disclosures heart failure in women · heart failure therapy treatment of underlying cause...

1

Heart failure in Women

The Melbourne Women’s and Children’s

Update 2018

Dr Hendrik Zimmet MBBS FRACP FCSANZ

Heart Failure Cardiologist

Associate Clinical Dean, Monash University Central Clinical School Epworth

Clinical Senior Lecturer, University of Melbourne

Disclosures

Speaking Honoraria

- Bristol-Myers Squibb

- Menarini

- Novartis

- Pfizer

- Vifor

- ZOLL

Sponsorship

- AstraZeneca

- Merck Sharp & Dohme

- Menarini

- Servier

2

Site Principal Investigator

- AMGEN

Advisory Board Membership

- Otsuka

SUMMARY

Terminology

Heart Failure in Women

ARNIs (ie. Entresto)

SGLT2 Inhibitors

Heart Failure in Pregnancy

3

TERMINOLOGY

“Heart Failure”

- a very frightening term

What does your patient think when they

hear this?

• mortally challenged

• kidney failure = dialysis

liver failure = transplant

heart failure = ??

5

“Heart Failure”

- a very frightening term

Rephrasing and explaining

•“The term "heart failure" is misleading”

• “It does NOT mean the heart has "failed" or stopped

working.”

• “It simply means that your heart does not work as well

as it should.”

• “Heart Dysfunction”

6

2

DEFINITIONS

Heart Failure is a SYNDROME

not a single disease

• combination of typical

symptoms and signs

• due to a number of different

underlying heart disorders

8

CAUSES OF HF

Causes of Heart Failure

Ischaemic Heart Disease

Hypertension

Valvular Heart Disease

Cardiomyopathy– Acute (typically myocarditis)

– Dilated

– Hypertrophic

– Restrictive

High-output Cardiac Failure– Tachycardia-induced

– Thyroid, other

Pericardial

10

CATEGORIZATION HFREF VS HFPEF

3

Ventricular Function

In Heart Failure

Systolic (HFREF - HF with reduced EF)

vs

Diastolic

- HF with preserved ejection fraction (HFPEF)

13

Systolic HF (aka HFREF)

• Heart failure with reduced left

ventricular ejection fraction

(ie. LVEF <50%)

• decreased ability of the heart

to contract

14

Diastolic HF (aka HFPEF)

• Patients with symptoms & signs of heart

failure and preserved LVEF (ie. LVEF >50%)

• Also known as HFPEF(heart failure with

preserved ejection fraction)

• decreased ability of the heart to fill, typically

due to impaired myocardial relaxation

15

Definition of HFrEF and HFpEF

HFpEF: heart failure with preserved ejection fraction; HFrEF: heart failure with reduced ejection

fraction; LVEF: left ventricular ejection fraction

Steinberg et al. Circulation 2012;126:65–75

0% 20% 40% 60% 80% 100%

Definite HFpEF

(LVEF ≥50%)

Definite HFrEF

(LVEF <40%)

Uncertain

(40% ≤LVEF <50%)

Proportion of patients

14%50% 36%

HEART FAILURE

IN WOMEN EPIDEMIOLOGY

4

HF in Women

- Epidemiology I

More likely to be diagnosed at an older age

More likely to be hypertensive and have

preserved systolic function

Less coronary artery disease

Prior MI associated with a higher risk of

developing HF

19

Taylor AL. Heart Failure in Women. Curr Heart Fail Rep. 2015 Jan 30;12(2):187–95.

HF in Women

- Epidemiology II

Have better survival after onset of HF,

with a mortality risk approximately 15-

20% less than men

Tend to be more symptomatic at

presentation

Have higher HF hospitalization rate

than men

20


CVD in women

with Diabetes Mellitus (DM)

CVD presents later in life in women however, this age-

related difference is attenuated in women with DM 1

DM increases the risk of cardiovascular disease 3-4x in

women compared with 2-3x in men 1

DM may reduce gender-related differences in prevalence of

CVD by fading the vascular protective effects afforded by

oestrogen in females 2

Relationship between changes of balance of oestrogen

receptors (ERα and ERβ) with dichotomous effects by

estrogen 2

21

1. Norhammar A, Schenck-Gustafsson K. Type 2 diabetes and cardiovascular disease in women.

Diabetologia. 2012 Sep 4;56(1):1–9.

2.Dantas APV, Fortes ZB, de Carvalho MHC. Vascular Disease in Diabetic Women:

Why Do They Miss the Female Protection? Experimental Diabetes Research. 2012;2012(11):1–10.

22

Heart failure affects a large number of Australians

each year, placing a significant burden on the

healthcare system1-5

†As there are no national data for heart failure in Australia, the Australian Institute of Health and Welfare has used overseas f indings to estimate incidence in Australia.4

1. BEACH. Management of heart failure in general practice patients. 2015. 2. Australian Bureau of Statistics. 3222.0 - Population Projections, Australia, 2012 to 2101. Available at http://w ww.abs.gov.au/AUSSTATS/[email protected]/Latestproducts/3222.0Main Features32012 (base)

to 2101?opendocument&tabname=Summary&prodno=3222.0&issue=2012%20(base)%20to%202101&num=&view=. Accessed September 2015. 3. Australian Bureau of Statistics, 3303.0 - Causes of Death, Australia, 2013 Available at

http://www.abs.gov.au/ausstats/[email protected]/Lookup/by%20Subject/3303.0~2013~Main%20Features~Leading%20Causes%20of%20Death~10001 Accessed July 2016. 4. Australian Institute of Health and Welfare 2011. Cardiovascular disease: Australian facts 2011.

Cardiovascular disease series. Cat. no. CVD 53. Canberra: AIHW. 5. National Heart Foundation of Australia. A systematic approach to chronic heart failure care: a consensus statement. Melbourne: National Heart Foundation of Australia, 2013. Available at

https://heartfoundation.org.au/images/uploads/publications/HF_CHF_consensus_web_FINAL_SP.pdf . Accessed June 2016. 6. National Heart Foundation of Australia. Australian Heart Disease Statistics 2014. Available at

http://www.heartfoundation.org.au/SiteCollectionDocuments/HeartStats_2014_web.pdf. Accessed June 2016.

>400,000

Australians(1.7%) had heart

failure

in 2014–151,2

3,244 deathswere listed as caused by

heart failure in Australia in

20133~30,000 Australians

are newly diagnosed

with chronic heart

failure every year4†

50,983

hospitalisationsWith primary diagnosis

of heart failure in

Australia in 2011–126

8.9 daysaverage length of stay4

>$1 billionper annum in costs to

the Australian

economy5

23

Mortality in Heart failureHF is associated with significant mortality

30% of patients discharged following

a HF hospitalization are readmitted

with the first 30 days

Vulnerable period

= 1st 30 days post discharge

Strategies

- Early review post-discharge

(within 2 weeks)

- Cardiac Rehab (ideally HF specific)

The Vulnerable Period

24

https://heartfoundation.org.au/images/uploads/publications/HF_CHF_consensus_web_FINAL_SP.pdf

http://www.heartfoundation.org.au/SiteCollectionDocuments/HeartStats_2014_web.pdf.

5

25

Many patients are discharged with unresolved congestion, which is associated with poor long-term outcomes

26

OFTEN DUE TO INEFFECTIVE FLUID REMOVAL

Lack of patient understanding of importance of daily weighs

and when to seek help

Lack of patient understanding of fluid restriction, and how

to follow it

Incomplete medication list, and lack of understanding of

importance of medications

Recurrent Hospital Admission- Causes

Heart failure imposes a significant economic

burden on the healthcare system

27

PATHOPHYSIOLOGY

HF in Women

- Pathophysiology

Growing body of evidence to suggest female

myocardium has distinct adaptive mechanisms

more robust than males

Differences in• Myocardial calcium handling due to oestrogens

• NO synthesis

• Reduction of matrix turnover by oestrogens

• Down-regulation of the RAAS by endogenous oestrogens

29

Shah RU, Klein L, Lloyd-Jones DM. Heart failure in women: epidemiology, biology and treatment. Womens

Health (Lond). 2009 Sep;5(5):517–27.

HFrEF SYMPTOMS&

PROGRESSION

Overactivation of the RAAS and SNS is detrimental in HFrEF

and underpins the basis of therapy

1. McMurray et al. Eur Heart J 2012;33:1787–847; Figure References: Levin et al. N Engl J Med 1998;339:321–8;

Nathisuwan & Talbert. Pharmacotherapy 2002;22:27–42; Kemp & Conte. Cardiovascular Pathology 2012;365–71;

Schrier & Abraham. N Engl J Med 2009;341:577–85

ACEI: angiotensin-converting-enzyme inhibitor; Ang: angiotensin; ARB: angiotensin receptor blocker; AT1R: angiotensin II

type 1 receptor; MRA: mineralocorticoid receptor antagonist; NPs: natriuretic peptides; NPRs: natriuretic peptide receptors;

RAAS: renin-angiotensin-aldosterone system; SNS: sympathetic nervous system

Epinephrine

Norepinephrineα1, β1, β2

receptors

Vasoconstriction

RAAS activityVasopressin

Heart rateContractility

Sympathetic nervous system

Ang II AT1R

Vasoconstriction

Blood pressureSympathetic tone

AldosteroneHypertrophy

Fibrosis

Renin-angiotensin-aldosterone-system

NPRs NPs

Vasodilation

Blood pressureSympathetic toneNatriuresis/diuresisVasopressinAldosteroneFibrosisHypertrophy

Natriuretic peptide system1

• The crucial importance of the RAAS is supported by the beneficial effects of ACEIs, ARBs and MRAs1

• Benefits of β-blockers indicate that the SNS also plays a key role1

6

CLINICAL PRESENTATION

Key Symptoms

Shortness of Breath– NYHA Class

– ORTHOPNOEA

– Paroxysmal nocturnal dyspnoea

(PND)

Oedema– Peripheral oedema

– (Ascites)

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Quantifying Oedema

DONT JUST CHECK THE ANKLES !!

Follow the oedema up the legs and ascertain how

high it goes.

Good places to look

- lateral and posterior lower leg

- lateral and medial thigh

- lower abdominal wall

- sacral region

Approximating amount of fluid

- Feet ~500ml each

- Lower leg ~ 1L each

- Thighs ~2-3L each

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Oedema extending above the knees

typically responds poorly to oral Frusemide

Once Oedema extends above the level of the knees, there is

usually a significant amount of gut / splanchnic oedema

This gut oedema results in reduced absorption of oral

Frusemide

Other medications appear to NOT be significantly affected

Patients with this degree of oedema / fluid overload

typically require intravenous Frusemide to achieve

effective diuresis

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INVESTIGATIONS

Investigations

Echo, echo, echo....

ABSOLUTE KEY

INVESTIGATION IN ANY

PATIENT WITH SUSPECTED

HEART FAILURE

– Cardiac size & structure

– Systolic & diastolic function

– Left side vs right side

– Pulmonary pressures

– Valves

– Pericardium

36

7

BNP (Brain Natriuretic Peptide)

Produced by Ventricular Muscle under stretch / strain

SUPPLEMENTS CLINICAL JUDGEMENT

When cause of dyspnoea uncertain

3 different assays: BNP, proBNP, NT-proBNP

- reference ranges NOT comparable

- only NT-proBNP can be used to track progress

in patients on ARNIs (Entresto)

NOT Medicare Rebatable

37

Utility of Cardiac MR in Cardiomyopathy

Highly accurate EF assessment

Detection of myocardial oedema and inflammation

(eg. myocarditis)

Patterns of fibrosis– characteristic appearances for ischaemia, DCM, HCM

and other aetiologies

– arrhythmic risk

38

TREATMENT

Tiers ofHeart Failure Therapy

TREATMENT OF UNDERLYING CAUSE

Non-pharmacological

• Fluid intake

• Salt intake

Pharmacological

• Tablets

• (Inotropes)

Devices

• ICDs

• Cardiac resynchronization (CRT) / Biventricular pacing

Cardiac Rehabilitation & MULTI-DISCIPLINARY CARE

Transplantation (& Mechanical Circulatory Support)

40

HF in Women

- TherapyWomen comprise <20% of patient in most major HF Clinical

Trials to date

β-blockers have the most data to support their use in women

Older women with heart failure are less likely to receive

guideline recommended treatments

Women are 3 times less likely than men to receive an ICD

Surgical therapies for advanced HF, such as high risk CABG,

mitral valve repair, left ventricular assist device implantation

and cardiac transplantation, are far less likely to

be used in women

41Taylor AL. Heart Failure in Women. Curr Heart Fail Rep. 2015 Jan 30;12(2):187–95.

NON-PHARMACOLOGICAL

8

Optimal Fluid Balance Management

43

KEY PRINCIPLE• 1L of fluid = 1kg of weight

PILLARS OF MANAGEMENT• Daily weighs• Fluid Restriction (1.5L/day)

NOT always requiredONLY required in patients with problemsof fluid overload

OPTIMIZATION

• Patient diary

• Medical review if weight increase‣>1kg/day for 2 days‣>2.5kg over 1 week

• Fluid Restriction patient education handout

• Track / Record Fluid Intake for 1 week until routine established

PHARMACOLOGICAL

45

TREAT CONGESTION !!

Euvolaemia is everything!

HFrEF survival rates have improved over

time with the introduction of new

therapies

Sinus Node Inhibitor

- reduces heart rate (HR)

Place in therapy

- patients intolerant of beta-blockers

- patients on max tolerated beta-blocker with HR > 70

bpm

‘SHIFT’ trial

- LVEF <35%

- HR > 70 bpm

47

The Addition of “I” for Ivabradine (aka Coralan)

37

ARNI: angiotensin receptor neprilysin inhibitor

9

Inactive

fragments

Angiotensinogen(liver secretion)

LCZ696 simultaneously inhibits neprilysin (via LBQ657) and

blocks AT1 receptors (via valsartan)

Sacubitril (AHU377; pro-drug)

Valsartan

N

NHN

N

N

O

OH

O

LCZ696

LBQ657(NEP inhibitor)

OH

OHN

O

HO

O

RAAS

Enhancing

Vasorelaxation

Blood pressure

Sympathetic tone

Aldosterone levels

Fibrosis

Hypertrophy

Natriuresis/diuresis

Ang II

Ang I

AT1 receptor

*Neprilysin substrates listed in order of relative affinity for NEP: ANP, CNP, Ang II, Ang I, adrenomedullin, substance P, bradykinin, endothelin-1, BNP

Ang: angiotensin; ANP: atrial natriuretic peptide; AT1: angiotensin II type 1; BNP: B-type natriuretic peptide; CNP: C-type natriuretic peptide; NEP: neprilysin; RAAS: renin-

angiotensin-aldosterone system

Levin et al. N Engl J Med 1998;339:321–8; Nathisuwan & Talbert. Pharmacotherapy 2002;22:27–42; Schrier & Abraham. N Engl J Med 2009;341:577–85; Langenickel &

Dole. Drug Discov Today: Ther Strateg 2012;9:e131–9; Feng et al. Tetrahedron Letters 2012;53:275–6

Inhibiting

Vasoconstriction

Blood pressure

Sympathetic tone

Aldosterone

Fibrosis

Hypertrophy

Sodium and water retention

ANP, BNP, CNP, othervasoactive peptides*

50

PARADIGM-HF TrialSummary of Results

51

52

Baseline demographics were similar between treatment groups1

Adapted from McMurray JJ et al. (2014).1

*The data for NYHA class reflect the status of patients at the time of randomisation. Patients were required to have at least NYHA Class II symptoms at screening. †Race or ethnic group was reported by the investigators.

LVEF: left ventricular ejection fraction; NYHA: New York Heart Association; SBP: systolic blood pressure.

1. McMurray JJ et al. N Engl J Med 2014;371(11):993–1004.

ENTRESTO®

(n=4187)

Enalapril(n=4212)

Age, mean 63.8±11.5 63.8±11.3

Female, % (n) 21.0 (879) 22.6 (953)

Heart rate, beats/min 72±12 73±12

SBP, mmHg 122±15 121±15

LVEF, % 29.6±6.1 29.4±6.3

Ischaemic cardiomyopathy, % (n) 59.9 (2506) 60.1 (2530)

NYHA class, % (n)*

I 4.3 (180) 5.0 (209)

II 71.6 (2998) 69.3 (2921)

III 23.1 (969) 24.9 (1049)

IV 0.8 (33) 0.6 (27)

Missing data 0.2 (7) 0.1 (6)

Race, % (n)†

White 66.0 (2763) 66.0 (2781)

Black 5.1 (213) 5.1 (215)

Asian 18.1 (759) 17.8 (750)

Other 10.8 (452) 11.1 (466)

Therapeutic

Algorithm for

patient with

symptomatic

HFREF

Diastolic Heart Failure (HFPEF)Management

>50%)

Consider reducing HR to <70 bpm

β-blocker

??

10

PRESCRIBING ENTRESTO

Prescribing EntrestoUse of Entresto

is very similar to ACEI & ARBs

Side effect profile of Entresto….

is very similar to ACEI & ARBs

2 Major Exceptions

must have 36 hour washout period between ACEI

Entresto has an additional diuretic effect which varies

between patients

57

58

*40% before protocol amendment. †25% before protocol amendment.

ACEI: angiotensin-converting enzyme inhibitor; ARB: angiotensin-receptor blocker; BNP: B-type natriuretic peptide; EF:

ejection fraction; eGFR: estimated glomerular filtration rate; HF: heart failure; NT-proBNP: N-terminal proBNP; NYHA:

New York Heart Association; SBP: systolic blood pressure.

1. McMurray JJ et al. N Engl J Med 2014;371(11):993–1004.

Inclusion

• At least 18 years of age

• NYHA Class II–IV

• EF ≤35%*

• BNP ≥150 pg/mL or NT-proBNP

≥600 pg/mL

OR

BNP ≥100 pg/mL or NT-proBNP

≥400 pg/mL (if hospitalised for HF

in previous 12 months)

PARADIGM-HF: Select inclusion

and exclusion criteria1

Exclusion

• Symptomatic hypotension

• SBP <100 mmHg at screening or

<95 mmHg at randomisation

• eGFR <30 mL/min per 1.73 m2 or a decrease

of >35% between screening

and randomisation†

• Serum K+ >5.2 mmol/L at screening or

>5.4 mmol/L at randomisation

• History of angioedema or unacceptable side

effects during treatment with

ACEIs or ARBs

59

Switching to ENTRESTO®:

Patients previously on an ACEI

Start ENTRESTO® at the recommended dose

of 49/51 mg twice daily1

Choose initial dose of ENTRESTO® based on current treatment and titrate to the target dose1

Patients receiving a total daily dose of ≤10

mg of enalapril or therapeutically

equivalent doses of another ACEI; for

example1,2

• Perindopril erbumine ≤4 mg

• Ramipril <5 mg

Patients receiving a total daily dose of >10

mg of enalapril or therapeutically

equivalent doses of another ACEI; for

example1,2

• Perindopril erbumine >4 mg

• Ramipril >5 mg

Stop ACEI

36 hours before

starting ENTRESTO®

Stop ACEI

36 hours before

starting ENTRESTO®

Start ENTRESTO® at

the recommended

dose of 24/26 mg

twice daily

Double the dose after

2 to 4 weeks to 49/51

mg twice daily, as

tolerated by the

patient

Double the dose

of ENTRESTO®

after 2 to 4 weeks

to

the target

maintenance

dose of 97/103

mg twice daily, as

tolerated by the patient

ACEI equivalent dose

Important safety information ENTRESTO® is contraindicated with concomitant use of an ACEIand in patients with a history of angioedema related to previous ACEI therapy.1

ACEI: angiotensin-converting enzyme inhibitor.

1. ENTRESTO® Product Information. TGA-approved Product Information. Novartis Pharmaceuticals

Australia Pty Limited. 2. Data on file. CSR CLCZ696B2228. Novartis Pharmaceuticals Corp; East

Hanover, NJ. November 2014.

60

Switching to ENTRESTO®:

Patients previously on an ARB

ARB: angiotensin-receptor blocker.

1. ENTRESTO® Product Information. TGA-approved Product Information. Novartis Pharmaceuticals

Australia Pty Limited. 2. Data on file. CSR CLCZ696B2228. Novartis Pharmaceuticals Corp; East

Hanover, NJ. November 2014.

Patients receiving a total daily dose of ≤160 mg of valsartan or therapeutically

equivalent doses of another ARB; for example2

• Irbesartan ≤150 mg

• Candesartan ≤16 mg

Patients receiving a total daily dose of >160 mg of valsartan or therapeutically

equivalent doses of another ARB; for example2

• Irbesartan >150 mg

• Candesartan >16 mg

Start ENTRESTO® at

the recommended

dose of 24/26 mg

twice daily

Double the dose after

2 to 4 weeks to 49/51

mg twice daily, as

tolerated by the

patient

Double the dose

of ENTRESTO®

after 2 to 4 weeks

to

the target

maintenance

dose of 97/103

mg twice daily, as

tolerated by the patient

Choose initial dose of ENTRESTO® based on current treatment and titrate to the target dose1

ARB equivalent dose

Start ENTRESTO® at the recommended dose

of 49/51 mg twice daily1

Important safety informationENTRESTO® is contraindicated in patients with a history of angioedema related to previous ARB therapy. Avoid use of ENTRESTO® with an ARB.1

11

Optimal Dosing / Uptitration

Clinical trial evidence is generally for highest / maximum tolerated dose.

UPTITRATE AS TOLERATED

Which medication first?- relieve symptoms- combination better than single agent- trials suggest outcomes equal whether

ACEI/ARB or beta-blocker first

61

Dealing with Side Effects

Most common

- Reduced BP, elevated K, increased Cr/Ur

- Reduced HR (only with beta-blockers & Ivabradine)

SEE IF ANOTHER NON-HF MEDICATION CAN BE

REDUCED OR CEASED

- eg. Slow K, Amlodipine, (even diuretic in patient on Entresto)

If no other option then consider

- reducing another HF medication

- that particular HF medication

- ceasing that particular HF medication if absolutely necessary

62

SGLT2 INHIBITORS

64

Mechanism of action

Clinical Trial Outcomes

Empagliflozin demonstrated an unprecedented 38%

reduction in CV mortality in patients with diabetes

Highly significant reductions in HF hospitalizations

and end-stage kidney disease

∼1% reduction in HbA1c levels, with favorable

reductions in both BP (∼3–6 mmHg) and body

weight (∼2–4 kg/m2).

65Zinman B, Wanner C, Lachin JM, Fitchett D, Bluhmki E, Hantel S, et al.

Empagliflozin, Cardiovascular Outcomes, and Mortality in Type 2 Diabetes.

N Engl J Med. 2015 Nov 26;373(22):2117–28.

EMPA-REG OUTCOME®: summary

3P-MACE, 3-point major adverse cardiovascular events

Empagliflozin is not indicated for CV risk reduction. CV, cardiovascular; T2D, type 2 diabetesZinman B et al. N Engl J Med 2015;doi:10.1056/NEJMoa1504720; Zinman B. EASD 2015; Oral presentation

66

Empagliflozin in addition to standard of care reduced CV risk and improved overall survival in adults with T2D at high CV risk

↓ 3P-MACE

14%

↓ CV death

38%

↓ All-cause

mortality

32%

↓ Heart failure

hospitalisations

35%

The overall safety profile of empagliflozin was consistent with previous clinical trials and current label information

12

Additional Observed EffectsInduces plasma volume contraction without

activation of the sympathetic nervous system

Might improve efficiency of myocardial energetics

Decreased vascular stiffness and improved

endothelial function

In future, might even be considered in HF or

chronic kidney disease patients without diabetes

67

1. Martens P, Mathieu C, Verbrugge FH. Promise of SGLT2 Inhibitors in Heart Failure:

Diabetes and Beyond. Current Treatment Options in Cardiovascular Medicine; 2017 Mar 22;:1–14.

HF IN PREGNANCY

HF and Pregnancy

2 major types

HF emerging during pregnancy in women

with documented preexistent CV disease

Development of HF in the peripartum

period in women without previous

evidence of heart disease

69


HF during pregnancy in women with

preexistent CV disease

May be due to pregnancy-related changes in

• volume status

• red cell mass

• peripheral vascular resistance

• heart rate

• circulatory hormones

• prostaglandins

• procoagulant factors

70


HF during pregnancy in women with

preexistent CV disease

Risk of HF dependent on

• type of pre-existing cardiac

• lesion phase of the pregnancy

Serious complication

Increased maternal and foetal mortality

71


Peripartum Cardiomyopathy

- Definition, Epidemiology, Risk Factors

HF with LV dysfunction occurring in the last months of

pregnancy or the first several months postpartum

Risk factors

- preeclampsia

- African ancestry

Aetiology remains unknown with multiple hypotheses

proposed

72


13

Peripartum Cardiomyopathy

- Treatment and Outcomes

Bromocriptine may offer a specific treatment though this will

requires further study

No evidence-based differences in the management with the

exception of

- anticoagulation, as pregnancy is associated with

hypercoagulability

- prohibition of the use of ACE inhibitors

Recovery of LV function quite variable

Risk of recurrence with subsequent pregnancies high and

woman should be advised of this

73


KEY POINTS

75

When To Refer to a Cardiologist?

• ALWAYS AT DIAGNOSIS

• WHENEVER THERE IS A SIGNIFICANT CHANGE

IN SYMPTOMS OR STATUS

• IDEALLY - A TEAM EFFORT & APPROACH

- Regular GP reviews

- Periodic Cardiologist review

Key Points

HF is a syndrome with multiple underlying causes

There are significant differences in HF between men and

women

Entresto is a new and power addition to current HF theapy

HOWEVER it should be used after standard therapies have

been trialled and fully uptitrated

SGLT2 Inhibitors produce unprecedented reduction in

Cardiac and HF events in diabetics AND may ultimately be

used to treat HF in their own right

76

77

SUMMARY

Terminology

Heart Failure in Women

ARNIs (ie. Entresto)

SGLT2 Inhibitors

Heart Failure in Pregnancy

Resources

UpToDate

Heart Failure Guidelines–National Heart Foundation of Australia

–Cardiac Society of Australia & New Zealand (CSANZ)

–American Heart Association (AHA)

–European Society of Cardiology (ESC)

iPhone & Android–AHA & ESC Guidelines

78