Type | Description | Common Causes / Mechanism |
---|---|---|
Type 1 MI | Primary coronary event due to atherothrombosis | Plaque rupture, erosion, fissuring, or spontaneous coronary artery dissection → intraluminal thrombus formation → acute coronary occlusion |
Type 2 MI | Ischaemia from oxygen supply-demand mismatch(not due to acute plaque rupture) | - ↓ Supply: respiratory failure, severe anaemia, coronary embolism, coronary spasm, microvascular dysfunction - ↑ Demand: tachyarrhythmia, severe hypertension ± LVH - Blood pressure extremes: malignant hypertension, severe hypotension, shock |
Type 3 MI | Sudden cardiac death with presumed ischaemia before biomarkers can be measured | Cardiac arrest before blood sample, often due to arrhythmia from acute ischaemia |
Type 4 MI | Related to PCI | 4a: During PCI procedure4b: Due to stent thrombosis |
Type 5 MI | Related to cardiac surgery | Peri-operative myocardial damage from coronary emboli, prolonged cross-clamping, or low perfusion |
Not all MIs are sure to obstructive coronary artery disease (CAD)
Mechanisms:
Coronary spasm (vasospastic angina / Variant angina)
A sudden, temporary tightening of a heart artery that reduces blood flow to the heart muscle.
Like a “cramp” in the artery wall, causing chest pain (often at rest)
Usually goes away with medicine that relaxes the artery (nitrates, calcium channel blockers)
Coronary embolism
A blood clot or other material travels through the blood stream and gets stuck in a heart artery, blocking blood flow
Can come from the heart itself (e.g. irregular heartbeat like atrial fibrillation) or from infected/abnormal heart valves
Coronary microvascular dysfunction
The very small blood vessels in the heart don’t open up properly to let blood through, even though the main heart arteries look normal
Like having a “traffic jam” in the tiny side streets, not the main road
Spontaneous coronary artery dissection (SCAD)
A sudden tear in the wall of a heart artery, which lets blood enter the wall and squeeze the channel where blood normally flows.
Often happens in younger women and can occur without the usual heart disease risk factors.
Takotsubo cardiomyopathy (Stress-induced)
A sudden weakening of the heart muscle, usually after extreme emotional or physical stress.
Also called “broken heart syndrome” — the heart’s main pumping chamber changes shape and doesn’t contract normally.
Usually temporary, with recovery in weeks.
Myocarditis
Inflammation of the heart muscle, usually from a viral infection or immune reaction.
The inflamed muscle can’t pump as well and may cause chest pain or heart failure symptoms.
Coronary slow flow phenomenon
Blood moves unusually slowly through the heart arteries, even though there are no blockages.
Caused by problems with the artery’s ability to widen or with tiny vessel resistance.
Can cause chest pain similar to heart disease.
Pulmonary embolism
A blood clot blocks an artery in the lungs, making it harder for blood to pick up oxygen.
The heart has to work harder, and the strain can cause heart injury.
Severe sepsis
A life-threatening reaction to infection where inflammation spreads throughout the body.
Drops blood pressure and diverts blood away from the heart, starving it of oxygen.
Stroke
When blood flow to part of the brain is cut off by a clot or bleed.
The stress on the body and the changes in blood flow can trigger heart damage.
Chronic kidney disease
Long-term kidney damage that causes waste and fluid buildup in the blood.
Can cause changes in blood pressure, inflammation, and blood chemistry that strain the heart.
Definition:
Acute myocardial injury with evidence of ischaemia, caused by an imbalance between myocardial oxygen supply and demand in the absence of acute atherothrombotic coronary occlusion
Causes:
Decreased supply
Severe anaemia leads to reduced oxygen carrying capacity
Respiratory failure causes hypoxaemia
Coronary spasm, embolism, or dissection
Microvascular dysfunction
Increased demand
Sustained tachyarrhythmia (e.g. AF with RVR, VT)
Severe hypertension with left ventricular hypertrophy
Perfusion pressure changes
Severe hypotension (shock, massive GI bleed)
Malignant hypertension damaging microvasculature
Pathophysiology:
Trigger (e.g. anaemia, arrhythmia, hypotension) leads to mismatch in oxygen supply/demand
Myocardial hypoxia causes impaired ATP production
Switch to anaerobic metabolism causes lactate accumulation, acidosis
Loss of contractile function and membrane instability causes myocyte necrosis
Release of cardiac troponins into circulation
Definition:
Transient vasoconstriction (>90% narrowing) of a coronary artery, leading to myocardial ischaemia, often without significant fixed atherosclerotic disease
Causes/risk factors:
Idiopathic (a condition with no identifiable cause after thorough investigation) (most common)
Smoking (major risk factor)
Cocaine or other sympathomimetic use
Endothelial dysfunction
Cold exposure
Hyperventilation
Vasoconstrictor drugs (e.g. triptans, ergot derivatives)
Symptoms:
Nitrate-responsive angina, often at rest (especially early morning)
Can be triggered by emotional stress or cold
May have exercise-induced or hyperventilation-induced angina
Episodes may show transient ST elevation or depression on ECG
Diagnosis:
Clinical history of rest angina + ECG changes during pain
Provocative testing during angiography (e.g. acetylcholine, ergonovine) showing:
Transient total/subtotal occlusion (>90%)
Reproduction of symptoms
Ischaemic ST changes
Treatment:
First line: Calcium channel blockers (e.g. diltiazem, amlodipine)
nitrates for acute relied
Avoid beta-blockers (can worsen spasm in some cases)