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ACCSAP > CAD > Flashcards

CAD Flashcards

1
Q

Coronary artery calcium scoring

A

detects subclinical atherosclerosis with MESA score
>400= silent ischemia, high risk of events
Good for asymptomatic, intermediate risk stratification

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2
Q

Don’t give nitro in ACS if

A

Recent use of PDE4 inhibitor

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3
Q

Bradycardia immediately after relief of occluded RCA

Treatment

A

Bezold-Jarisch reflex
Stimulation of vagal fibers in inferior LV wall
Atropine, fluids-> isoprotenerol-> pacing

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4
Q

Papillary muscle rupture

Treatment

A

Posteromedial-only supplied by pda (inferior MI)

Surgery, can temporize with Afterload reduction and IABP

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5
Q

Micro vascular angina diagnosis

Treatment

A

coronary flow reserve by positron emission tomography or Doppler flow wire during angiography.

aggressive risk-factor modification, alpha-BETA-BLOCKERS and calcium channel blockers, and novel therapies (including potassium channel openers, metabolic agents, rho-kinase inhibitors, angiotensin-converting enzyme inhibitors, late sodium channel modifiers, ivabradine, phosphodiesterase-5 inhibitors, and statins).

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6
Q

No exercise stress test if

A

Risk stratification for suspected ACS (elevated troponin, recent chest pain)
Do pharmacological instead

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7
Q

P2Y12 inhibitor mechanism of action
Aspirin
GpIIa/ IIIb

A

Inhibits ADP induced platelet activation
and aggregation

Inhibits COX1 and production of thromboxane A2( which causes platelet aggregation)

block the cross-linking of platelets by inhibiting platelet binding to the dimeric fibrinogen molecule. (Figure 1)

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8
Q

Antiplatelets for stable angina itself

A

One (aspirin or P2Y12) to prevent MI and death

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9
Q

Duke treadmill score calculation

A

exercise duration (minutes) - (4 x angina index) - (5 x maximum ST deviation). The angina index is 0, 1, or 2 (no angina, non exercise limiting angina, exercise limiting angina)

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10
Q

Duke treadmill score interpretation

A

A low-risk DTS is >5 and indicates a 5-year survival of >97%.
An intermediate-risk DTS of -10 to +4 is associated with a 5-year survival of 90%.
A high-risk DTS score of -11 or lower is associated with a 5-year survival of 65%.

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11
Q

Concave ST elevations with PR depression 1-8 weeks post MI

A

Dressler syndrome

Aspirin high dose (750 TID), can consider addition of PPI

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12
Q

No thrombolysis in NSTEMI, only STEMI

Anticoagulation choices

A

1) enoxaparin for hospitalization or until (PCI)
2) bivalirudin, only in patients managed with an early invasive strategy, continued until diagnostic angiography or PCI;
3) fondaparinux for hospitalization or until PCI (with unfractionated heparin or bivalirudin administered during PCI because of the risk of catheter thrombosis);
4) unfractionated heparin for 48 hours or until PCI

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13
Q

Myocardial injury due to ischemia vs not

A

rise and/or fall of cardiac troponin +
at least one of the following:
symptoms of acute myocardialischemia, new ischemic ECG changes,
pathological Q waves,
imaging evidence of new loss of viable myocardium or new regional wall motion abnormality in a pattern consistent with an ischemic etiology.

For a type I myocardial infarction, coronary thrombus must also be identified (acute atherothrombosis)

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14
Q

Plaque vulnerability to rupture

A

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

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15
Q

LBBB stress test

Agent
Image: echo or perfusion imaging or ECG

A

No ECG testing/ exercise radionuclide myocardial perfusion imaging (increased false positives)

Vasodilator myocardial perfusion imaging is ok
Dobutamine would be ok but increases risk of arrhythmias

CT coronary can also be used to assess ischemia

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16
Q

Late reperfusion

A

In asymptomatic patients, do not if after 12 hours

Do in cardiogenic shock or acute severe heart failure, intermediate- or high-risk findings on predischarge noninvasive imaging, or myocardial ischemia that is spontaneous or provoked by minimal exertion.

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17
Q

Cardiac PET for

A

Viability

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18
Q

Stress testing in known CAD

A

Imaging, not treadmill ECG

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19
Q

Predictors of mortality in ACS

Biggest predictors

A

TIMI
>75 yo, SBP <100

a score of 0 to >8 is associated with a 30-day mortality of 0.8-36%, whereas the 1-year mortality among those surviving the first 30 days ranges from 1% to 17%.

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20
Q

Risk discussion

CAC scores

A

40-75 years of age without diabetes who are at a 10-year ASCVD risk of 7.5-19.9%

1-99 favors statin therapy
>=100 Agatston units or ≥75th percentile, statin therapy

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21
Q

ST elevations with q waves

A

LV aneurysm

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22
Q

Inferior STEMI (1/3 will have RV infarct)

A

Avoid nitro and diuretics

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23
Q

Inferior ST elevation + ST elevation in V1

greater ST-segment elevation in lead III than lead II

A

RV infarct, get right sided EKG (STE in V4R)

RCA, not lcx

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24
Q

LV aneurysm vs pseudoaneurysm

increased risk of

A

broad neck, anticoagulate vs narrow,contained rupture-> surgery
ventricular arrhythmias, heart failure, and thromboembolism

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25
Q

restricted motion of the posterior mitral valve leaflet MI

A

inferior- ischemic mitral regurg

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26
Q

ACS mechanisms

A

SCAD, plaque rupture with overlying thrombosis, vasospasm, coronary embolus, myocardial bridging

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27
Q

myxoma

A

vascular mass

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28
Q

takotsubo CM

A

REGIONAL (mid-apex) motion abnormality, can form thrombus in 2 days
neuro disorders and pheo can be triggers

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29
Q

aldosterone antagonist

A

STEMI, already on ACEI/ARB+BB, EF less than or equal to 40% and either symptomatic heart failure (HF) or diabetes mellitus (Class I)

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30
Q

intermediate- high coronary artery calcium score (>100)

A

CAD, treat medically if asymptomatic, high intensity statin

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31
Q

prior to revascularization in SIHD

A

should be on GDMT

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32
Q

women with angina, normal cath
mechanism
diagnosis

A

microvascular dysfunction
endothelial or nonendothelial dysfunction
coronary flow reserve with adenosine (<2.5)/ diameter decrease with nitro- nonendo
decreased diameter with acetylcholine-endo

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33
Q

microvascular dysfunction increases risk of

A

progression to epicardial coronary disease, major adverse cardiovascular events, and hospitalization.

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34
Q

Apical variant of takotsubo

Treatment

A

LV outflow tract obstruction

Avoid dobutamine/norepinephrine
Use beta blockers to decrease HR
Decrease after load with things like phenylephrine if possible

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35
Q

Chest pain in the setting of an argument and strong smoking history

A 
Coronary vasospasm (smooth muscle hyperreactivity) 
Disappearing EKG changes
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36
Q

TIMI risk score

A

> 65 years of age; three or more risk factors for coronary artery disease; prior coronary stenosis ≥50%; ST deviation on electrocardiography; two or more anginal events in the prior 24 hours; use of aspirin in the prior 7 days; and elevated cardiac biomarkers.

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37
Q

Localizing MI

AVL elevation

A

ST depressions do not localize - reciprocal
Elevations do

High lateral (Ostial OM)

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38
Q

NSTEMI cath strategy

Immediate invasive (within 2 hours )

Early invasive (within 24 hours)

Delayed invasive (after)

A

Sick

Not sick, but high risk score

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39
Q

patients with MI. ST-segment depressions of ≥2 mm

AVR elevation

Inferior MI, III>II

A

Posterior MI

subtotal occlusion of the left main or proximal left anterior descending artery.

RCA

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40
Q

Suspected RV infarct

Hypotension caused by

A

Inferior STEMI + (hypotension, JVD, clear lungs)-> get right sided ECG-> ST elevation in lead V4R (RV involvement).

Decreased preload
Increased RVEDP-> septal bowing-> decreased LV filling
RV dilation-> increased pericardial pressure-> restricts LV filling

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41
Q

Beta blocker duration post MI

A

At least 3 years

Indefinitely if EF <40%

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42
Q

Strongest predictor of survival post MI

A

EF

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43
Q

Hibernating myocardium

Predictor of recovery

A

resting LV) dysfunction due to reduced coronary blood flow that improves with revascularization.

Extent of fibrosis

44
Q

Hibernating myocardium dobutamine stress echo

A

Hypokinetic at rest, improves with low dose dobutamine, akinetic at peak

45
Q

ACS diagnosis

A

Clinical, can be made without EKG changes or trop elevation or typical symptoms

46
Q

No reflow phenomenon

Due to

A

Slow flow after revasc

Microvascular obstruction

47
Q

Intervening on stenosis
<40%
40-70%

A

No
FFR <0.8/ iFr < 0.89/ intravascular ultrasound area <6
anything >50% in left main is considered significant

48
Q

Sgarbossa criteria

A

1) concordant ST elevation >1mm in leads with a positive QRS complex (score 5);
2) concordant ST depression >1 mm in leads V1-V3 (score 3); and
3) excessively discordant ST elevation >5 mm in leads with a negative QRS complex (score 2).

49
Q

Negative ECG+ high suspicion for ACS

A

get posterior EKG (V7-V9)

Prominent R waves with ST depression in V1-V3

50
Q

Cardiac rehab timing
Phase I

Phase II/III

Phase IV

A

while hospitalized: patient assessment, education; a follow-up plan

2 weeks post MI, supervised exercise, 1 year

Self-motivated maintenance

51
Q

Biggest prognosticator in ETT

A

exercise duration

52
Q

NSTEMI peak troponin

A

12-24 hours after onset

53
Q

Evolucumab

A

PCSK9 inhibitor

intolerant to statin therapy or does not achieve adequate LDL lowering with statin therapy

54
Q

Rise and fall of troponin w/o positive EKG/symptoms

A

myocardial injury, type II NSTEMI

Stress test before discharge

55
Q

Strongest risk factor for death in ACS

A

Age

56
Q

Reduce myocardial oxygen requirements (ischemia) w/o affecting hemodynamics

A

Ranexa

57
Q

Post MI TTE timing

A

2-3 days

Then 40 days after

58
Q

Recurrent angina after thrombolytics for STEMI

A

Cath

59
Q

Post MI bradycardia

Permanent pacing if

A

Due to increased vagal tone, self-limited

persistent sinus node dysfunction or high-degree AV block after a waiting period

60
Q

Prinzmetal angina

Diagnosis

Treatment

A

At rest in the early morning hours, cigarettes.
transient STE with no epicardial CAD
Narrowing that resolves with nitro -> Provocative testing with ergonovine or acetylcholine.

smoking cessation and CCB, nitrates

61
Q

Killip class

A

Spectrum of HF in acute MI, increased mortality if higher, strongest predictor of mortality at 90 days

62
Q

Killip I
II
III
IV

A

No clinical signs of heart failure
Rales (crackles), an S3, and JVD
Acute pulmonary edema
Cardiogenic shock or hypotension (systolic blood pressure <90 mm Hg) and evidence of peripheral vasoconstriction.

63
Q

Typical angina

Atypical angina

Noncardiac chest pain

Unstable angina

Stable

A

Exertional/emotional substernal chest discomfort relieved by rest/relaxation/nitroglycerin

meets two of the above characteristics

meets one of the above characteristics, no further testing

new in onset (within 2 months), increasing, or occurring at rest (doesn’t have to be persistent, just worsening qualifies)

Occurs predictably and reproducibly at a certain level of exertion and relieved with rest

64
Q

What portends the highest risk of future CV events in stable angina?

A

patients with a history of prior ischemic event (such as MI or stroke)

65
Q

Cocaine effects

A

Platelet activation-> thrombosis
Htn
Thin vascular walls due to smooth muscle apoptosis and cystic medial necrosis-> coronary or aortic dissection
Increased Myocardial oxygen demand-> ischemia Coronary vasospasm
Myocarditis
Arrhythmia
Bradycardia, prolonged qtc-> torsades

66
Q

Aspiration thrombectomy before PCI in STEMI

A

Increases risk of stroke, don’t do

67
Q

Post anterior STEMI LVOT complication

Treatment

A

LVOT obstruction and SAM due to increased contractility of the preserved myocardial segments

to decrease inotropy, increase preload, and increase afterload.

68
Q

Hydra/dinitrate

A

Fourth line for heart failure in blacks after BB, ACEI, MRA

69
Q

Coronary microvasc disease provocative tests

A

Acetylcholine for impaired endothelial-dependent reactivity

nitroglycerin, papaverine, adenosine, or dipyridamole for vascular smooth muscle mediated disease

70
Q

Symptoms and EKG changes in likely multi vessel disease with normal perfusion

A

Balanced ischemia

If pretest prob is high, ignore perfusion findings, go straight to cath

71
Q

GDMT for stable CAD

A

aspirin, statin, BP control

Cath is not indicated unless meds fail

72
Q

Post MI ventricular arrhythmias

A

Bb or nondihydro CCB

If sustained VT/VF-> amio -> lidocaine. ICD before d/c

73
Q

Takotsubo mot consistent if

A

There is pheochromocytoma or myocarditis.

74
Q

Reversible P2Y12 inhibitor

A

Cangrelor , function returns within an hour

75
Q

PAD with or without stenting

A

Plavix period (or aspirin)

76
Q

Ticagrelor to plavix

A

SOB

77
Q

STEMI fibrinolytic therapy, other meds

A

anticoagulant therapy for entire hospitalization, up to 8 days, or until revascularization if performed.
Heparin/lovenox/fonda

78
Q

Prasugrel CI

A

Prior TIA/ stroke

79
Q

High risk findings on perfusion imaging

A

large (>12% of myocardium) or severe reversible defects
abnormal EF
increased lung uptake of tracer, and/or transient ischemic dilation (TID) (>1.2) -> subendocardial ischemia

80
Q

SCA due to coronary spasm in ppl who can’t tolerate meds

A

ICD

81
Q

AIVR vs VT

A

slow (60-100) bpm

82
Q

Iatrogenic coronary occlusion during MV repair/replacement

A

direct injury/distortion from suturing and/or coronary embolization (bone, suture material, silicone, thrombus, and air embolism).

83
Q

most likely mechanism of chronic stable angina

A

stable coronary plaque that limits augmentation of blood flow

84
Q

RCA vs lcx lesion

A

STE in III more than II

85
Q

SCAD screening

A

Extracoronary vascular disease

CTA/MRA of carotids and renal arteries

86
Q

Post MI recurrent chest pain with rapid progression to hemodynamic collapse

A

LV free wall rupture

87
Q

Empiric echo

A

Suspected CHF or valvular disease

88
Q

ACS + LV thrombus

A

DAPT + AC (DOAC/heparin ok)

Triple therapy is ok

89
Q

Absolute CI to fibrinolysis

A

H/o intracranial hemorrhage

90
Q

Highest negative predictive value for MI

A

Troponin

91
Q

Full dose alteplase

A

15 mg

92
Q

SCAD mechanism

A

intimal tear with blood subsequently entering a false lumen or spontaneous hemorrhage of the vaso vasorum causing intramural hematoma within coronary artery

93
Q

Takotsubo mechanism

A

Catecholamine-induced myocardial stunning

94
Q

Most common NSTEMI mechanism

A

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

95
Q

Late reperfusion (>12 hours) increases risk of

A

Mechanical complications

96
Q

Intermediate risk statin decision

Get

A

40-75 years without DM and with LDL between 70-189 mg/dL and a 10-year ASCVD risk between 7.5-19.9%

CAC 0- no statin…except in smokers, and those with a strong family history of premature ASCVD.

97
Q

Cocaine intoxication

Cocaine ACS treatment

A

hypertension, tachycardia, and altered mental status

Benzos, nitro

98
Q

Coronary spasm caused by

A

alcohol, hyperventilation, epinephrine, norepinephrine, ephedrine, cocaine, and/or methamphetamines.

99
Q

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

A

Cath w/in 2 hours

100
Q

Post medically managed ACS stress test indicated if

A

Low and intermediate risk NSTEMI, free of ischemia for 12-24 hours

Medically managed STEMI without high risk features

For prognosis, eval residual ischemia

101
Q

Takotsubo pathophysiology

MRI

A

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

No late gadolinium enhancement.

102
Q

Bio markers for intermediate risk stratification

A

An elevated hs-CRP >/= 2 mg/L

serum triglycerides >/= 175 mg/L, lipoprotein(a) > 50 mg/dl or > 125 nmol/L, apolipoprotein B >/=130 mg/dl, and ankle brachial index <0.9

103
Q

Fragmented QRS complexes=

A

Pathological qs

104
Q

EKGs in ACS eval

A

repeated every 15-30 minutes for the first hour

105
Q

EKG segment

A

TP interval

ACCSAP (11 decks)

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