Group A2

Non-Plaque Coronary Causes

Heart attacks caused by problems of the artery itself but not from plaque cracking/eroding. This group includes spasm (sudden tightening), SCAD (a split in the artery wall), and blood clots that arrive or form without a plaque trigger.

1) What does “A2” mean?

Group A2 MINOCA covers coronary causes of heart-muscle injury where the artery looks non-obstructed (<50% narrowed on the dye x-ray test called an angiogram) but blood flow still drops enough to injure the heart. Typical mechanisms are:

  • Coronary vasospasm — a sudden squeeze of a heart artery (like cramp) that briefly narrows the vessel and reduces blood flow. This can happen in the big surface arteries (epicardial) or in the small vessels deep in the heart muscle (microvascular spasm).
  • SCAD — Spontaneous Coronary Artery Dissection: a split in the inner wall that lets blood collect within the wall (intramural haematoma = a bruise inside the wall), squeezing the true channel (lumen = the hollow inside of the artery).
  • “Lone” thrombus or embolus — a blood clot forming in, or travelling to, a coronary artery even when plaque isn’t the trigger (e.g., from an irregular heartbeat like atrial fibrillation, a heart valve infection, or via a small hole in the heart called a PFO).

2) Tests you might have

Coronary angiography

  • X-ray dye test showing the outline of the arteries.
  • In SCAD it may show a long smooth narrowing or step-down appearance; in spasm it can look normal unless the spasm is caught in the moment.

Inside-artery imaging

  • OCT (optical coherence tomography) = tiny light-based camera; best for seeing a tear, flap, or clot.
  • IVUS (intravascular ultrasound) = mini ultrasound from inside the artery; shows the wall and any bruise.
  • In SCAD, these are used carefully to avoid worsening the split.

Spasm testing

  • Acetylcholine test (performed in expert centres): a very small, short-acting dose is given into the artery to see if it spasms — helps diagnose epicardial or microvascular spasm.
  • Flow measures like CFR/IMR check how well blood moves through the small vessels.

Heart MRI (CMR)

  • Confirms if there’s a true heart-attack pattern or another cause like inflammation (myocarditis) or stress-related weakness (Takotsubo).
  • Stress perfusion MRI can show reduced small-vessel flow.

CTCA / vessel screening

  • CTCA (CT coronary angiography) can monitor healing after SCAD without invasive catheters.
  • Ultrasound/CT of other arteries may look for FMD (fibromuscular dysplasia), which can be linked to SCAD.

Find the source of a clot

  • Heart rhythm monitoring for AF (atrial fibrillation).
  • Echo to check for a heart-chamber clot or valve infection.
  • Bubble study if a PFO (small heart hole) is suspected.

Not everyone needs every test — your team will tailor this to your situation.

3) Treatment (based on the cause)

SCAD (artery wall split)

  • Conservative first if safe: most heal on their own over weeks.
  • Avoid clot-dissolving injections (thrombolysis) — can worsen the split.
  • Stents only if ongoing poor flow or high-risk features — done cautiously.
  • Antiplatelet therapy (usually aspirin; two tablets if a stent was needed, for a limited time).
  • Beta-blocker to reduce stress on the artery and lower recurrence risk.
  • Screen for FMD; cardiac rehab; pregnancy/contraception counselling where relevant.

Epicardial vasospasm (big-artery spasm)

  • Calcium-channel blockers (e.g., diltiazem, amlodipine) and long-acting nitrates to relax the artery.
  • Short-acting GTN spray/tablets for pain episodes.
  • Avoid triggers: cold exposure, tobacco, cocaine/amphetamines; avoid some non-selective beta-blockers.
  • Consider statins and ACEi/ARB to support vessel health; address sleep and stress.

Microvascular spasm/dysfunction (small vessels)

  • Calcium-channel blockers (either type) and sometimes ranolazine for symptoms.
  • ACEi/ARB and statin to support the vessel lining; low-dose beta-blocker only if helpful and spasm isn’t worsened.
  • Cardiac rehab with gradual exercise; track triggers (cold, stress, poor sleep).

“Lone” clot / embolus

  • Treat the source: anticoagulation for AF; antibiotics for valve infection; consider PFO pathway if a proven paradoxical embolus.
  • Anticoagulant vs antiplatelet depends on the cause and imaging (e.g., a clot inside the left ventricle needs an anticoagulant).
  • Thrombophilia testing if events are unexplained or keep recurring.

Care that helps everyone

  • Stop smoking; optimise blood pressure, cholesterol, and diabetes control.
  • Psychological support and peer community; plan a paced return to work/exercise.
  • Follow-up scans (echo ± MRI) to confirm recovery and guide medicines.

4) What’s the outlook?

SCAD usually heals, though it can recur; long-term survival is good with careful follow-up. Vasospasm is very treatable but may need ongoing tablets and trigger management. For clot/embolus causes, success depends on controlling the source and preventing another event.

5) Quick FAQs

  • Why did my angiogram look normal? Spasm can come and go, and SCAD may appear as a smooth narrowing — extra tests can reveal the real cause.
  • Do I need a stent? Often no. SCAD and spasm are frequently best treated with medicines and time.
  • Can it come back? Sometimes, yes — especially SCAD/spasm. Medicines, avoiding triggers, and follow-up reduce the risk.

6) What we still don’t know (research)

  • How to make spasm testing (acetylcholine) accessible and consistent across centres.
  • The best clot-prevention plan in SCAD without stents (how strong/how long).
  • Long-term outcomes for microvascular spasm using MRI-guided treatment.
  • Best pathways for PFO-related clots in the context of MINOCA.
  • Why SCAD/spasm are more common in women; hormonal and genetic factors.

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