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PHRM 845 > Pathophysiology, Pharmacology, Pharmacotherapy of CAD > Flashcards

Pathophysiology, Pharmacology, Pharmacotherapy of CAD Flashcards

1
Q

What is chronic coronary disease?

A

Heterogeneous group of conditions that includes:
- obstructive and nonobstructive CAD with or without previous MI or revascularization,
- ischemic heart disease diagnosed only by noninvasive testing,
- and chronic angina syndromes with varying underlying causes

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2
Q

What are the types of angina?

A
  1. Printzmetal’s variant angina (vasospasm)
  2. Chronic stable angina (fixed stenosis)
  3. Unstable angina (thrombus)
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3
Q

What is printzmetal’s variant angina also known as?

A

Supply ischemia

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4
Q

What is chronic stable angina also known as?

A

Demand ischemia

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5
Q

What is unstable angina also known as?

A

Supply ischemia

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6
Q

Describe printzmetal’s variant angina

A

Artery closes bc of spasm(s)

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7
Q

Describe chronic stable angina

A

Plaque blockage that results in ischemia with exertion

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8
Q

Describe unstable angina

A

Plaque + thrombus that causes vessel to fully close

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9
Q

What causes increased oxygen demand that leads to ischemia?

A

Increased HR, contractility, afterload, preload

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10
Q

What causes decreased coronary blood flow that leads to ischemia?

A

Fixed stenosis, vasospasm, thrombus

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11
Q

What are the components of ischemia and describe them

A
  • Angina -> chest pain
  • Anginal equivalents -> Sx like SOB that is normally caused by another disease like HF
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12
Q

How does contractility impact myocardial O2 supply/demand ratio?

A

Decrease in contractility will decrease O2 consumption

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13
Q

How does HR impact myocardial O2 supply/demand ratio?

A
  • Decreased HR will decrease O2 consumption
  • Decreased HR will increase coronary perfusion
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14
Q

How does preload-LVEDV impact myocardial O2 supply/demand ratio?

A
  • Decreased by venodilation
  • Decrease leads to decrease in O2 consumption
  • Decrease leads to increase in myocardial perfusion
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15
Q

How does afterload impact mycardial O2 supply/demand ratio?

A
  • Decreased by dilation of arteries
  • Decrease leads to decrease in O2 consumption
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16
Q

What is stable pectoris usually associated with?

A

Large single to multivessel ASCAD

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17
Q

What do approx 85% of pts with angina pectoris have?

A

Significant coronary artery disease (defined as >70-75% atherosclerotic reduction) in a major epicardial coronary vessel

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18
Q

What are major epicardial coronary vessels?

A

Vessels that sit and are connected to epicardial surface of the heart

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19
Q

What does not usually cause ischemia?

A

Atherosclerotic reductions between 50-70%

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20
Q

What is the pathophysiology of myocardial ischemia?

A
  • Imbalance between myocardial oxygen supply and demand
  • Produces disturbances in myocardial function without causing myocardial necrosis
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21
Q

What is the pathophysiology of angina?

A
  • Resulting symptoms from ischemia
  • Is a clinical syndrome of chest discomfort
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22
Q

What is the definition of stable angina pectoris?

A
  • Discomfort in the chest and/or adjacent areas
  • Caused by myocardial ischemia and associated with a disturbance in myocardial function WITHOUT myocardial necrosis
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23
Q

What is the definition of stable in stable angina pectoris?

A

Characteristics of an anginal episode (quality, frequency, severity, duration of Sx, time of day, etc) have not changed recently

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24
Q

What is the first P in PPQRST?

A

Precipitating factors

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25
Q

Presentations of precipitating factors?

A
  • Exercise/exertion
  • Weather factors (cold, warm, and humid)
  • Walking against wind
  • Large meal
  • Emotional factors involved with exercise
  • Fright, anger
  • Coitus
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26
Q

What is the second P in PPQRST?

A

Palliative measures

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27
Q

Presentations of palliative measures?

A

Rest and/or sublingual nitroglycerin/nitrates

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28
Q

What is the Q in PPQRST?

A

Quality and quantity of pain

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29
Q

Presentations of quality and quantity of pain?

A

Squeezing, heaviness, tightening

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30
Q

What is the R in PPQRST?

A

Region and radiation

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31
Q

Presentations of region and radiation?

A
  • Substernal
  • Anywhere between epigastrium and pharynx
  • Sometimes limited to left shoulder and arm
  • Rarely limited to right arm
  • Limited to lower jaw
  • Lower cervical and upper thoracic spine
  • Left interscapular or suprascapular area
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32
Q

What is S in PPRQST?

A

Severity of pain

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33
Q

Presentations of severity of pain?

A

Subjective, >5 out of 10

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34
Q

What is the T in PPRQST?

A

Timing and temporal pattern

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35
Q

Presentations in timing and temporal pattern?

A

Lasts <20 min, usually relieved in 5-10 min

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36
Q

What is the classic clinical characteristics of typical angina?

A
  • Substernal
  • Duration of 0.5 to 20 min
  • Nitroglycerin/rest gives relief
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37
Q

What is the typical ECG findings of typical ischemia/angina?

A

ST segment depression during event

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38
Q

What is typical ECG findings during variant angina?

A

ST segment elevation in variant angina

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39
Q

What are the endpoints of exercise tolerance testing

A

Duration, workload achieved, ECG changes, BP and HR responses, and Sxs

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40
Q

What are the diagnostic procedures for CHD?

A
  • Cardiac imaging
  • Echocardiography
  • Cardiac catheterization and coronary angiography
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41
Q

What does cardiac imaging consist of in CHD diagnostic procedures?

A
  • Pharmacologic stress testing
  • Nuclear imaging
  • Electron beam computerized tomography (calcium score)
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42
Q

What does cardiac catheterization and coronary angiography accomplish?

A
  • Definitive assessment of coronary anatomy
  • Invasive
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43
Q

Where is cardiac catheterization typically inserted?

A

Radial artery in the wrist

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44
Q

What is the desired outcome 1 of CCD tx?

A
  • Risk factor modification
  • Prevent ACS and death
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45
Q

What is the desired outcome 2 of CCD tx?

A
  • Management of anginal episodes
  • Alleviate acute Sxs and prevent recurrent Sxs of ischemia
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46
Q

What is the desired outcome 3 of CCD tx?

A

Avoid/minimize adverse tx effects

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47
Q

What is the tx goal of dyslipidemia risk factor?

A

> = 50% reduction in LDL

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48
Q

What is the preferred tx for dyslipidemia risk factor?

A
  • Lifestyle modifications
  • Low (<7%) sat fat, low (<200 mg/dL) cholesterol
  • Moderate to high intensity statins
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49
Q

What is the tx goal for HTN risk factor?

A

BP <130/80 mmHg

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50
Q

What is the preferred tx for HTN risk factor?

A
  • Lifestyle modifications
  • BBs, ACEi, ARBs, and others as necessary
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51
Q

What is the tx goal for DM risk factor?

A

A1c <7%

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52
Q

What is the preferred tx for DM risk factor?

A
  • Individualize to reach goal
  • SGLT2 or GLP-1 for T2DM with ASCVD
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53
Q

What is the tx goal for smoking risk factor?

A

Complete smoking cessation/exposure

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54
Q

What is the preferred tx for smoking risk factor?

A

Systematic strategy, pharmacotherapy

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55
Q

What is the tx goal for weight management risk factor?

A
  • BMI 18.5 to 24.9
  • Waist circumference of 40 or less in men and 35 or less in women
  • Wt loss of 5-10% initially
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56
Q

What is the preferred tx for high weight risk factor?

A
  • Diet/lifestyle modifications
  • Printed educational materials
  • Encouragement
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57
Q

What is the tx goal for low physical activity risk factor?

A
  • 30 to 60 min moderate intensity 5 to 7 days a week
  • Cardiac rehab/supervised
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58
Q

What is the preferred tx for low physical activity risk factor?

A
  • Brisk walking, swimming, cycling
  • Increased daily activities in general
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59
Q

How can a pt lower their risk for CAD?

A
  • Yearly influenza vaccination
  • Lower alcohol consumption
  • Lower exposure to air pollution
  • Management of psychological factors
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60
Q

What is aspirin’s MOA?

A
  • Acetylation and irreversible inactivation of platelet COX-1
  • Antiplatelet activity by blocking TXA2 synthesis
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61
Q

What does aspirin achieve through its MOA?

A
  • Interferes with platelet aggregation
  • Prolongs bleeding time
  • Blocks arterial thrombi formation
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62
Q

What is a downside of aspirin?

A

It does not treat currently formed thrombus

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63
Q

What are effects of COX-1?

A
  • Increases platelet aggregation
  • Vasoconstriction
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64
Q

What are effects of COX-2?

A
  • Inhibits platelet aggregation
  • Vasodilation
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65
Q

What is the loading dose of aspirin?

A

160-325 mg

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66
Q

What is the maintenance dose of aspirin?

A

75-162 mg daily

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67
Q

What are the AEs of aspirin?

A
  • GI bleeding
  • Hematologic bleeding (intracranial and extracranial)
  • Hypersensitivity
  • Major bleeding in 2-3% of pts in year 1
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68
Q

What is the MOA of P2Y12 inhibitors?

A

Selectively inhibit adenosine diphosphate induced platelet aggregation with no direct effect on TXA2

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69
Q

What is the loading dose of clopidogrel (Plavix)?

A

300-600 mg

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70
Q

What is the maintenance dose of clopidogrel (Plavix)?

A

75 mg daily

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71
Q

What is the loading dose of prasugrel (Effient)?

A

60 mg

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72
Q

What is the maintenance dose of prasugrel (Effient)?

A

10 mg daily

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73
Q

What is the loading dose of ticagrelor (Brilinta)?

A

180 mg

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74
Q

What is the maintenance dose of ticagrelor (Brilinta)?

A

90 mg BID

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75
Q

How is cangrelor (Kengreal) administered that is different from the other P2Y12 inhibitors?

A

IV only

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76
Q

When is prasugrel (Effient) and cangrelor (Kengreal) indicated?

A

Following ACS

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77
Q

When is ticagrelor (Brilinta) indicated?

A

Following ACS or prior MI

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78
Q

Why can 2 or more platelet inhibitors be used together?

A

Different MOAs

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79
Q

What drug class is clopidogrel and prasugrel?

A

Thienopyridine

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80
Q

What is the pharmacology of clopidogrel?

A
  • It is CYP dependent
  • Converted to active (prodrug)
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81
Q

What is the time to peak inhibition of clopidogrel?

A
  • 4 to 5 hours for 300 mg
  • 2 to 3 hours for 600 mg
82
Q

What is the time required for effect dissipation for clopidogrel?

A

5 days

83
Q

What is the pharmacology of prasugrel?

A
  • “less” CYP dependent (still a prodrug)
  • Converted to active
84
Q

What is the time to peak inhibition of prasugrel?

A

2-4 hours

85
Q

What is the time required for effect dissipation for prasugrel?

A

7 days

86
Q

What drug class is ticagrelor?

A

Cyclopentyl-triazole-pyrimidine

87
Q

What is the pharmacology of ticagrelor?

A
  • Direct acting
  • Not a prodrug
88
Q

What is the time to peak inhibition for ticagrelor?

A

2-4 hours

89
Q

What is the time required for effect dissipation of ticagrelor?

A

5 days

90
Q

What are AEs of clopidogrel?

A
  • Bleeding, diarrhea, rash
  • About 1% increase in major bleeding when used with aspirin
91
Q

What are AEs of prasugrel?

A
  • Bleeding, diarrhea, rash
  • About 0.6% increase (absolute risk) in major bleeding and about 0.5% increase (vs. clopidogrel) in life-threatening bleeding when used with aspirin
92
Q

What are AEs of ticagrelor?

A

Bleeding, bradycardia, heart block, dyspnea (SOB)

93
Q

What is the REQUIRED dose of aspirin if it is taken with ticagrelor (Brilinta)?

A

<= 100 mg

94
Q

Why does aspirin dose need to be <= 100 mg if taken with ticagrelor (Brilinta)?

A

Increased risk of cerebral hemorrhage and therefore stroke

95
Q

What improvements should pts show before being given ACEi/ARBs?

A

Stabilized plaque, improved ET function, inhibition of VSM cell growth, decreased macrophage migration, and anti-ox properties

96
Q

What do ACEi and ARBs not do in ischemia?

A

Does not improve symptomatic ischemia

97
Q

What do ACEi and ARBs do in ischemia?

A

Lowers CV events in high risk pts with or without LV dysfunction

98
Q

When are ACEi and ARBs considered in ischemia?

A
  • Considered in all pts with CCD
  • Esp in pts with LVEF <40%, HTN, DM, CKD
99
Q

What does colchicine do in ischemia?

A

Heart disease is inflammation and colchicine reduces inflammation

100
Q

How does colchicine reduce inflammation?

A

Via reduction in IL-1beta and IL-18

101
Q

When is colchicine considered?

A

When pt presents with elevated levels of hsCRP (>2)

102
Q

What is hsCRP?

A

An inflammation marker

103
Q

What is the pharmacology of colchicine?

A

CYP3A and P-gp substrate

104
Q

What is something to watch out for with colchicine?

A

Caution in concomitant use with strong inhibitors of CYP3A and P-gp

105
Q

When is colchicine CI?

A

CI in severe renal and hepatic disease

106
Q

What is the pharmacotherapy behind preventing and/or reducing ischemia and angina sx?

A
  • Increase myocardial O2 supply
  • But MAINLY by decreasing myocardial O2 demand
107
Q

What is the MOA of organic nitrates?

A
  • Nitric oxide donors/releasers
  • Activation of guanylate cyclase
108
Q

What are the effects of organic nitrates?

A
  • Marked venodilation (decreased preload)
  • Less arteriole dilation, coronary and peripheral
  • Inhibition of platelet aggregation (minor)
109
Q

Where is NO produced?

A

In the endothelial cells

110
Q

How does NO cause vasodilation?

A
  • It interacts with GC+, making it sGC
  • sGC converts GTP to cGMP
111
Q

What are the clinical effects of nitrates?

A
  • Increased myocardial O2 supply
  • Decreased myocardial O2 demand
112
Q

Explain how nitrates increase myocardial O2 supply.

A

Endothelium-dependent vasodilation; dilates epicardial arteries and coronary collateral vessels

113
Q

Explain how nitrates decrease myocardial O2 demand.

A

Venous vasodilation causes reduced preload and decreased LV volume

114
Q

What do nitrates not tx/reverse?

A

Nitrates has no effect on the natural progression of the disease; it only tx sxs

115
Q

What is the biggest advantage of a spray NTG over other dosage forms

A

Spray NTG has a shelf life of about 3 years

116
Q

What are the AEs of nitrates?

A
  • Headache (throbbing, pulsating)
  • Hypotension, dizziness, lightheadedness, facial flushing
  • Reflex tachycardia
117
Q

What should be done if a pt gets headache while using NTG?

A
  • Use APAP meds like acetaminophen/tylenol
  • DO NOT USE NSAIDs
118
Q

Why is there extreme caution exercised when using PDEi + nitrates?

A

Substantially enhanced vasodilatory effects (hypotension; 25 mmHg drop in SBP)

119
Q

How long should a pt wait to take Avanafil after taking a nitrate?

A

12 hours

120
Q

How long should a pt wait to take Sildenafil or Vardenafil after taking a nitrate?

A

24 hours

121
Q

How long should a pt wait to take Tadalafil after taking a nitrate?

A

48 hours

122
Q

What is the bottom line clinical recommendation for nitrates?

A
  • SL NTG or SL spray should be utilized in all pts with CCD
  • Can be taken prior to exertion to prevent acute angina
123
Q

What drugs are used to PREVENT RECURRENT ischemia and angina Sx?

A

BBs, CCBs, nitrates

124
Q

Explain the action of B-adrenergic receptors in cardiac myocytes.

A
125
Q

What are the pharmacologic effects on B-adrenergic receptors?

A
126
Q

Explain the mechanism of B-adrenergic receptors in smooth muscle cells.

A
127
Q

What is the MOA of BBs?

A

Competitive, reversible inhibitors of beta-adrenergic stimulation by catecholamines

128
Q

What are the desired effects of BBs on myocardial O2 demand?

A
  • Reduce HR, myocardial contractility, arterial BP
129
Q

What are the undesired effects of BBs on myocardial O2 demand?

A
  • Increase in preload; this negates some positive effects of BBs
130
Q

What is the main reason BBs are used to keep pts alive?

A

BBs are associated with reduced ventricular arrhythmias and remodeling

131
Q

What are cardiac related AEs of BBs?

A

Sinus bradycardia (HR <60), sinus arrest, AV block, reduced LVEF

132
Q

How should a BB be initiated?

A

Initiate at lowest dose and titrate to Sx reduction

133
Q

What is the goal HR of a pt on BBs?

A
  • Rest: 50-60 bpm
  • Exercise: <= 100 bpm or 75% of HR that causes angina
134
Q

What is the brand name of atenolol?

A

Tenormin

135
Q

What is the receptor selectivity of atenolol?

A

B1

136
Q

What is the ISA (intrinsic sympathomimetic activity) of atenolol?

A

0

137
Q

What is the lipid solubility of atenolol?

A

Low

138
Q

What is the primary route of elimination of atenolol?

A

Renal

139
Q

What is the usual maintenance dose of atenolol?

A

50-100 mg QD

140
Q

What is the brand name of metoprolol and metoprolol XL?

A

Lopressor and Toprol XL, respectively

141
Q

What receptor(s) are metoprolol and metoprolol XL selective for?

A

B1

142
Q

What is the ISA of metoprolol and metoprolol XL?

A

0

143
Q

What is the lipid solubility of metoprolol and meto XL?

A

Moderate

144
Q

What is the primary route of elimination of metoprolols?

A

Hepatic

145
Q

What are the usual daily maintenance doses of metoprolol and meto XL?

A
  • 50-100 mg BID
  • 100-200 mg QD
146
Q

What are the brand names of propranolol and propranolol LA?

A

Inderal and Inderal LA

147
Q

What receptors are propranolol and propranolol LA selective for?

A

B1, B2

148
Q

What is the ISA of the propranolols?

A

0

149
Q

What is the lipid solubility of the propranolols?

A

High

150
Q

What is the primary route of elimination for the propranolols?

A

Hepatic

151
Q

What is the usual maintenance dose of the propranolols?

A
  • Variable for regular
  • 80-160 mg BID for the LA
152
Q

What is MOA of CCBs?

A
153
Q

What is the pharmacologic characteristics of CCBs?

A
154
Q

Myocardial selectivity of calcium channel antagonists:

A
155
Q

Vascular selectivity of calcium channel antagonists:

A
156
Q

What are the AEs of DHP CCBs?

A
  • Hypotension, flushing, headache, dizziness
  • Peripheral edema, likely related to arteriolar vasodilation
  • Reduced myocardial contractility
  • Reflex adrenergic activation
157
Q

What are the AEs of non-DHP CCBs?

A
  • Reduced myocardial contractility (V>D)
  • AV/SA nodal conduction disturbances: bradycardia and atrioventricular block (V>D)
  • Hypotension, flushing, headache, dizziness
  • Constipation (V>D)
158
Q

How should CCBs be initiated?

A

Initiate at lowest dose and titrate to Sx reduction

159
Q

Explain nitrate tolerance.

A

Decreased response in the presence of continuously or frequently administered nitrates

160
Q

How is nitrate tolerance prevented?

A
  • Nitrate free period of at least 10-12 hours
  • Biopharmaceutics and PK contribute to the amount of time required to be dosage-free
161
Q

What is the pharmacology of nitrate tolerance?

A
  • Reversible (hours) in absence of drug
  • ALDH2 inactivation in mitochondria
  • ISMN and ISDN also elicit tolerance but via a slower, less understood process
162
Q

What is the dosing interval of SL NTG tabs/caps?

A

2-4 times/day

163
Q

What is the dosing interval of NTG ointment?

A

3-4 times/day

164
Q

What is the dosing interval of NTG patch?

A

Once daily

165
Q

What is the dosing interval of ISDN tabs?

A

2-3 times/day

166
Q

What is the dosing interval of ISDN SR caps/tabs?

A

1-2 times/day

167
Q

What is the dosing interval of ISMN tabs?

A

2 times/day 7 hours apart

168
Q

What is the dosing interval of ISMN SR tabs?

A

Once daily

169
Q

What are patient counseling points of nitrate patches?

A
  • Discussion of nitrate free interval
  • Apply patch between elbows and knees
  • Apply patch to clean, dry, hairless skin
  • Choose diff area every day
  • Showering is allowed with patch on
  • Do not cut patch
  • Wash hands before and after
170
Q

What are patient counseling points of NTG ointment?

A
  • Same as patches
  • Do not rub or massage ointment
  • Do not cover area
171
Q

Describe the cellular events during ischemia.

A
172
Q

What is the MOA of ranolazine?

A
  • Inhibition of inward Na+ current in ischemic myocytes
  • Decreased intracellular Na+ -> decreased Ca2+ influx
  • DOES NOT affect HR, BP, inotropy, or perfusion
173
Q

What is the brand name, strength, and dosage form of ranolazine?

A

Ranexa 500mg ER tabs

174
Q

How is ranolazine administered?

A

Titration from 500 BID to 1000 BID over 1-2 weeks

175
Q

What is the indication for ranolazine?

A

Tx of chronic angina

176
Q

What is the EMA’s indication for ranolazine?

A

Add on therapy for sx tx of pts with stable angina pectoris who are inadequately controlled or intolerant to 1st line antianginal therapies

177
Q

How is ranolazine used in combo therapy?

A

Add to CCBs, BBs, or nitrates when inadequate response to monotherapy

178
Q

When is ranolazine used as monotherapy?

A

When BP/HR too low with first line agents

179
Q

How is ranolazine metabolized?

A
  • 70-85% by CYP3A4
  • 10-15% by CYP2D6
  • Substrate for P-gp
180
Q

What should ranolazine not be used with?

A

Strong 3A inhibitors (KTZ, ITZ, PIs, clarithomycin) or inducers (CBZ, RIF, st. john’s wart)

181
Q

What dose should ranolazine be limited to if used with moderate inhibitors (Dilt, Ver, ERY and FLZ)?

A

500 mg BID

182
Q

What does ranolazine inhibit?

A

CYP3A and/or P-gp

183
Q

What are the AEs of ranolazine?

A
  • Constipation, nausea, dizziness, headache
  • Dose related increase in QT interval; should not be used with other drugs that prolong QT interval
184
Q

How is an agent selected for stable angina?

A
  • BBs, CCBs, and nitrates can be used
  • Selection should be based upon pt characteristics and concomitant conditions
185
Q

When should BBs be used in stable angina?

A
  • Compelling indications: stable HF, MI hx
  • Esp useful in afib, high resting HR, migraine HAs
  • Avoid in vasospastic/printzmetal’s angina, conduction disturbances
186
Q

What are the CIs of BBs in stable angina?

A
  • Bradycardia (HR <50 bpm)
  • High degree of AV block or sick sinus syndrome (w no pacemaker)
187
Q

When should CCBs be used in stable angina?

A

Non-DHP CCBs preferred instead of BBs if:
- CIs to BBs
- Unacceptable SEs to BBs
- Potentially useful in chronic lung disease, HTN, DM, and peripheral vascular disease

188
Q

What are the CIs of CCBs in stable angina?

A
  • Non-DHPs: HFrEF, bradycardia (HR <50 bpm), high degree of AV block or sick sinus syndrome (w no pacemaker)
  • DHPs: HFrEF (except amlodipine and felodipine)
189
Q

When should nitrates be used in stable angina?

A

Preferred as:
- Combo with BBs/non-DHPs (to blunt nitrate induced increase in HR)
- Short acting prn nitrates to relieve discomfort or prevent ischemia before exertion

190
Q

Why is nitrate monotherapy challenging?

A

Due to nitrate free period and tolerance

191
Q

What are the cautions of nitrates in stable angina?

A

Hypertrophic obstructive cardiomyopathy (HOCM), severe aortic stenosis, PDI use

192
Q

Is ivabradine approved in the US?

A

No

193
Q

What is ivabradine?

A

HCN channel inhibitors - reduces diastolic depolarization:
- slows HR
- prolongs diastole and improves ventricular filling
- reduces myocardial o2 consumption
- no hemodynamic or conduction abnormalities (vs BBs and CCBs)

194
Q

What is ivabradine approved for?

A

Approved for angina in Europe and other countries

195
Q

What is ivabradine indicated for?

A

Indicated for Sx tx of chronic stable angina pectoris in CAD adults w normal sinus rhythm and HR >= 70 bpm
- adults unable to tolerate/CI to use of BBs
- combo w BBs in pts inadequately controlled w an optimal BBs dose

196
Q

What is ivabradine approved for by the FDA?

A

HF tx, but not SIHD

197
Q

When does ischemia/angina occur in prinzmetal’s angina?

A
  • Usually occurs at rest
  • Not precipitated by physical exertion or emotional stress
198
Q

What is the ECG associated with prinzmetal’s angina?

A

ST segment elevation

199
Q

At what time of day do prinzmetal angina ischemic episodes most frequently occur?

A

In the early morning hours

200
Q

What is prinzmetal’s angina not necessarily associated with?

A

Atherosclerosis

201
Q

How is vasospastic angina managed?

A
  • Acute tx: SL NTG, etc
  • Chronic tx: CCBs, nitrates, combo therapy
  • NEVER BBs

PHRM 845 (48 decks)

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