CAD Flashcards

1
Q

TIMI risk score

A

> 65 years
3 risk factors
known CAD (stenosis >50%)
aspirin use in the prior 7 days
recent (previous 24 hours) angina
increased cardiac markers, and ST elevation >0.5 mm (Figure 1)

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2
Q

TIMI risk score >2

A

early invasive strategy-cath w/in 48 hours

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3
Q

vasospastic angina/ Prinzmetal or variant angina

A

spasm, transient ECG changes and symptoms.
Smoking cessation, CCBs, nitrates.
BBs can exacerbate symptoms

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4
Q

Avoid exercise stress test in

A

abnormal resting ECG

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5
Q

Angina treatment
Antianginal which is independent of hemodynamics and myocardial oxygen consumption

A

Nitrates, BB, CCBs
Ranexa

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6
Q

typical chest pain/angina

A

substernal chest discomfort provoked by exertion or emotional stress and relieved by rest or nitroglycerin.

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7
Q

ludwig angina

A

cellulitis involving the floor of the oral cavity; fever, a swollen and painful neck, a raised tongue, and trouble swallowing.

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8
Q

chronic stable angina mechanism

A

stable coronary plaque that limits augmentation of blood flow

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9
Q

ACS mechanism

Vasospasm

A

Atherosclerotic plaque rupture
coronary artery vascular smooth muscle hyper-reactivity

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10
Q

Highest risk of future CV events

A

Prior ischemic event

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11
Q

Microvascular dysfunction/ microvascular angina

A

symptoms+ evidence of ischemia but no epicardial coronary disease.
PET CFR for diagnosis. Treat risk factors, BBs, CCBs

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12
Q

PAD antiplatelet

A

Either aspirin or plavix

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13
Q

CAD patients all get

A

echo

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14
Q

CCTA and stress testing are equivalent.

A
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15
Q

Left main intervention

A

CABG unless high surgical risk (reduced EF)

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16
Q

ASCVD risk enhancing factors

A

hs-CRP level ≥2 mg/L
triglyceride levels ≥175 mg/L,
lipoprotein(a) >50 mg/dL (>125 nmol/L), apolipoprotein (b) ≥130 mg/dL, and ankle-brachial index <0.9 (Figure 1)

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17
Q

SIHD allergic to aspirin

A

Give plavix

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18
Q

strongest predictor of survival following a STEMI

A

EF

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19
Q

strongest prognostic exercise test variable

A

duration

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20
Q

To assess risk for CAD

A

CAC, CRP. Do not do this in patients who already have high risk per h/o or symptoms

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21
Q

impaired endothelial-dependent reactivity test for microvascular disease

abnormal vascular smooth muscle

A

Acetylcholine

Nitroglycerin

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22
Q

treatment of LVOT obstruction

A

BB, fluids, phenylephrine

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23
Q

SCAD

A

1/4 of ACS in F <50 yo
intimal tear or bleeding of the vasa vasorum with intramedial hemorrhage

pregnant or early post partum

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24
Q

NSTEMI troponin peak

A

24-48 hours after onset of symptoms
correlates with the size of the infarction.

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25
Q

Cardiac rehab onset post MI

A

> 2 weeks

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26
Q

RCA occlusion

A

consider RV infarct. hypotension with clear lungs. give fluids, get echo

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27
Q

inferior STEMI + hypotension +jugular venous distention + a normal lung =

A

RV infarct
Avoid diuretics, nitrates, and opiates

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28
Q

highest sensitivity lead for lcx occlusions

A

V8

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29
Q

ST-segment elevation in lead III greater than that seen in lead II

A

RCA occlusion

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30
Q

Lead V4R (i.e., ECG with the V4 lead in the right rather than left midclavicular line) STEMI

A

RV infarct

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31
Q

takotsubo mechanism

A

catecholamine excess, derangement of myocardial glucose and fatty acid metabolism, microcirculatory dysfunction, coronary vasospasm, and estrogen deficiency.

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32
Q

STEMI + PCI >120 mins away

A

full dose alteplase or tenecteplase. Administer w/in 30 mins of arrival. Transfer ASAP afterwards. Give AC for at least 48 hours, ideally entire hospitalization. Bival if HIT on others.

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33
Q

PCI related MI

A

Troponin > 5x normal/baseline +
ECG changes OR new WMAs OR cath evidence of complication

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34
Q

Inferolateral akinesis MR due to

A

restricted posterior leaflet

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35
Q

strongest risk factor in GRACE

A

Age

36
Q

HDUS Brady can be treated with

Wait 5 days post MI to place PPM if patient has AV block.

A

dopamine

37
Q

Highest negative predictive value for MI.
Most sensitive and specific

A

Troponin

38
Q

NSTEMI AC

A

lovenox while hospitalized or until PCI or bival until early PCI or fonda while hosptialized or until PCI, or heparin for 48 hours or until PCI.

39
Q

SCAD.
SCAD mechanism.

A

Screen for FMD in renals and carotids with CT or MRA.
intimal tear with blood subsequently entering a false lumen or spontaneous hemorrhage of the vaso vasorum causing an intramural hematoma within the coronary arteries

40
Q

NSVT/PVCs post MI in the acute period

A

BB or CCB

41
Q

Low risk SIHD cath

A

Cannot cath until refractory symptoms on GDMT

42
Q

Abnormal coronary flow reserve (adenosine)

A

< 2.5 = nonendothelial microvasc dysfunction

43
Q

Microvascular dysfunction types

A

nonendothelial dysfunction (nitro),
endothelial macrovascular dysfunction (acetylcholine)

44
Q

recurrent chest pain with rapid progression to hemodynamic collapse post PCI

A

LV free wall rupture. may see equalization of diastolic pressures (tamponade). Give fluids

45
Q

inferior + V1 (or V4R) STEMI=

A

RV infarct
III STE> II (RCA instead of lcx)

46
Q

Exercise NST CI

Dobutamine stress echo CI

A

LBBB: reduced specificity, false positive septum
recent afib

47
Q

BB duration post MI in normal EF

A

3 years

48
Q

regadenoson and adenosine CI

A

active wheezing, severe COPD/asthma

49
Q

Prasugrel CI

A

H/o stroke

50
Q

NST high risk findings

A

large (>12% of myocardium) or severe reversible defects, EF reduction on stress, increased lung uptake of tracer, and/or transient ischemic dilation (TID) >1.2.

51
Q

Dressler syndrome

A

post MI pericarditis
Treat with high dose aspirin (750 mg TID).

52
Q

late reperfusion increases the risk of

posteromedial pap muscle rupture

A

mechanical complications

inferior infarct

53
Q

Low EF during hospitalization for STEMI

A

Repeat >90 days after revasc

54
Q

Aspiration thrombectomy associated with

A

increased stroke rate

55
Q

hypertension, tachycardia, and altered mental status+ vasospasm

A

cocaine, also causes platelet activation. hold metop, use benzos and nitro

56
Q

Nitro CI

A

within 24 hours of sildenafil or vardenafil use or within 48 hours of tadalafil use

57
Q

Most common mechanism for NSTEMI

A

disruption of the fibrous cap (plaque rupture or erosion), which stimulates thrombogenesis

58
Q

Plaque formation mechanism

A

initial xanthoma formation and initial intimal thickening->extracellular lipid accumulation in the subintima-> fibrofatty stage-> procoagulant expression and weakening of the fibrous cap

59
Q

SCD due to vasospasm

A

ICD

60
Q

40-70% stenosis PCI

A

FFR < 0.8, iFR < 0.89, IVUS < 6

61
Q

Duke treadmill score

A

exercise duration (minutes) - (4 x angina index) - (5 x maximum ST deviation). The angina index is 0, 1, or2.
>5: low risk, <3% mortality
4 to -10: intermediate, 10%
-11: high, 35%

62
Q

Increased plaque rupture

A

increased macrophage infiltration, larger necrotic lipid cores, thinner fibrous caps, fewer smooth muscle cells, neoangiogenesis, and intraplaque hemorrhage

63
Q

MI

A

rise or fall in troponin +
symptoms of ischemia or imaging evidence or ECG changes.
Differentiate into type 1 (must have coronary thrombus) and type 2.

64
Q

typical chest pain

atypical
noncardiac

A

substernal, exertion/stress, rest/nitro
2/3
1/3

65
Q

To reclassify ASCVD risk

A

CAC score

66
Q

Dobu response in hibernating myocardium

A

Hypokinetic-> improves at low dose-> akinetic at high dose
loss of sarcomeres and myofibrils, increased glycogen stores, and extracellular fibrosis`

67
Q

sudden onset of symptoms, infarcts in two different arterial territories on head imaging, and hemorrhagic transformation of infarct.

A

EMBOLIC stroke

68
Q

HCM histology

A

Myofibril disarray

69
Q

Highest risk for future CVD events

A

CAC score > 400

70
Q

Noncardiac chest pain=

A

no further testing

71
Q

Need to rule out myocarditis and pheo to diagnose

A

stress cardiomyopathy

72
Q

Medical management of ACS

A

active GIB, >12 hours from onset of symptoms if hemodynamically stable

73
Q

exertional chest pain following thrombolytic therapy for a STEMI

A

Cath

74
Q

STEMI c/b cardiogenic shock treatment

A

Meds-> IABP

75
Q

strongest predictors of ACS mortality

A

Age ≥75 years and systolic blood pressure <100 mm Hg

76
Q

Kilip class

A

heart failure signs and symptoms in the setting of acute MI
Class I: No clinical signs of heart failure
Class II: Rales (crackles) in the lungs, an S3, and elevated jugular venous pressure
Class III: Acute pulmonary edema
Class IV: Cardiogenic shock or hypotension (systolic blood pressure <90 mm Hg) and evidence of peripheral vasoconstriction.

77
Q

Pap muscle rupture temporizing measures

A

diuretics, nitrates, and afterload reduction with nitroprusside, and an intra-aortic balloon pump

78
Q

reversible inhibitor of the platelet P2Y12 receptor
specific inhibitor of the protease-activated receptor 1 (PAR1)

A

cangrelor, return to normal within 1 hour
vorapaxar

79
Q

NSTEMI cath w/in 2 hours

A

refractory angina, signs/symptoms of HF or new/worsening mitral regurgitation, hemodynamic instability, recurrent angina at rest, or ventricular tachycardia/fibrillation

80
Q

“no-reflow” phenomenon

A

suboptimal myocardial perfusion despite restoration of lumen patency in the infarct-related artery due to microvascular obstruction, vasospasm or myocyte reperfusion injury.

81
Q

Cardiac rehab phases

A

phase I (inpatient phase) -PT and education
Phase II (outpatient phase)- individualized exercise prescription and risk-factor reduction
Phases III and IV (maintenance phase)- long-term lifestyle changes

82
Q

Fibrinolytic CI

A

Any history of intracranial hemorrhage, no matter how old

83
Q

P2Y12 receptor inhibitor mechanism

A

inhibits ADP induced platelet aggregation. Ticagrelor has rapid onset and greater platelet inhibition compared to clopidogrel

84
Q

Serial troponin timing

A

At presentation and 3-6 hours if old trop, 1-3 hours if high sensitivity

85
Q

HF GDMT

A

BB, ACEI/ARB/ARNI, MRA, dapa, hydral/nitrate

86
Q

Post MI HF pathophysiology

A

activation of the sympathetic nervous system with increase in norepinephrine and beta1-adrenergic activity+ decrease in parasympathetic activity through decreased acetylcholine signaling-> (RAAS) system is activated. Endothelin 1 is also increased.

87
Q

LV aneurysm increases risk for

A

ventricular arrhythmias, heart failure, and thromboembolism