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ECG Findings in Myocardial Infarction (STEMI & NSTEMI)

The Underlying Mechanism

Three simultaneous electrical defects occur in infarcted myocardium, all producing the same net result - ST elevation in leads overlying the infarct:

Defect in Infarcted Cells	Current Flow	ECG Change (leads over infarct)
Rapid repolarization (accelerated K+ channel opening)	Out of infarct	ST elevation
Decreased resting membrane potential (K+ loss)	Into infarct	TQ depression - recorded as ST elevation
Delayed depolarization	Out of infarct	ST elevation

Ganong's Review of Medical Physiology, 26th ed., p. 534

Leads on the opposite side of the heart show reciprocal ST depression.

Current of Injury: Subendocardial vs. Transmural

Current of injury diagram - subendocardial vs transmural

Panel A (subendocardial ischemia / NSTEMI): The ST vector points inward toward the ventricular cavity. Overlying leads show ST depression.
Panel B (transmural ischemia / STEMI): The ST vector points outward (epicardial). Overlying leads show ST elevation.
Harrison's Principles of Internal Medicine, 22E, p. 1916

Temporal Evolution of ECG Changes in STEMI

The changes evolve in a predictable sequence:

Minutes - Hours (hyperacute phase): Tall, peaked hyperacute T waves - often the very first sign. Then ST elevation develops.
Hours - Days: ST elevation with formation of Q waves. T waves may start to invert.
Days - Weeks: ST normalizes. T-wave inversions persist. Q waves deepen.
Weeks - Months: Q waves may persist permanently (scar). T waves may normalize or remain inverted.

Note: Reversible transmural ischemia (e.g., Prinzmetal/vasospastic angina) can cause transient ST elevation without Q wave formation.

STEMI: Localization by Leads

Territory	ECG Leads with ST Elevation
Anteroseptal	V1, V2, (V3)
Anterior	V1, V2, V3, V4
Anterolateral	V1-V6, I, aVL
Lateral	I, aVL
Inferior	II, III, aVF
Inferolateral	II, III, aVF, V5, V6
True posterior	Tall R wave in V1-V2, R/S ≥ 1, ST depression V1-V3 (mirror image)
Right ventricular	ST elevation II, III, aVF + ST elevation in right-sided leads V3R-V6R

Tintinalli's Emergency Medicine, p. 378

Tip: For inferior STEMI, always obtain a right-sided ECG (V3R-V6R) to rule out RV infarction, which increases morbidity significantly and changes management (avoid nitrates, give fluids).

Identifying the Culprit Vessel

ECG Pattern	Likely Culprit Artery
ST elevation III > II + ST depression in I, aVL	Right coronary artery (RCA)
Above + ST elevation V1 or V4R	Proximal RCA (with RV infarction)
Inferior MI + ST elevation in I, aVL, V5/V6	Left circumflex (LCx)
ST elevation aVR > V1	Left main or proximal LAD
ST elevation V1-V4 + absence of above inferior pattern	LAD (distal)

Tintinalli's Emergency Medicine, p. 378-379

NSTEMI / Unstable Angina: ECG Findings

Diagnosis of NSTEMI depends primarily on elevated troponin + compatible symptoms; the ECG may show changes but does NOT meet STEMI criteria.
Common findings:
- ST depression (subendocardial ischemia)
- T-wave inversions (may be deep and widespread)
- Non-specific ST-T changes
- ECG may be completely normal in up to 20% of NSTEMIs
Tintinalli's Emergency Medicine, p. 378

Wellens T-Wave Sign (High-Risk NSTEMI Pattern)

Wellens pattern - deep precordial T-wave inversions V1-V6

Deep symmetric T-wave inversions in V1-V4 (and sometimes I, aVL) suggest critical proximal LAD stenosis. This is the Wellens sign - patient may be pain-free at the time of ECG but is at high risk for massive anterior MI. Do not stress test these patients.

Harrison's Principles of Internal Medicine, 22E, p. 1916

Q Waves: What They Mean

Pathological Q wave: ≥ 0.04 s wide and ≥ 25% of R-wave height - indicates myocardial necrosis (scar).
Old teaching: Q waves = transmural; no Q waves = subendocardial. This is now known to be unreliable - transmural infarcts can occur without Q waves, and NSTEMIs can produce Q waves.
More accurate classification: Q-wave MI vs. Non-Q-wave MI
Harrison's Principles of Internal Medicine, 22E

Key Mimics to Exclude (STEMI Mimics)

Condition	Distinguishing Feature
Left bundle branch block (LBBB)	New LBBB can mimic STEMI (Sgarbossa criteria help)
Pericarditis	Diffuse saddle-shaped ST elevation, PR depression, no reciprocal changes
Brugada pattern	ST elevation V1-V2 with RBBB morphology, no ischemic context
Benign early repolarization	ST elevation V2-V5, J-point notching, young patient, stable
LVH with strain	ST depression/T inversion in lateral leads, no chest pain

Summary mnemonic - STEMI evolution: "HyperT → STE → Q + Tinv → Q scar"

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Ischaemic Heart Disease (IHD) - Overview & Pathophysiology

What is IHD?

IHD (also called Coronary Artery Disease / CAD) is a condition in which myocardial oxygen demand exceeds supply, most commonly due to atherosclerotic narrowing of the coronary arteries. It is the leading cause of death worldwide - myocardial infarction alone accounts for roughly one-quarter of all deaths in Western nations.

Robbins & Kumar Basic Pathology, p. 314

The Central Concept: Supply vs. Demand Mismatch

Factor	What Happens in IHD
O2 supply	Reduced - atherosclerotic stenosis limits coronary blood flow
O2 demand	Normal or increased - heart still needs to pump
Net result	Myocardial ischaemia → angina or infarction

The myocardium is unique in that it extracts nearly all available O2 from coronary blood even at rest, so it cannot compensate by extracting more - the only way to increase supply is to increase coronary flow. Stenosis blocks this ability.

Stage 1 - Endothelial Dysfunction (The Trigger)

The process begins with injury to the vascular endothelium, driven by risk factors such as:

Hyperlipidaemia (elevated LDL)
Hypertension
Cigarette smoking
Diabetes mellitus

Endothelial cells normally produce nitric oxide (NO), a potent vasodilator that maintains vascular tone and inhibits platelet aggregation. Injury reduces bioavailable NO, causing:

Vasoconstriction
Pro-inflammatory signalling
Increased vascular permeability (allows LDL to enter the intima)
Sabiston Textbook of Surgery, p. 2484

Stage 2 - Inflammation & Foam Cell Formation

Once LDL enters the intima, it is oxidised to oxLDL, which:

Triggers release of adhesion molecules - VCAM-1 and ICAM-1 - on the endothelium
Recruits monocytes and T lymphocytes from the bloodstream
Monocytes differentiate into macrophages, which engulf oxLDL via scavenger receptors
Lipid-laden macrophages become foam cells - the initial visible lesion, called a fatty streak

T cells activated in this environment release TNF-α, IL-1β, IL-6, perpetuating the inflammatory cycle.

Stage 3 - Plaque Formation (Atheroma)

Atherosclerotic plaque structure - fibrous cap and necrotic core

With persistent injury, smooth muscle cells (SMCs) migrate from the media into the intima, driven by cytokines and growth factors. These SMCs then:

Proliferate
Synthesise collagen and proteoglycans (extracellular matrix)
Form a fibrous cap over the accumulated lipid and necrotic debris

The mature atheromatous plaque has two key structural components:

Fibrous cap - SMCs, macrophages, foam cells, lymphocytes, collagen, elastin
Necrotic (lipid) core - cell debris, cholesterol crystals, foam cells, calcium

The shoulder areas of the plaque (junction between plaque and normal wall) are the most structurally vulnerable - richest in macrophages and most prone to rupture.

Robbins & Kumar Basic Pathology, p. 314

Stage 4 - Plaque Instability and Acute Coronary Syndromes

Plaque stability depends on the balance between fibrous cap synthesis and degradation. MMPs (matrix metalloproteinases) secreted by activated macrophages degrade the fibrous cap. Three mechanisms can trigger ACS:

Mechanism	What Happens	Typical Presentation
Plaque rupture (most common, ~75%)	Fibrous cap tears, exposing lipid core to blood → thrombus	STEMI (complete occlusion)
Plaque erosion (~25%)	Superficial endothelial loss, no frank rupture	NSTEMI, more common in women/younger patients
Calcified nodule (rare)	Hard calcified deposits breach the cap → sudden occlusion	Variable

Sabiston Textbook of Surgery, p. 2485

Risk Factors

Non-Modifiable	Modifiable
Family history (strongest independent factor)	Hyperlipidaemia
Increasing age	Hypertension
Male sex	Cigarette smoking
Genetic disorders (e.g. familial hypercholesterolaemia)	Diabetes mellitus
	Obesity, sedentary lifestyle
	Inflammation (elevated hsCRP)

Risk factors are multiplicative, not additive. Three simultaneous factors (hyperlipidaemia + hypertension + smoking) increase MI risk 7-fold.

Robbins & Kumar Basic Pathology, p. 315

Spectrum of Clinical Presentations

Atherosclerosis produces a spectrum of disease depending on how much and how fast the artery is occluded:

Stable Angina → Unstable Angina → NSTEMI → STEMI → Sudden Cardiac Death
   (chronic          (plaque           (partial      (complete
   fixed stenosis)    destabilising)    occlusion)    occlusion)

Stable angina: Fixed stenosis (>70% lumen reduction) - chest pain only on exertion, relieved by rest/nitrates
Unstable angina: Plaque disruption + partial thrombus - pain at rest or minimal exertion, troponin normal
NSTEMI: Same as UA but with myocardial necrosis (troponin elevated), subendocardial
STEMI: Complete occlusion, transmural infarction, ST elevation on ECG
Sudden cardiac death: Lethal arrhythmia (VF) from acute ischaemia or scar-related re-entry

Key Molecular Summary

Risk factors
    ↓
Endothelial injury → ↓ Nitric Oxide → Vasoconstriction + inflammation
    ↓
LDL enters intima → oxLDL → Monocyte recruitment → Foam cells → Fatty streak
    ↓
SMC migration + ECM synthesis → Fibrous cap + Lipid core = Atheroma
    ↓
Plaque grows → Luminal stenosis → Stable angina (demand ischaemia)
    ↓
Plaque rupture/erosion → Thrombosis → ACS (supply failure)

Sabiston Textbook of Surgery; Robbins & Kumar Basic Pathology

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ECG Findings in Ischaemic Heart Disease (IHD) - Full Spectrum

The ECG in IHD varies based on where the patient sits on the ischaemia spectrum - from normal at rest in stable disease, through dynamic changes during angina, all the way to STEMI with Q waves.

1. Stable Angina / Chronic IHD - Resting ECG

The resting ECG can be completely normal even with severe coronary stenosis. When abnormal, look for:

Finding	Significance
ST depression (focal)	Fixed subendocardial ischaemia
T-wave inversions	Chronic ischaemic change, old territory
Pathological Q waves	Evidence of previous MI (scar)
LBBB or left anterior fascicular block	Common conduction disturbance from IHD
Ventricular ectopics (VPBs)	Low sensitivity/specificity for CAD

Key point: A normal resting ECG does NOT exclude significant CAD. The ECG becomes abnormal in ≥50% of patients with normal resting ECGs only during stress or a spontaneous anginal episode.

Goldman-Cecil Medicine, p. 1736

2. During an Anginal Episode (Dynamic Changes)

The most important feature is dynamic (i.e., it appears with symptoms and resolves with rest/nitrates):

ST depression - most common finding; represents subendocardial ischaemia
Transient ST elevation - rare in stable angina; more typical of Prinzmetal (vasospastic) angina
Pseudonormalization - a previously inverted T wave becomes "normal" during ischaemia; a subtle but important sign of acute ischaemia

3. NSTEMI / Unstable Angina - ECG Changes

ST Depression (Subendocardial Ischaemia)

Three morphologies of ST depression in ACS:

(A) Horizontal ST depression - most specific for ischaemia (e.g., unstable angina)
(B) Horizontal ST depression - NSTEMI pattern
(C) Downsloping ST depression - high specificity for ischaemia
(D) Upsloping ST depression - less specific but can occur in ischaemia
(E) Reciprocal ST depression - horizontal STD in a remote lead (e.g., inferior lead depression with anterior STEMI)

The most ischaemic patterns are horizontal and downsloping. Upsloping is the least specific.

T-Wave Inversions

(A & B) T-wave inversions in ACS - narrow, symmetrical
(C) T-wave inversion in NSTEMI
(D) Deep symmetrical T-wave inversions - Wellens syndrome (proximal LAD stenosis)

Classic ACS T-wave inversions are narrow, symmetrical, with an isoelectric preceding ST segment.

Rosen's Emergency Medicine, p. 1001

Distinction between UA and NSTEMI: Both may show identical ECG changes (or even a normal ECG). The difference is made by serial troponins - elevated in NSTEMI, normal in UA.

4. STEMI - Hyperacute Phase

Hyperacute T waves (earliest sign - minutes after occlusion)

Panel A: Broad, tall, peaked T waves in V3 and V4 - the hyperacute T waves of early STEMI. ST segment just beginning to rise in V3/V4.
Panel B: Same patient 30 minutes later - now prominent ST elevation in V1-V4 (fully evolved STEMI).

Hyperacute T waves are broad-based and asymmetric (unlike hyperkalaemia T waves which are narrow and peaked).

5. STEMI - Full Evolution

Time	ECG Change
Minutes	Hyperacute (tall, broad) T waves
Hours	ST elevation (convex/tombstone morphology)
Hours - Days	Q wave formation + T wave inversion begins
Days - Weeks	ST normalises; deep T inversions; Q waves persist
Months - permanent	Q waves (scar); T waves may normalise

ST Elevation Morphology

ST elevation in STEMI is typically flat or convex upward (tombstone/domed). In contrast, benign causes of STE (pericarditis, early repolarisation) tend to show concave (smiley-face) ST elevation - though this is a guideline, not a rule.

STEMI Localisation

Territory	Leads with STE	Culprit Artery
Anteroseptal	V1, V2 (±V3)	Proximal LAD
Anterior	V1-V4	LAD
Anterolateral	V1-V6, I, aVL	Proximal LAD
Lateral	I, aVL	LCx or diagonal
Inferior	II, III, aVF	RCA (most) or LCx
Posterior	ST depression V1-V3 + tall R in V1	LCx or RCA
Right ventricular	II, III, aVF + V3R-V6R	Proximal RCA

6. Wellens Syndrome (High-Risk NSTEMI Pattern)

Wellens syndrome - deep T inversions and biphasic T waves

Type I (75%): Deeply inverted symmetrical T waves in V2/V3 (panel A, B)
Type II (25%): Biphasic T waves in V2/V3 (panels C, D)

The patient is often pain-free at the time of ECG. This pattern indicates critical proximal LAD stenosis and carries a high risk of imminent anterior STEMI if not revascularised. Do not perform stress testing - it can precipitate complete occlusion.

Rosen's Emergency Medicine, p. 1002

7. Q Waves - Marker of Necrosis

Pathological Q wave: ≥ 0.04 sec (1 small box) wide AND ≥ 25% of R-wave amplitude in the same lead
First appear at 1 hour post-MI but usually complete by 8-12 hours
Presence of Q waves + STE does not mean reperfusion is too late - always treat STEMI urgently
Can regress over months, especially after successful reperfusion

8. Reciprocal Changes in STEMI

Reciprocal ST depression in leads opposite to the infarct territory indicates:

More extensive infarction
More severe underlying CAD
Greater haemodynamic compromise
Higher mortality

Example: Inferior STEMI (STE in II, III, aVF) → reciprocal ST depression in aVL (classically ≥1 mm depression in aVL is very specific for inferior STEMI).

Summary Table - IHD ECG by Syndrome

Syndrome	Resting ECG	During Episode	Key Feature
Stable angina	Normal or non-specific ST-T	ST depression / T inversion	Dynamic, resolves with rest
Prinzmetal angina	Usually normal	Transient ST elevation	Resolves completely, no Q waves
Unstable angina	Normal, ST depression, or T inversion	Worsening	Normal troponin
NSTEMI	ST depression ± T inversion	Same	Elevated troponin
STEMI	Hyperacute T → STE → Q waves	Ongoing	Convex STE ≥1 mm in ≥2 contiguous leads
Old MI	Persistent Q waves, T inversions	Stable	Scar; no acute change

Rosen's Emergency Medicine; Goldman-Cecil Medicine

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