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Spring 2024 Therapeutics 3 > Exam 1: Coronary Artery Disease > Flashcards

Exam 1: Coronary Artery Disease Flashcards

1
Q

What is angina?

A

Chest pain/ shortness of breath caused when heart muscles receive insufficient oxygen-rich blood

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2
Q

What is ischemia?

A

Condition where blood flow and oxygen are reduced to a part of the body

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3
Q

What is the number one cause of death in both men and men?

A

Atherosclerotic CAD
(coronary artery disease)

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4
Q

How does age impact the incidence of Atherosclerotic CAD?

A

Increases with age

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5
Q

How does gender impact the incidence of Atherosclerotic CAD?

A

More common in men than women until menopause

-After menopause the incidence is equal

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6
Q

What fraction of deaths in the US are caused by Atherosclerotic CAD each year?

A

1 in every 3 deaths (1/3)

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7
Q

What is the main factor contributing to the increase in Atherosclerotic CAD over time?

A

Diet

-has changed over the last centuries and CAD has increased with it

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8
Q

What type of disease is Stable angina pectoris considered?

A

Macrovascular disease

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9
Q

What type of disease is Variant or Printzmetal’s angina considered?

A

Vasospastic disease

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10
Q

What type of disease is Cardiac Syndrome X considered?

A

Microvascular disease

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11
Q

What are the 3 types of angina?

A

-Printzmetal’s Variant Angina
-Chronic Stable Angina
-Unstable Angina

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12
Q

What is Printzmetal’s Variant Angina?

A

Vasospasm

*Supply ischemia

-There is a spastic coronary artery, the artery becomes closed by a spasm, and this alters the supply of blood to muscle

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13
Q

What is Chronic Stable Angina?

A

Fixed Stenosis (fixed narrowing of artery from a plaque)

*Demand Ischemia (only one)

-Fixed threshold

-Blockage resulting in ischemia upon exertion

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14
Q

What is Unstable Angina?

A

*Thrombus

*Supply Ischemia

-Atherosclerotic plaque progresses and forms a thrombus in the artery

-The thrombus added to the plaque eventually causes the vessel to fully close which can lead to tissue death (infarction)

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15
Q

What 3 factors contribute to oxygen demand ?

A

*Wall tension
(affected by systolic pressure and left ventricular volume)

*Contractility

*Heart Rate

(all can be targeted by drugs)

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16
Q

What 3 things lead to Decreased Coronary Blood Flow?

A

-Fixed Stenosis
-Vasospasm
-Thrombus

(these are all related to the 3 types of angina)

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17
Q

What 4 things lead to Increased Oxygen Consumption?

A

-Increased Heart Rate
-Increased Contractility
-Increased Afterload
-Increased Preload

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18
Q

How would a patient know they have ischemia?

A

If they experience:

-Angina (chest pain)
-Anginal Equivalents (normally due to other diseases they have like heart failure, ex: SOB)

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19
Q

How will a decrease in heart contractility affect O2 consumption?

A

O2 consumption will decrease

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20
Q

What affect will a decreased heart rate have on O2 consumption and coronary perfusion?

A

O2 consumption will decrease

Coronary perfusion will increase

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21
Q

How is preload decreased?

A

Venodilation

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22
Q

What effect does decreasing preload have on O2 Consumption and Myocardial Perfusion?

A

O2 consumption decreases

Myocardial perfusion increases

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23
Q

How is afterload decreased?

A

Dilation of arteries

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24
Q

A decrease in afterload has what affect on O2 consumption?

A

Decrease in O2 consumption

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25
Q

What disease is stable angina pectoris usually associated with?

A

Single to Multivessel ASCAD (atherosclerotic coronary artery disease)

(plaque buildup in the arteries)

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26
Q

What percentage of patients experiencing angina have significant coronary artery disease?

A

85%

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27
Q

What percent of atherosclerotic reduction is defined as “significant coronary artery disease”?

*hint: this is also the percent of blockage typically required to develop a thrombus

A

> 70-75%

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28
Q

True or False: 50-70% blockage in a vessel can cause ischemia

A

FALSE

> 70-75% of blockage in a vessel is required to cause ischemia

*this is typically caused by plaque buildup

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29
Q

What is myocardial ischemia?

A

An imbalance between myocardial oxygen supply and demand

-Usually effort induced!!! when there is a decrease in oxygen supply

-Typically caused by atherosclerotic plaque accumulation

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30
Q

What are the effects of myocardial ischemia?

A

Disturbances in myocardial function without causing myocardial necrosis

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31
Q

What is angina?

A

-The resulting symptoms from ischemia
(chest discomfort)

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32
Q

What is the relationship between ischemia and angina?

A

Ischemia is what happens

Angina is the outward symptom that the patient describes

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33
Q

What is the difference between stable and unstable angina?

A

Stable: occurs predictably with physical activity or emotional stress. Lasts a short time and is typically helped by medication

Unstable: Occurs unpredictably, even at rest or with minimal exertion. It worsens in frequency and severity and is a medical emergency. patient should seek medical attention

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34
Q

What is an important thing to remember about stable angina regarding symptom characteristics?

A

Angina is considered “stable” when characteristics of an anginal episode (quality, frequency, severity, duration, time of day, etc) HAVE NOT CHANGED RECENTLY

(typically over the course of a few months)

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35
Q

True or False: Stable angina does not cause myocardial necrosis

A

TRUE

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36
Q

What is the clinical presentation of stable angina?

A

PQRST

P: precipitating factors: exertion

P: palliative measures: rest and/or sublingual nitroglycerin

Q: quality and quantity of the pain: squeezing, heaviness, tightening

R: region and radiation: substernal

S: severity of the pain: subjective, >5 out of 10 typically

T: timing and temporal pattern: lasts <20min, usually relieved in 5-10min

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37
Q

How long does stable angina normally last and how does this differ than MI?

A

Stable angina: usually relieved in 5-10 minutes

MI: Lasts LONGER than 20 minutes

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38
Q

What are some precipitating factors of stable angina?

A

-Exercise
-Effort involving use of arms above the head
-Weather (cold, warm and humid)
-Walking against wind
-Large meal
-Emotions with exercise
-Fright, anger
-Coitus
*Smoking

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39
Q

Where does the pain associated with angina typically radiate to?

A

-Left arm and shoulder
-Jaw
-Right arm (occasionally but less common)

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40
Q

What qualities are typically associated with angina?

A

-Pressure/heavy weight on chest
-SOB with feelings of constriction in the larynx or upper trachea
-Burning, tightness, crushing or visceral quality
-Gradual increase in intensity followed by gradual fading away
-Anginal equivalents present

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41
Q

What is one of the most common causes of hospitalization for patients with CAD?

A

Snow shoveling

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42
Q

Why are women and patients with diabetes often less likely to be properly diagnosed with CAD?

A

-They tend to have more silent episodes and report pain in different ways
-Providers are often biased toward diagnosing men and not women since men experience it earlier

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43
Q

What ECG finding is typically shown with angina?

A

ST-segment depression during event

-The ST-segment occurs directly before the beginning of the T wave

-Normally the ST-segment is flat, but with angina there is a curve downward

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44
Q

How do we diagnose CCD?

A

-History and physical examination
(determine risk factors)

-Electrocardiogram
(look for ST segment depression [ischemia] or elevation [variant angina])

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45
Q

How do we diagnose CHD?

A

-Treadmill or bicycle exercise testing

-Endpoints (duration, workload achieved, ECG changes, BP and HR responses, Symptoms)

-Double product (HR and Systolic BP used as an index of MVO2)

-Assessment of drug therapy

Beta-blockers and CCBs may complicate interpretation by decreasing HR

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46
Q

How may beta-blockers and CCBs complicate diagnostic procedures for CHD testing?

A

They make interpretation of the results of exercise testing and heart rate evaluation difficult since they lower heart rate

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47
Q

What are the diagnostic procedures for CHD?

A

-Cardiac imaging
—Stress testing
—Nuclear imaging
—Electron beam computerized
tomography (EBCT)

-Echocardiography

-Cardiac catheterization and coronary angiography

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48
Q

How is stress testing conducted?

A

-Patient is given dobutamine to increase their heart rate
-This is done when a patient cannot undergo exercise testing

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49
Q

How is EBCT (electron beam computerized tomography) conducted?

A

Non-invasive CT scan that allows you to quantify calcification (via a calcium score) that could be associated with plaque formation

-higher score=higher chance that plaque is more significant

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50
Q

How is coronary catheterization and coronary angiography conducted?

A

Catheterization: A catheter is introduced into the heart through the groin or wrist. Used to clear clogged arteries

Coronary angiography: A picture/visualization of the vessel. Is the only way to definitively assess a patient’s coronary anatomy
**very invasive and expensive, most commonly performed medical procedure in US

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51
Q

What is the first desired outcome for treatment of chronic coronary disease?

A

PREVENT DEATH
-Risk factor modification
-Prevent future events/death

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52
Q

What is the second desired outcome for treatment of chronic coronary disease?

A

ALLEVIATE OR PREVENT SYMPTOMS
-Manage anginal episodes
-Alleviate acute symptoms
-Prevent recurrent symptoms of ischemia

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53
Q

What is the MOA of aspirin?

A

Acetylates and irreversibly inactivates platelet COX-1

Has antiplatelet activity (blocks TXA2 synthesis)
–interferes with platelet aggregation
-prolongs bleeding time
-blocks arterial thrombi formation

***Aspirin DOES NOT affect thrombi that are already formed, only blocks creation of new ones

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54
Q

True or False: Aspirin will break up thrombi that are already formed

A

FALSE
-only blocks the formation of thrombi
-does not affect already made thrombi
-must be used chronically

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55
Q

What is the function of TXA2?

A

Formed by COX-1 to recruit and activate platelets

(COX-1 is blocked by aspirin which indirectly blocks TXA2)

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56
Q

Why do we only use low dose (81mg) aspirin and not high dose aspirin for CAD?

A

Low dose aspirin only inhibits COX-1 whereas high doe aspirin will inhibit both COX-1 and COX-2

COX-1 increases platelet aggregation and vasoconstriction which we want inhibited by aspirin

COX-2 inhibits platelet aggregation and induces vasodilation which we do not want inhibited!! Inhibiting this increases the risk of a thrombosis

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57
Q

What molecule does COX-1 synthesize?

A

Thromboxan A2 (TXA2)

-this promotes platelet aggregation and vasoconstriction)
-pro-thrombotic

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58
Q

What molecule does COX-2 synthesize?

A

Prostacyclin PGI2

-this inhibits platelet aggregation and increases vasodilation
-anti-thrombotic

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59
Q

What drugs are selective COX-2 inhibitors?

A

“coxibs”

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60
Q

What is the loading dose of aspirin? (soluble or EC)

A

162-325mg

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61
Q

What are the P2Y12 Inhibitor Platelet Drugs?

A

Clopidogrel (Plavix)
Prasugrel (Effient)
Ticagrelor (Brilinta)
Cangrelor (Kengreal)

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62
Q

What is the MOA of the P2Y12 inhibitors?

A

Selectively inhibit adenosine diphosphate (ADP) induced platelet aggregation

*no direct effect on TXA2

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63
Q

What is the loading and regular dose of Clopidogrel (Plavix)?

A

L: 300-600mg *

R: 75 mg daily

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64
Q

What is the loading and regular dose of Prasugrel (Effient)?

A

L: 60mg *

R: 10 mg daily

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65
Q

What is the loading and regular dose of Ticagrelor (Brilinta)?

A

L: 180mg*

R: 90 mg BID

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66
Q

What is the dosing of Cangrelor (Kengreal)?

A

IV only

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67
Q

What are the adverse effects of aspirin?

A

-GI bleeding
-Hematologic: bleeding (intracranial and extracranial)
-Hypersensitivity
-Major bleeding (2-3% in first year)

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68
Q

What is the purpose of enteric coated aspirins?

A

They do not dissolve in the stomach and only dissolve in the small intestine (alkaline environment)

-Reduces GI side effects and GI bleeding

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69
Q

If a patient thinks they are having a heart attack, how should we instruct them to take an aspirin?

A

-Tell the patient to take a low dose aspirin and CHEW it
-Otherwise the aspirin will take 4 hours to pass through the stomach and dissolve which is too much time

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70
Q

What is the recommended dose of aspirin for cardiovascular prevention?

A

81 mg

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71
Q

True or False: Antiplatelet medications can be used together

A

TRUE
-because they have different mechanisms of action in the aggregation cascade

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72
Q

Which two P2Y12 inhibitors are members of the Thienopyridine class?

A

Clopidogrel (Plavix)

Prasugrel (Effient)

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73
Q

Which two P2Y12 Inhibitors need to be activated by CYP (prodrugs)?

A

Clopidogrel (Plavix)

Prasugrel (Effient)

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74
Q

What P2Y12 Inhibitor does NOT need to be activated by CYP/ is direct acting?

A

Ticagrelor (Brilinta)

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75
Q

What is the typical half-lives of the P2Y12 Inhibitors?

A

5 days or 7 days

**keep this in mind before surgery

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76
Q

True or False: P2Y12 Inhibitors increase the risk of bleeding more significantly than aspirin

A

True

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77
Q

What are the adverse effects of the P2Y12 inhibitors?

A

Clopidogrel: Bleeding, Diarrhea, rash

Prasugrel: Bleeding, Diarrhea, Rash

Ticagrelor: Bleeding, Bradycardia, Heart Block, Dyspnea (SOB)

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78
Q

When added to aspirin, by how much do the P2Y12 inhibitors increase the risk of major bleeding?

A

Clopidogrel: 1% increase

Prasugrel: 0.6% increase

Ticagrelor: 1% increase

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79
Q

All patients with a history of CCD should receive which medication?

A

Aspirin 75-100 mg/day indefinitely

(prefer 81mg)

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80
Q

If a patient has an absolute contraindication to aspirin or a significant intolerance, what medication should they be started on instead?

A

Clopidogrel 75 mg/day indefinitely

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81
Q

What medication is considered SAPT (Single-Antiplatelet Therapy)?

A

Aspirin 75-100mg/day

OR

Clopidogrel 75 mg/day
(when aspirin is contraindicated)

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82
Q

What two medications are considered DAPT (Dual-Antiplatelet Therapy)?

A

Aspirin 81mg/day
+
P2Y12 Inhibitor (ex: Clopidogrel 75 mg/day)

*certain high risk patients receive both

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83
Q

What treatment should patients with No History of Stent Implantation receive?

(secondary prevention)

A

SAPT (Single-Antiplatelet Therapy)

High-risk patients: DAPT (Dual-Antiplatelet Therapy)

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84
Q

How is a stent placed?

A

-The stent (metal tubing) is put over an uninflated balloon and inserted into an artery
-The balloon is expanded at the site
-Cells surround the stent (endothelialize) and leave the vessel open
-Need to use antiplatelet therapy after the fact

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85
Q

What are the 2 types of stents?

A

Bare Metal Stents (rarely used)

Drug Eluting Stents
–3 generations
–2nd and 3rd mostly used
–Contain antiproliferative drugs to
prevent cell proliferation at site
–“limus” drugs

86
Q

Before an elective PCI (Percutaneous Coronary intervention) + Drug Eluting Stent, what medications are a patient given?

A

Aspirin loading dose (325mg)
and
P2Y12 Inhibitor loading dose

87
Q

After an elective PCI (percutaneous coronary intervention) + Drug Eluting Stent, if a patient has a LOW BLEEDING RISK, what medications are they given and for how long?

A

DAPT: Minimum 6 months

SAPT: Indefinitely

88
Q

After an elective PCA (percutaneous coronary intervention) + Drug Eluting Stent, if a patient has a HIGH BLEEDING RISK/OVERT BLEEDING, what medications are they given and for how long?

A

DAPT: 1-3 months

SAPT: P2Y12 inhibitor until 12 months

SAPT: Aspirin indefinitely

89
Q

Which P2Y12 Inhibitor is preferred for use with Elective PCI + Drug Eluting Stent placement?

A

NO DISTINGUISHMENT BETWEEN CHOICES, ANY ARE CORRECT

*Prefer to avoid Ticagrelor 90 mg BID because of dosing

Prefer: Clopidogrel 75mg daily or Prasugrel 10 mg daily

90
Q

When a patient undergoes CABG (coronary artery bypass graft), what medication regimen should they be put on?

A

DAPT for 12 MONTHS!
(aspirin 81 mg/day + clopidogrel 70 mg/day)

SAPT indefinitely
(aspirin 81 mg/day for life)

91
Q

If a patient is on both ticagrelor (Brilinta) and aspirin, how does this affect the dosing of aspirin used?

KNOW THIS

A

The dose of aspirin must be BELOW 100mg

92
Q

When a patient is taking both ticagrelor (Brilinta) and aspirin, the risk of which disease states increase?

A

-Cerebral Hemorrhage
-Stroke

**this is why the aspirin dose must be below 100mg!!!

93
Q

What are the benefits provided by ACE inhibitors and ARBs for CCD?

A

-Stabilize plaque formation

-Improve endothelial function

-Inhibit VSM (vascular smooth muscle) cell growth

-Decrease macrophage migration

-Anti-oxidant properties??

DO NOT PROVIDE SYMPTOM RELIEF

94
Q

Why are ACEi and ARBs used for CCD?

A

They reduce the progression of the disease and decrease the likelihood of having cardiovascular events

They do not reduce symptoms

95
Q

True or False: ACEi and ARBs improve symptomatic ischemia

A

FALSE

-they do not reduce angina or other disease symptoms

96
Q

True or False: All patients with CCD should receive an ACEi or an ARB

A

TRUE

-these drugs should be considered in all patients with CCD

-may have a lower benefit in lower risk patients though

97
Q

What patient populations have the greatest benefit from receiving an ACEi or an ARB?

A

LVEF <40% (left ventricular ejection fraction)

HTN

DM

CKD

98
Q

Who should receive ARBs instead of ACEi’s?

A

-Patients intolerant to ACEi
(cough or adverse effects)

99
Q

True or False: ACEi and ARBs can be used together to treat CCD

A

FALSE

-never use these drugs together

100
Q

What is colchicine normally used to treat?

A

Gout

101
Q

What is the mechanism of action of colchicine/ how does it work?

A

Reduces inflammation

by: reducing IL-1B and IL-18

102
Q

What is the role of colchicine in treating CCD, and which patients should this medication be considered in?

A

This medication is reserved for high risk patients with elevated levels of hsCRP (>2)

(hsCRP is an inflammatory marker)

*Note: atherosclerosis and CV disease are inflammatory diseases

103
Q

What level of the inflammatory marker hsCRP is considered “elevated”?

A

> 2

**consider initiating colchicine when patients are at this level and have high risk CCD

104
Q

When is colchicine contraindicated?

A

Severe renal disease

Severe hepatic disease

105
Q

What is the role of statins in CCD?

A

All patients should be on a high intensity statin!!!

(if high intensity is not tolerated, moderate intensity statins can be used)

106
Q

Which patients have beta blockers been shown to reduce mortality in?

A

Post-ACS

Heart failure (with reduced ejection fraction) (HFrEF)

***data has not shown reduced mortality in any other patient populations regarding CCD

107
Q

True or False: If a patient experiences angina from CCD while exercising, we want them to stop exercising

A

FALSE, we want to treat the symptom so that the patient can continue exercising

(still may be difficult with heart rate lowering effects of beta blockers)

108
Q

What 3 conditions lead to decreased coronary blood flow?

A

-Fixed stenosis
-Vasospasm
-Thrombus

109
Q

What 4 states contribute to increased oxygen consumption?

A

Increased Heart Rate
Increased Contractility
Increased Afterload
Increased Preload

110
Q

What two things contribute to ischemia?

A

-Decreased coronary blood flow

-Increased oxygen consumption

111
Q

What drugs decrease heart rate?

A

Beta Blockers

Verapamil + Diltiazem

112
Q

What drugs increase heart rate?

A

Nitrates

*Nifedipine (DHP CCB)

113
Q

What drugs decrease myocardial contractility?

A

Beta blockers

Nifedipine (DHP CCB) (or no effect)

Verapamil

Diltiazem (or no effect)

114
Q

What is another term for afterload?

A

Systolic blood pressure

115
Q

What is another term for preload?

A

Left-ventricular end-diastolic volume

(LV volume)

116
Q

What drugs decrease preload the most?

A

Nitrates

117
Q

What drugs INCREASE preload?

A

Beta-blockers

118
Q

What drug classes are used to prevent ACUTE ischemia and angina symptoms?

A

Nitrates

(nitroglycerin)

119
Q

What is the mechanism of action of nitrates?

A

Nitric oxide donors/releasers

-Activate guanylate cyclase

120
Q

What action of nitrates decreases preload?

A

Venodilation

121
Q

What are the 3 activities of nitrates?

A

-Marked venodilation (decreases preload)

-Less arteriole dilation (coronary and peripheral)

-Inhibition of platelet aggregation (minor)

122
Q

What molecule leads to the relaxation caused by nitrates?

A

Increase in cGMP

-impacts the myosin chain contraction

*NOTE: PDE5i do this as well

123
Q

Do nitrates affect the natural history of CAD?

A

NO

*do not keep people alive, only treat symptoms!!!!!

124
Q

What is the dosing for SL Nitroglycerine Tablets?

A

0.3-0.6 mg

125
Q

What is the dosing interval/frequency of SL Nitroglycerin Tablets and Spray?

A

PRN, repeat dose 1-3 times every 5 minutes

126
Q

What is the dosing for SL Nitroglycerin Spray?

A

0.4 mg/spray

127
Q

If patient experiences lasting chest pain and is instructed to chew an aspirin, what dose should they chew?

A

162-325 mg

128
Q

If patient is experiencing chest pain, when should they call 911?

A

If the pain is unimproved or worsening after 5 minutes

*this goes for both patients prescribed NTG and not

129
Q

What are 6 important counseling points for nitroglycerin tablets?

A

-Keep tablets in original container

-Do not swallow, place under tongue

-Do not store in bathroom or humid area

-Sit down before taking

-Keep the tablets on you at all times

-Take up to 3 doses 5 mins apart

130
Q

What are 2 important unique counseling points for nitroglycerin spray?

A

-Spray under tongue, do not inhale

-DO NOT SHAKE

131
Q

What are the adverse effects of nitrates?

A

-Headache (throbbing or pulsing)
-Hypotension
-Dizziness/ lightheadedness
-Facial flushing!
Reflex tachycardia

132
Q

What drug class causes reflex tachycardia?

A

Nitrates

-BP reduced and baroreceptors sense it. catecholamines get released and BP goes up

**want to use lowest dose possible

133
Q

What drug class should be used with extreme caution with PDE5 inhibitors?

A

Nitrates

*risk of hypotension and death

*vasodilatory effects of nitrates are substantially enhanced when used in combo

134
Q

If a patient takes Avanafil (PDE5i), how long do they have to wait before taking a nitrate?

A

12 hours

135
Q

If a patient takes Sildenafil or Vardenafil, how long do they have to wait before taking a nitrate?

A

24 hours

136
Q

If a patient takes Tadalafil, how long do they have to wait before taking a nitrate?

A

48 hours

137
Q

What patients should receive sublingual nitroglycerin?

A

ALL patients with CCD

(either spray or tablet)

138
Q

True or False: nitroglycerin can be useful for the prevention of angina by taking it right before a patient exerts themself

A

True

139
Q

Which beta receptor is more present in heart cells (B1 or B2)?

A

B1

(80% B1 and 20% B2)

140
Q

What drug classes are used to prevent RECURRENT/CHRONIC ischemia and angina symptoms?

A

-Beta blockers
-Calcium channel blockers
-Nitrates

141
Q

How does the distribution of beta cells change in heart failure?

A

B1: 60%
B2: 40%

*B2 becomes more important

142
Q

What affect do beta blockers have in cardiac myocytes?

A

Block B1 (and possibly B2) receptors which prevents release of cAMP

This decreases heart rate, contractility, and conduction velocity

143
Q

What is chronotropy?

A

Changes made to heart rate

144
Q

What is inotropy?

A

A change in contractility

145
Q

What is dromotropy?

A

A change in conduction velocity/speed

146
Q

What affect do beta blockers have in vascular smooth muscle cells?

A

B2 receptors in smooth muscles (vascular, GI, uterine) cause relaxation

-beta blockers block this

147
Q

What is the mechanism of action of beta blockers?

A

Competitive, reversible inhibitors of beta-adrenergic stimulation by catecholamines

148
Q

In what 3 ways do beta blockers decrease myocardial oxygen demand?

A

Reduce HR

Reduce myocardial contractility

Reduce arterial BP (afterload)

149
Q

What negative effect do beta blockers have on myocardial oxygen demand?

A

They reduce heart rate which increases diastolic filling time

*ultimately this INCREASES preload

150
Q

What affects do beta blockers have on preload and afterload?

A

Preload: increase it (bad)

After load: decrease it

151
Q

Beta blockers are associated with a reduction of what two (bad) events in the heart?

A

Ventricular arrhythmias

Remodeling

152
Q

What two prototype beta blockers are cardio selective for B1?

A

Atenolol

Metoprolol

153
Q

What two prototype beta blockers are nonselective?

A

Propranolol

Carvedilol

154
Q

What two prototype beta blockers have intrinsic sympathomimetic activity?

A

Pindolol

Acebutolol

155
Q

What contraindications are associated with intrinsic sympathomimetic activity beta blockers?

A

Contraindicated in post-MI patients

*May increase heart rate at rest
*May cause angina

DO NOT USE THESE FOR ANGINA EITHER

(pindolol, acebutolol)

156
Q

Which non-selective beta blocker has both alpha and beta blocking effects?

A

Carvedilol

157
Q

Which two prototype beta blockers are lipid soluble and how are they removed from the body?

A

Propranolol
Carvedilol

(removed by the kidneys)

158
Q

Which two prototype beta blockers are water soluble?

A

Atenolol
Bisoprolol

(removed unchanged)

159
Q

What cardiac adverse effects do beta blockers have?

A

-Sinus bradycardia
(<60)

-Sinus arrest
(no sinus pulse, all comes from below sinus node)

-AV block
(no beats conducted from atrium to ventricle)

-Reduced LVEF

160
Q

What general side effects do beta blockers have (not cardiac related)?

A

-Bronchoconstriction
-Fatigue
-Depression
-Nightmares
-Sexual dysfunction
-Exercise intolerance

161
Q

Why should patients be tapered off of beta blockers?

A

Beta blocker withdrawal syndrome

-androgen hypersensitivity due to increased receptors being made while on beta blockers to try and overcome the beta blocker

-When the beta blocker is removed, all of these receptors are activated

-causes a rise in BP and HR

162
Q

How should beta blocker dosing be handled?

A

Start at lowest dose

-titrate to symptom reduction

163
Q

What are the goal heart rates for beta blockers?

A

Rest: 50-60 bpm

Exercise: <100 bpm

164
Q

What is the MOA of Calcium Chanel Blockers?

A

Block L-type calcium channels

*this blocks the contraction effects of calcium

165
Q

What effects do calcium channel blockers have in cardiac cells?

A

-Decrease influx of Ca
-Decrease chronotropy and inotropy

166
Q

What effects do calcium channel blockers have in vascular cells?

A

Vasodilation (relaxation)

167
Q

Which group of CCB is a more potent vasodilator?

A

DHPs

*non-DHPs act more like beta blockers, still vasodilate but less

168
Q

What two CCBs do we never use in CCD?
And why?

A

Nifedipine (Procardia, Adalat)

Nicardipine (Cardene)

*cause substantial reflex tachycardia

169
Q

What are the side effects of DHPs?

A

-Hypotension
-Flushing
-Headache
-Dizziness
*Peripheral edema (due to vasodilation)
*Reduced myocardial contractility
*Reflex adrenergic activation

170
Q

If a patient develops peripheral edema while on a DHP CCB what should be done?

A

Decrease the dose

-this is a dose-related side effect
-some patients may not tolerate any dose

171
Q

What are the side effects of Non-DHPs?

A

*Reduce myocardial contractility (V>D)
*Bradycardia and AV block (V>D)
-Hypotension
-Flushing
-Headache
-Dizziness
Constipation (V>D)

172
Q

Which two drug classes have constipation as a side effect?

A

Non-DHP CCB

Ranolazine

*note: may not be great in elderly patients

173
Q

How should CCB dosing be initiated?

A

-Initiate at lowest dose
-Titrate to symptom relief

174
Q

In what patients can calcium channel blockers have an added benefit?

A

-Patients with increased BP

175
Q

What causes the biggest challenge in a patient taking a nitrate?

A

Nitrate tolerance

*this can happen within a single day, patients need to be given increasingly higher doses

*why nitrate-free periods are important

176
Q

To prevent nitrate tolerance, how long should a nitrate free period last each day?

A

10-12 hours

177
Q

For a NTG patch, how long should it be on and how long should it be off?

-What times should it be put on and taken off?

A

On for 12-14 hrs, off for 10-12 hrs

On: 7 am

Off: 7-9 pm

178
Q

For ISDN tablets dosed TID, what times should they be taken?

A

8am, 12pm, 4pm

179
Q

For ISMN tablets dosed BID, what times should they be taken?

A

8am, 3pm

180
Q

For ISMN SR tablets taken once daily, what time should they be taken?

A

8am

*so that drug is out of system by 8pm

181
Q

Why are nitrates typically only used as combination therapy?

A

Because patients do not get any protection at night with nitrates alone due to the nitrate free period

182
Q

What are the important counseling points for nitroglycerin patches?

A

-Apply between elbows and knees
-Apply to clean, dry, hairless, unmarked area
-Choose different area each day
-You CAN shower with the patch
-Do not cut
-Wash hands before and after

183
Q

What are 2 additional important counseling points for application of nitroglycerin ointment?

A

-Do not rub or massage in ointment

-Do not cover the area with any kind of wrap

184
Q

How can vasodilators cause tachycardia?

A

Reduce arterial pressure which leads to increased heart rate

-ultimately increases cardiac output and increases demand

185
Q

Which drugs can cause vasodilator induced tachycardia?

A

-Nitrates

-Dihydropyridines

186
Q

What is the mechanism of action of Ranolazine (Ranexa)

A

Inhibits late inward sodium channels in ischemic myocytes (this leads to a decreased Ca influx)

-interrupts the cycle leading to ischemia

187
Q

What is the titration for ranolazine dosing?

A

Start at 500mg BID and increase to 1000mg BID over 1-2weeks

188
Q

What is Ranolazine (Ranexa) indicated for in the US?

A

Treatment of chronic angina

189
Q

When do we use Ranolazine (Ranexa)?

A

-As an add-on to CCBs, BBs, or Nitrates

*Monotherapy only when patients have a BP/HR too low with first-line options

*Typically only add on when BP or HR is low but patient is uncontrolled

190
Q

What drugs should Ranolazine not be used with?

A

3A inhibitors:
-Ketoconazole + Itraconazole
-Clarithromycin

3A Inducers:
-Carbamazepine
-Rifampin
-St John’s Wort

191
Q

With what drugs should the dosing of Rifampin be limited to 500 mg BID?

A

*Diltiazem + Verapamil
-Erythromycin
-Fluconazole

192
Q

What are the adverse effects of Ranolazine (Ranexa)?

A

*Constipation
-Nausea
-Dizziness
-Headache
Increases QT-Interval

193
Q

What is the first drug class we choose for treatment of stable angina?

A

Beta Blockers

194
Q

What drug classes do not have any effect on the natural progression of CCD?

A

-BBs
-CCBs
-Nitrates
-Ranolazine

195
Q

When should beta blockers be avoided?

A

-Prinzmetal’s Angina (vasospastic)

-Conduction Disturbances (SA node block, AV node block)

196
Q

What are the contraindications for beta blockers?

A

-Bradycardia (HR<50)

-High degree AV block/sick sinus syndrome (with no pacemaker)

197
Q

When are non-DHPs preferred?

A

*If a beta blocker cannot be used due to contraindications or side effects

198
Q

When are Non-DHPs and DHPs contraindicated?

A

Non-DHP:
-HFrEF
-Bradycardia (HR < 50)
-AV node block or sick sinus syndrome (with no pacemaker)

DHP:
-HFrEF (except amlodipine and felodipine)

199
Q

Which two drug classes should never be combined?

A

Beta blockers
+
Non-DHP CCB

200
Q

When using NSAIDs in CV disease, what considerations should be made?

A

-Only use temporarily!
-Lowest dose for shortest time period
*Check for Benefit or AEs within one week of initiation

201
Q

What two NSAIDs should be chosen first to be used with CV disease?

A

Ibuprofen

Naproxen

*with gastroprotection

202
Q

What other NSAID can be used and at what dose to have similar cardiovascular risk as Ibuprofen and Naproxen?

A

Celecoxib doses up to 200mg per day

*Note: this medication seems to have poorer analgesic effects

*Note: Increasing dose above 200mg increases CV risk

203
Q

What NSAID should be absolutely avoided in CV disease?

A

Diclofenac

*highest risk of aspirin interaction

204
Q

If a patient is taking both Aspirin and an NSAID, how much time should they space the doses out by?

A

Take aspirin AT LEAST 2 HOURS BEFORE the NSAID

*this gives aspirin the chance to acetylate the COX so the NSAID has less of a chance to compete with it

205
Q

What CV drug do NSAIDs interact with?

A

Aspirin

(minimize its effects)

206
Q

What are the 3 names for ischemia associated with vasospasm?

A

-Prinzmetal’s angina
-Vasospastic angina
-Variant angina

207
Q

What are the symptoms of vasospastic angina?

A

-Ischemia/angina occurs at rest
(not brought on by exercise or emotional stress)

-ECG ST-segment elevation

-Ischemic episodes occur mostly in the early morning hours

-Does not have to be associated with atherosclerosis (plaque buildup)

208
Q

What affect does vasospastic angina have on an ECG?

A

ECG ST-segment elevation

209
Q

What time of day does vasospastic angina typically occur?

A

Early morning hours

210
Q

What is the first-line treatment for vasospastic angina?

A

BP > or =130/80: CCB
*most patients

BP <130/80: LA Nitrate

211
Q

What drug class should be avoided in vasospastic angina?

A

Beta Blockers

Spring 2024 Therapeutics 3 (24 decks)

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