Myocardial Infarction

Timing of morphologic changes in MI

Partially based on Schoen FJ. The Heart. Chapter in Kumar V, et al. Pathologic Basis of Disease. 7th ed. Elsevier Saunders. Philadelphia. 2005. With additions and modifications. Calvin E. Oyer, M.D. 7/05


Gross findings


Clinical correlations

1½- 4 hours

None for 1st 12 hours by direct examination.

None or wavy fibers. Wavy fibers as early as 1-3 hours. Contraction bands, when present, can occur early (as early as after 2 minutes of reperfusion in animal experiments). .

Mural thrombi can form early and embolize at any time

4-12 hours

Special staining shows lack of dehydrogenase as early as 2-3 hours.

Early coagulation necrosis, edema, hemorrhage, Earliest sign is hypereosinophilia of myocytes.

CK and CK-MB elevated 4-48 hours. Troponin I

8-72 hours.

12-24 hours

Pallor or red-blue hue. Occasionally, hemorrhage, especially when thrombolysis was administered.

Coagulation necrosis, hypereosinophilia, pyknosis as early as 5 hours, loss of striations later, contraction band necrosis, polys as early as 6-8 hours 

Serious arrhythmias can occur at any time. Primary ventricular fibrillation – usually in 1st 12 hours.

1-3 days


Coagulation necrosis, loss of nuclei 24-48 hours, more loss of striations, polys peak at 48 hours 

Pericardial friction rub, due to fibrinous pericarditis, most common on days 2-3

3-7 days

As macrophages and necrotic tissue predominate, tissue is soft and appears yellow with red border due to hyperemia. Prone to rupture.

Early disintegration of dead muscle, dying polys. Macrophages appearing and increasing.


Rupture of free wall, ventricular septum, or papillary muscle at 3-6 days

7-10 days


Macros with phagocytosis, early granulation tissue. Proliferation of blood vessels as early as 3 days.

Fibroblasts as early as 4 days.


10-14 days


Granulation tissue recognized as early as 7-10 days. Collagen fibers as early as 9 days.

Dressler syndrome, an autoimmune-based pericarditis, at 1-8 weeks

2-8 weeks

Appearance evolves to that of a white, fibrous scar.

Increased collagen and decreased cellularity. Peak granulation tissue at 2-4 weeks. Dense scar as early as 6 weeks.

Ventricular aneurysms are a late complication.


Myocardial infarction  (~48hrs)

Illustrates maximum acute inflammation, loss of nuclei and striations; hypereosinophilia still present.

Myocardial infarction (7-10 days)

Macrophages, granulation tissue, and hyperemia. Acute inflammation has subsided.

Myocardial infarction (7-10 days; high-mag)

Macrophages, fibroblasts, and debris from dead myocytes.

Myocardial Infarction (3 days; gross)

A hemorrhagic inferolateral infarct at 3 days. In this case, the patient had been treated with thrombolytic agents, which result in an increased incidence of hemorrhage in the myocardium.  The hemorrhage, however, is usually of no clinical significance.

Myocardial infarction (contraction band)

Contraction bands are associated with reperfusion. In myocardial infarction, they are most likely seen at margin of infarct. They can also be seen in cases of sudden cardiac death and perioperative ischemia during cardiac surgery. They represent hypercontraction due to massive calcium influx.

Contraction band lesions, a.k.a. myofibrillar degeneration, coagulative myocytolysis, kinetic cell death, and contraction band necrosis, can be regarded as accelerated necrosis of irreversibly injured myocytes. They represent hypercontraction with massive influx of calcium within injured myocytes which were still viable prior to reperfusion. They appear as early as after only 2 minutes of reperfusion and are to be distinguished from coagulation necrosis which histologically requires hours for appearance. Contraction band lesions are most numerous in margins of infarcts between dead and viable myocardial zones, in infarcts in patients treated with thrombolytic agents, in hearts of sudden cardiac death, and in hearts of patients with perioperative ischemia during cardiac surgery. They are not seen in non-cardiac CPR cases.

Myocardial infarction (myocytolysis)

Note swollen, vacuolar appearance. Results from ischemia. Myocyte injury considered not yet irreversible.  Seen in subendocardial region (as here) and at margins of infarcts. A.k.a. vacuolar degeneration or colliquative myocytolysis.

Myocytolysis, a.k.a. vacuolar degeneration or colliquative myocytolysis, is characterized by a nucleus seen within a sarcolemmal tube which otherwise appears empty. Myocytolysis is seen most frequently in the left ventricular subendocardium and at the perimeter of MI’s. These cells are thought to be still viable. Their staining for creatine kinase (CK), lactic dehydrogenase (LD), and aspartate aminotransferase (AST) is the same as for normal fibers whereas fibers with coagulation necrosis, which is irreversible, are negative for these stains.

Myocardial infarction - wavy myofibers

Though wavy fibers, illustrated here, occur as early as 2-3 hours, this infarct is older as indicated by occasional polys and loss of nuclei and striations.

Acute myocardial infarction (MI) results from prolonged ischemia of myocardial tissue due to reduced coronary artery perfusion. Decreased oxygen flow to myocardium results in anaerobic metabolism. ATP synthesis decreases within 1-2 minutes, and is reduced to 50% by 10 minutes. ATP loss leads to membrane channel (Na/K ATPase) disruption and subsequent increase in cell membrane permeability. Calcium ion influx ensues, which activates various degradative enzymes to further disrupt cellular function. Irreversible cell death occurs in about 15-20 minutes. Risk factors for MI include: age (>50), gender (M>F), CAD, diabetes, HTN, previous MI, obesity, smoking, and hyperlipidemia. Patient with an acute MI typically present with substernal chest pressure radiating to left arm or jaw that lasts for more than 30 minutes. These symptoms are often associated with diaphoresis, dyspnea and palpitations. However, symptoms vary widely. Prompt and accurate assessment is key to reducing mortality. Patients suspected of an MI should be given morphine, oxygen, nitroglycerine, and ASA (MONA therapy). Beta-blockers, ACE-I, and statins also play a crucial role in the medical management of MI. A stat EKG should be obtained to look for ST changes (always compare with previous EKGs, if available). Cardiac enzymes (e.g., CK-MB and troponin-I) should be ordered. When the diagnosis of MI is made, revascularization should be attempted, either via t-PA (best within first 6hrs, up to 24hrs) or via percutaneous transluminal coronary angioplasty (PTCA).