Coronary STEMI ♥  real-geometry sim

Myocardial injury — cardiac troponin (cTn) above the 99th-percentile upper reference limit. Called acute when there is a rise and/or fall.
Myocardial infarction — acute myocardial injury plus clinical evidence of acute myocardial ischaemia, i.e. cTn rise/fall (≥1 value > 99th percentile) and at least one of:

• symptoms of ischaemia;
• new ischaemic ECG changes;
• development of pathological Q waves;
• imaging evidence of new loss of viable myocardium / new regional wall-motion abnormality in an ischaemic pattern;
• coronary thrombus on angiography or autopsy (types 1 & 2).

Type 1 — atherothrombotic MI: plaque rupture or erosion with intraluminal thrombus.
Type 2 — MI from oxygen supply/demand mismatch without acute atherothrombosis (e.g. tachyarrhythmia, hypotension, anaemia, coronary spasm/embolism, severe hypertension).
Type 3 — cardiac death with ischaemic symptoms and presumed new ischaemic ECG changes or VF, before biomarkers could be obtained.
Type 4a — PCI-related (cTn > 5× 99th percentile + evidence of ischaemia). 4b — stent thrombosis. 4c — restenosis.
Type 5 — CABG-related (cTn > 10× 99th percentile + evidence of ischaemia).

In the absence of LVH or LBBB:

• ≥1 mm (0.1 mV) in any two contiguous leads, except V2–V3;
• V2–V3: ≥2 mm (men ≥40 y), ≥2.5 mm (men <40 y), or ≥1.5 mm (women, any age);
• Right-sided V3R–V4R: ≥0.5 mm (≥1 mm in men <30 y) — RV infarction;
• Posterior V7–V9: ≥0.5 mm — inferobasal (posterior) infarction.

ST-depression / T-changes: horizontal or down-sloping ST-depression ≥0.5 mm in two contiguous leads and/or T-inversion >1 mm in leads with a dominant R.

De Winter — up-sloping ST-depression + tall symmetric T in V1–V6 (proximal-LAD occlusion equivalent).
Posterior MI — ST-depression with tall R in V1–V3, confirmed by ST↑ in V7–V9.
Left-main / proximal triple-vessel — ST↑ in aVR (> V1) with diffuse ST-depression.
Hyperacute T-waves — broad, tall, symmetric T early in occlusion, before ST-elevation.
Wellens — biphasic (type A) or deep symmetric T-inversion (type B) in V2–V3 during a pain-free period — critical proximal-LAD stenosis, a pre-infarction warning.

Concordant ST-elevation ≥1 mm in any lead (most specific);
Concordant ST-depression ≥1 mm in V1–V3;
Discordant ST-elevation — modified (Smith) criterion: ST/S ratio ≤ −0.25 (i.e. discordant STE ≥25 % of the preceding S-wave depth).

Inferior STEMI — RCA vs LCx:

• RCA — ST↑ in lead III > lead II, with reciprocal ST↓ in I and aVL. ST↑ in V1/V4R adds RV involvement (proximal RCA).
• LCx — the opposite: ST↑ in lead II ≥ lead III, often with ST↑ in I / V5–V6 and little or no reciprocal change in I/aVL (frequently posterior extension, ST↓ V1–V3).

aVR & V1 — left main vs proximal LAD:

• Left main / severe 3-vessel — ST↑ in aVR > V1 with diffuse ST depression.
• Proximal LAD (before the first septal) — ST↑ in V1 ≥ aVR (V1 elevation from septal ischaemia), typically with anterior ST↑ rather than diffuse depression.

Not every ST-elevation is a coronary occlusion. Common non-ischaemic causes:

• Benign early repolarisation — concave ST↑ with J-point notching/slurring, mainly V2–V5, young patients.
• Acute pericarditis — diffuse (non-territorial) concave ST↑ with PR-segment depression; PR↑ in aVR.
• LV hypertrophy / LBBB / ventricular paced rhythm — discordant (secondary) ST-T changes; apply Sgarbossa in LBBB/paced.
• LV aneurysm — persistent ST↑ with well-formed Q-waves weeks after an old MI.
• Brugada syndrome — coved ST↑ in V1–V2 (type 1).
• Hyperkalaemia — ST↑ with peaked T-waves, widened QRS.
• Takotsubo (stress) cardiomyopathy — anterior ST↑ mimicking LAD, but no culprit lesion.
• Myopericarditis, coronary vasospasm (Prinzmetal), raised ICP/SAH, hypothermia (Osborn/J waves).

Troponin is organ-specific but not disease-specific — an elevation means myocardial injury, not necessarily atherothrombotic infarction. Non-type-1 causes:

• Type-2 MI — supply/demand mismatch (tachyarrhythmia, hypotension, anaemia, severe hypertension, spasm/embolism).
• Cardiac non-ischaemic — myocarditis, acute/decompensated heart failure, Takotsubo, cardiac contusion, infiltrative disease, post-PCI/CABG/ablation.
• Pulmonary — pulmonary embolism, pulmonary hypertension (RV strain).
• Systemic / critical illness — sepsis, shock, extensive burns, strenuous endurance exercise.
• Chronic kidney disease — reduced clearance and chronic structural change.
• Neurological — stroke, subarachnoid haemorrhage.

The rise-and-fall pattern plus clinical context distinguishes these from acute infarction.