Pathology · Year 2 · from Pathology
Case 1: Acute Myocardial Infarction with Coagulative Necrosis
Patient Demographics
- Age: 62 years old
- Sex: Male
- Occupation: Accountant
Chief Complaint
"Crushing chest pain for 3 hours"
History of Present Illness
A 62-year-old male with a history of hypertension and hyperlipidemia presents to the emergency department with severe substernal chest pain that began 3 hours ago while climbing stairs. The pain radiates to his left arm and jaw and is associated with diaphoresis and nausea. He describes the pain as "an elephant sitting on my chest." He has never experienced this type of pain before.
Physical Examination
- Vital Signs: BP 100/70 mmHg, HR 95 bpm, RR 22/min, SpO2 94% on room air
- General: Diaphoretic, anxious male in moderate distress
- Cardiovascular: S1, S2 present, S4 gallop heard, no murmurs
- Lungs: Bilateral basilar crackles
- Extremities: Cool, clammy, no edema
Diagnostic Workup
Laboratory Studies:
| Test | Result | Reference Range |
|---|---|---|
| Troponin I | 8.5 ng/mL | <0.04 ng/mL |
| CK-MB | 45 U/L | 0-25 U/L |
| BNP | 450 pg/mL | <100 pg/mL |
| Lactate | 3.2 mmol/L | 0.5-2.0 mmol/L |
Electrocardiogram:
- ST-segment elevation in leads V1-V4 (anterior leads)
- Reciprocal ST depression in leads II, III, aVF
Echocardiogram:
- Akinesis of the anterior wall and apex
- Ejection fraction 35%
- Mild mitral regurgitation
Pathology Correlation
This case demonstrates coagulative necrosis following acute myocardial ischemia:
- Mechanism: Coronary artery occlusion leads to ATP depletion in cardiomyocytes
- Cellular changes: Within 30 minutes - cell swelling, glycogen depletion
- Irreversible injury: After 20-40 minutes of severe ischemia
- Histology: Coagulative necrosis preserves tissue architecture; "ghost cells" visible by 24-48 hours
- Contraction bands: May appear with reperfusion injury
Clinical Image
Gross pathology of myocardial infarction showing pale, mottled area of coagulative necrosis in the left ventricular wall. The necrotic tissue appears pale compared to viable myocardium.
Image Source: Wikimedia Commons - "Myocardial infarction" License: CC BY-SA 3.0 URL: https://commons.wikimedia.org/wiki/File:AMI_gross_(1).jpg
Diagnosis
ST-Elevation Myocardial Infarction (STEMI) - Anterior wall
Treatment
- Emergent percutaneous coronary intervention (PCI) with stent placement
- Dual antiplatelet therapy (aspirin + P2Y12 inhibitor)
- Anticoagulation (heparin)
- Beta-blocker (metoprolol)
- ACE inhibitor (lisinopril)
- High-intensity statin therapy
Teaching Points
- Coagulative necrosis is the predominant pattern in solid organs (heart, kidney, spleen) following ischemia
- Tissue architecture is preserved because structural proteins resist enzymatic degradation
- Troponin release indicates irreversible myocyte injury and membrane damage
- The "point of no return" involves severe membrane damage and mitochondrial dysfunction
- Reperfusion injury can cause additional damage through reactive oxygen species generation