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CAD Flashcards

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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
Cardiac rehab onset post MI
> 2 weeks
26
RCA occlusion
consider RV infarct. hypotension with clear lungs. give fluids, get echo
27
inferior STEMI + hypotension +jugular venous distention + a normal lung =
RV infarct Avoid diuretics, nitrates, and opiates
28
highest sensitivity lead for lcx occlusions
V8
29
ST-segment elevation in lead III greater than that seen in lead II
RCA occlusion
30
Lead V4R (i.e., ECG with the V4 lead in the right rather than left midclavicular line) STEMI
RV infarct
31
takotsubo mechanism
catecholamine excess, derangement of myocardial glucose and fatty acid metabolism, microcirculatory dysfunction, coronary vasospasm, and estrogen deficiency.
32
STEMI + PCI >120 mins away
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.
33
PCI related MI
Troponin > 5x normal/baseline + ECG changes OR new WMAs OR cath evidence of complication
34
Inferolateral akinesis MR due to
restricted posterior leaflet
35
strongest risk factor in GRACE
Age
36
HDUS Brady can be treated with Wait 5 days post MI to place PPM if patient has AV block.
dopamine
37
Highest negative predictive value for MI. Most sensitive and specific
Troponin
38
NSTEMI AC
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
SCAD. SCAD mechanism.
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
NSVT/PVCs post MI in the acute period
BB or CCB
41
Low risk SIHD cath
Cannot cath until refractory symptoms on GDMT
42
Abnormal coronary flow reserve (adenosine)
< 2.5 = nonendothelial microvasc dysfunction
43
Microvascular dysfunction types
nonendothelial dysfunction (nitro), endothelial macrovascular dysfunction (acetylcholine)
44
recurrent chest pain with rapid progression to hemodynamic collapse post PCI
LV free wall rupture. may see equalization of diastolic pressures (tamponade). Give fluids
45
inferior + V1 (or V4R) STEMI=
RV infarct III STE> II (RCA instead of lcx)
46
Exercise NST CI Dobutamine stress echo CI
LBBB: reduced specificity, false positive septum recent afib
47
BB duration post MI in normal EF
3 years
48
regadenoson and adenosine CI
active wheezing, severe COPD/asthma
49
Prasugrel CI
H/o stroke
50
NST high risk findings
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
Dressler syndrome
post MI pericarditis Treat with high dose aspirin (750 mg TID).
52
late reperfusion increases the risk of posteromedial pap muscle rupture
mechanical complications inferior infarct
53
Low EF during hospitalization for STEMI
Repeat >90 days after revasc
54
Aspiration thrombectomy associated with
increased stroke rate
55
hypertension, tachycardia, and altered mental status+ vasospasm
cocaine, also causes platelet activation. hold metop, use benzos and nitro
56
Nitro CI
within 24 hours of sildenafil or vardenafil use or within 48 hours of tadalafil use
57
Most common mechanism for NSTEMI
disruption of the fibrous cap (plaque rupture or erosion), which stimulates thrombogenesis
58
Plaque formation mechanism
initial xanthoma formation and initial intimal thickening->extracellular lipid accumulation in the subintima-> fibrofatty stage-> procoagulant expression and weakening of the fibrous cap
59
SCD due to vasospasm
ICD
60
40-70% stenosis PCI
FFR < 0.8, iFR < 0.89, IVUS < 6
61
Duke treadmill score
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
Increased plaque rupture
increased macrophage infiltration, larger necrotic lipid cores, thinner fibrous caps, fewer smooth muscle cells, neoangiogenesis, and intraplaque hemorrhage
63
MI
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
typical chest pain atypical noncardiac
substernal, exertion/stress, rest/nitro 2/3 1/3
65
To reclassify ASCVD risk
CAC score
66
Dobu response in hibernating myocardium
Hypokinetic-> improves at low dose-> akinetic at high dose loss of sarcomeres and myofibrils, increased glycogen stores, and extracellular fibrosis`
67
sudden onset of symptoms, infarcts in two different arterial territories on head imaging, and hemorrhagic transformation of infarct.
EMBOLIC stroke
68
HCM histology
Myofibril disarray
69
Highest risk for future CVD events
CAC score > 400
70
Noncardiac chest pain=
no further testing
71
Need to rule out myocarditis and pheo to diagnose
stress cardiomyopathy
72
Medical management of ACS
active GIB, >12 hours from onset of symptoms if hemodynamically stable
73
exertional chest pain following thrombolytic therapy for a STEMI
Cath
74
STEMI c/b cardiogenic shock treatment
Meds-> IABP
75
strongest predictors of ACS mortality
Age ≥75 years and systolic blood pressure <100 mm Hg
76
Kilip class
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
Pap muscle rupture temporizing measures
diuretics, nitrates, and afterload reduction with nitroprusside, and an intra-aortic balloon pump
78
reversible inhibitor of the platelet P2Y12 receptor specific inhibitor of the protease-activated receptor 1 (PAR1)
cangrelor, return to normal within 1 hour vorapaxar
79
NSTEMI cath w/in 2 hours
refractory angina, signs/symptoms of HF or new/worsening mitral regurgitation, hemodynamic instability, recurrent angina at rest, or ventricular tachycardia/fibrillation
80
“no-reflow” phenomenon
suboptimal myocardial perfusion despite restoration of lumen patency in the infarct-related artery due to microvascular obstruction, vasospasm or myocyte reperfusion injury.
81
Cardiac rehab phases
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
Fibrinolytic CI
Any history of intracranial hemorrhage, no matter how old
83
P2Y12 receptor inhibitor mechanism
inhibits ADP induced platelet aggregation. Ticagrelor has rapid onset and greater platelet inhibition compared to clopidogrel
84
Serial troponin timing
At presentation and 3-6 hours if old trop, 1-3 hours if high sensitivity
85
HF GDMT
BB, ACEI/ARB/ARNI, MRA, dapa, hydral/nitrate
86
Post MI HF pathophysiology
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
LV aneurysm increases risk for
ventricular arrhythmias, heart failure, and thromboembolism

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