Group A1

Plaque-Mediated Causes (Type 1 MI)

Heart attacks caused by changes in artery “plaque” (fatty build-up) that cracks or wears away, causing a small blood clot. This can still happen even when the angiogram (x-ray dye test of the heart arteries) doesn’t show a big blockage.

1) What does this mean?

Group A1 MINOCA is a heart attack where a plaque (fatty deposit in the artery wall) either ruptures (cracks open) or erodes (the surface wears away). This triggers a thrombus (blood clot) that reduces blood flow to the heart muscle. On angiography (a dye test under x-ray) the artery can still look non-obstructed (<50% narrowed), but the plaque event has still caused damage. Doctors call this a Type 1 myocardial infarction (Type 1 MI = classic heart attack from a plaque-related clot).

2) What actually happens?

Plaque rupture

  • A thin “cap” over a soft, fatty core breaks open.
  • A fresh clot forms and may briefly block blood flow before dissolving or moving.
  • Later, the artery may only look mildly narrowed on the scan, but the injury has already happened.

Plaque erosion

  • The surface gets irritated and the protective lining wears away.
  • Platelets (sticky blood cells) cling on and form a non-blocking clot (the lumen — the inner channel of the artery — can still be more than 50% open).
  • More often seen in younger people and in women.

Both situations reduce oxygen to part of the heart (ischaemia = low oxygen), which is why troponin (a heart-injury blood test) rises and then falls.

3) Tests you might have

Coronary angiography

  • X-ray dye test to see the arteries; shows if narrowing is <50% (non-obstructive).
  • Can miss small cracks or surface wear of plaque, or tiny clots that have moved.

Inside-artery imaging

  • OCT = optical coherence tomography (a tiny camera with light) — best at seeing cracks/erosion and clots from inside the artery.
  • IVUS = intravascular ultrasound (mini ultrasound probe) — shows plaque build-up and vessel shape.

Heart MRI (CMR)

  • Looks for the pattern of a true heart attack (typical scar pattern called LGE = late gadolinium enhancement).
  • Helps exclude look-alikes such as myocarditis (inflammation) or Takotsubo (stress-induced weakness).
  • Blood tests: high-sensitivity troponin (injury marker), cholesterol profile (LDL-C = “bad” cholesterol), HbA1c (diabetes screen), CRP (inflammation).
  • Pressure tests in the artery (FFR/iFR) in selected cases — check if a narrowing really limits flow.

Not everyone needs every test — your team chooses what adds value for you.

4) Treatment & prevention

4.1 In hospital (acute care)

  • Clot-preventing medicines (antithrombotic therapy): usually aspirin plus a second “platelet blocker” (a P2Y12 inhibitor, e.g., clopidogrel/ticagrelor). The course length is personalised to balance clot-risk and bleeding-risk.
  • Opening an artery (revascularisation) with a stent (tiny metal tube) is only done if scans show a clear culprit causing ongoing reduced blood flow or high risk. Many A1 cases are best treated with medicines alone.
  • Comfort care and monitoring: pain relief, blood pressure and rhythm control, observation if needed.

4.2 Long-term medicines (secondary prevention)

  • Antiplatelets: aspirin long-term; add a second tablet for a set time as advised.
  • Statin: lowers LDL-C and stabilises plaque.
  • ACE inhibitor or ARB: particularly helpful if you have high blood pressure, diabetes or a weaker heart pump.
  • Beta-blocker: for heart protection, rhythm control, or if the pump is weaker.

4.2 If needed

  • Ezetimibe or PCSK9 inhibitor if cholesterol targets aren’t met on a statin.
  • Blood thinner (anticoagulant) only for specific reasons (e.g., a clot inside the heart, or atrial fibrillation — an irregular rhythm).
  • Lifestyle care: stopping smoking, blood pressure and sugar control, healthy weight.
  • Cardiac rehab and support for mood, sleep and confidence.

4.3 Follow-up goals

  • Clinic review at 6–12 weeks: symptoms, medicines, blood pressure, cholesterol.
  • LDL-C target set by your team (often ≤1.8 mmol/L, sometimes lower if risk is high).
  • Repeat scans (echo ± MRI) if symptoms persist or the heart pump looked weak before.

5) What’s the outlook?

With the right medicines and lifestyle support, future risk can be greatly reduced. Risk depends on age, risk-factor control, and whether the event was a rupture (usually higher risk) or erosion. Sticking with follow-up and rehab really helps.

6) Quick FAQs

  • Why didn’t my angiogram show a big blockage? The clot may have been small, short-lived, or the problem was on the surface of the plaque. Inside-artery scans (OCT/IVUS) can reveal this.
  • Do I need a stent? Only if there’s a clear, ongoing flow problem. Many A1 cases do well with medicines alone.
  • How long do I need two antiplatelet tablets? Your team will personalise this to balance clot-prevention and bleeding risk.
  • Will this happen again? Risk falls with consistent medicines and risk-factor control. Keep your follow-ups.

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

  • When everyone should get inside-artery imaging (OCT/IVUS) and how to standardise it.
  • Best length of dual antiplatelet therapy (two platelet-blockers) for rupture vs. erosion.
  • Long-term outcomes after erosion without stents; best cholesterol targets/therapies.
  • Whether new anti-inflammatory treatments help stabilise plaque in MINOCA.

Research & clinical trials

Interested in research or new treatments? Visit our research hub or speak to your care team about local studies.