IHD Therapeutics Lecture 1 Flashcards

1
Q

t/f as ischemic heart disease progresses, the symptoms severity and risk of death increases

A

true

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2
Q

people with a diagnosis of ischemic heart disease are ___x more likely to die prematurely

A

3

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3
Q

people who have had a heart attack are ___X more likely to die prematurely

A

4

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4
Q

people who have been diagnosed with heart failure are ___X more likely to die prematurely

A

6

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5
Q

what are some modifiable risk factors for CVD?

A

tobacco use, dyslipidemia, HTN, physical inactivity, diet, obesity, depression, medications

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6
Q

what are some non-modifiable risk factors for CVD?

A
  1. Males >45, females >55
  2. MI or stroke in 1st degree relative in men <55 or <65 in females
  3. Ethnicity
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7
Q

what are the 2 branches of ischemic heart disease?

A

stable angina and acute coronary syndromes

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7
Q

what are the 2 branches of ischemic heart disease?

A

stable angina and acute coronary syndromes

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8
Q

what is included under acute coronary syndromes?

A

non-ST elevation ACS and STEMI

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8
Q

what is included under acute coronary syndromes?

A

non-ST elevation ACS and STEMI

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9
Q

what are the 2 types of non-ST elevation ACS?

A

unstable angina and NSTEMI

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10
Q

what 4 things affect myocardial oxygen supply?

A
  1. arterial oxygen content
  2. coronary blood flow
  3. diastole
  4. vasospasm
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11
Q

what 3 things affect myocardial demand?

A

heart rate
contractility
myocardial wall tension

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12
Q

conditions like hyopthermia, hyperthyroidism, sympathomimetic toxicity, HTN, hypertrophic cardiomyopathy, aortic stenosis, sustained tachycardia, anxiety _______(increase/decrease) myocardial oxygen ____(supply or demand)

A

increase demand

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13
Q

conditions like anemia, hypoxemia, sympathomimetic toxicity, sickle cell disease, hypertrophic cardiomyopathy, aortic stenosis and polycythemia ______(increase or decrease) myocardial oxygen _____(supply or demand)

A

decrease oxygen supply

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14
Q

what are the 4 trademarks of the pathophysiology of atherosclerosis?

A
  1. repeated injury to endothelium
  2. chemical signals due to injury
  3. plaque formation
  4. reduced lumen size
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15
Q

what are some cardiac non-atherosclerotic conditions that cause angina-like syndromes?

A

aortic dissection, pericarditits, coronary artery vasospasm (Prinzmetal’s), valvular heart disease

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16
Q

what are some examples of non-cardiac non-atherosclerotic conditions that cause angina-like syndromes?

A

pulmonary embolism, pneumonia, pleuritic, esophageal reflux, PUD, anxiety, anemia

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17
Q

what is vasospastic angina (Prinzmetal’s pr variant angina)?

A

severe chest pain secondary to ischemia. Occurs at rest and cannot be reproduced by exercise. ECG with have ST elevations

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18
Q

what are some risk factors for vasospastic angina?

A

cigarette smoking, cocaine and alcohol use

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19
Q

what is syndrome X (microvascular angina)?

A

typical angina symptoms, ST depression on ECG, but no significant CAD seen on angiogram

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20
Q

microvascular angina (syndrome X) is more common in what patient population?

A

premenopausal women

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21
Q

what is silent myocardial ischemia?

A

ischemia is present, but patient doesnt experience angina. Typical ST changes on ECG at rest or with exercise

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22
Q

compare treatment of silent ischemia to IHD

A

treated similary, but there is less nitrate use bc symptoms relief is not needed at much

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23
Q

Describe the typical presentation of stable angina

A
  1. pressure or heavy weight on chest (crushing, burning, tightness)
  2. substernal, may radiate to jaw, shoulder, back, or arms
  3. 30 sec up to 20 min
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24
Q

what are some atypical symptoms of stable angina?

A

nausea, diaphoresis, SOB, anxiety

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25
Q

the atypical symptoms of stable angina are typically seen in what patient populations?

A

women and diabetic patients

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26
Q

the atypical symptoms of stable angina are typically seen in what patient populations?

A

women and diabetic patients

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26
Q

the atypical symptoms of stable angina are typically seen in what patient populations?

A

women and diabetic patients

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27
Q

what are some precipitating factors of stable angina?

A

exercise, cold weather, after meals, emotional stress, sexual activity

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28
Q

what provides relief for stable angina?

A

rest and or nitroglycerin

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28
Q

what provides relief for stable angina?

A

rest and or nitroglycerin

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28
Q

what provides relief for stable angina?

A

rest and or nitroglycerin

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28
Q

what provides relief for stable angina?

A

rest and or nitroglycerin

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28
Q

what provides relief for stable angina?

A

rest and or nitroglycerin

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28
Q

what provides relief for stable angina?

A

rest and or nitroglycerin

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28
Q

what provides relief for stable angina?

A

rest and or nitroglycerin

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28
Q

what provides relief for stable angina?

A

rest and or nitroglycerin

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28
Q

what provides relief for stable angina?

A

rest and or nitroglycerin

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28
Q

what provides relief for stable angina?

A

rest and or nitroglycerin

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28
Q

what provides relief for stable angina?

A

rest and or nitroglycerin

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28
Q

what provides relief for stable angina?

A

rest and or nitroglycerin

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29
Q

what provides relief for stable angina?

A

rest and or nitroglycerin

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30
Q

what provides relief for stable angina?

A

rest and or nitroglycerin

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31
Q

describe Grade I stable angina

A

ordinary physical activity (walking, climbing stairs) does not cause angina, but strenuous, rapid, or prolonged exertion causes angina

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32
Q

describe Grade I stable angina

A

ordinary physical activity (walking, climbing stairs) does not cause angina, but strenuous, rapid, or prolonged exertion causes angina

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33
Q

describe Grade II angina

A

slight limitation of ordinary activity. Angina occurs when walking, climbing stairs rapidly, walking uphill, walking or going up stairs after meals, in the cold, under emotional stress, or only during the few hours after waking. Can walk more than 2 blocks on a level surface, and can climb more than one flight of stairs under normal conditions

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34
Q

describe Grade III angina

A

marked limitation of ordinary physical activity. Walking one or two blocks on a level surface and climbing one flight of stairs in normal conditions causes angina

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35
Q

describe Grade IV angina

A

inability to carry on any physical activity without discomfort. Angina may be present at rest

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36
Q

what are the diagnostic tests for IHD?

A

ECG, exercise stress test, pharmacologic stress test, nuclear stress test, cardiac CT/MRI, cardiac catheterization

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37
Q

what are the main goals of therapy for stable angina?

A
  1. prevent disease progression (ex: ACS, stroke, MI etc and prevent worsening atherosclerosis)
  2. alleviate acute symptoms of ischemia (angina)
  3. prevent future symptoms of myocardial ischemia
  4. minimize ADRs of therapy
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38
Q

what are some lifestyle modifications that can reduce IHD risk?

A

smoking cessation, exercise, weight management, alcohol management, diet to control dyslipidemia, HTN, diabetes etc.

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39
Q

what are some lifestyle modifications that can reduce IHD risk?

A

smoking cessation, exercise, weight management, alcohol management, diet to control dyslipidemia, HTN, diabetes etc.

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40
Q

what are two types of revascularization?

A

PCI (percutaneous coronary intervention) and CABG (coronary artery bypass graft)

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41
Q

what are 4 classes of medications used to prevent progression of IHD?

A
  1. anti-platelets
  2. statins (cholesterol management)
  3. ACE-Is
  4. antianginals
42
Q

what are 5 classes of medications used for symptoms control of IHD?

A
  1. beta blockers
  2. CCBs
  3. nitrates
  4. ranalozine
  5. Ivabridine
    These are all used as antianginals
43
Q

in stable angina, all patients are given what dose of ASA? For how long?

A

81mg daily; indefinitely

44
Q

what was found out in the COMPASS trial about rivaroxaban for stable angina?

A

NNT CV events = 77
NNH major bleeding = 84
5mg BID showed no benefit, currently not guideline recommended

45
Q

all patients should with IHD should have ACE-I considered as an option, but especially which patient populations?

A

HTN, diabets, left ventricular ejection fraction <40%, CKD

46
Q

what were the landmark trials that showed the benefits of ACE-I in prevention of CAD?

A

HOPE, EUROPA, PEACE

47
Q

can ARBs be used for IHD if ACE-I are not tolerated?

A

yes

48
Q

what monitoring needs to be done with ACE-i?

A

Scr and K at baseline and within 1-2 weeks of starting treatment or dose adjustment

49
Q

do ACE-i need to be held for diabetic patients when they experience GI distress/dehydration to minimize kidney damage?

A

yes!! They are on the SADMANs list and patient must be educated on this

50
Q

beta blockers are considered 1st line for chronic stable angina if there is previous history of ______

A

MI, reduced ejection fraction, heart failure

51
Q

when are long-acting nitrates added for management of stable angina?

A

if a combination of B blocker & CCB is not working or is contraindicated

52
Q

what is the effect of beta blockers on coronary blood flow?

A

no change

53
Q

what is the effect of B blockers on HR?

A

decrease

54
Q

what is the effect of B blockers on wall tension?

A

decrease

55
Q

what is the effect of B blockers on myocardial contractility?

A

decrease

56
Q

what is the effect of DH CCB on coronary blood flow, HR, wall tension, and myocardial contractility?

A

increase coronary blood flow, increase HR, decrease wall tension, decrease myocardial contractility

57
Q

what is the effect of non-DHP CCB on coronary blood flow, HR, wall tension, and myocardial contractility?

A

increase coronary blood flwo, decrease everything else

58
Q

what is the effect of nitrates on coronary blood flow, HR, wall tension, myocardial contractility?

A

increase coronary blood flow, increase HR, decrease wall tension, no change on contractility

59
Q

what is the effect of ranolazine on coronary blood flow, HR, wall tension, and myocardial contractility?

A

decrease wall tension, no change in anything else

60
Q

In what 2 ways do B blockers increase myocardial oxygen supply?

A
  1. prolongs diastole (which may improve perfusion to ischemic areas)
  2. ventricular relaxation which results in a modest sub-endocardial blood flow
61
Q

what are the effects of B blockers on oxygen demand?

A
  1. decrease HR
  2. decrease contractility
  3. decrease BP
62
Q

what are some ADRs of B blockers?

A

impotence, sleep disturbances, exercise intolerance, bradycardia, postural hypotension, masked hyoglycemia

63
Q

what are some C/i for B blocker use?

A

bradycardia, hypotension, AV block, sick sinus syndrome, vasospastic angina, cardiogenic shock, decompensated HF

64
Q

caution should be used when giving B blockers to what patient populations?

A

diabetes, asthma/COPD, peripheral vascular disease. Avoid agents with sympathomimetic activity

65
Q

B blockers are especially useful if a patient has what comorbid conditions>

A

migraines, hyperthyroidism, tachycardia, ACS/MI, aortic/mitral stenosis

66
Q

what are the cardio-selective B blockers?

A

bisoprolol, metoprolol, atenolol

67
Q

what are the non-selective B blockers?

A

propranolol, timolol, nadolol

68
Q

what are the mixed B blockers (a/b)?

A

carvediolol, labetolol

69
Q

what are the effects of CCBs on oxygen supply?

A
  1. decreased HR (verapamil/diltiazem), which increases diastolic perfusion time, enhancing LV perfusion
  2. decrease coronary vascular resistance
  3. increase vasodilation of coronary arteries
70
Q

what are theeffects of CCBs on oxygen demand?

A
  1. vasodilation of systemin arteries decreases SV and arterial BP
  2. decrease contractility (verapamil/diltiazem) oxygen requirement decreased (varying negative ionotropic effects)
  3. decreased HR (diltiazem/verapamil)
71
Q

what are the non-DHP CCBs?

A

verapamil and diltiazem

72
Q

what are the C/i for non-DHP CCBs?

A

bradycardia, AV block, HF, cardiogenic shock

73
Q

what are the ADRs of non-DHP CCBs?

A

bradycardia, constipation, hypotension (avoid in B blocker use)

74
Q

what are the DHP-CCBs?

A

amlodipine and nifedipine

75
Q

what are the C/i pf DHP CCBs?

A

severe aortic stenosis

76
Q

what are the ADRs of DHP-CCBs?

A

headache, flushing, peripheral edema, hypotension, CYP3A4 interactions

77
Q

when are non-DHP CCBs especially beneficial?

A

HTN, SVT, vasospastic angina, PVD, DM, severe asthma/COPD

78
Q

when are DHP CCBs especially beneficial?

A

HTN, DM< bradycardia, severe asthma/COPD, vasospactic angina, PVD

79
Q

why should short-acting CCBs not be used?

A

they increase the number of angina episodes per week

80
Q

t/f all patients with a hx of symptomatic angina should be given SL nitroglycerin

A

t

81
Q

what is the dosing for SL nitroglycerin?

A

can give 1 spray or 1 tablet 5 min before activity and that should last 30 min. For symptom relief, you can use 1 spray or 1 tablet q5min up to three times (if you are not better, you need to call 911)

82
Q

use of nitrates is C/i if what class of medications have been used in the past 24-48 hours?

A

phosphodiesterase 5 inhibitors

83
Q

what is the effect of nitrates on oxygen supply?

A

dilates large coronary arteries and areas of stenosis to increase o2 supply

84
Q

what are the effects of nitrates on O2 demand?

A
  1. venous vasodilation decreases blood return to the heart (preload), reducing LV volume, wall stress and therefore demand
  2. decreases arterial vasodialtion, decreases peripheral resistance, reducing BP nad demand
85
Q

what are the ADRs of nitrates?

A

headache, hypotension, syncope, dizziness, lightheadedness, flushing, tachycardia

86
Q

what are the C/i of nitrates?

A

hemodynamic instability, combination with PDE-5 inhibitors

87
Q

what cautions need to be exercised when using a nitrate?

A

tolerance can develop, so there should be a nitrate free period (patch 10-12hrs, paste 6-8hrs, dinitrate BID-TID, mononitrate UID)

88
Q

why should nitrates not be used as a monotherapy?

A

no protection during the off periods

89
Q

t/f the antianginal effects of Ranolazine are not fully known

A

t

90
Q

what is the MOA of Ranolazine?

A

inhibits the late phase of inward Na channels in ischemic myocytes during repolarization. This reduction in Na causes an influx of Ca, decreasing ventrucular tension and myocardial O2 consumption

91
Q

when using ranolazine, the oxygen ____ is increased

A

efficiency

92
Q

what is the place in therapy for Ranolazine?

A

to be used in combination with B blockers, CCbs or nitrates when these agents are not working, or are not tolerated

93
Q

what are the ADRs of Ranolazine?

A

constipation, dizziness, nausea, headache, SOB, peripheral edema, QT prolongation

94
Q

what are the C/i for Ranolazine?

A

strong CYP3A4 inhibitors/inducers, moderate to severe hepatic impaorment, CrCl <30mL/min

95
Q

caution should be used if ranolazine is goinf to be used with other medications that prolong ___

A

QT interval

96
Q

does ranolazine have significant effects on HR and BP?

A

no

97
Q

what is the typical dose of ranolazine for angina?

A

500mg po BID titrated q2-4 weeks to 1000mg BID

98
Q

what is the effect of Ibavridine on oxygen supply?

A

increases diastole time, increasing coronary perfusion

99
Q

what is the effect of ibavridine on oxygen demand?

A

decreases HR by inhibiting sinus node

100
Q

what are the ADRs of Ibavridine?

A

decreased HR (risk increased if over 75 yo), headache, dizziness, visual disturbances

101
Q

what are the c/i for ibavridine?

A

resting HR below 70BPM, non-DHP CCB, strong CYP3A4 agents, severe hepatic dx, prolonged QT interval

102
Q

Ibavridine is especially beneficial for what patient populations?

A

patients with tachycardia, approved fro HF with reduced EF (EF <35%). No benefit in mortality for CAD

103
Q

ibavridine is meant to be used in combination with ____ or ____ if those agents have not been successful

A

B blockers, CCBs

104
Q

what will the cardiac enzymes look like if the patient has stable angina?

A

normal (no myocardial death at this point)

105
Q

what is pharmacological stress testing?

A

Use of dobutamine to increase blood flow to normal arteries and will show a decrease to sites of stenosis. Uses Echo imaging

106
Q

what is nuclear stress testing?

A

uses radio-active substances to see what area of heart muscle are not getting enough O2 at rest or during exercise

107
Q

what is shown by a cardia CT?

A

3D images of the heart

108
Q

what is cardiac catheterization?

A

contrast dye is injected into radial or femoral artery to visualize coronary artery anatomy. AKA an angiogram. This is the gold standard to testing IHD

109
Q

patients suspected of IHD should have non-invasive diagnostic testing within ____weeks of initial assessment, should see a speacialist in anaother _____ weeks and should have a cardiac angiogram within another ____ weeks

A

2; 6; 6

110
Q

the 12-16 week period between suspected IHD diagnosis and angiogram is enough time to do what?

A

titrate indicated medications, determine if there is enough symptom relief and identify patients who may require re-vasculariation

111
Q

risk for heart disease is increased ___x in an active smoker and ___x for passive environmental smoke exposure

A

1.8, 1.3

112
Q

How does nicotine increase oxygen demand?

A

raises HR and BP

113
Q

what comormid condition is the most common and most powerful contributor to atherosclerotic coronary vascular dx?

A

Hypertension

114
Q

explain what happens in a PCI

A

a catheter is placed into a BV in the groin or in the arm and is threaded through the blood vessels into the narrowed coronary artery of interest, then a balloon tip with a stent is inflated, the stent is left and the balloon removed. This moved plaque out of the way and artery is re-opened

115
Q

explain what happens during a CABG

A

a piece of healthy blood vessel (from patients arm, leg, chest etc.) is removed and placed above and below the blocked artery so blood flow is redirected (bypassed)

116
Q

in what situations is CABG performed?

A

if there are many blockages or if the blockages are hard for the catheter to reach

117
Q

do revascularization techniques get rid of atherosclerosis or atherosclerotic risk?

A

no!

118
Q

treatment of IHD is considered ____(primary or secondary) prevention

A

secondary

119
Q

if the PCI is elective and there is not a high bleeding risk, how long will DAPT be?

A

6 months

120
Q

if a patient has high risk or angiographic features for thrombotic CV events and not at high bleeding risk, how long may DAPT be continued?

A

3 years

121
Q

If a patient is at high risk for bleeding, what is the minimum DAPT treatment for a bare metal stent? For a drobuluting stent?

A

1 month bare metal, , 3 months drobuluting

122
Q

what is the goal LDL for IHD?

A

<1.8 mmol/L