Acute myocardial infarction indicates irreversible myocardial injury resulting in necrosis of a significant portion of myocardium (generally >1 cm).
Coagulative necrosis begins approximately 30 minutes after coronary occlusion, followed by a robust inflammatory response that begins with the release of reactive oxygen species and neutrophil invasion.
Loss of viability (irreversible injury) takes at least 20-40 minutes after total occlusion of blood flow.1
| Stage | Gross Changes | Microscopic Changes | Clinical Correlations |
| 0–6 hours | None | No morphologic changes at first; vascular congestion at perimeter of lesion after the first few hours | Arrhythmia most common cause of death in early hours; mural thrombi can form and embolize |
| After 12 hours | None | First appearance of neutrophils in viable tissue adjacent to the lesion | |
| 12–24 hours | Slight swelling and change of color | Cytoplasm displays increasing affinity for acidophilic dyes, and striations are lost; nuclei disappear; neutrophils infiltrate the lesion | |
| By 24 hours | Pale or reddish-brown infarct with surrounding hyperemia | Well-developed changes of coagulative necrosis; progressive infiltration by neutrophils | |
| By third day | Increasingly yellow color of infarct | Replacement of neutrophils by macrophages; phagocytosis of debris begins | Pericardial friction rub due to fibrinous pericarditis most common on days 2–3 |
| From 7 days | Yellow infarcted area surrounded by congested red border | Beginning of growth of young fibroblasts and newly formed vessels into the lesion; replacement of neutrophils by macrophages and phagocytosis of debris continues | Risk for myocardial rupture (free wall, ventricular septum, papillary muscle) greatest within first 4–7 days |
| From 10 days | Red, newly formed vascular connective tissue encircles and gradually replaces yellow necrotic tissue | Growth of fibrovascular tissue continues; replacement of neutrophils by macrophages and phagocytosis of debris are almost complete | Dressler syndrome, an autoimmune-based pericarditis can occur 1–8 weeks |
| Between second and fourth weeks | Progressive synthesis of collagen and other intracellular matrix proteins | ||
| From fifth week | Increasing pallor of infarct because of progressive fibrosis | Progressive fibrosis | |
| Within 3–6 months | Well-developed gray-white scar | Mature fibrous tissue replaces area of infarction | Ventricular aneurysm may occur in scarred area |
Following a myocardial infarction (MI), the myocardium undergoes several progressive changes, both at the gross and microscopic levels. These changes occur in a well-defined sequence over time:
1. **Initial Changes (Minutes to Hours):**
- Myocardial ischemia leads to the cessation of myocardial contractility. Within 10-15 minutes of ischemia, ultrastructural changes such as diminished cellular glycogen, relaxed myofibrils, and sarcolemmal disruption begin to appear[5].
- Mitochondrial abnormalities can be observed as early as 10 minutes after coronary occlusion[5].
2. **Early Changes (Hours to Days):**
- Coagulative necrosis becomes apparent within 6 to 12 hours[1].
- Neutrophilic infiltration occurs around 12 to 24 hours post-infarction[1].
- Loss of nuclei and continued necrosis are seen from day 1 to day 3, followed by phagocytosis by macrophages from day 3 to day 7[1].
- Myocyte necrosis progresses from the subendocardium to the subepicardium over several hours[5].
3. **Intermediate Changes (Days to Weeks):**
- Granulation tissue begins to form at the margins of the infarcted area by the end of the first week[1].
- Progressive infiltration by macrophages and fibroblasts leads to the deposition of collagen and formation of scar tissue[2].
4. **Late Changes (Weeks to Months):**
- The infarcted area is replaced by fibrous scar tissue, which is typically complete by around 2 months post-MI[1].
- The fibrous scar results in reduced compliance and increased stiffness of the affected myocardial region, contributing to potential complications such as heart failure[2][3].
These changes are crucial in determining the structural and functional outcomes of the heart post-MI, influencing the risk of complications such as heart failure, arrhythmias, and further ischemic events[2][3].
Citations:
[1] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7750744/
[2] https://webpath.med.utah.edu/TUTORIAL/MYOCARD/MYOCARD.html
[3] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7251228/
[4] https://www.sciencedirect.com/science/article/pii/000287039290916J
[5] https://www.ahajournals.org/doi/10.1161/CIR.0000000000000617