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PY366 Heart Failure > Therapeutics of Heart failure > Flashcards

Therapeutics of Heart failure Flashcards

1
Q

what are the 3 types of heart failure

A
  1. heart failure with reduced ejection fraction (HFrEF)
  2. heart failure with mildly reduced ejection fraction (HFmrEF)
  3. heart failure with preserved ejection fraction (HFpEF)
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2
Q

what is the diagnostic criteria for HFrEF

A
  1. symptoms and signs
  2. LVEF <40%
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3
Q

what is the diagnostic criteria of HFmrEF

A
  1. symptoms and signs
  2. LVEF 41-49%
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4
Q

what is the diagnostic criteria for HFpEF

A
  1. symptoms and signs
  2. LVEF>50%
  3. objective evidence of cardiac structural/functional abnormalities consistent with the presence of LV diastolic dysfunction/raised LV filling pressures, including raised natriuretic peptides
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5
Q

is heart failure a progressive condition

A

often a persistent and progressive conditionm

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6
Q

what are the aims of therapy for treating heart failure

A

1, improve life expectancy
2. improve quality of life

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7
Q

how can we achieve these aims of therapy

A
  1. early and accurate diagnosis
  2. prescribe in line with the evidence base- drugs, monitoring, exercise and devices
  3. encourage self management
  4. good access to professional health
    - reduce admissions, readmissions and length of stay
  5. good end of life care
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8
Q

what is involved in the history and examination of heart failure

A
  1. detailed history- current symptoms and PMH
  2. patient examination
    - signs and symptoms
    - ECG
    - chest x ray
  3. blood tests- renal function, FBC, thyroid, HbA1c, LFT
  4. natriuretic peptides
    - NT- pro BNP
  5. echocardiogram- dimensions/function of heart
    - valves, systolic and diastolic function
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9
Q

what investigations can be conducted to evaluate possible aggravating factors or alternative diagnosis

A
  1. ECG
  2. Chest X ray
  3. urinalysis
  4. peak flow or spirometry
  5. blood tests
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10
Q

what does NT pro BNP stand for

A

n-terminal pro B type natriuretic peptide

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11
Q

what do natriuretic peptides do

A
  • they promote natriuresis
  • inhibit ADH and aldosterone release
  • cause arterial and vasodilation
  • synthesised in myocardial cells in response to raised ventricular pressure
  • levels can be raised in heart failure
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12
Q

what do high levels of Natriuretic peptides suggest

A

suggests heart failure
- levels don’t differentiate between HFrEF or HFpEF
- can also be raised for other reasons (AF, renal impairment)

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13
Q

what can reduce natriuretic peptide levels

A
  • obesity
  • afro caribbean patients
  • patients already on treatment with diuretics, ACE inhibitors, beta blockers, ARBs and aldosterone antagonists
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14
Q

why is an echocardiogram performed

A
  • transthoracic doppler 2d echocardiogram
  • performed to exclude important valve disease, assess systolic and diastolic function of heart
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15
Q

what are the heart failure classifications in terms of physical activity

A
  1. class I- no limitation of physical activity, ordinary physical activity doesn’t cause symptoms
  2. class II- slight limitation of physical activity, comfortable at rest, ordinary physical activity causes symptoms
  3. class III- marked limitation of physical activity, comfortable at rest, but less than ordinary activity causes symptoms
  4. class IV- Severe limitation and discomfort with any physical activity, symptoms persist even at rest
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16
Q

what is the 1st step in pharmacological intervention in heart failure

A

offer diuretics to control symptoms
- reduce fluid retention and minimise congestive symptoms

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17
Q

what needs to be carefully monitored in use of diuretics

A
  • renal function
  • weight
  • electrolytes
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18
Q

what are the different types of diuretics used for heart failure

A
  1. loop diuretics- furosemide, bumetanide
  2. thiazide diuretics- bendroflumethiazide
  3. combination of loop and thiazide diuretics
  4. mineralocorticoid receptor antagonists- spironolactone, epleronone
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18
Q

describe the absorption of loop diuretics and how they are given

A
  1. furosemide has inter and intra patient variability of absorption
    - in hospital, given as IV: bolus or continuous infusion
    - step down to oral: 48 hour rule
  2. bumetanide better absorbed in fed state
    - 40mg of furosemide= bumetanide 1mg
  3. monitor electrolytes
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18
Q

describe how thiazides are used in heart failure

A
  1. only used alone in mild HF (usually for hypertension)
  2. ineffective in poor renal function
  3. monitor potassium, sodium, magnesium and calcium
  4. may exacerbate diabetes and gout
  5. metolazone alone is a weak diuretic but very potent when combined with loop diuretic
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18
Q

what does raised aldosterone lead to

A

leads to sodium and water retention
- peripheral oedema and congestion
- vasoconstriction, causing hypertension
- hypokalaemia and hypomagnesia which may induce electrical instability and death of cardiac myocytes
- myocardial hypertrophy and fibrosis
. blocking of aldosterone shown to be beneficial in HFrEF

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18
Q

what can be added to reduce fluid retention and abdominal oedema

A

can add mineralocorticoid receptor antagonists

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19
Q

how are ACE inhibitors used in heart failure

A
  1. prevent myocardial hypertrophy and remodelling
  2. relieve symptoms and hospitalisations
  3. improve exercise tolerance
  4. reduce acute exacerbations
  5. reduce mortality
  6. improve survival and prevent progression of symptoms
  7. used in all patients with HFrEF, EF<40% regardless of symptoms
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20
Q

outline examples of ACE inhibitor survival trials

A
  1. SAVE trial- first ACE inhibitor post MI study
    - pts EF<40% post MI
    - captopril vs placebo
    - captopril reduced mortality BY 25%
    - results replicated in other studies
  2. ATLAS trial- more benefit with higher doses
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21
Q

give examples of ACE inhibitor prevention trials

A
  1. HOPE trial- pts aged >55 years with high risk for CV events
    - ramipril 10mg vs placebo
    - no HF patients at inclusion
    - in high risk patients, ramipril prevents heart failure and reduced primary endpoint
22
Q

what needs to be monitored in use of ACE inhibitors

A
  1. renal function
  2. potassium
  3. cough
  4. blood pressure
  5. titrate to target dose every 2-4 weeks
23
Q

when should specialist initiation of ACE inhibitors be conducted

A
  1. diuretic therapy
  2. Cr>150
  3. hyponatraemia
  4. hypotension
24
Q

what are the contraindications of ACE inhibitors

A
  • bilateral renal artery stenosis
  • pregnancy
  • angio-oedema
25
Q

outline angiotensin II antagonist studies

A
  1. CHARM ADDED trial- pts NYHA classification II-IV and LVEF<40%
    - candesartan vs placebo
    - candesartan in addition to ACE reduces CV events in heart failure patients with reduced LVEF and reduced total number of hospital admissions
26
Q

describe the use of angiotensin II antagonists in heart failure

A
  1. ACE inhibitors are gold standard first line
  2. not superior to ACE inhibitors
  3. use if intolerant of ACE inhibitor
  4. if patient remains symptomatic, add MRA or switch to sacubitril valsartan
27
Q

describe how beta blockers are used in heart failure

A
  1. cause bradycardia which will improve the filling of the ventricle and increase coronary blood flow
    - cardiac output is maintained and force of contraction is reduced
  2. block RAS system and aldosterone effects
  3. reduce arrhythmias/SCD
  4. reduce mortality
  5. used in all patients with HFrEF, EF<40% regardless of symptoms
28
Q

outline beta blocker trials

A
  1. CIBIS II- bisoprolol
  2. MERIT HF- metoprolol
  3. clear evidence of benefit of adding BB to ACE inhibitor
29
Q

what should be monitored in use of beta blockers

A
  1. care in unstable heart failure
  2. start low and go slow
  3. monitor heart rate and blood pressure
  4. monitor wheeze/bronchospasm
30
Q

outline examples of MRA trials

A
  1. EMPHASIS HF- pts, NYHA II
    - age >55 and EF<35% receiving recommended therapy
    - randomised to epleronone 25mg or placebo
    - reduced primary endpoint of death and hospitalisation
31
Q

what needs to be monitored in MRA use

A
  1. renal function
  2. potassium and sodium
  3. weight
  4. fluid balance
32
Q

describe the use of nitrates in heart failure

A
  1. vasodilator
  2. give IV in acute exacerbations, short term only
  3. monitor blood pressure
    - avoid in hypotension
  4. oral for maintenance therapy with hydralazine
33
Q

describe the use of hydralazine in heart failure

A
  1. vasodilator
    - may be used if poor renal function as alternative to ACEi
  2. useful in patients of Afro-caribbean
  3. poorly tolerated
    4.avoid after acute event as can provoke angina
  4. can cause lupus like syndome
  5. monitor liver
34
Q

describe the use of digoxin in heart failure

A
  1. recommended for worsening or severe heart failure due to LVSD despite 1st and 2nd line treatment
  2. slows heart rate, better filling of ventricles and increases force of contraction and ionotropic effects
  3. monitor potassium and heart rate
  4. used in sinus rhythm at low dose
  5. doesn’t improve mortality but reduces hospital admissions
35
Q

outline the digoxin trials

A
  1. DIG trial- NYHA I-II, EF<45%
    - heart failure patients in sinus rhythm
    - digoxin vs placebo
    - reduced rate of hospital admisisons
    - no evidence that reduces mortality
36
Q

outline the ivabradine trials

A
  1. chronic heart failure, EF<35% and in sinus rhythm
  2. randomised to ivabradine or placebo
  3. primary endpoint of CV death or hospital admissions reduced
37
Q

what is ivabradine licensed for

A
  1. chronic heart failure NYHA II-IV with EF<35%
    - must also be in sinus rhythm and heart rate >75bpm and maximum BB tolerated
  2. angina
38
Q

how does Entresto (angiotensin- neprilysin inhibitor) work

A

inhibits the RAAS and also neprilysin with sacubitril, which increases levels of natriuretic peptides

39
Q

describe the sacubitril and valsartan trail

A

PARADIGM trail- lowered rate of primary endpoint of CV death or hospitalisation for HF
- also lowered premature death from any cause
- favourable effects on quality of life measures and functional status
- no additional adverse effects on renal function
- more potent effect on blood pressure

40
Q

when is sacubitril valsartan use recommended

A
  1. recommended for treating symptomatic chronic heart failure with reduced ejection fraction in people:
    - with New York heart association class II-IV symptoms and
    - with a left ventricular ejection fraction of 35% or less and
    - who are already taking a stable dose of ACEi or ARBs
41
Q

describe the switch to sacubitril valsartan

A
  1. replaces any ACE or other ARB
  2. Discontinue any ACE inhibitor for at least 36 hours prior to initiating
    - risk of angio-oedema if coprescribed
  3. discontinue any other ARB
42
Q

when is a dose of 24mg sacubitril and 26mg valsartan used

A
  1. starting dose if on low dose ACEi/ARB prior to initiation
  2. also consider this dose if any concerns about low blood pressure, renal function or hyperkalaemia
43
Q

when is a dose of 49mg sacabitril and 51mg valsartan used

A

starting dose if on high dose ACE/ARB prior to initiation

44
Q

when is a dose of 97mg sacabitril and 103mg valsartan used

A

target dose

45
Q

what cautions should be considered when using sacabitril valsartan

A
  • hypotension
  • hyperkalaemia
  • worsening renal failure
  • over diuresis
46
Q

give examples of SGLT2 inhibitors

A

dapagliflozin, empagliflozin

47
Q

describe how dapagliflozin works

A
  • acts in the kidneys
  • reduces glucose and sodium reabsorption
  • downregulation of sympathetic activity
  • lowers preload and afterload of the heart
48
Q

outline the dapagliflozin study

A

DAPA-HF- assessing dapagliflozin in HFrEF patients with or without T2D
- dapagliflozin 10mg vs placebo
- significant reduction in primary endpoint of CV death and worsening HF

49
Q

what are the common side effects of SGLT2 inhibitors

A
  • dizziness
  • rash
  • back pain
  • UTI
  • dysuria or polyuria
  • initial dip in CrCl
  • hypoglycaemia
  • risk of DKA
50
Q

what are the 4 pillars of heart failure

A
  1. ARNI
  2. BB
  3. MRA
  4. SGLT2I
51
Q

what is the process of treatment following the 4 pillars of heart failure

A
  1. initiate
  2. optimise
  3. re-assess
52
Q

give examples of device therapy

A
  1. Implantable cardioverter defibrillator (ICD)
  2. cardiac resynchronisation therapy pacemaker/defibrillator (CRT-P and CRT-D)
53
Q

how does ICD devices work

A
  • prevent bradycardia
  • can identify and stop ventricular arrhythmias to reduce risk of sudden death and all cause mortality in pts with heart failure
54
Q

how do CRT devices work

A
  • improve hearts pumping efficiency and blood flow
  • leads to improved symptoms and quality of life
  • compared with optimal medical treatment alone, CRT devices reduce mortality in pts with HF
55
Q

describe the management of HFmrEF and HFpEF

A
  1. diuretics for fluid congestion
  2. manage comorbidities
  3. SGLT2 inhibitors
    - empagliflozin licenced
56
Q

outline a empagliflozin study

A

EMPEROR-empagliflozin vs placebo in pts with HFpEF
- LVEF>40%
- empagliflozin showed 21% RRR in primary endpoint of CV death or HHF
- reduced 1st and recurrent HHF by 27% in a confirmatory secondary endpoint

PY366 Heart Failure (6 decks)

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