CAD Flashcards
Coronary artery calcium scoring
detects subclinical atherosclerosis with MESA score
>400= silent ischemia, high risk of events
Good for asymptomatic, intermediate risk stratification
Don’t give nitro in ACS if
Recent use of PDE4 inhibitor
Bradycardia immediately after relief of occluded RCA
Treatment
Bezold-Jarisch reflex
Stimulation of vagal fibers in inferior LV wall
Atropine, fluids-> isoprotenerol-> pacing
Papillary muscle rupture
Treatment
Posteromedial-only supplied by pda (inferior MI)
Surgery, can temporize with Afterload reduction and IABP
Micro vascular angina diagnosis
Treatment
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).
No exercise stress test if
Risk stratification for suspected ACS (elevated troponin, recent chest pain)
Do pharmacological instead
P2Y12 inhibitor mechanism of action
Aspirin
GpIIa/ IIIb
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)
Antiplatelets for stable angina itself
One (aspirin or P2Y12) to prevent MI and death
Duke treadmill score calculation
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)
Duke treadmill score interpretation
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%.
Concave ST elevations with PR depression 1-8 weeks post MI
Dressler syndrome
Aspirin high dose (750 TID), can consider addition of PPI
No thrombolysis in NSTEMI, only STEMI
Anticoagulation choices
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
Myocardial injury due to ischemia vs not
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)
Plaque vulnerability to rupture
Inflammation : increased macrophage infiltration, larger necrotic lipid cores, thinner fibrous caps, fewer smooth muscle cells, neoangiogenesis, and intraplaque hemorrhage
LBBB stress test
Agent
Image: echo or perfusion imaging or ECG
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
Late reperfusion
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.
Cardiac PET for
Viability
Stress testing in known CAD
Imaging, not treadmill ECG
Predictors of mortality in ACS
Biggest predictors
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%.
Risk discussion
CAC scores
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
ST elevations with q waves
LV aneurysm
Inferior STEMI (1/3 will have RV infarct)
Avoid nitro and diuretics
Inferior ST elevation + ST elevation in V1
greater ST-segment elevation in lead III than lead II
RV infarct, get right sided EKG (STE in V4R)
RCA, not lcx
LV aneurysm vs pseudoaneurysm
increased risk of
broad neck, anticoagulate vs narrow,contained rupture-> surgery
ventricular arrhythmias, heart failure, and thromboembolism
restricted motion of the posterior mitral valve leaflet MI
inferior- ischemic mitral regurg
ACS mechanisms
SCAD, plaque rupture with overlying thrombosis, vasospasm, coronary embolus, myocardial bridging
myxoma
vascular mass
takotsubo CM
REGIONAL (mid-apex) motion abnormality, can form thrombus in 2 days
neuro disorders and pheo can be triggers
aldosterone antagonist
STEMI, already on ACEI/ARB+BB, EF less than or equal to 40% and either symptomatic heart failure (HF) or diabetes mellitus (Class I)
intermediate- high coronary artery calcium score (>100)
CAD, treat medically if asymptomatic, high intensity statin
prior to revascularization in SIHD
should be on GDMT
women with angina, normal cath
mechanism
diagnosis
microvascular dysfunction
endothelial or nonendothelial dysfunction
coronary flow reserve with adenosine (<2.5)/ diameter decrease with nitro- nonendo
decreased diameter with acetylcholine-endo
microvascular dysfunction increases risk of
progression to epicardial coronary disease, major adverse cardiovascular events, and hospitalization.
Apical variant of takotsubo
Treatment
LV outflow tract obstruction
Avoid dobutamine/norepinephrine
Use beta blockers to decrease HR
Decrease after load with things like phenylephrine if possible
Chest pain in the setting of an argument and strong smoking history
Coronary vasospasm (smooth muscle hyperreactivity) Disappearing EKG changes
TIMI risk score
> 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.
Localizing MI
AVL elevation
ST depressions do not localize - reciprocal
Elevations do
High lateral (Ostial OM)
NSTEMI cath strategy
Immediate invasive (within 2 hours )
Early invasive (within 24 hours)
Delayed invasive (after)
Sick
Not sick, but high risk score
patients with MI. ST-segment depressions of ≥2 mm
AVR elevation
Inferior MI, III>II
Posterior MI
subtotal occlusion of the left main or proximal left anterior descending artery.
RCA
Suspected RV infarct
Hypotension caused by
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
Beta blocker duration post MI
At least 3 years
Indefinitely if EF <40%
Strongest predictor of survival post MI
EF
Hibernating myocardium
Predictor of recovery
resting LV) dysfunction due to reduced coronary blood flow that improves with revascularization.
Extent of fibrosis
Hibernating myocardium dobutamine stress echo
Hypokinetic at rest, improves with low dose dobutamine, akinetic at peak
ACS diagnosis
Clinical, can be made without EKG changes or trop elevation or typical symptoms
No reflow phenomenon
Due to
Slow flow after revasc
Microvascular obstruction
Intervening on stenosis
<40%
40-70%
No
FFR <0.8/ iFr < 0.89/ intravascular ultrasound area <6
anything >50% in left main is considered significant
Sgarbossa criteria
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).
Negative ECG+ high suspicion for ACS
get posterior EKG (V7-V9)
Prominent R waves with ST depression in V1-V3
Cardiac rehab timing
Phase I
Phase II/III
Phase IV
while hospitalized: patient assessment, education; a follow-up plan
2 weeks post MI, supervised exercise, 1 year
Self-motivated maintenance
Biggest prognosticator in ETT
exercise duration
NSTEMI peak troponin
12-24 hours after onset
Evolucumab
PCSK9 inhibitor
intolerant to statin therapy or does not achieve adequate LDL lowering with statin therapy
Rise and fall of troponin w/o positive EKG/symptoms
myocardial injury, type II NSTEMI
Stress test before discharge
Strongest risk factor for death in ACS
Age
Reduce myocardial oxygen requirements (ischemia) w/o affecting hemodynamics
Ranexa
Post MI TTE timing
2-3 days
Then 40 days after
Recurrent angina after thrombolytics for STEMI
Cath
Post MI bradycardia
Permanent pacing if
Due to increased vagal tone, self-limited
persistent sinus node dysfunction or high-degree AV block after a waiting period
Prinzmetal angina
Diagnosis
Treatment
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
Killip class
Spectrum of HF in acute MI, increased mortality if higher, strongest predictor of mortality at 90 days
Killip I
II
III
IV
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.
Typical angina
Atypical angina
Noncardiac chest pain
Unstable angina
Stable
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
What portends the highest risk of future CV events in stable angina?
patients with a history of prior ischemic event (such as MI or stroke)
Cocaine effects
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
Aspiration thrombectomy before PCI in STEMI
Increases risk of stroke, don’t do
Post anterior STEMI LVOT complication
Treatment
LVOT obstruction and SAM due to increased contractility of the preserved myocardial segments
to decrease inotropy, increase preload, and increase afterload.
Hydra/dinitrate
Fourth line for heart failure in blacks after BB, ACEI, MRA
Coronary microvasc disease provocative tests
Acetylcholine for impaired endothelial-dependent reactivity
nitroglycerin, papaverine, adenosine, or dipyridamole for vascular smooth muscle mediated disease
Symptoms and EKG changes in likely multi vessel disease with normal perfusion
Balanced ischemia
If pretest prob is high, ignore perfusion findings, go straight to cath
GDMT for stable CAD
aspirin, statin, BP control
Cath is not indicated unless meds fail
Post MI ventricular arrhythmias
Bb or nondihydro CCB
If sustained VT/VF-> amio -> lidocaine. ICD before d/c
Takotsubo mot consistent if
There is pheochromocytoma or myocarditis.
Reversible P2Y12 inhibitor
Cangrelor , function returns within an hour
PAD with or without stenting
Plavix period (or aspirin)
Ticagrelor to plavix
SOB
STEMI fibrinolytic therapy, other meds
anticoagulant therapy for entire hospitalization, up to 8 days, or until revascularization if performed.
Heparin/lovenox/fonda
Prasugrel CI
Prior TIA/ stroke
High risk findings on perfusion imaging
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
SCA due to coronary spasm in ppl who can’t tolerate meds
ICD
AIVR vs VT
slow (60-100) bpm
Iatrogenic coronary occlusion during MV repair/replacement
direct injury/distortion from suturing and/or coronary embolization (bone, suture material, silicone, thrombus, and air embolism).
most likely mechanism of chronic stable angina
stable coronary plaque that limits augmentation of blood flow
RCA vs lcx lesion
STE in III more than II
SCAD screening
Extracoronary vascular disease
CTA/MRA of carotids and renal arteries
Post MI recurrent chest pain with rapid progression to hemodynamic collapse
LV free wall rupture
Empiric echo
Suspected CHF or valvular disease
ACS + LV thrombus
DAPT + AC (DOAC/heparin ok)
Triple therapy is ok
Absolute CI to fibrinolysis
H/o intracranial hemorrhage
Highest negative predictive value for MI
Troponin
Full dose alteplase
15 mg
SCAD mechanism
intimal tear with blood subsequently entering a false lumen or spontaneous hemorrhage of the vaso vasorum causing intramural hematoma within coronary artery
Takotsubo mechanism
Catecholamine-induced myocardial stunning
Most common NSTEMI mechanism
disruption of the fibrous cap (plaque rupture or erosion), which stimulates thrombogenesis
Late reperfusion (>12 hours) increases risk of
Mechanical complications
Intermediate risk statin decision
Get
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.
Cocaine intoxication
Cocaine ACS treatment
hypertension, tachycardia, and altered mental status
Benzos, nitro
Coronary spasm caused by
alcohol, hyperventilation, epinephrine, norepinephrine, ephedrine, cocaine, and/or methamphetamines.
NSTEMI patients with refractory angina, signs/symptoms of HF or new/worsening mitral regurgitation, hemodynamic instability, recurrent angina at rest, or ventricular tachycardia/fibrillation
Cath w/in 2 hours
Post medically managed ACS stress test indicated if
Low and intermediate risk NSTEMI, free of ischemia for 12-24 hours
Medically managed STEMI without high risk features
For prognosis, eval residual ischemia
Takotsubo pathophysiology
MRI
catecholamine excess, derangement of myocardial glucose and fatty acid metabolism, microcirculatory dysfunction, coronary vasospasm, and estrogen deficiency.
No late gadolinium enhancement.
Bio markers for intermediate risk stratification
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
Fragmented QRS complexes=
Pathological qs
EKGs in ACS eval
repeated every 15-30 minutes for the first hour
EKG segment
TP interval
