Therapy of Chronic Heart Disease Flashcards

1
Q

Heart failure (HF) is a progressive clinical syndrome associated with:

A

Impairment of the ability of the ventricle to fill with or eject blood

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2
Q

HF may be caused by an abnormality in:

A

1) Systolic function
2) Diastolic function
3) Both

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3
Q

What are the leading causes of HF?

A

1) Coronary artery disease
2) Hypertension

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4
Q

In heart failure with reduced ejection fraction (HFrEF) there is a decrease in:

A

Cardiac output

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5
Q

What compensatory responses happen due to heart failure with reduced ejection fraction (HFrEF)?

A

1) Activation of the sympathetic nervous system (SNS) and the renin–angiotensin–aldosterone system (RAAS)

2) Vasoconstriction
3) Sodium and water retention
4) Ventricular hypertrophy and remodeling

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6
Q

Pharmacotherapy targeted at ____ has slowed the progression of HFrEF and improved survival.

A

Antagonizing the neurohormonal activation

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7
Q

Heart failure with preserved ejection fraction (HFpEF) is primarily due to:

A

1) Diastolic dysfunction
2) Disturbances in relaxation

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8
Q

What are the causes of systolic dysfunction (decreased contractility)?

A

1) Reduction in muscle mass (MI)
2) Dilated cardiomyopathies
3) Ventricular hypertrophy
4) Pressure overload (systemic or pulmonary hypertension, aortic or pulmonary valve stenosis)
5) Volume overload (valvular regurgitation, shunts, high-output states)

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9
Q

What are the causes of diastolic dysfunction (restriction in ventricular filling)?

A

1) Increased ventricular stiffness
2) Ventricular hypertrophy (hypertrophic cardiomyopathy, others)
3) Infiltrative myocardial diseases (amyloidosis, sarcoidosis, endomyocardial fibrosis)
4) Myocardial ischemia and infarction
5) Mitral or tricuspid valve stenosis
6) Pericardial disease (pericarditis, pericardial
tamponade)

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10
Q

What are the factors precipitating/exacerbating
heart failure?

A

1) Cardiac events
2) Noncardiac events
3) Nonadherence with prescribed HF medications or with dietary recommendations
4) Drugs

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10
Q

How can drugs precipitate or exacerbate HF?

A

1) Negative inotropic effects
2) Direct cardiotoxicity
3) Increased sodium and/or water retention

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11
Q

Which drugs have negative inotropic effects?

A

1) Antiarrhythmics
2) Beta-blockers
3) Calcium channel blockers

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12
Q

Which Antiarrhythmics have negative inotropic effects?

A

1) Disopyramide
2) Flecainide
3) Propafenone

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13
Q

Which Beta-blockers have negative inotropic effects?

A

1) Propranolol
2) Metoprolol
3) Carvedilol

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14
Q

Which Calcium channel blockers have negative inotropic effects?

A

1) Verapamil
2) Diltiazem

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15
Q

Which drugs can cause cardiotoxicity?

A

1) Doxorubicin
2) Epirubicin
3) Daunomycin
4) Ethanol
5) Cyclophosphamide
6) Trastuzumab
7) Bevacizumab
8) Ifosfamide
9) Lapatinib
10) Sunitinib
11) Imatinib
12) Amphetamines
13) Cocaine

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16
Q

Which drug contains high sodium?

A

Ticarcillin disodium

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16
Q

Which drugs can cause sodium and/or water retention?

A

1) NSAIDs
2) COX2-inhibitors
3) Rosiglitazone
4) Pioglitazone
5) Glucocorticoids
6) Androgens and Estrogens
7) High dose Salicylates
8) High sodium-containing drugs

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17
Q

___ and _____ are part of
CHF therapy.

A

Medication history; Discontinuation of medications known to exacerbate HF

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18
Q

What are key elements in the pathogenesis of progressive myocardial failure?

A

Left ventricular hypertrophy and remodeling

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19
Q

Ventricular remodeling is a broad term describing:

A

Changes in both:
1) Myocardial cells
2) Extracellular matrix

= changes in the size, shape, structure, and function of the heart.

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20
Q

What is the normal shape of the left ventricle?

A

Ellipse

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21
Q

What is the shape of the left ventricle after remodeling?

A

Sphere

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22
Q

The change in ventricular size and shape during remodeling further:

A

1) Depresses the mechanical performance of the heart
2) Increases regurgitant flow through the mitral valve
3) Sustains progression of remodeling

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23
Q

The onset of the ___ precedes
the development of HF symptoms.

A

Remodeling process

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24
Q

Which mediators play an important role in initiating the signal transduction cascade responsible for ventricular remodeling?

A

1) Angiotensin II
2) NE
3) Endothelin
4) Aldosterone
5) Vasopressin
6) Numerous inflammatory cytokines

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25
Q

The goals of therapy in management of chronic
HF are to:

A

1) Improve the patient’s quality of life
2) Relieve or reduce symptoms
3) Prevent or minimize hospitalizations
4) Slow progression of the disease
5) Prolong survival

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26
Q

The general principles used to guide the treatment of HFrEF are based on:

A

Numerous large, randomized, double-blind, multicenter clinical trials.

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27
Q

The guidelines for the management of HFpEF are based primarily on:

A

Studies in relatively small groups of patients and on clinical experience.

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28
Q

The complexity of the HF syndrome necessitates a comprehensive approach to management, which includes:

A

1) Accurate diagnosis
2) Identification and treatment of risk factors
3) Elimination or minimization of precipitating factors
4) Appropriate pharmacologic and nonpharmacologic therapy
5) Close monitoring and follow up

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29
Q

What is the first step in management of chronic HF?

A

Determine the etiology and/or precipitating factors

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30
Q

___ in patients with CHD may reduce HF symptoms.

A

Revascularization or anti-ischemic therapy

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31
Q

___ reduces cardiac workload and is recommended for all patients with acute congestive symptoms, until patient’s symptoms have stabilized and excess fluid is removed.

A

Restriction of physical activity

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32
Q

What may improve functional status & quality of life, and may reduce hospitalizations and death from cardiovascular causes?

A

Exercise training

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33
Q

In patients with hyponatremia (Na ˂130 mEq/L) or those with persistent volume retention despite high diuretic doses and sodium restriction, daily fluid intake should be:

A

Limited to 2 L/day from all sources.

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34
Q

You should be careful with sodium and fluid restriction in patients with:

A

HFpEF

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35
Q

Why should you be careful with sodium and fluid restriction in patients with HFpEF?

A

Because excessive restriction can lead to:
1) Hypotension
2) Low-output state
3) Renal insufficiency

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36
Q

What are the four identified stages of HF?

A

1) Patients at Risk for HF
2) Patients With Pre-HF
3) Stage C HF
4) Stage D (Advanced) HF

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37
Q

What is the first stage of HF? (Patients at Risk for HF)

A

Patients with cardiac disease but without limitations of physical activity

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38
Q

What interventions can be taken to prevent the first stage of HF from progressing?

A

1) If Hypertensive: Reduce BP
2) If type 2 diabetes: SGLT2i
3) Healthy life style habits
4) Risk factor identification and prevention

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39
Q

Risk factors act ___(additively/synergistically) to develop both HFrEF and HFpEF.

A

Synergistically

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40
Q

___ and ___ are recommended for HF prevention in patients with multiple cardiovascular risk factors.

A

ACE inhibitors/ARBs; Statins

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41
Q

What is the second stage of HF? (Patients With Pre-HF)

A

Patients with cardiac disease that results in slight limitations of physical activity.

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42
Q

Patients with the second stage of HF (Patients With Pre-HF) have:

A

Structural heart disease but NOT
HF symptoms.

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43
Q

What does structural heart disease include in patients with the second stage of HF (Patients With Pre-HF)?

A

1) Left ventricular hypertrophy
2) Recent or old MI
3) Valvular heart disease
4) LVEF ˂ 0.4

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44
Q

How can you prevent clinical HF in patients with Pre-HF (2nd stage) with LVEF ≤ 40%?

A

ACEIs should be used to prevent symptomatic HF and reduce mortality

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45
Q

How can you prevent clinical HF in patients with Pre-HF (2nd stage) with a history of MI or ACS?

A

Statins should be used to prevent symptomatic HF and adverse cardiovascular events.

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46
Q

How can you prevent clinical HF in patients with Pre-HF (2nd stage) with a history of MI or ACS and LVEF ≤ 40%?

A

Evidence-based beta blocker should be used to reduce mortality

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47
Q

Which drugs should not be used in patients with LVEF ≤50%?

A

1) Thiazolidindiones
2) Non-hydropyridine calcium channel blockers

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48
Q

What is the third stage of HF? (Stage C HF)

A

Patients with cardiac disease that results in marked limitation of physical activity.
Although patients are comfortable at rest, less than ordinary activity will lead to symptoms

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49
Q

Patients with structural heart disease and previous or current symptoms are classified as ___ and can have HFrEF or HFpEF.

A

Stage C

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50
Q

Patients with HF should receive vaccination for ___ to reduce mortality.

A

Respiratory illnesses

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51
Q

Patients with HF should be screened for ___ and other risk factors for poor self care.

A

Depression

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52
Q

Which drugs are recommended in patients with heart failure with fluid retention?

A

1) Loop diuretics
2) Metolazone (If no response)

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53
Q

In patients with HFrEF and NYHA class II-III symptoms, the use of ___ is recommended to reduce morbidity and mortality.

A

ARNi (angiotensin receptor/neprilysin inhibitor)

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54
Q

In patients with previous or current symptoms of chronic HFrEF, the use of ___ is beneficial to reduce morbidity and mortality when the use of ARNi is not feasible.

A

ACEIs/ARBs

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55
Q

ARNi should not be coadministered with __ or within ____.

A

ACEIs; the last 36 hours of the last dose of ACEIs.

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56
Q

ARNi should not be administered in any patient with a history of ___.

A

Angioedema

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57
Q

___ should not be administered in any patient with a history of angioedema.

A

ACEIs

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58
Q

In patients with previous or current symptoms of chronic HFrEF, use of one of the three ____ is recommended to reduce mortality and hospitalization

A

Beta blockers

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59
Q

In patients with HFrEF and NYHA class II-IV symptoms, which drug is recommended to
reduce morbidity and mortality if eGFR is > than 30 mL/min and serum potassium < 5 mEq/L?

A

Aldosterone receptor antagonist (Spironolactone or Eplerenone)

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60
Q

For African-American patients with NYHA class III-IV HFrEF who receive optimal therapy, the combination _____ is recommended to improve symptoms and reduce morbidity and mortality,

A

Hydralazine and Isosorbide dinitrate

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61
Q

In patients who can not receive ACEIs, ARNi or ARB, ___ is recommended to reduce morbidity and mortality.

A

Hydralazine and isosorbide dinitrate

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62
Q

For patient with symptomatic (NYHA class II-III) stable chronic HFrEF (≤ 35%) who are receiving GDMT, including beta blocker at maximum tolerated dose, and who are in sinus rhythm with a heart rate of ≥ 70 bpm at rest, ___ can be beneficial to reduce heart failure hospitalization and cardiovascular death.

A

Ivabradine

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63
Q

In patients with symptomatic HFrEF despite GDMT (or who are unable to tolerate GDMT), ___ may be considered to decrease hospitalization for HF.

A

Digoxin

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64
Q

In selected high risk patients with HFrEF and recent worsening of HF already on GDMT an ____ may be considered to decrease HF hospitalization and cardiovascular death.

A

Oral soluble guanylate cyclase stimulator

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65
Q

Nonpharmacologic therapy with devices such as _____is also indicated in certain patients with HFrEF in Stage C.

A

1) Implantable cardioverter-defibrillator (ICD)
2) Cardiac resynchronization therapy (CRT) with a biventricular pacemaker

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66
Q

What is Stage D (Advanced) HF?

A

Patients with cardiac disease that results in an inability to carry on physical activity without discomfort.
Symptoms of congestive heart failure are present even at rest

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67
Q

In patients with advanced heart failure, when consistent with patient’s goal of care, timely
referral for HF specialty care is recommended to:

A

1) Review HF management
2) Assess suitability for advanced HF therapies (left ventricular assist device [LVAD], cardiac
transplantation, palliative care and palliative inotropes).

68
Q

Guidelines for Stage D HFpEF recommend treating co-morbid
conditions by:

A

1) Controlling HR and BP
2) Alleviating causes of myocardial ischemia
3) Reducing volume
4) Restoring and maintaining sinus rhythm in patients with atrial fibrillation

69
Q

What are the 3 treatment approaches for HFpEF?

A

1) Symptom-targeted treatment
2) Disease-targeted treatment
3) Mechanism-targeted treatment

70
Q

What is the symptom-targeted treatment for HFpEF?

A

1) Decrease pulmonary venous pressure
2) Reduce myocardial oxygen demand
3) Maintain atrial contraction
4) Improve exercise tolerance

71
Q

What is the rationale for decreasing pulmonary venous pressure in HFpEF?

A

Reduce left ventricular volume

72
Q

What is the rationale for reducing myocardial oxygen demand in HFpEF?

A

1) Reduce HR
2) Control BP

73
Q

What is the rationale for maintaining atrial contraction in HFpEF?

A

Restore sinus rhythm

74
Q

Which agents can decrease pulmonary venous pressure?

A

1) Diuretics
2) Nitrates
3) Salt restriction

75
Q

Which agents can reduce myocardial oxygen demand?

A

1) Beta-Blockers
2) Verapamil
3) Diltiazem
4) ACEi/ARBs
5) CCBs

76
Q

Which agents can maintain atrial contraction?

A

Cardioversion of A-fib

77
Q

Which agents can improve exercise tolerance?

A

Use positive inotropic agents with caution

78
Q

What is the disease-targeted treatment for HFpEF?

A

1) Prevent or treat myocardial ischemia
2) Prevent or regress ventricular hypertrophy

79
Q

Which agents can prevent or treat myocardial ischemia?

A

1) Beta-Blockers
2) Nitrates
3) Verapamil
4) Diltiazem

80
Q

Which agents can prevent or regress ventricular hypertrophy?

A

Antihypertensives

81
Q

What is the mechanism-targeted treatment for HFpEF?

A

1) Modify myocardial and extramyocardial mechanisms
2) Modify intracellular and extracellular mechanisms

82
Q

Which agents can modify myocardial and extramyocardial mechanisms?

A

1) ACEis/ARBs
2) Diuretics
3) Spironolactone

83
Q

Which agents can modify intracellular and extracellular mechanisms?

A

1) ACEis/ARBs
2) Diuretics

84
Q

In patients with atrial fibrillation who are intolerant to or have NOT responded to a βblocker; ____ may be considered.

A

1) Diltiazem
2) Verapamil

85
Q

A nondihydropyridine or dihydropyridine calcium channel blocker can be considered for ___.

A

Angina and hypertension

86
Q

___ and __ are recommended for the treatment of both HFrEF and HFpEF.

A

β-blockers and diuretics

87
Q

In HFpEF, β-blockers are used to:

A

1) Decrease HR
2) Prolong diastole
3) Modify hemodynamic response to exercise

88
Q

In HFrEF, β-blockers are used in the long term to:

A

1) Improve the inotropic state
2) Modify LV remodeling

89
Q

The doses of diuretics used to treat ___ are much smaller than those used to treat ___.

A

HFpEF; HFrEF

90
Q

____ are useful in lowering BP and reducing LVH.

A

Antagonists of the RAAS

91
Q

___ may be useful in the treatment of HFpEF.

A

Calcium channel blockers

92
Q

Which calcium channel blockers are usefulin HFpEF?

A

1) Diltiazem
2) Amlodipine
3) Verapamil

93
Q

The natriuretic peptides ANP and BNP cause:

A

1) Vasodilation
2) Natriuresis
3) Diuresis

94
Q

What do the natriuretic peptides ANP and BNP do?

A

1) Inhibit renin secretion
2) Inhibit aldosterone production
3) Attenuate ventricular hypertrophy and fibrosis

95
Q

What is Neprilysin?

A

A zinc-dependent metalloprotease

96
Q

Function of Neprilysin?

A

1) Breaks down the natriuretic peptides ANP & BNP, bradykinin and other peptides
2) Clearance of amyloid-β from the brain and CSF

97
Q

ARB/Neprilysin Inhibitor such as ___ can be used for the treatment of patients with HFrEF.

A

Valsartan/Sacubitril

98
Q

___ is a prodrug, which inhibits the action of neprilysin.

A

Sacubitril

99
Q

What are the adverse effects of Valsartan/Sacubitril?

A

1) Hypotension
2) Dizziness
3) Hyperkalemia
4) Worsening renal function
5) Cough
6) Angioedema

100
Q

Valsartan/Sacubitril should not be used with:

A

1) ACEis or ARBs
2) Aliskiren

101
Q

Valsartan/Sacubitril contraindications?

A

1) History of angioedema
2) Pregnancy
3) Hyperkalemia
4) Renal artery stenosis
5) Severe hepatic impairment
6) Renal dysfunction
7) Diabetic patients taking Aliskiren

102
Q

Where does Ivabradine act?

A

Blocks the If current in the SA node that is responsible for controlling the heart rate.

103
Q

What does Ivabradine do?

A

Slows the spontaneous depolarization of the sinus node = dose-dependent slowing of HR

104
Q

Ivabradine’s effects are specific to the If current and does not affect:

A

1) Myocardial contractility
2) AV conduction

105
Q

Ivabradine is extensively metabolized by intestinal and hepatic ___.

A

CYP3A4

106
Q

Ivabradine is contraindicated in which patients?

A

1) Patients taking CYP3A4 inhibitors = bradycardia
2) Patients taking CYP3A4 inducers = prolongs QT

107
Q

Adverse effects of Ivabradine?

A

1) Bradycardia
2) Effects on vision primarily manifesting as phosphenes (transient brightness in portions of the visual field)
3) Atrial fibrillation

108
Q

In the heart, natriuretic peptides lead to the activation of the ___ pathway.

A

Nitric Oxide-soluble Guanylate Cyclase-cGMP

109
Q

Soluble Guanylate Cyclase (sGC) stimulators activate:

A

sGC independent of NO by binding to a non-heme site in sGC

110
Q

Which sGC stimulator has been in use for pulmonary hypertension?

A

Riociguat

111
Q

What is Vericigaut?

A

sGC stimulator

112
Q

Vericigaut has significant benefits in reducing hospitalizations in patients with ___ that are at high risk of cardiovascular events.

A

HFrEF

113
Q

Does Vericiguat have a mortality benefit?

A

NO

114
Q

Vericigaut is contraindicated in which patients?

A

1) Those with concomitant use of other soluble guanylate cyclase (sGC) stimulators
2) Pregnancy

115
Q

Unless contraindicated, ___ should be initiated early as part of the foundational therapy in all patients with HF.

A

SGLT2 inhibitors

116
Q

SGLT2 inhibitors have been shown to reduce risks of clinical events in patients with heart failure (HF), with early and sustained benefits regardless of:

A

1) Ejection fraction
2) Diabetic status
3) Care setting

117
Q

Contraindications for SGLT2 inhibitors?

A

1) Type 1 DM or history of ketoacidosis
2) Hypotension (systolic BP<100mmHg)
3) Severe kidney disease (eGFR <20-25mL/min/1.73m2)
4) Pregnancy, risk of pregnancy, breast feeding
5) Caution in patients with a history of recurrent UGS infections

117
Q

Association of ____ was the best combination for reducing all-cause death and the composite outcome of cardiovascular death or hospitalization for HF, and serious adverse renal outcomes in patients with a broad spectrum of severity of HFrEF.

A

1) ARNi
2) β-blockers
3) Aldosterone receptor antagonists
4) SGLT2 inhibitors

118
Q

What should you monitor when giving SGLT2 inhibitors?

A

1) Check renal function when starting therapy and after 1-2 weeks
2) Blood glucose
3) Observe for acute illness or major surgery

119
Q

Patient/caregiver counselling for SGLT2 inhibitors?

A

1) Ensure adequate daily genital hygiene
2) Watch for symptoms of volume depletion, urogenital infection, and diabetic ketoacidosis
3) Avoid dehydration, low carbohydrate (ketogenic) diet, and excessive alcohol consumption

120
Q

What are the benefits of diuretics?

A

1) Reduction of symptoms associated with fluid retention
2) Improvement of exercise tolerance and quality of life
3) Reduction of hospitalizations from HF
4) Reduction of pulmonary and peripheral edema through reduction of preload

121
Q

True or False:
Diuretics prolong survival and alter disease progression.

A

False

122
Q

Over-diuresis may produce __ with ACE inhibitor or β-blocker therapy.

A

Hypotension

123
Q

Hypotension can be a significant problem in the treatment of HFpEF because:

A

A small change in volume causes a large change in filling pressure and cardiac output.

124
Q

___(Loop/Thiazide) diuretics may be preferred in patients with mild fluid retention and elevated BP because of their
more persistent antihypertensive effects.

A

Thiazide

125
Q

____ or ____ can inhibit delivery of loop diuretics to their site of action and decrease effectiveness.

A

1) Probenecid
2) Organic by-products of uremia

126
Q

Loop diuretics should not be given with:

A

NSAIDs

127
Q

Unlike thiazides, loop diuretics maintain their effectiveness in the presence of:

A

Impaired renal function

128
Q

The most common cause of HFrEF is:

A

Ischemic heart disease

129
Q

Which ACEi’s benefit post-MI patients whether therapy is initiated early or late after the infarct?

A

1) Captopril
2) Ramipril
3) Trandolapril

130
Q

CKD patients should be monitored carefully for the development of:

A

1) Worsening renal function
2) Hyperkalemia

131
Q

True or False: ACEi’s improve survival rate.

A

True

132
Q

Do ARBs cause cough or angioedema?

A

No

133
Q

Do ACEi’s cause cough or angioedema?

A

Yes

134
Q

Which drugs are ARBs?

A

1) Candesartan
2) Losartan
3) Valsartan

135
Q

ARBs are indicated in which patients?

A

Those who are unable to tolerate cough produced by ACE inhibitors.

136
Q

____ should be used in all stable patients with HF and a reduced left ventricular EF in the absence of contraindications.

A

β-blockers

137
Q

___ are recommended for asymptomatic patients with a reduced left ventricular EF to decrease the risk of progression to HF.

A

β-blockers

138
Q

Three β-blockers have been shown to significantly reduce mortality compared with placebo:

A

1) Carvedilol
2) Metoprolol succinate (CR/XL)
3) Bisoprolol

139
Q

What have the 3 main β-blockers been shown to do?

A

Reverse modeling:
1) Decrease ventricular mass
2) Reverse the sphericity of the ventricle
3) Reduce systolic and diastolic volumes

140
Q

What does reverse modeling mean?

A

Return of the heart toward more normal size, shape, and function

141
Q

Initiating a β-blocker first may be of benefit for which patients?

A

1) Those with evidence of excessive SNS activity (tachycardia)
2) Those whose renal function or potassium concentrations preclude starting an ACEi (or ARB) at that time

142
Q

The risk for decompensation during β-blocker initiation may be greater in the absence of:

A

Preexisting ACE inhibitor therapy

143
Q

β-Blockers favorable effects include:

A

1) Antiarrhythmic effects
2) Attenuating or reversing ventricular remodeling
3) Decreasing myocyte death from catecholamine-induced necrosis or apoptosis
4) Preventing fetal gene expression
5) Improving left ventricular systolic function
6) Decreasing HR and ventricular wall stress thereby reducing myocardial oxygen demand
7) Inhibiting plasma renin release

144
Q

β-blockers should NOT be started in patients on:

A

IV inotropic support

145
Q

How should β-blockers be started?

A

1) In very low doses with slow upward dose titration (not ˂ 2 weeks)
2) Close monitoring to minimize acute decompensation

146
Q

Dose up-titration is a __(long/short) process.

A

Long

147
Q

In patients with HFpEF, How might β-blockers help lower and maintain low pulmonary venous pressure?

A

By decreasing HR and increasing the duration of diastole

148
Q

Why is tachycardia poorly tolerated in patients with HFpEF?

A

Because rapid HRs cause an increase in myocardial oxygen demand and a decrease in coronary perfusion time, which can promote ischemia even in the absence of epicardial CAD

149
Q

Excessive bradycardia when using beta-blockers can result in:

A

A fall of cardiac output despite an increase in LV filling

150
Q

Which aldosterone antagonists have potassium sparing effects?

A

1) Spironolactone
2) Eplerenone

151
Q

Aldosterone antagonists inhibit ____, thereby attenuating cardiac fibrosis and ventricular remodeling.

A

Cardiac extracellular matrix and collagen deposition

152
Q

What are the most common adverse effects of Spironolactone?

A

1) Gynecomastia
2) Hyperkalemia

153
Q

What is the most common adverse effect of Eplerenone?

A

Hyperkalemia

154
Q

There are NO clear guidelines on aldosterone antagonist use for patients with:

A

HFpEF

155
Q

What are the factors contributing to the high incidence of hyperkalemia with aldosterone antagonists?

A

1) The initiation of aldosterone antagonists in patients with impaired renal function or high serum K+

2) The failure to decrease or stop potassium supplements when starting aldosterone antagonists

3) Diabetes mellitus

4) High potassium intake with food

5) Concomitant use of ACEi/ARBs and NSAIDs.

156
Q

Strategies for reducing the risk for hyperkalemia with aldosterone antagonists:

A

1) Avoid starting aldosterone antagonists in patients with abnormal labs

2) Start with low doses

3) Decrease or discontinue potassium supplements when starting an aldosterone antagonist

4) Avoid concomitant use of NSAIDs (COX-1 or COX-2 inhibitors) or high-dose ACEi or ARBs

5) Monitor serum K+ and renal function

6) If K+ exceeds 5.5 mg/dL at any point during therapy, reduce or stop aldosterone antagonist therapy

157
Q

What abnormal labs prevent you from starting aldosterone antagonists out of fear of hyperkalemia?

A

1) Serum creatinine concentration >2.0 mg/dL in women or >2.5 mg/dL in men or a CrCL <30 mL/min

2) Recent worsening of renal function

3) Serum K+ >5 mEq/L

4) History of severe hyperkalemia

158
Q

How should you counsel patients taking aldosterone antagonists?

A

1) Limit intake of high potassium-containing foods and salt substitutes
2) Avoid the use of over-the-counter NSAIDs
3) Temporarily discontinue aldosterone antagonist therapy if diuretic therapy is interrupted

158
Q

__ and __ are combined in the treatment of HFrEF because of their complementary hemodynamic actions.

A

1) Nitrates
2) Hydralazine

159
Q

Nitrates cause:

A

Venodilation = decrease preload

160
Q

Hydralazine causes:

A

Arterial vasodilation = decreased afterload

161
Q

Hydralazine is a:

A

Direct-acting arterial vasodilator

162
Q

Nitric oxide attenuates myocardial remodeling by reducing:

A

1) Cardiac myocyte hypertrophy
2) Cardiac dilation
3) Mortality

163
Q

Digoxin has a:

A

Positive inotropic effect on the heart

164
Q

What is the benefit of digoxin on hospitalizations and mortality?

A

NONE

165
Q

True or False: Digoxin is a first line agent in HF.

A

False

166
Q

There is NO established role for Digoxin in ___ when patients are in normal sinus rhythm.

A

HFpEF

167
Q

What does Digoxin help control?

A

Ventricular response in patients with HFrEF and supraventricular arrhythmias