Drug-Induced Cardiac Disease- Drug-Induced HF Flashcards

1
Q

3 causes of drug-induced HF

A

Sodium and volume retention

Direct cardiotoxicity

Negative inotropy

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2
Q

Drugs that can cause sodium and volume retention

A

NSAIDs, steroids, TZDs

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3
Q

Mechanism of drug-induced HF for NSAIDs and steroids

A

Both of them are global anti-inflammatory agents

Decreases prostaglandins in the kidney → allows for vasodilation of the afferent and efferent arterioles and Na and H2O excretion –> increase the rate of sodium and water retention –> symptoms of fluid overload and HF exacerbation

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4
Q

In drug-induced HF, NSAIDs also do what?

A

Increase systemic vascular resistance by increasing the pressure the LV has to push against

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5
Q

In HF patients, what should you do with NSAIDs and steroids?

A

Avoid use if possible, but if necessary, use at minimum doses and duration

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6
Q

Drugs that can cause direct cardiotoxicity

A

chemo agents, biologics, alcohol

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7
Q

Chemo agents that can cause direct cardiotoxicity

A

doxorubicin, daunorubicin (anthracyclines)

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8
Q

Anthracycline mechanism of damage

A

Inhibition of TOP2B causes DNA breakdown and cell death. When the cells die…

Increased free radicals of O2
Defective mitochondrial biogenesis
Causing cell death of cardiac myocytes and we’re releasing free radicals → damages the adjacent cardiac myocytes

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9
Q

Medication to prevent cardiotoxicity

A

Dexarozane, binds to TOP2B to prevent anthracycline binding

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10
Q

Anthracycline cardiotoxicity treatment-related risk factors

A

Cumulative dose of anthracyclines (>400mg/m2)

Dosing schedules

Previous anthracycline therapy

Radiation therapy

Coadministration of potentially cardiotoxic agents

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11
Q

Anthracycline cardiotoxicity patient-related risk factors

A

Older age
Preexisting CVD or risk factors
Obesity
Smoking
Gender (but there’s not a lot of clear cut evidence on this)

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12
Q

Lifetime cumulative dose max of anthracyclines

A

550mg/m2

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13
Q

Biologic that can cause drug-induced HF

A

Trastuzumab

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14
Q

Is cardiotoxicity caused by anthracyclines reversible?

A

No

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15
Q

Is cardiotoxicity caused by trastuzumab reversible?

A

Yes, just very slowly once it’s D/C’ed

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16
Q

Risk factors for trastuzumab-induced cardiotoxicity

A

Advanced age, presence of CV comorbidities, previous treatment with anthracyclines

17
Q

Trastuzumab mechanism

A

Inhibition of HER2 proteins and human ERBB2 (?) signaling in cardiac myocytes, both necessary for growth and repair of cardiac muscles. When they can’t grow and repair → increases breakdown and cell death

18
Q

Trastuzumab’s effects on ROS, NOS, NO, and angiotensin II

A

Increased ROS
Reduced NOS expression
Reduced NO bioavailability
Increased angiotensin II

19
Q

Trastuzumab CIs

A

There are no CIs based on the manufacturer, but it’s best to be avoided in patients with HF history

20
Q

Trastuzumab monitoring

A

Evaluate LVEF in all patients prior to and during treatment

21
Q

Trastuzumab treatment

A

dose adjust based on LVEF
Consider dose reduction or D/C if HF develops
Consider using HF medications during treatment if EF declines

22
Q

Alcohol mechanism to cause cardiotoxicity

A

direct toxic effect on the myocardium

23
Q

Drugs that can cause negative inotropy

A

Non-DHP CCBs (diltiazem, verapamil), beta-blockers

24
Q

How do non-DHP CCBs cause negative inotropy?

A

Decrease amount of squeeze the heart has to do; makes the muscle more tired so it can’t work as effectively

25
Q

Avoid non-DHP CCBs in patients with what EF?

A

<40% (HFrEF)

26
Q

Beta-blockers and HF

A

In stable HF, they can decrease long-term cardiomyopathy; over time, they can increase or maintain heart function

27
Q

Avoid beta-blockers in what patients?

A

Patients with acute HF exacerbations