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Ischemic Heart Disease & MI

Name: Ischemic Heart Disease & MI
Creator: Veli Bakalov, MD

From angina to the hour-by-hour histology of a dying myocardium

Cardiovascular·Ischemic Heart Disease & Heart Failure·5 min read·9 high-yield points·Reviewed by Veli Bakalov, MD @HemeOncBuddy

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Stable angina = fixed stenosis over 70%, troponin negative; unstable angina = plaque rupture with thrombus, rest pain, troponin still negative; a positive troponin makes it NSTEMI.
Prinzmetal angina = vasospasm with transient ST elevation at rest (smoking, cocaine, triptans); treat with calcium channel blockers and nitrates, avoid nonselective β-blockers.
LAD is the most commonly occluded artery (anterior wall, anterior two-thirds of septum, apex); RCA supplies the inferior wall and AV node, so inferior MI causes bradycardia and AV block.
ECG territories: anterior V1–V4 (LAD), septal V1–V2, lateral I/aVL/V5–V6 (circumflex), inferior II/III/aVF (RCA); posterior = tall R and ST depression in V1–V2.
STEMI = transmural infarct from complete occlusion; NSTEMI = subendocardial (inner third) infarct with ST depression and positive troponin.
Troponin rises at 3–4 h, peaks ~24 h, stays up 7–10 days; CK-MB normalizes in 48–72 h, so a new CK-MB rise flags reinfarction.
MI histology: wavy fibers (0–4 h) → coagulative necrosis (4–24 h) → neutrophils (1–3 d) → macrophages and granulation (3–14 d, weakest) → type I collagen scar (weeks).
Ruptures in days 3–14: free wall → tamponade, septum → VSD with O2 step-up, posteromedial papillary muscle (single PDA supply) → acute MR; VF is the top killer in the first 48 h.
Reperfusion injury (free radicals, Ca2+ overload) → contraction band necrosis; pericarditis at 1–3 days vs Dressler autoimmune pericarditis at 2–10 weeks; true aneurysm → persistent ST elevation and mural thrombus.

Angina and the acute coronary syndromes

Supply and demand. Ischemia occurs when myocardial O2 demand outstrips coronary flow. The left ventricle is perfused mainly in diastole, so tachycardia worsens ischemia twice — raising demand and shortening diastole. The subendocardium, farthest from the epicardial arteries and compressed during systole, is the most vulnerable layer.

Stable angina. A fixed atherosclerotic stenosis over 70% limits flow when demand rises: exertional chest pain relieved by rest or nitroglycerin, ST depression during pain, and a negative troponin.

Unstable angina. Thrombus on a ruptured plaque partially occludes the artery: pain at rest or in a crescendo pattern and ST depression, but troponin stays negative. The same picture with a positive troponin is NSTEMI.

Prinzmetal (variant) angina. Coronary vasospasm rather than fixed stenosis: chest pain at rest with transient ST elevation, often in younger patients, triggered by smoking, cocaine, or triptans. Treat with calcium channel blockers and nitrates.

Avoid nonselective β-blockers in Prinzmetal angina: losing β2-mediated vasodilation leaves α-mediated vasoconstriction unopposed and can worsen spasm.

Ischemic syndromes compared

Syndrome	Mechanism	Pain	ECG	Troponin
Stable angina	Fixed stenosis over 70%	Exertional, relieved by rest or nitroglycerin	ST depression	Negative
Unstable angina	Thrombus on ruptured plaque, incomplete occlusion	At rest or crescendo	ST depression	Negative
Prinzmetal	Vasospasm	At rest	Transient ST elevation	Usually negative
NSTEMI	Partial occlusion or demand ischemia; subendocardial infarct	At rest, prolonged	ST depression or T-wave inversion	Positive
STEMI	Complete occlusion; transmural infarct	At rest, severe	ST elevation, later pathologic Q waves	Positive

Coronary territories and ECG localization

LAD, the widowmaker. The left anterior descending is the most commonly occluded coronary artery. It supplies the anterior LV wall, the anterior two-thirds of the septum, and the apex, and shares the anterolateral papillary muscle with the circumflex.

Circumflex and RCA. The left circumflex feeds the lateral wall. The right coronary artery supplies the inferior wall, the RV, and usually the SA and AV nodes, so an inferior MI can cause bradycardia and AV block.

Dominance. Whichever artery gives rise to the posterior descending artery (PDA) is dominant; about 85% of people are right-dominant. The PDA supplies the posterior septum and the posteromedial papillary muscle, which depends on this single vessel.

Localizing the infarct

Wall	ECG leads	Usual artery
Anterior	V1–V4	LAD
Septal	V1–V2	LAD
Lateral	I, aVL, V5–V6	Left circumflex
Inferior	II, III, aVF	RCA
Posterior	Tall R waves and ST depression in V1–V2 (reciprocal)	Left circumflex or PDA (from RCA or LCx)

Proximal RCA occlusion can add an RV infarct: hypotension, raised JVP, and clear lungs. The RV is preload-dependent, so nitrates can precipitate collapse and IV fluid supports output.

Infarct depth and cardiac biomarkers

STEMI. Complete occlusion produces a transmural (full-thickness) infarct with ST elevation and, later, pathologic Q waves.

NSTEMI. Partial occlusion or demand ischemia produces a subendocardial infarct of the inner one-third, with ST depression or T-wave inversion and a positive troponin.

Troponin I/T. The most sensitive and specific marker: it rises 3–4 hours after infarction, peaks at about 24 hours, and stays elevated for 7–10 days.

CK-MB. Rises on a similar schedule but normalizes within 48–72 hours. Because troponin is still high for over a week, a re-rising CK-MB is what flags reinfarction.

3–4 htroponin begins to rise

~24 htroponin peak

7–10 dtroponin stays elevated

48–72 hCK-MB back to normal

Pathology: the infarct timeline

0–4 hoursNo gross or light-microscopic change apart from early wavy fibers, yet the risk of lethal ventricular arrhythmia is high.
4–24 hoursDark mottling; coagulative necrosis begins; contraction bands, especially with reperfusion; neutrophils start arriving by about 24 hours.
1–3 daysNeutrophils peak amid extensive coagulative necrosis; fibrinous pericarditis may follow a transmural infarct.
3–14 daysMacrophages clear debris, then granulation tissue grows in: yellow soft center with a red hyperemic border; the wall is weakest around days 5–7.
2 weeks to monthsGray-white scar of type I collagen.

Reperfusion injury. Restoring flow by thrombolysis or PCI salvages myocardium but paradoxically injures it through oxygen free radicals and calcium overload. The histologic hallmark is contraction band necrosis: hypercontracted sarcomeres with thick eosinophilic transverse bands.

Stunned myocardium is viable tissue that stays dysfunctional for hours to days after reperfusion. Hibernating myocardium is chronically underperfused but viable, with reduced contraction that recovers after revascularization.

Complications by time

Post-MI complications

Complication	Typical timing	Key features
Ventricular arrhythmia (VF)	First 48 hours	Most common cause of early death
Peri-infarction pericarditis	1–3 days	Fibrinous; friction rub after transmural MI
Papillary muscle rupture	About days 2–7	Posteromedial muscle (single PDA supply) → acute severe MR, pulmonary edema
Interventricular septal rupture	About days 3–5	Acute VSD with left-to-right shunt and O2 step-up in the RV
Free wall rupture	About days 5–14	Hemopericardium → cardiac tamponade
True LV aneurysm	Weeks to months	Scarred, bulging wall; persistent ST elevation; mural thrombus → embolic stroke
Dressler syndrome	2–10 weeks	Autoimmune fibrinous pericarditis: fever, pleuritic pain, high ESR, anti-heart antibodies

Ruptures cluster in days 3–14 (peak risk around days 5–7), when macrophages have softened the wall but collagen has not yet replaced it.

Mechanical ruptures. Both papillary muscle and septal rupture produce a new holosystolic murmur; the septal lesion is distinguished by the oxygen step-up from right atrium to right ventricle. Free wall rupture usually presents as sudden tamponade and electromechanical collapse.

Two pericarditis windows. Early fibrinous pericarditis (1–3 days) reflects necrosis extending to the epicardium; Dressler syndrome weeks later is immune-mediated, driven by antibodies to newly exposed myocardial antigens.