV

• 48h PO prior discharge

• Do not fluid restrict (unless refractory)

• Refractory: add MRA or thiazide (metolazone)

• No evidence to support Ultrafiltration over diuretics

• Aim for Euvolaemia before discharge

1985 1990 1995 2000 2005 2010 2015

V-HeFT IHydralazine and

isosorbide dinitratevs placebo or prazosin

CONSENSUSEnalapril vs placebo V-HeFT II

Enalapril vs hydralazineand isosorbide dinitrate

SOLVD-TEnalapril vs placebo

SOLVD-PEnalapril vs placebo

Packer et al.Carvedilol vs

placebo

DIGDigoxin vs placebo

RALESSpironolactone vs

placebo

Val-HeFTValsartan vs

placebo

REMATCHLVAD vs medical

therapy alone

COPERNICUSCarvedilol vs placebo

COMPANIONCRT-D vs CRT-P

A-HeFTHydralazine and

isosorbide dinitratevs placebo

CARE-HFCRT vs medical therapy alone

SCD-HeFTICD vs amiodarone

or placebo

SHIFT2

Ivabradine vs placebo

MADIT-CRTCRT-D vs ICD

PARADIGM-HFEntresto (sacubitril / valsartan)

vs enalapril

EMPHASIS-HFEplerenone vs placebo

RAFTCRT-D vs ICD

EchoCRTCRT turned on vs off

ACEi or ARB Hydralazine or nitrate

βB

MRA

Devices

Other inventions

1. Sacks CA et al. New Engl J Med 2014;371:989-991; 2. Swedberg K et al. Lancet 2010;376;875-885.

Optimising treatment in Decompensated HF

Treatment of HFrEF

81. ACE inhibitors/ARBs

2. Beta-blockers

3. Mineralocorticoid receptor antagonists

4. Cardiac resynchronisation therapy

5. Implantable cardioverter defibrillator

Class I evidence A

Class I evidence B

6. Entresto/ARNIs

Class II evidence B

7. Ivabradine

Class II evidence C

8. LVAD/Cardiac Transplant

Evidenced based treatments

• Improve Prognosis

• Lower Hospital admissions

• Improve QoL/Symptoms



Think HR control!

Sinus rhythm: 60 bpm

AF: 70 - 80 bpm


Ivabradine: If LVEF<35% (or intolerant BB) + NYHA II + HR>70


Sacubitril/Valsartan (Entresto): LVEF<35% + NYHA II + ACEi




Cardiac Resynchronisation therapy (CRT)

OMTNot improving

In AHF would not consider ICD


Think iron deficiency

Iron deficiency defined:

• Ferritin <100 μg/L or

• 100-300 if Tsats<20%CONFIRM HF EHJ 2015;36:657-68

Optimising care of AHF

AKI or WRF Hyponatraemia Hypotension

Expect it! Poor prognosisTreat patient not

number

↑30% Creattemporarily stop RAASi

Congestion = diluted, needs diuretic

Stop non-HF antiHTNmedications

Congested, don’t stop diuretic, give more

Congested = continue RAASi

Prioritise aims, if congested – diuretics

most important


3. Adults with AHF have input <24 hours of admission from a dedicated specialist heart failure team.

Heart Failure Out Reach Service

Community HF Service


End stage HF (Palliative care)

ACEi/ARB/ARNi, BB, MRA

CRT/ICDs

Diuretics

LVADs/Cardiac Tx

SGLT2i

AF Ablation

MitraClip

Palliative Care

Treatments for underDx conditions,

e.g. TTR

Remote patient care strategies

Life long care

Outline

• Definition

• Why important

• What you need to know

Thankyou

The Failing Heart - RCP London

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