A 74-year-old man presents with complaints of sudden severe crushing retrosternal pain. The pain radiated to his left arm shortly after it began, and he was subsequently rushed to the emergency department for evaluation. His troponins and creatine kinase-MB (CK-MB) were elevated. Unfortunately, the patient died within the next 2 hours and an autopsy was performed immediately. The gross examination of the heart will show?

White, patchy, non-contractile scar

Red granulation tissue surrounding the infarction

A 49-year-old man was brought to the emergency department by ambulance with complaints of sudden-onset chest pain that radiates into his neck and down his left arm. This substernal pain started 2 hours ago while he was having dinner. His past medical history is remarkable for hypercholesterolemia that is responsive to therapy with statins and coronary artery disease. His temperature is 37.0°C (98.6°F), blood pressure is 155/90 mm Hg, pulse is 112/min, and respiratory rate is 25/min. Troponin I levels are elevated. A 12-lead ECG was performed (see image). What is the most likely etiology of this patient’s presentation?

Right coronary artery occlusion

Left circumflex artery occlusion

Left anterior descending artery occlusion

Left main coronary artery occlusion

A 78-year-old man with a history of myocardial infarction status post coronary artery bypass grafting and a 60-pack-year history of smoking is found deceased in his apartment after not returning calls to his family for the last 2 days. The man was last known to be alive 3 days ago, when his neighbor saw him getting his mail. The family requests an autopsy. On autopsy, the man is found to have a 100% blockage of his left anterior descending artery of his heart and likely passed from sudden cardiac death 2 days prior. Which of the following findings is expected to be found on histologic examination of his damaged myocardium?

Uniform binding of acidophilic dyes

Cellular debris and lymphocytes

Cellular debris and macrophages

Two days after being admitted for acute myocardial infarction, a 61-year-old man has sharp, substernal chest pain that worsens with inspiration and improves when leaning forward. Cardiac examination shows a scratchy sound best heard over the left sternal border. Histopathological examination of the infarcted myocardial tissue is most likely to show which of the following findings?

Granulation tissue with macrophages

A 73-year-old man with coronary artery disease and hypertension is brought to the emergency department by ambulance 90 minutes after the acute onset of substernal chest pain and dyspnea. He has smoked 2 packs of cigarettes daily for 52 years. Shortly after arriving at the hospital, he loses consciousness and is pulseless. Despite attempts at cardiopulmonary resuscitation, he dies. Examination of the heart at autopsy shows complete occlusion of the left anterior descending artery with a red thrombus overlying a necrotic plaque. Which of the following pathophysiologic mechanisms is most likely responsible for this patient's acute coronary condition?

Secretion of matrix metalloproteinases

Influx of lipids into the endothelium

Release of platelet-derived growth factor

Proliferation of smooth muscle cells

A 69-year-old man is scheduled to undergo radical retropubic prostatectomy for prostate cancer in 2 weeks. He had a myocardial infarction at the age of 54 years. He has a history of GERD, unstable angina, hyperlipidemia, and severe osteoarthritis in the left hip. He is unable to climb up stairs or walk fast because of pain in his left hip. He had smoked one pack of cigarettes daily for 30 years but quit 25 years ago. He drinks one glass of wine daily. Current medications include aspirin, metoprolol, lisinopril, rosuvastatin, omeprazole, and ibuprofen as needed. His temperature is 36.4°C (97.5°F), pulse is 90/min, and blood pressure is 136/88 mm Hg. Physical examination shows no abnormalities. A 12-lead ECG shows Q waves and inverted T waves in leads II, III, and aVF. His B-type natriuretic protein is 84 pg/mL (N < 125). Which of the following is the most appropriate next step in management to assess this patient's perioperative cardiac risk?

Radionuclide myocardial perfusion imaging

24-hour ambulatory ECG monitoring

A 50-year-old man presents the emergency department for intense chest pain, profuse sweating, and shortness of breath. The onset of these symptoms was 3 hours ago. The chest pain began after a heated discussion with a colleague at the community college where he is employed. Upon arrival, he is found conscious and responsive; the vital signs include a blood pressure of 130/80 mm Hg, a heart rate at 90/min, a respiratory rate at 20/min, and a body temperature of 36.4°C (97.5°F). His medical history is significant for hypertension diagnosed 7 years ago, which is well-controlled with a calcium channel blocker. The initial electrocardiogram (ECG) shows ST-segment depression in multiple consecutive leads, an elevated cardiac troponin T level, and normal kidney function. Which of the following would you expect to find in this patient?

Incomplete occlusion of a coronary artery

Myocardial infarction pathology for USMLE Step 2 CK: High-Yield Pathology Lessons

MI Pathogenesis - The Clot Thickens

Initiating Event: Rupture or erosion of an unstable atherosclerotic plaque exposes its thrombogenic lipid core.
Thrombosis: Platelet adhesion, activation, and the coagulation cascade rapidly form a thrombus, leading to coronary artery occlusion.
Infarct Progression:
- Subendocardial Infarct: Involves the inner third of the myocardium, the region most vulnerable to ischemia. Often due to incomplete or transient occlusion.
- Transmural Infarct: Infarction spans the entire myocardial wall thickness, resulting from complete and prolonged occlusion (typically >6 hours).

Thin-cap fibroatheroma vs. stable plaque

⭐ The Left Anterior Descending (LAD) artery is the most commonly occluded coronary artery, typically leading to an anteroseptal MI.

Infarct Evolution - A Scar is Born

Histological Evolution of Acute Myocardial Infarction

Time Post-MI	Gross Changes	Microscopic Findings	Key Complications
0-24h	Dark mottling	Early coagulative necrosis; edema, hemorrhage. Contraction bands with reperfusion.	Arrhythmia, cardiogenic shock, sudden death
1-3d	Hyperemia, yellow-tan center	Coagulative necrosis, acute inflammation (neutrophils).	Fibrinous pericarditis
3-14d	Yellow-tan, soft, with hyperemic border	Macrophages, granulation tissue formation.	Ventricular free wall rupture, papillary muscle rupture, interventricular septum rupture
>2w	Gray-white scar	Dense collagenous scar (fibrosis).	True aneurysm, Dressler syndrome, heart failure

MI Complications - When the Heart Breaks

Ventricular Free-Wall Rupture Phenotypes and Management

⭐ Papillary muscle rupture (posteromedial papillary muscle is most susceptible) leads to acute, severe mitral regurgitation.

Free wall rupture: Leads to cardiac tamponade.
Interventricular septum rupture: Creates a VSD (shunt).
Mural thrombus: Risk of systemic embolization.
Dressler syndrome: Autoimmune fibrinous pericarditis, weeks to months post-MI.

📌 Mnemonic (DARTH VADER): Death, Arrhythmia, Rupture, Tamponade, Heart failure, Valve disease, Aneurysm, Dressler's syndrome, Embolism, Recurrence.

High‑Yield Points - ⚡ Biggest Takeaways

Coagulative necrosis and wavy fibers are the earliest changes (4-24 hours), followed by neutrophilic infiltrate.

Macrophages dominate at 3-7 days, creating the highest risk period for myocardial rupture.

Granulation tissue (type III collagen) appears at 1-2 weeks, maturing into a dense type I collagen scar.

Reperfusion injury is characterized by contraction band necrosis due to massive calcium influx.

The LAD artery is the most commonly occluded vessel, typically causing an anteroseptal MI.

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