Type 2 MI and SCAD — viva

Stem

Practice viva. The examiner shows you two troponin-positive patients: an older man in fast atrial fibrillation with pneumonia, and a young woman with chest pain and non-obstructive-looking arteries. You are asked how to name, investigate and manage each.^[8][1][5]

Branch A — Injury or infarction?

Examiner: How do you define acute myocardial injury, and when does it become infarction?^[1]

Strong answer:

• Fifth UDMI Box 1: a rise and/or fall in cardiac troponin I or T with at least one value above the sex-specific 99th percentile URL.^[1]
• MI requires acute myocardial injury plus one or more of: symptoms or other evidence of acute ischaemia, including new ischaemic ECG changes or pathological Q waves; imaging evidence of an acute coronary pathology; or new loss of viable myocardium or a new regional wall motion abnormality in a pattern consistent with an ischaemic aetiology.^[1]
• Non-ischaemic mechanisms include inflammation, physiological stress response, catecholamine stress, cardiotoxic agents and trauma.^[1]

Follow-up: Why did the 2026 definition drop "type 2"?^[1]

• Grouping non-atherosclerotic coronary causes such as dissection, embolism or vasospasm with supply–demand imbalance as type 2 MI limited its adoption, because these patients follow very different diagnostic pathways and need different treatments; the numerical classification was replaced by primary, secondary and procedure-related MI.^[1]

Branch B — The man in fast AF

Examiner: How would you confirm secondary MI, and what would you do?^[1]

Strong answer:

• Fifth UDMI Box 4 confirms it, where imaging is feasible and appropriate, by obstructive disease (≥70% stenosis in an epicardial vessel by angiography, or ≥50% stenosis in an epicardial vessel that is flow-limiting on physiological assessment) without an acute coronary pathology, or by a new or presumed new regional wall motion abnormality or absent viable myocardium in a pattern consistent with an ischaemic aetiology.^[1]
• Troponin alone cannot separate ischaemic from non-ischaemic injury, and ECG changes are often global.^[1]
• If ischaemia is persistent or recurrent and primary MI is a differential diagnosis, invasive angiography is indicated; otherwise imaging is often deferred until the acute condition is treated, for example to CCTA.^[1]
• ESC 2023 says there are currently no specific recommended pharmacological interventions for type 2 MI and directs management to treating precipitants alongside strict control of CV risk factors.^[2]

Follow-up: Why bother confirming it?^[1]

• A secondary MI confirmed by coronary and/or cardiac imaging would have treatment implications for those with coronary disease and/or LV systolic dysfunction, and imaging may also identify non-obstructive but clinically relevant coronary disease or other previously unrecognized cardiac conditions, such as non-ischaemic cardiomyopathy or valvular heart disease (Fifth UDMI).^[1]
• ESC 2023 also notes that type 2 MI is common and associated with a prognosis similar to type 1 MI.^[2]

Branch C — The young woman: MINOCA or SCAD?

Examiner: The angiogram has no stenosis of 50% or more. What is your working diagnosis and next step?^[2][1]

Strong answer:

• A working diagnosis of MINOCA: ESC 2023 uses stenosis <50% in any major epicardial vessel, and the Fifth UDMI renames it myocardial injury with non-obstructive coronary arteries.^[2][1]
• But first look again at the angiogram for SCAD: type 2 is the commonest pattern, and relying on multiple lumens or contrast staining would miss more than 70% of SCAD (AHA 2018).^[5]
• In a working diagnosis of MINOCA, ESC 2023 recommends CMR imaging after invasive angiography if the final diagnosis is not clear (Class I, Level B); its text adds that CMR should be performed as soon as possible after presentation to maximize diagnostic yield, ideally during the index admission.^[2]

Follow-up: The angiogram shows a type 3 focal stenosis in a large proximal vessel, and you are unsure. What now?^[5]

• AHA 2018, weighing risks and benefits, limits intracoronary imaging to an uncertain angiographic diagnosis (eg, type 3 or unclear lesions) in a vessel large enough; OCT is the preferred method when the angiographic diagnosis is uncertain and it is believed that intravascular imaging can be safely undertaken.^[5]
• If the decision is made to image, ESC 2023 says the guide wire must be confirmed in the true lumen before the imaging catheter is advanced.^[2]

Branch D — SCAD management

Examiner: It is SCAD. She is stable with preserved flow. Do you stent?^[2]

Strong answer:

• No. ESC 2023 recommends PCI in SCAD only with symptoms and signs of ongoing ischaemia, a large area of myocardium in jeopardy and reduced antegrade flow (Class I, Level C); NHFA/CSANZ 2025 separately says that in people with acute coronary occlusion MI (ACOMI) due to SCAD who are otherwise stable, routine revascularisation is not recommended (consensus).^[2][10]
• PCI in SCAD carries more complications: coronary complications followed PCI in >30% in an international case series (ESC 2023), and AHA 2018 describes how guidewires may enter the false lumen and balloons or stents can propagate the haematoma.^[2][5]
• I would monitor her in hospital for 3–5 days, because early recurrent MI may develop in 5% to 10% of conservatively managed patients, mostly from extension of dissection within the first 7 days after the acute episode (AHA 2018).^[5]

Follow-up: Which drugs?^[2]

• ESC 2023 says that, until evidence from ongoing prospective trials becomes available, SCAD should receive the same pharmacological therapy as other ACS patients; ESC 2025 pregnancy, in its section on pregnancy-associated SCAD, notes evidence favouring single antiplatelet therapy with aspirin in conservatively managed SCAD; the 2018 statements describe divergent antiplatelet practice.^[2][7][6][5]
• AHA 2018: β-blockers should be considered with LV dysfunction, arrhythmias or hypertension; in the prospective Vancouver cohort of 327 patients with nonatherosclerotic SCAD (Saw 2017; observational, median follow-up 3.1 years, multivariate modelling), β-blocker use was associated with less recurrent SCAD (hazard ratio 0.36).^[5][11]
• Thrombolysis is contraindicated in acute SCAD (ESC ACCA 2018).^[6]

Follow-up: And after discharge?^[5]

• Vascular imaging from the brain to pelvis should be considered for FMD and aneurysm (AHA 2018), cardiac rehabilitation referral, and counselling about pregnancy and hormones.^[5]
• Recurrent SCAD means de novo dissection; in the Mayo Clinic series SCAD recurred in 17% of patients, with a median time to the second episode of 2.8 years (AHA 2018).^[5]