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
Describe the typical presentation of stable angina
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
24
what are some atypical symptoms of stable angina?
nausea, diaphoresis, SOB, anxiety
25
the atypical symptoms of stable angina are typically seen in what patient populations?
women and diabetic patients
26
the atypical symptoms of stable angina are typically seen in what patient populations?
women and diabetic patients
26
the atypical symptoms of stable angina are typically seen in what patient populations?
women and diabetic patients
27
what are some precipitating factors of stable angina?
exercise, cold weather, after meals, emotional stress, sexual activity
28
what provides relief for stable angina?
rest and or nitroglycerin
28
what provides relief for stable angina?
rest and or nitroglycerin
28
what provides relief for stable angina?
rest and or nitroglycerin
28
what provides relief for stable angina?
rest and or nitroglycerin
28
what provides relief for stable angina?
rest and or nitroglycerin
28
what provides relief for stable angina?
rest and or nitroglycerin
28
what provides relief for stable angina?
rest and or nitroglycerin
28
what provides relief for stable angina?
rest and or nitroglycerin
28
what provides relief for stable angina?
rest and or nitroglycerin
28
what provides relief for stable angina?
rest and or nitroglycerin
28
what provides relief for stable angina?
rest and or nitroglycerin
28
what provides relief for stable angina?
rest and or nitroglycerin
29
what provides relief for stable angina?
rest and or nitroglycerin
30
what provides relief for stable angina?
rest and or nitroglycerin
31
describe Grade I stable angina
ordinary physical activity (walking, climbing stairs) does not cause angina, but strenuous, rapid, or prolonged exertion causes angina
32
describe Grade I stable angina
ordinary physical activity (walking, climbing stairs) does not cause angina, but strenuous, rapid, or prolonged exertion causes angina
33
describe Grade II angina
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
34
describe Grade III angina
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
35
describe Grade IV angina
inability to carry on any physical activity without discomfort. Angina may be present at rest
36
what are the diagnostic tests for IHD?
ECG, exercise stress test, pharmacologic stress test, nuclear stress test, cardiac CT/MRI, cardiac catheterization
37
what are the main goals of therapy for stable angina?
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
38
what are some lifestyle modifications that can reduce IHD risk?
smoking cessation, exercise, weight management, alcohol management, diet to control dyslipidemia, HTN, diabetes etc.
39
what are some lifestyle modifications that can reduce IHD risk?
smoking cessation, exercise, weight management, alcohol management, diet to control dyslipidemia, HTN, diabetes etc.
40
what are two types of revascularization?
PCI (percutaneous coronary intervention) and CABG (coronary artery bypass graft)
41
what are 4 classes of medications used to prevent progression of IHD?
1. anti-platelets 2. statins (cholesterol management) 3. ACE-Is 4. antianginals
42
what are 5 classes of medications used for symptoms control of IHD?
1. beta blockers 2. CCBs 3. nitrates 4. ranalozine 5. Ivabridine These are all used as antianginals
43
in stable angina, all patients are given what dose of ASA? For how long?
81mg daily; indefinitely
44
what was found out in the COMPASS trial about rivaroxaban for stable angina?
NNT CV events = 77 NNH major bleeding = 84 5mg BID showed no benefit, currently not guideline recommended
45
all patients should with IHD should have ACE-I considered as an option, but especially which patient populations?
HTN, diabets, left ventricular ejection fraction <40%, CKD
46
what were the landmark trials that showed the benefits of ACE-I in prevention of CAD?
HOPE, EUROPA, PEACE
47
can ARBs be used for IHD if ACE-I are not tolerated?
yes
48
what monitoring needs to be done with ACE-i?
Scr and K at baseline and within 1-2 weeks of starting treatment or dose adjustment
49
do ACE-i need to be held for diabetic patients when they experience GI distress/dehydration to minimize kidney damage?
yes!! They are on the SADMANs list and patient must be educated on this
50
beta blockers are considered 1st line for chronic stable angina if there is previous history of ______
MI, reduced ejection fraction, heart failure
51
when are long-acting nitrates added for management of stable angina?
if a combination of B blocker & CCB is not working or is contraindicated
52
what is the effect of beta blockers on coronary blood flow?
no change
53
what is the effect of B blockers on HR?
decrease
54
what is the effect of B blockers on wall tension?
decrease
55
what is the effect of B blockers on myocardial contractility?
decrease
56
what is the effect of DH CCB on coronary blood flow, HR, wall tension, and myocardial contractility?
increase coronary blood flow, increase HR, decrease wall tension, decrease myocardial contractility
57
what is the effect of non-DHP CCB on coronary blood flow, HR, wall tension, and myocardial contractility?
increase coronary blood flwo, decrease everything else
58
what is the effect of nitrates on coronary blood flow, HR, wall tension, myocardial contractility?
increase coronary blood flow, increase HR, decrease wall tension, no change on contractility
59
what is the effect of ranolazine on coronary blood flow, HR, wall tension, and myocardial contractility?
decrease wall tension, no change in anything else
60
In what 2 ways do B blockers increase myocardial oxygen supply?
1. prolongs diastole (which may improve perfusion to ischemic areas) 2. ventricular relaxation which results in a modest sub-endocardial blood flow
61
what are the effects of B blockers on oxygen demand?
1. decrease HR 2. decrease contractility 3. decrease BP
62
what are some ADRs of B blockers?
impotence, sleep disturbances, exercise intolerance, bradycardia, postural hypotension, masked hyoglycemia
63
what are some C/i for B blocker use?
bradycardia, hypotension, AV block, sick sinus syndrome, vasospastic angina, cardiogenic shock, decompensated HF
64
caution should be used when giving B blockers to what patient populations?
diabetes, asthma/COPD, peripheral vascular disease. Avoid agents with sympathomimetic activity
65
B blockers are especially useful if a patient has what comorbid conditions>
migraines, hyperthyroidism, tachycardia, ACS/MI, aortic/mitral stenosis
66
what are the cardio-selective B blockers?
bisoprolol, metoprolol, atenolol
67
what are the non-selective B blockers?
propranolol, timolol, nadolol
68
what are the mixed B blockers (a/b)?
carvediolol, labetolol
69
what are the effects of CCBs on oxygen supply?
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
what are theeffects of CCBs on oxygen demand?
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
what are the non-DHP CCBs?
verapamil and diltiazem
72
what are the C/i for non-DHP CCBs?
bradycardia, AV block, HF, cardiogenic shock
73
what are the ADRs of non-DHP CCBs?
bradycardia, constipation, hypotension (avoid in B blocker use)
74
what are the DHP-CCBs?
amlodipine and nifedipine
75
what are the C/i pf DHP CCBs?
severe aortic stenosis
76
what are the ADRs of DHP-CCBs?
headache, flushing, peripheral edema, hypotension, CYP3A4 interactions
77
when are non-DHP CCBs especially beneficial?
HTN, SVT, vasospastic angina, PVD, DM, severe asthma/COPD
78
when are DHP CCBs especially beneficial?
HTN, DM< bradycardia, severe asthma/COPD, vasospactic angina, PVD
79
why should short-acting CCBs not be used?
they increase the number of angina episodes per week
80
t/f all patients with a hx of symptomatic angina should be given SL nitroglycerin
t
81
what is the dosing for SL nitroglycerin?
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
use of nitrates is C/i if what class of medications have been used in the past 24-48 hours?
phosphodiesterase 5 inhibitors
83
what is the effect of nitrates on oxygen supply?
dilates large coronary arteries and areas of stenosis to increase o2 supply
84
what are the effects of nitrates on O2 demand?
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
what are the ADRs of nitrates?
headache, hypotension, syncope, dizziness, lightheadedness, flushing, tachycardia
86
what are the C/i of nitrates?
hemodynamic instability, combination with PDE-5 inhibitors
87
what cautions need to be exercised when using a nitrate?
tolerance can develop, so there should be a nitrate free period (patch 10-12hrs, paste 6-8hrs, dinitrate BID-TID, mononitrate UID)
88
why should nitrates not be used as a monotherapy?
no protection during the off periods
89
t/f the antianginal effects of Ranolazine are not fully known
t
90
what is the MOA of Ranolazine?
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
when using ranolazine, the oxygen ____ is increased
efficiency
92
what is the place in therapy for Ranolazine?
to be used in combination with B blockers, CCbs or nitrates when these agents are not working, or are not tolerated
93
what are the ADRs of Ranolazine?
constipation, dizziness, nausea, headache, SOB, peripheral edema, QT prolongation
94
what are the C/i for Ranolazine?
strong CYP3A4 inhibitors/inducers, moderate to severe hepatic impaorment, CrCl <30mL/min
95
caution should be used if ranolazine is goinf to be used with other medications that prolong ___
QT interval
96
does ranolazine have significant effects on HR and BP?
no
97
what is the typical dose of ranolazine for angina?
500mg po BID titrated q2-4 weeks to 1000mg BID
98
what is the effect of Ibavridine on oxygen supply?
increases diastole time, increasing coronary perfusion
99
what is the effect of ibavridine on oxygen demand?
decreases HR by inhibiting sinus node
100
what are the ADRs of Ibavridine?
decreased HR (risk increased if over 75 yo), headache, dizziness, visual disturbances
101
what are the c/i for ibavridine?
resting HR below 70BPM, non-DHP CCB, strong CYP3A4 agents, severe hepatic dx, prolonged QT interval
102
Ibavridine is especially beneficial for what patient populations?
patients with tachycardia, approved fro HF with reduced EF (EF <35%). No benefit in mortality for CAD
103
ibavridine is meant to be used in combination with ____ or ____ if those agents have not been successful
B blockers, CCBs
104
what will the cardiac enzymes look like if the patient has stable angina?
normal (no myocardial death at this point)
105
what is pharmacological stress testing?
Use of dobutamine to increase blood flow to normal arteries and will show a decrease to sites of stenosis. Uses Echo imaging
106
what is nuclear stress testing?
uses radio-active substances to see what area of heart muscle are not getting enough O2 at rest or during exercise
107
what is shown by a cardia CT?
3D images of the heart
108
what is cardiac catheterization?
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
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
2; 6; 6
110
the 12-16 week period between suspected IHD diagnosis and angiogram is enough time to do what?
titrate indicated medications, determine if there is enough symptom relief and identify patients who may require re-vasculariation
111
risk for heart disease is increased ___x in an active smoker and ___x for passive environmental smoke exposure
1.8, 1.3
112
How does nicotine increase oxygen demand?
raises HR and BP
113
what comormid condition is the most common and most powerful contributor to atherosclerotic coronary vascular dx?
Hypertension
114
explain what happens in a PCI
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
explain what happens during a CABG
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
in what situations is CABG performed?
if there are many blockages or if the blockages are hard for the catheter to reach
117
do revascularization techniques get rid of atherosclerosis or atherosclerotic risk?
no!
118
treatment of IHD is considered ____(primary or secondary) prevention
secondary
119
if the PCI is elective and there is not a high bleeding risk, how long will DAPT be?
6 months
120
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?
3 years
121
If a patient is at high risk for bleeding, what is the minimum DAPT treatment for a bare metal stent? For a drobuluting stent?
1 month bare metal, , 3 months drobuluting
122
what is the goal LDL for IHD?
<1.8 mmol/L