Coronary Artery Occlusion
A ruptured plaque triggers thrombus formation that blocks coronary flow.
- Seconds: Typical onset (Plaque rupture to clot)
- LAD/RCA/LCx: Vessel (Culprit artery)
- 0%: Flow (Total occlusion)
- Chest pain: Symptom (Classic presentation)
Thrombus formation
Ruptured plaque exposes lipid core, platelets aggregate, clot forms.
Time zero for the ischemic clock starts here.
Myocardial Ischemia Onset
Oxygen deprivation begins within seconds downstream of the blockage.
- <2 min: ATP depletion (Anaerobic shift)
- High early: Reversibility (If reperfused fast)
- ST shift: ECG change (Early marker)
- Minutes: Pain onset (Symptom trigger)
Metabolic starvation
Cells switch to anaerobic metabolism as oxygen supply collapses.
Ischemia is reversible if flow returns quickly.
Cell Necrosis Begins
Sustained ischemia causes myocyte membranes to rupture irreversibly.
- ~20-40 min: Necrosis start (Wavefront begins)
- Subendo→epi: Pattern (Wavefront spread)
- ~20 min: Point of no return (Irreversible injury)
- Begins: Marker leak (Membrane rupture)
Wavefront necrosis
Death spreads from inner to outer heart wall the longer flow stays blocked.
Time is muscle — every minute of occlusion adds necrotic tissue.
Troponin Release Into Blood
Dying cells spill troponin, which diffuses into the bloodstream over hours.
- ~1-3h: First detectable (High-sensitivity assay)
- ~12-24h: Peak level (After occlusion)
- ~2h: Half-life (Clearance rate)
- High: Specificity (Cardiac-specific)
Blood-level kinetics
Troponin rises steeply after a lag, tracking infarct size and time.
Bigger infarcts release troponin faster and higher.
Diagnostic Window & Serial Testing
Serial troponin draws close the early diagnostic gap of normal first tests.
- 0h & 1-3h: Serial draw (hs-cTn protocol)
- Low: Early sensitivity (Before ~3h)
- >95%: Late sensitivity (By ~6h)
- ESC 0/1h: Guideline (Rapid rule-out/in)
Serial testing protocol
Repeat draws catch infarcts missed by a single early troponin.
A single early-negative troponin never excludes MI.