Lec 16+18 Stable CAD Flashcards

1
Q

What is order of severity:

  • MI
  • asymptomatic ischemia
  • unstable angina
  • angina pectoris
A

asymptomatic ischemia –> angina pectoris –> unstable angina –> MI

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2
Q

What is definition ischemic heart disease?

A

clinical expression of imbalance between myocardial ox supply and demand

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3
Q

What is angina pectoris?

A

uncomfortable sensation in chest produced by myocardial ischemia

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4
Q

What is stable angina?

A

chronic pattern of angina associated with physical activity or emotional upset usually radiates to L arm or jaw

relieved by rest w/in minutes or nitroglycerin

temporary ST depression on EKG
no permanent mycocardial damage = reversible

usually when stenosis > 70%

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5
Q

What is variant [prinzmetal] angina?

A

angina occurs at rest secondary to coronary artery vasospasm

transient ST elevation on EKG

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6
Q

What is silent ischemia?

A

asymptomatic episdoes of myocardial ischemia

only detect by EKG or other lab

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7
Q

What is unstable angina?

A

increase frequency + duration of angina at low exertion or at rest

ST depression on EKG

high risk of progression to MI

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8
Q

What is myocardial infarction?

A

region of myocardial necrosis usually due to prolonged cessation blood supply from acute thrombus at site of coronary atherosclertic stenosis + complete occlusion of coronary artery

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9
Q

What are the determinants of myocardial oxygen supply?

A
  • blood O2 content

- coronary flow

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10
Q

What determines the O2 content of blood?

A
  • hemoglobin level and O2 sat

- affected by lung disease, anemia, hemorrhage

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11
Q

What determines coronary flow?

A

Q = P/R

  • direct relation to perfusion pressure
  • indirect to vascular resistance
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12
Q

What determines perfusion pressure?

A
  • coronary perfusion occurs during diastole
  • can be approximated by diastolic pressure in aorta

decrease by anything that: decreases diastolic P [hypotension or aortic regurgitation] OR increases LVEDP [diminishes flow]

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13
Q

What are some conditions that decrease diastolic pressure and thus perfusion pressure?

A

hypotension

aortic regurgitation

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14
Q

What determines coronary vascular resistance?

A
  • vascular tone

- degree of coronary stenosis

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15
Q

What metabolic factors mediate vascular tone?

A

adenosine = produced in hypoxia = vasodilator

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16
Q

What is syndrome X?

A

chest pain and evidence of ischemia but normal coronary arteries

abnormal response to adenosine
microvascular dysfunction

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17
Q

What are endothelial factors that mediate vascular tone?

A

endothelium-dependent vasodilators: ACh, serotonin, thrombin, sheer stress –> cause endothelium to produce NO, prostacyclin, EDHF

endothelium-dependent vasoconstrictors: Thrombin, angiotensin II, epinephrin –> cause endothelium to produce endothelin I

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18
Q

What 3 factors released from endothelium cause smooth muscle relaxation?

A

NO, prostacyclin, EDHF

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19
Q

What factor released from endothelium causes smooth muscle contraction?

A

endothelin 1

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20
Q

What factors act on endothelial cells to cause vasodilation?

A

ACh
serotonin
shear stress

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21
Q

What factors act on endothelial cells to cause vasoconstriction?

A

thrombin
angiotensin II
epinephrine

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22
Q

How does endothelial response to ACh changed in normal vs at risk?

A

normal = ACh is a vasodilator

in pt with lots of risk factors for heart disease –> give ACh –> vasoconstriction

example of endothelial dysfunction

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23
Q

What are 3 major determinants of myocardial oxygen demand?

A
  • ventricular wall stress
  • heart rate
  • contractility
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24
Q

What is ventricular wall stress? What are some states that increase it?

A

wall stress = P * r / 2h

  • increase by pressure overload [aortic stenosis/HTN]
  • increase by volume overload [mitral regurgitation]
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25
How does HR affect oxygen demand?
more ox required in higher HR
26
How does fixed atherosclerotic plaque affect coronary blood flow?
increases resistance mostly by reduction in lumen diameter also by length of lesion R= L / r^4
27
What does the hemodynamic consequences of arterial narrowing depend on?
- degree of stenosis | - compensatory vasodilation
28
At what level of stenosis is maximal blood flow decreased under conditions of stress?
70% stenosis = stable angina, fine in normal but when you exert yourself you don't have enough O2 to support increased need
29
At what level of stenosis is resting blood flow impaired?
90% stenosis
30
What dysfunction in endothelial cells in chronic CAD?
- impaired release of endothelium-dependent vasodilators in response to normal stimuli - impaired vasodilatory effects of adenosine + other metabolites - vasoconstriction over vasodilation [usually opposite] - loss of inherent antithrombic effect of endothelial cells --> promotes thrombosis
31
What are some causes of non-atherosclerotic myocardial ischemia?
- reduced O2 supply | - increased O2 demand
32
What are 2 things that can cause reduced O2 supply?
- aortic regurgitation [decrease diastolic BP --> decrease perfusion P] - acute blood loss [GI bleeding]
33
What are 3 things that can cause increase O2 demand?
- tachyarrythmias = rapid aFib - acute rise in BP = HTN crisis - severe aortic stenosis [LV hypertrophy]
34
What is myocyte necrosis?
irreversible cell death with prolonged episode = infarct - detect by cardiac imaging or Q wave on ECG
35
What is stunned myocardium?
episode of systolic dysfunction after some degree of transient ischemia but no necrosis functionally can gradually recover back to normal
36
What is hibernating myocardium?
chronic dysfunction, has many years of CAD and chronic lack of O2 supply --> abnormal ventricular function if you revascularize you can restore ventricular function
37
What should you look for in history for diagnosis of chronic stable angina?
- sensation pain/pressure in chest - diffuse localization can radiate to left arm/neck - lasts few min - associated: SOB, fatigue, nausea, diaphoresis - precipitated by physical activity or emotional stress
38
What is differential diagnosis for chronic stable angina?
cardiac spasm= occurs only at rest pericarditis = positional / bad with deep inspiration GI: associated with meal, antacids help MSK: focal
39
What do you see on EKG in chronic stable angina?
ST depression or T wave inversion = myocardial ischemia infarct = ST elevation may be normal in most pt if not having acute episode
40
What is stress testing?
- try to induce stress by exercise or pharmacologic so you can look at EKG or echo or nuclear perfusion to check for ischemia
41
What is gold standard for chronic stable angina diagnosis?
coronary angiography = need contrast media, visualize lumen but can't assess atherosclerotic disease in vascular wall to look for vulnerability
42
What are the 2 goals for treatment of stable CAD?
- improve QOL --> reduce symptoms angina | - improve quantity of life --> reduce fatal events
43
What is use of nitrates in stable CAD treatment?
venodilation --> reduce LV volume --> lower wall stress + ox demand
44
What are most common side effects nitrates?
lightheadedness, headache | tolerance
45
What effect of nitrates on long term MI survival?
none = no mortality benefit | just for symptom release
46
What is use of B blockers in stable CAD treatment
inhibit B receptors --> decrease HR and contractility [B1]; vasoconstriction in vasculature and bronchial tree [B2] --> decrease myocardial ox demand by slowing HR + decrease force of contraction + increase ox supply by increase duration of diastole
47
``` How do nitrates affect the following: end diastolic volume blood pressure contractility heart rate ejection time oxygen demand ```
``` end diastolic volume: decrease blood pressure: decrease contractility: increase [reflex response] heart rate: increase [reflex response] ejection time: decrease oxygen demand: decrease ```
48
``` How do beta blockers affect the following: end diastolic volume blood pressure contractility heart rate ejection time oxygen demand ```
``` end diastolic volume: increase blood pressure: decrease contractility: decrease heart rate: decrease ejection time: increase oxygen demand: decrease ```
49
``` How do nitrates and Bblocker together affect the following: end diastolic volume blood pressure contractility heart rate ejection time oxygen demand ```
``` end diastolic volume: no effect or decrease blood pressure: decrease contractility: little/none heart rate: decrease ejection time: little/no effect oxygen demand: big decrease ```
50
Which patients have greatest benefit from B-blockers?
- pts with symptoms, with prior MI, or with heart failure
51
Do Bblockers improve mortality or symptoms or both?
both improve mortality and symptoms
52
What are side effects of B blockers?
- bronchospasm --> caution in asthmatics - decompensated LV dysfunction --> make it worse = DO NOT USE IN DECOMPENSATED LV - significant bradycardia - fatigue - sexual dysfunction - may mask reflex tachycardia from hypoglycemia
53
What is particular use of dihydropyridines?
coronary spasm
54
Why caution when use Ca channel blocker with B blocker?
may accentuate negative chronotropy and inotropy
55
What is effect of ranolazine?
decreases anginal frequency and improves exercise tolerance - does not reduce mortality but does improve symtpoms
56
What is effect of antiplatelet therapy?
reduce risk of thrombotic complications by inhibition of platelet aggregation = no benefit to symptoms but significant reduction mortality
57
Who should use thienopyridine [clopidogrel]?
pts intolerant to aspirin inhibits platelet P2Y12 receptor monotherapy = equivalent to aspirin, no benefit to use together
58
What is effect of lipid lowering therapy on pt with stable angina?
lower risk for death/MI in pt at risk or wtih established CAD
59
Who should get beta blockers?
post-MI, in heart failure
60
Who should get ACE inhibitors?
post MI, with LV dysfuntion, in heart failure, DM, chronic kidney disease, HTN
61
What 4 drugs give symptom relief in stable CAD?
- nitrates, B Blocker, CCB, ranolazine
62
What are the 2 methods of revascularization?
balloon angioplasty stent | coronary artery bypass graft
63
What are problems with previous iterations balloon angioplasty?
balloon alone --> get elastic recoil, restenosis bare metal --> get restenosis due to inflammation and proliferation smooth muscle around it drug eluting --> coated with anti-proliferative, inhibits restonosis but also delays normal endothelialization --> increase risk for thrombosis = need long term DAPT
64
Is there reduction in death from stent [percutaneous coronary intervention]?
nope! just reduce anginal symptoms
65
Who should get percutaneous coronary intervention?
pt with refratory symptoms despite optomizing medical therapy OR intolerant to medical therapy
66
What is difference in venous vs arterial grafts?
venous = from saphenous; patency at 10 yrs 50% arterial = from raidal, internal mammary; very high patency 90% at 10 yrs = used for left main stenoses
67
Which people have greatest mortality advantage from revascularization?
- left main stenosis - 2 vessel stenosis involving LAD - 3 vessel CAD - diabetic with multivessel CAD
68
What are advantages/disadvantages of PCI?
advantage: low risk procedure, minimal recuperation disadvantage: need dual antiplatelet threapy = bleeding risk; higher revascularization rates
69
What are advantages/disadvantages of CABG?
advantages = complete revascularization, no need for long term anti-platelet therapy, proven mortality benefit in certain pts disadvantages: higher procedure risk, longer recuperation