NSTEMI Flashcards
(195 cards)
1
Q
What is required to diagnose myocardial infarction (MI)?
A
A: Troponin elevation above the 99th percentile with rise/fall pattern plus evidence of ischemia (angina, ECG changes, imaging abnormalities, or intracoronary thrombus).
2
Q
Is a rise in troponin alone diagnostic of MI?
A
A: No, troponin rise indicates myocardial injury but not MI unless ischemia is also evident.
3
Q
What is the significance of a chronically elevated but stable troponin?
A
A: It suggests chronic myocardial injury (e.g., heart failure, LVH, CKD) but not MI.
4
Q
What troponin change pattern suggests MI?
A
A: A rise above the 99th percentile with a rise/fall >20% (or 50–80% if troponin < 0.1 ng/ml).
5
Q
What is “non-MI troponin elevation”?
A
A: Troponin rise without ischemia; also called non-ischemic myocardial injury.
6
Q
What defines a Type 1 MI?
A
A: MI due to atherosclerotic plaque rupture/erosion causing thrombosis and ischemia.
7
Q
What distinguishes NSTEMI from STEMI?
A
A: NSTEMI: No persistent ST elevation.
STEMI: Persistent (>20 min) ST elevation due to occlusive thrombus.
8
Q
What is a Type 2 MI?
A
A: MI due to oxygen supply/demand mismatch, often without acute plaque rupture.
9
Q
What are cardiac causes of Type 2 MI?
A
A: Severe hypertension, acute heart failure, arrhythmias, aortic stenosis, HCM.
10
Q
What are non-cardiac causes of Type 2 MI?
A
A: Anemia, sepsis, GI bleed, hypoxemia.
11
Q
How is Type 2 MI managed acutely?
A
A: Treat the underlying cause (e.g., transfusion for anemia); antithrombotics usually avoided acutely.
12
Q
How does prognosis differ between Type 2 MI with and without CAD?
A
A: Without CAD: Good prognosis.
With CAD: Similar cardiac mortality to Type 1 MI.
13
Q
What is non-ischemic myocardial injury?
A
A: Myocardial injury not due to ischemia, often from myocarditis, trauma, shock, CKD.
14
Q
What is coronary vasospasm?
A
A: Transient coronary constriction, often at a site of atherosclerosis, causing angina or MI.
15
Q
How is vasospasm definitively diagnosed?
A
A: Angiographic provocation test with reproduction of symptoms and ST changes.
16
Q
What does MINOCA stand for?
A
A: Myocardial Infarction with Non-Obstructive Coronary Arteries (<50% stenosis).
17
Q
What percentage of MI patients have MINOCA?
A
A: 6–10%, higher in women and younger patients.
18
Q
What are possible causes of MINOCA?
A
A: Plaque rupture with distal embolization, coronary embolus, vasospasm, myopericarditis, takotsubo, type 2 MI causes.
19
Q
What is the role of cardiac MRI in MINOCA?
A
A: Diagnoses myocarditis, infarction, takotsubo; useful when coronary angiogram is normal.
20
Q
What is the typical troponin level in overlooked type 2 MI?
A
A: Mildly elevated, usually <1 ng/ml.
21
Q
How common is plaque disruption in MINOCA on OCT?
A
A: Seen in 46–50% of patients, even with normal angiography.
22
Q
What are clinical presentations of unstable angina?
A
A: Crescendo angina, new-onset severe exertional angina, or rest angina with normal troponin.
23
Q
What makes MI more likely than unstable angina?
A
A: Troponin elevation; in sensitive assays, rest angina without troponin rise is rarely true ACS.
24
Q
What defines reinfarction?
A
A: CK/CK-MB re-elevation or >20% rise in troponin from prior nadir.
25
What is Type 3 MI?
A: Sudden cardiac death with preceding MI symptoms or ECG changes.
26
What defines Type 4 MI (post-PCI)?
A: Troponin >5× normal plus ischemic features or procedural complication.
27
What defines Type 5 MI (post-CABG)?
A: Troponin >10× normal with new Q waves or wall motion abnormality.
28
What troponin elevation after PCI is considered clinically meaningful by expert consensus?
A: Troponin ≥70× or CK-MB ≥10× normal.
29
Can MINOCA be associated with thrombophilia?
A: Yes, ~14% of MINOCA patients have thrombophilic conditions.
30
What is a rare cause of falsely elevated troponin?
A: Heterophile antibodies interfering with the assay.
31
How is troponin elevation in takotsubo typically seen on MRI?
A: Edema without late gadolinium enhancement; non-ischemic pattern
32
What does a subendocardial or transmural MRI pattern suggest?
A: Infarction (ischemic).
33
What MRI pattern suggests myocarditis?
A: Subepicardial or mid-wall involvement in non-vascular distribution.
34
What clinical context differentiates Type 1 MI from Type 2 MI?
A: Type 1 MI occurs without acute noncardiac illness; Type 2 MI occurs in the setting of acute noncardiac illness.
35
What type of MI includes STEMI and NSTEMI?.
A: Type 1 MI
36
Can a Type 1 MI be reclassified as Type 2 MI after angiography?
A: Yes, if coronary angiography shows non-obstructive findings and an acute noncardiac illness is present.
37
What troponin I level typically indicates ischemic imbalance without CAD?
A: <0.5–1 ng/ml.
38
What does a troponin I level >1 ng/ml suggest?
A: Obstructive CAD, regardless of whether the MI is Type 1 or Type 2.
39
How reliable is troponin I >1 ng/ml for predicting CAD?
A: High positive predictive value (~90%), unless renal dysfunction is present.
40
What does a mild troponin rise (e.g., 0.04 ng/ml) with angina and no secondary ischemia suggest?
A: Type 1 MI until proven otherwise by angiography.
41
What features in a Type 2 MI setting may suggest underlying CAD and favor Type 1 MI diagnosis?
A: Pronounced angina, ST abnormalities, or wall motion abnormalities.
42
What is the first priority in a patient with stable angina destabilized by acute bleed, severe anemia, or tachyarrhythmia?
A: Treat the anemia or arrhythmia before CAD.
43
What causes troponin elevation in acute heart failure?
A: Microcirculatory compression (high LVEDP), wall stretch, and neurohormonal injury.
44
What percentage of HF patients may have troponin >1 ng/ml without CAD?
A: 6%.
45
Does an elevated troponin in HF always indicate MI?
A: No, most elevations are "non-MI troponin elevation."
46
When should coronary angiography be considered in HF with troponin rise?
A: If CAD hasn't been addressed previously, preferably after diuresis and before discharge.
47
What features in HF suggest Type 1 MI?
A: Ischemic ST changes, new Q waves, high troponin, or new segmental akinesis.
48
Does chest tightness in acute HF always imply CAD?
A: No, it often reflects dyspnea rather than ischemia.
49
What type of chest discomfort suggests CAD in HF?
A: Crescendo exertional chest discomfort preceding HF.
50
Can acute severe hypertension cause MI?
A: Yes, it can cause Type 2 MI, but can also result from Type 1 MI via catecholamine surge.
51
How does hypertension behave in Type 1 MI vs malignant hypertension?
A: In Type 1 MI, it improves with nitroglycerin; in malignant hypertension, it remains refractory.
52
What does a sustained BP drop with nitroglycerin suggest?
A: Hypertension was secondary to MI.
53
What is a troponin rise without clinical or ECG features of MI called?
A: Myocardial injury, not MI.
54
Are most troponin elevations in HF Type 2 MI?
A: No, they are usually non-MI troponin elevations.
55
Is the term NSTEMI used for Type 2 MI?
A: No, NSTEMI refers only to Type 1 MI.
56
What microvascular flow gradient results in zero-flow?
A: A gradient <40 mmHg between diastolic BP and LVEDP.
57
Why is measuring LVEDP important in ACS with normal coronaries?
A: Elevated LVEDP may explain mild troponin elevation via impaired microvascular flow.
58
What does negative troponin in suspected ACS usually indicate today?
A: Non-cardiac pain or stable angina rather than true unstable angina.
59
How has the role of unstable angina changed in the era of sensitive troponin assays?
A: It is now rare; most true ACS cases show troponin rise.
60
How does prognosis differ between unstable angina and NSTEMI?
A: Unstable angina has a better prognosis.
61
What are grouped together under NSTE-ACS?
A: Unstable angina and NSTEMI.
62
When is the term MINOCA appropriately used?
A: Only in Type 1 MI presentations with no obstructive CAD; not in Type 2 MI or non-MI injury.
63
What diagnosis should be considered in AF or severe LV dysfunction with high troponin and no CAD?
A: Coronary embolus.
64
Is ST depression during or after tachyarrhythmias specific for MI?
A: No, it may reflect cardiac memory and is not MI-specific.
65
Can MI type be reclassified after new clinical information or angiography?
A: Yes, Type 1 can be reclassified as Type 2, and vice versa.
66
How is Type 2 MI with CAD managed compared to Type 1 MI?
A: Differently in the acute setting (no antithrombotics or revascularization), but similar in chronic management and prognosis.
67
What ECG findings are diagnostic of non-ST elevation ischemia?
-ST depression ≥ 0.5 mm (transient/dynamic, not secondary to LVH)
-Deep T-wave inversion ≥ 3 mm
-Transient ST elevation < 20 minutes
-ST depression in ≥6 leads with ST elevation in aVR/V1 (suggests left main or 3-vessel CAD)-
68
What is the most likely culprit artery in ischemic ECGs in NSTEMI?
A: LAD or multivessel disease
69
What percent of acute LCx occlusions are missed on a standard 12-lead ECG?
A: Up to 40%
70
How can diagnostic yield of ECG be improved in patients with ongoing chest pain?
Record leads V7–V9
Repeat ECG every 10–30 minutes
Repeat during pain episodes
Compare with previous ECGs
71
What suggests a STEMI-equivalent missed by ECG?
A: Acute coronary occlusion (especially LCx) presenting without significant ST-T changes
72
What does ST depression in ≥6 leads with ST elevation in aVR suggest?
A: Left main or triple-vessel disease
73
What is the ECG sensitivity during active chest pain?
A: Higher sensitivity and specificity for ischemia detection
74
What does an undetectable hs-troponin (<5 ng/L) + symptom onset >3 hrs indicate?
A: MI ruled out; patient can be safely discharged
75
When does troponin typically rise post-ischemia?
Conventional: ≥3 hours
hs-Troponin: within 1 hour
76
What is the peak timing of troponin in MI?
-Non-reperfused: 18–24 hrs, remains for 7–14 days
-Small MI: Normalizes in 2–3 days
-Reperfused MI: Peaks in 12–18 hrs, resolves faster
77
Is CK-MB recommended for routine MI diagnosis?
A: No, troponin is superior. CK-MB only rises in large MIs.
78
When is CK-MB useful?
A: To estimate infarct timing in subacute symptom onset (e.g., a normal CK-MB with high troponin = older infarct)
79
How does the hs-troponin delta aid in MI rule-in?
Delta ≥10 ng/L → MI ruled in
Delta <4 ng/L → MI ruled out
Delta 4–9 ng/L → Observe and recheck
80
What does absence of wall motion abnormalities during chest pain suggest?
A: Rules against ischemia (if pain is ongoing)
81
What is the 0/1-hour hs-troponin strategy for ruling out MI؟
-Check at 0 and 1 hour
-Rule out if troponin is undetectable or change <4 ng/L
-Rule in if ≥52 ng/L or delta ≥10 ng/L
82
When is serial troponin not needed?
hs-Tn <5 ng/L
Pain onset >3 hours
ECG not suggestive of ischemia
83
If initial hs-troponin is 14–52 ng/L with delta 4–9 ng/L, what is next step?
Observe
Recheck in 3 hrs
Consider non-invasive testing if still <52
84
What percent of MI rule-in cases are true type 1 MI?
A: 70–75% in healthy patients, only 50% in all comers
85
When is conventional troponin repeated?
3–6 hrs after symptom onse
Later (6+ hrs) if symptoms recur or ECG is Worrisom
86
How long before surgery should eptifibatide be held before CABG?
A: 4 hours.
87
What percentage of high-risk ACS patients undergo no revascularization post-angiography?
A: Approximately 25–30%.
88
What percentage of NSTEMI patients have normal or insignificant coronary arteries?
A: ~10%
89
What is MINOCA?
A: Myocardial infarction with nonobstructive coronary arteries (<50% stenosis).
90
What imaging can help diagnose MINOCA?
A: Cardiac MRI (most useful), IVUS, and coronary vasospasm testing.
91
What do ESC guidelines recommend for multivessel PCI in NSTEMI?
A: Complete revascularization, flexible timing (Class IIa recommendation).
92
What did MRI studies reveal about identifying culprit arteries?
A: Angiography misidentified the culprit artery in 35% of NSTEMI cases.
93
Is culprit-only PCI always preferred in multivessel NSTEMI?
A: No. Multivessel PCI is often justified when culprit is unclear.
94
What did the DAPT trial show about extended therapy (1–2.5 years)?
A: Reduced MI by 50%, including at stent and non-stent sites.
95
When can de-escalation to clopidogrel be considered?
A: After 1 month if bleeding risk is high (TOPIC trial).
96
What is the long-term mortality of non-revascularized significant CAD patients?
A: ~20% at 3–4 years (3–4x higher than revascularized patients).
97
Are thrombolytics used in NSTEMI?
A: No. Thrombolytics are contraindicated in NSTEMI due to non-occlusive thrombus and risk of distal embolization.
98
What does an initial invasive strategy in NSTEMI involve?
A: Coronary angiography within 72h (or 24h in high-risk), followed by PCI, CABG, or medical therapy based on findings.
99
When is an immediate invasive strategy (<2h) indicated?
A: 1) ST elevation develops, 2) recurrent angina despite therapy, 3) hemodynamic instability or sustained VT.
100
When is a delayed invasive strategy (<72h) acceptable?
A: In intermediate-risk patients (e.g., typical angina, negative troponin).
101
What risk score supports an early invasive strategy (<24h)?
A: GRACE risk score >140.
102
What is aspirin’s MOA in ACS?
A: Irreversibly acetylates COX-1, blocking TXA2 production → inhibits platelet activation.
103
Which P2Y12 inhibitors are prodrugs?
A: Clopidogrel and prasugrel.
104
Which P2Y12 inhibitor is reversible?
.
A: Ticagrelor
105
Which P2Y12 inhibitor is IV and has rapid onset/offset?
A: Cangrelor (half-life ~5 min, 90% inhibition).
106
Is routine pre-treatment with P2Y12 inhibitors recommended?
A: No. ACCOAST and ISAR-REACT-5 show no benefit; ESC recommends against it (class III).
107
What patients respond poorly to clopidogrel?
A: Those with CYP2C19 mutation (poor metabolizers).
108
Which anticoagulant inactivates thrombin most?
A: UFH.
109
Which anticoagulant inhibits Xa exclusively?
A: Fondaparinux
110
Which anticoagulant binds thrombin directly (including clot-bound)?
A: Bivalirudin.
111
When is switching between enoxaparin and UFH discouraged?
A: Always – increases bleeding risk.
112
When is cangrelor used?
A: IV, during PCI; switch to oral P2Y12 afterward if not already given.
113
When is prasugrel/ticagrelor loaded?
A: At PCI, even if clopidogrel was previously given.
114
What is the mortality benefit of aldosterone antagonists in MI?
A: Shown in EF <40% (EPHESUS trial); not in EF >40% (ALBATROSS trial).
115
What is the role of nitrates in NSTEMI?
A: Sublingual or IV NTG for angina; avoid if SBP <100 or HR <50 bpm.
116
When are ACE-Is avoided?
A: SBP <100 or acute renal failure.
117
When are beta-blockers avoided in NSTEMI?
A: On day 1 in patients with signs of HF, SBP <120, HR >110, or age >70.
118
When can ADP receptor antagonists be discontinued early in NSTEMI patients with DES?
After 3 months in stable CAD
After 6 months in ACS
After 1 month if high bleeding risk (ESC class IIa recommendation)
119
In what trial was de-escalation from ticagrelor/prasugrel to clopidogrel supported at 1 month if bleeding risk is high?
A: TOPIC trial
120
Do CKD patients benefit from an invasive strategy?
A: Yes, especially in mild/moderate CKD (GFR 30–60), despite higher bleeding risk.
121
What glycoprotein IIb/IIIa inhibitor requires dose reduction in CKD?
A: Eptifibatide (cut dose in half if GFR < 50 ml/min)
122
Preferred anticoagulant if GFR < 30 ml/min?
A: UFH (lower bleeding risk than enoxaparin)
123
What anticoagulants are safest in NSTEMI with CKD?
Fondaparinux (non-PCI)
Bivalirudin (PCI)
124
In low-risk women with NSTE-ACS, what strategy may be harmful?
A: Initial invasive strategy (RITA 3 trial).
125
What % of NSTEMI patients have multiple complex angiographic plaques?
A: ~40%
126
What is the 8-month progression risk of an untreated culprit lesion >50% stenosis in ACS?
A: 25%, mostly to total occlusion.
127
What is risk of death or MI at 1 year post-NSTEMI?
A: 10–15%
128
What is 1-year mortality after NSTEMI?
A: ~5%
129
When can most patients resume normal/sexual activity post-NSTEMI?
A: 1–2 weeks if no significant LV dysfunction.
130
What do STOP DAPT-2, SMART-CHOICE, and TWILIGHT trials suggest about aspirin?
A: Stopping aspirin after 1–3 months (continuing ticagrelor or clopidogrel alone) reduces bleeding without ischemic harm.
131
What combination is preferred in AF patients undergoing PCI?
A: Clopidogrel + oral anticoagulant (e.g., apixaban, rivaroxaban) — avoid triple therapy beyond 1 week.
132
What did the WOEST, PIONEER-AF, RE-DUAL PCI, and AUGUSTUS trials show?
A: Dual therapy (clopidogrel + anticoagulant) is safer than triple therapy, with similar efficacy and less bleeding.
133
When can triple therapy (ASA + clopidogrel + anticoagulant) be used?
A: Considered for 1 month only in high ischemic risk/low bleeding risk patients.
134
What is recommended beyond 1 year in patients with PCI or MI + AF?
A: Oral anticoagulant monotherapy.
135
When should PPIs be used with clopidogrel?
A: Only in patients with a clear indication (e.g., GI bleeding history), despite concerns about CYP2C19 interaction.
136
When are aldosterone antagonists indicated?
A: EF < 40% with clinical HF or diabetes and Cr < 2 mg/dL.
137
LDL goal after ACS?
A: <60–70 mg/dL (start high-intensity statin regardless of initial LDL).
138
When are ACE inhibitors indicated post-NSTEMI?
Hypertension or LV dysfunction
For 6 weeks after MI regardless of EF (ISIS-4)
139
How long are beta-blockers continued post-NSTEMI?
A: 1–3 years if EF normal; indefinitely if EF ≤40% or HF.
140
What is bivalirudin’s key pharmacologic advantage?
Direct thrombin inhibition, short half-life (25 min), no platelet activation → less bleeding.
141
What is fondaparinux’s limitation during PCI?
Requires additional UFH or bivalirudin during PCI.
142
What is fondaparinux’s advantage in ACS?
Comparable ischemic reduction to enoxaparin, less bleeding, and lower mortality (OASIS-5 trial).
143
Why is SQ enoxaparin suboptimal when PCI is imminent?
First dose has delayed peak; IV UFH is better when early PCI is planned.
144
When is enoxaparin preferred over UFH?
In medically managed NSTE-ACS (not invasive).
145
What is the recommended PTT goal for UFH in ACS?
46–70 seconds (1.5–2× normal).
146
Is tailored therapy superior in clopidogrel resistance?
No; TAILOR-PCI showed no benefit of genotype-guided escalation.
147
How common is clopidogrel resistance?
~30% of patients.
148
When are GP IIb/IIIa inhibitors used?
During PCI in patients with large thrombus or complications; not upstream
149
When should clopidogrel or prasugrel be started after cangrelor?
At the end of infusion (ticagrelor can be given during infusion).
150
What is cangrelor and when is it used?
IV ADP antagonist used during PCI; indicated for ADP-naïve patients in ACS/stable CAD (Class IIb).
151
When should prasugrel be administered in ACS workup?
Only after coronary angiography confirms no need for CABG.
152
How does ticagrelor compare to prasugrel?
Reversible binding, adenosine release (↑bronchospasm), usable in medical management, no harm in stroke/elderly.
153
Who should not receive prasugrel?
History of stroke/TIA, age >75, weight <60 kg.
154
Which P2Y12 inhibitors are more potent than clopidogrel?
Prasugrel and ticagrelor (75% vs. 35% platelet inhibition)
155
When should clopidogrel be stopped before CABG?
Preferably 5 days; 3 days may suffice in high-risk patients.
156
What usually causes elevated troponin in GI bleeding?
Demand ischemia from anemia/tachycardia in stable CAD.
157
After lower GI bleed, when can antiplatelets be restarted?
7–10 days, based on lesion size and endoscopic treatment success.
158
After upper GI bleed, when can antiplatelets be restarted?
3–7 days after successful endoscopic therapy and no recurrent bleeding.
159
In chronic GI bleeding with recent DES, what should be done?
Continue DAPT; perform endoscopy on therapy; start PPI; test for H. pylori.
160
In ACS or PCI, how does the prognostic impact of major bleeding compare to that of a new MI?
Major bleeding has at least the same prognostic impact as a new MI.
161
What is the mortality risk in patients who experience major bleeding during ACS/PCI?
Up to 5× higher in-hospital and late mortality compared to those without bleeding.
162
What are the most common bleeding sites in ACS/PCI?
Femoral access site (50–66%), GI or GU bleeds, unexplained Hb drop, intracranial bleed (rare but fatal).
163
How does radial access influence bleeding risk?
Radial access significantly reduces bleeding and improves outcomes when done by experienced operators.
164
Is transfusion always beneficial in ACS patients with anemia?
No; transfusion may worsen outcomes due to proinflammatory and prothrombotic effects.
165
What hemoglobin threshold supports a restrictive transfusion strategy in ACS (per REALITY trial)?
Hb ≤8 g/dL.
166
When should transfusion be avoided in ACS patients?
When Hb >8 g/dL or Hct >25%, unless hemodynamically unstable or symptomatic.
167
Can warfarin be continued in ACS managed conservatively?
Yes, if appropriately anticoagulated, continue warfarin and avoid adding another anticoagulant.
168
What was shown in the SYNERGY trial regarding dual anticoagulants?
Dual anticoagulants increased bleeding risk without reducing ischemic events.
169
For transfemoral catheterization, when can an angiogram be performed on warfarin?
When INR ≤1.6.
170
In transradial catheterization, is warfarin held?
Often not held or only one dose withheld (Class IIa ESC).
171
How is NOAC managed around radial PCI?
NOAC may be continued without interruption; UFH is given during PCI.
172
How is NOAC managed for femoral PCI?
Hold NOAC for 1–2 days before the procedure.
173
What is seen in marathon runners with elevated troponin?
Transient LV dysfunction, RV dilation, no MRI enhancement.
174
When can troponin exceed MI cutoff without necrosis?
After marathon running in non-elite individuals.
175
What does undetectable hs-troponin suggest?
Very low cardiovascular risk—lower than even a normal stress test.
176
Does hs-troponin rise above MI cutoff in stress-induced ischemia?
Rarely—unless injury is sustained.
177
What activities can raise hs-troponin without MI?
Atrial pacing, stress testing, fast heart rate, myocardial stretch.
178
What percentage of troponin is cytosolic?
About 8%.
179
What happens if aspirin is given after NSAIDs?
Aspirin cannot bind COX-1 due to NSAID blockade and is cleared before acting.
180
Why are COX-2 inhibitors harmful in CAD?
They reduce prostacyclin without reducing thromboxane A2, increasing thrombotic risk.
181
What is the function of COX-2?
Produces inflammatory prostanoids and protective prostacyclin (vasodilatory, antiplatelet).
182
Is pregnancy advised after SCAD?
No, generally contraindicated.
183
What condition is SCAD highly associated with?
Fibromuscular dysplasia (renal ~70%, carotid ~50%).
184
What is the recurrence risk of SCAD at 5 years?
About 30%.
185
How is SCAD follow-up typically done?
Coronary CT at 6 weeks.
186
What is the healing rate of SCAD?
A: 70–97% spontaneous healing on angiography after ≥35 days.
187
What is the first-line management for stable SCAD?
Conservative: aspirin, clopidogrel, beta-blocker, 5–7 days monitoring.
188
What are the common presentations of SCAD?
A: NSTEMI (~60%) and STEMI (~40%).
189
Which coronary artery is most commonly affected in SCAD?
Mid-to-distal LAD.
190
Which SCAD type involves a visible flap or contrast stain?
Type 1 SCAD (~30%).
191
What is the most common SCAD type and feature?
A: Type 2 (~70%)—long, smooth stenosis (>30 mm), mimicking vasospasm or plaque erosion.
192
What is SCAD?
A split in the coronary artery wall without atheroma, due to intramural bleeding or intimal tear.
193
What angiographic feature is typical of plaque erosion?
Uncomplicated morphology with smooth borders.
194
Who is most commonly affected by plaque erosion?
A: Young female smokers (<50 years old).
195
What angiographic feature is typical of plaque rupture?
Complex, eccentric morphology with overhanging borders.
