Cardiology 4 - Heart Failure Flashcards

1
Q

What are features of neurohormonal imbalance in heart failure?

A

excess AT2, aldosterone, endothelin and noradrenaline and relative deficit of ANP, BNP, CNP, bradykinin and NO

also proinflammatory cytokines TNFa, IL-1, 6, 18

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2
Q

What are features of neurohormonal imbalance in heart failure?

A

excess AT2, aldosterone, endothelin and noradrenaline and relative deficit of ANP, BNP, CNP, bradykinin and NO

also proinflammatory cytokines TNFa, IL-1, 6, 18

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3
Q

What are common index events in heart failure?

A

Pressure load - AS, HTN
Volume load - AR, MR
Myocardial failure - MI (75%), DCM, Myocarditis
Impaired filling - Restrictive CM, Pericardial disaese

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4
Q

What is the relationship between end-systolic volume and mortality/CHF

A

increasing rates of CHF and mortality with increasing end systolic volume

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5
Q

What are determinants of cardiac output?

A

Contractility + preload + afterload = stroke volume

stroke volume x heart rate and synergic LV contraction/valve function = cardiac output.

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6
Q

Through was structures does a swan-ganz catheter pass during RHC?

A

R atrium, RV, main pulm artery, PA branch = wedge

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7
Q

What is the normal value for PCWP?

A
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8
Q

What is the most Sn clinical sign for heart failure, correlated with PCWP?

A

Orthopnoea identifies 90% of patients with PCWP >=22

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9
Q

What are features of DHF on doppler mitral flow?

A

initially increased Dt, and increased A with impaired relaxation, transitioning to severe restriction with E significantly greater than A and shorter Dt

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10
Q

What are features of DHF on doppler mitral flow?

A

initially increased Dt, and increased A with impaired relaxation, transitioning to severe restriction with E significantly greater than A and shorter Dt

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11
Q

What are common index events in heart failure?

A

Pressure load - AS, HTN
Volume load - AR, MR
Myocardial failure - MI (75%), DCM, Myocarditis
Impaired filling - Restrictive CM, Pericardial disaese

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12
Q

What is the relationship between end-systolic volume and mortality/CHF

A

increasing rates of CHF and mortality with increasing end systolic volume

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13
Q

What are determinants of cardiac output?

A

Contractility + preload + afterload = stroke volume

stroke volume x heart rate and synergic LV contraction/valve function = cardiac output.

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14
Q

Through was structures does a swan-ganz catheter pass during RHC?

A

R atrium, RV, main pulm artery, PA branch = wedge

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15
Q

What is the normal value for PCWP?

A

greater than or equal to 12

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16
Q

What is the most Sn clinical sign for heart failure, correlated with PCWP?

A

Orthopnoea identifies 90% of patients with PCWP >=22

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17
Q

What are features of diastolic HF?

A

stiffened ventricle, leading to impaired filling (need for increased pressures)
isolated DHF occurs in

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18
Q

What are features of DHF on doppler mitral flow?

A

initially increased Dt, and increased A with impaired relaxation, transitioning to severe restriction with E significantly greater than A and shorter Dt

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19
Q

What are features of ANP, BNP and CNP?

A

ANP - origin = cardiac atria, stimulated by atrial distension
BNP - ventricular myocardium - ventricular overload
CNP - endothelium - endothelial stress.

Higher BNP levels are seen in age, females and post menopause.

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20
Q

What are features of BNP cutoffs?

A

400 - CHF is very likely

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21
Q

What are the most significant modifiable risk factors for HF?

A

Hypertension - 39% HF in men, 59% in women
Coronary artery disease 34% in men, 13% in women

Obesity and diabetes mediate HF through HTN

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22
Q

What were the outcomes of the HOPE trial?

A

Compared ramipril to placebo in patients with high risk patients for CHF

23% reduction in patients developing heart failure.
NNT = 40, for heart failure prevention, NNT=13 for preventing 1 CV death, AMI, stroke or HF

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23
Q

What is the role of digoxin in CHF?

A

has been shown to reduce hospitalisations in CHF, in patients already taking diuretics and ACEi - does not reduce death.

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24
Q

What are two receptor polymorphisms associated with HF?

A

a2cdel322-325 - decreased function - increased norad at synapse
B1ARG389 - increased function wiht increased response at myocite.

If homozygous for both polymorphisms, OR 10.11 for HF

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25
Q

What are causes of diuretic resistance in CHF?

A

presence of gut oedema reduces aborption
frusemide absorption is variable, bumetanide better
may need temporary IV dosing
Na and fluid restriction are crucial

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26
Q

What is the role of ACEi in systolic heart failure?

A
indicated in all grades of heart failure and for prevention in high risk groups.
16% overall reduction in mortality for class overall (but no clear reduction in sudden cardiac death)

prevent diseases causing LV dysfucntion, prevent progression to symptomatic HF, reduce Sx, reverse remodelling and improve survival.

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27
Q

What was the outcome of the CHARM trial?

A

Found no increase in mortality in patients receiving a BB, ACEi and Candesartan, with significant benefits wrt to CV eath, CHF hospitalisation.

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28
Q

What are general principles of ARB in HF?

A

only losartan, valsartan and candesartan have been evaluated in clinical trials
strongest data for candesartan, valsartan also has HF indication.
benefits are greatest in ACEi naive patients.
Modest additional benefit when added to standard therapy
benefits only in systolic blood pressure.

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29
Q

What is the role of beta blockers in heart failure?

A

improves cardiac function, symptoms and clinical status.
Mortality reduction by 30-35%
reduced sudden death, reduced death and hospitalisation by 25-30%.
Not class effect - proven with carvedilol, bisoprolol, nebivolol, metoprolol succinate

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30
Q

What is the relative selectivity of B-blockers?

A

SR Metoprolol and bisoprolol are selective for B1 only, carvedilol is non-selective (B1, B2 and a1) but has vasidolatory and antioxidant properties.
Nebivolol has B1 and vasodilatory properties.

31
Q

at what point is benefit with respsect to mortality evident in beta blocker use in HF?

A

Two weeks, generally

Sx of dizziness and SOB fade over 3 months

32
Q

Is COPD contraindicated in b-blocker therapy in HF?

A

carvedilol introduced safely in COPD patients

Asthma continues to be a C/I to b-blocker use.

33
Q

What are two receptor polymorphisms associated with HF?

A

a2cdel322-325 - decreased function - increased norad at synapse
B1ARG389 - increased function wiht increased response at myocite.

If homozygous for both polymorphisms, OR 10.11 for HF

34
Q

In what classes of HF are B-blockers indicated?

A
Class II-IV and class I post MI
stage IV must be stable before commencing B-blocker
dose related benefit
35
Q

What was the outcome of the RALES study?

A

spironolactone + standard therapy in Class 3-4 CCF and LVEF 25% shown to improve survival by 10%

36
Q

What is the MoA of neprolysin inhibitors in HF?

A

inhibition of neprolysin increases levels of vasoactive peptides, including natriuretic peptides, bradykinin, and adrenomedullin

37
Q

What is the role of eplerenone in mild heart failure?

A
38
Q

What were issues post RALES in spironolactone in HF?

A

bradycardia, some requiring pacing
renal insufficiency
discontinuation

39
Q

What are the two most common mutations causing HCM?

A

b-myosin heavy chain ~35% of cases

followed by Myosin binding protein C, troponin T

40
Q

What is the mechanism of action of ivabradine?

A

inhibits If channel in sinus node - slows sinus rate without having any other effects upon neurohormones or BP

41
Q

What were outcomes in the ivabradine SHIFT trial?

A

Reduction in hospitalisation and death in patients on treatment arm with Class II to IV HF, sinur rhythm and HR >70 and EF 50% adequate dose of beta blocker.

minor improvement in patients with HR>77/min on subgroup analysis on study entry

42
Q

When should ivabradine be used given limitations of SHIFT trial?

A

When heart rate remains high, despite adequate BB dose (>77/min after 5 mins with ECG)
Lung disease precludes B-blocker (Asthma only)
Beta blockers are not truly tolerated (unacceptable symptomatic hypotension, etc.)

43
Q

What is the role of serelaxin in HF?

A

serelaxin = human recombinant relaxin-2
- naturally occuring vasodilatory peptide.

significant change in patient reported dyspnoea, and no change in secondary endpooints - days out of hopsital at 60 days and CVS death/readmission for HF at day 60.

Significant reduction in CVS death and all cause mortality at 180 days.

44
Q

What is the role of neprolysin inhibitors in HF?

A

in patients with HF with reduced ejection fraction, administration of Sacubitril-valsartan has been shown to reduce mortality and morbidity compared to ACEi in addition to standard medical therapy in patients with HF with reduced ejection fraction.

45
Q

What are risk factors for SCD in HCM?

A
FHX SCD
recurrent syncope in young
NSVT in adults
Severe LVH (septum 2.5-3cm)
Severe obstruciton
abnormal exercise blood pressure responses (decreased w exercise)
level of myocardial fibrosis on MRI
Arg719Trp mutation worse prognosis
46
Q

What are causes of cardiomyopathy?

A
Intrinsic to myocardium
- dilated CM
- hypertrophic CM
- Arrhytmogenic RV dysplasia
- obliteravie (restrictive) CM
Specific (secondary to external processes)
- hypertensive CM
- valvular CM
- ischaemic CM
- Systemic disease
- Inflammatory CM
47
Q

What are features of hypetrophic cardiomyopathy?

A

Idiopathic (AD)
50-60% of cases are AD
>80% have genetic features on detailed pedigree analysis
Sproadic disease is uncommon
incomplete penetrance and age related expression

48
Q

What are the two most common mutations causing HCM?

A
  1. cardiac myosin binding protein C (MYBPC3) - up to 48%

2. b-myosin heavy chain (MYH7) - up to 25%

49
Q

What are features of HOCM on echo?

A

Asymmetrical septal thickening (IVS:PW >1.5)
can be midventricular, apical (giant -ve t waves), concentric
+/- LVOTO
w diastolic dysfunction

50
Q

What are symptoms of HCM?

A
asymptomatic screening
palpitations and syncope
sudden death in young pts
endocarditis
dysponoea (high diastolic pressures, small vessel disease, abnormal vascular responses, myocardial bridges, increased coronary vascular resistance)
angina
51
Q

What are signs of HCM?

A

ejection systolic murmur
variability -increased contractility, decreased preload, decreased afterload (murmur is decreased with squatting, isometric exercise), louder with standing
Mitral regurgitation is almost universal if obstructive

52
Q

What are IX in HCM?

A

Echo
MRI
ECG - can show anything
genetic studies

53
Q

What are principles of management of HCM?

A

treat heart failure - no impact on survival
B-blockers and CCB to improve filling and reduce ischaemia
reduce outflow obstruction - avoid digoxin, diuretics (increase obstruction) - alcohol septal ablation, surgical septoplasty
Prevent sudden death - b-blockers, AICD (risk assessment)
Screen 1st degree relatives

54
Q

What are risk factors for SCD in HCM?

A
FHX SCD
recurrent syncope in young
NSVT in adults
Severe LVH (septum 2.5-3cm)
Severe obstruciton
abnormal exercise blood pressure responses (decreased w exercise)
level of myocardial fibrosis on MRI
Arg719Trp mutation worse prognosis
55
Q

When should restrictive CM be suspected?

A
Predominantly right heart failure
LV systolic function preseved
ventricular wall thickness increased
diastolic dysfunction
atrial dilated (AF common)
AV regurgitation common, and may be severe
56
Q

What are differential diagnoses for restrictive CM?

A

Pericardial disease, esp constriction

Pulmonary arterial HTN

57
Q

What proportion of HF patients have LBBB?

A

up to 50%

increased mortality with LBBB, QRS >140 even adjusted for other factors

58
Q

What sport should be avoided in HF?

A

swimming!

59
Q

What effect does CPAP have on OSA in HF?

A

improves EF

60
Q

What are inotropes used in advanced CCF?

A

B-agonists - dobutamine, dopamine, adrenaline, noradrenaline - increased cyclic AMP
Phosphodiesterase inhibitors - milrinone, enoximone, amrinone

Calcium sensitisers - levosimendad - ino-dilator, not arrhythmogenic

61
Q

What are outcomes of inotrope use in HF?

A

generally increased mortality and side effects (except levosimendan)
should be used as critical support until definitive therapy
acute decompensation with poor tissue perfusion
a/w secondary condition resolution
bridging to transplant etc.

62
Q

What is the role of levosimendan?

A
Troponin C calcium sensitiser
enhanced SR release of Ca and reuptake
PDE III inhibitor at high doses
long t1/2 - 13 days
not arrhythmogenic
63
Q

What is the predominant mode of death in HF according to class?

A

Class II and III - sudden cardiac death

Class IV - heart failure

64
Q

What two studies support the use of AICD therapy in CHF primary prevention?

A

MADIT 2 - RR 30% in pts post AMI with LVEF

65
Q

What are indications for AICD in heart failure?

A

ICD in all mild-mod HF with EF 40 days post MI, EF measured more than 3 months post revascularisation
Add CRT if QRS wide, class 3-4
Class 4 without wide QRS - no device

66
Q

What proportion of HF patients have LBBB?

A

up to 50%

increased mortality with LBBB, QRS >140

67
Q

In what patients is BiV pacing recommended?

A

Wide QRS >=120-150msec
Low EF 150msec
Sx despite optimal therapy

most benefit in those with QRS >150msec

68
Q

What are benefits of CRT in HF?

A

increased NYHA class and improved LVED on echo with CRT.

Reduced death and hospitalisation.

Benefits also extend to patients with NYHA class II (mild HF)

69
Q

What is the benefit of Bi-V pacing in patients with AV block and systolic dysfunction (high degree AV block)

A

Improved all cause death, HF hospitalisation

70
Q

What are current indications for cardiac transplant in australia?

A
Refractory class III-IV NYHA HF
VO2 max
71
Q

What are inadequate indications for transplantation?

A

EF 15ml/min/kg without any other indication

72
Q

What is overall survival in patients post cardiac transplantation?

A

Death rate is ~4%/year, with half dead at 9 years

73
Q

What is the effect of LVADs in heart failure?

A
improved mortality (decreased by 48%)
higher neurological rates and device malfunction