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Pathology of Myocardial Infarction

Dr Sampurna Roy MD

 
Cardiac Pathology Online

 

http://www. histopathology-india.net/ HeartIndex. htm

               
Myocardial infarction may occur at any age but frequency rises with increasing age.

Women are remarkably protected against myocardial infarction during reproductive life.

Myocardial infarct is the ischemic necrosis of an area of myocardium.

 

This is a section of the subepicardial myocardium from an autopsy case of a 71 year old Asian male. The features are those of acute myocardial infarction showing neutrophilic infiltrate along with areas of necrosis, diffuse interstitial edema and pale myocytes with fading nuclei and decreased striations.

 

 

Assessment of Ischaemic Myocardial Damage

Sudden Cardiac Death

On the basis of morphology, pathogenesis and clinical significance, there are two types of infarct.

1. Transmural infarct- This is the infarction of the full thickness of the ventricular wall, usually caused by severe coronary atherosclerosis, worsened by acute plaque disruption and superimposed occlusive thrombosis.

2. Subendothelial infarct- This is limited to the inner one third to one half of the ventricular wall (an area of diminished perfusion).

Pathogenesis:

 

Commonest cause (at least 90%) is due to coronary atherosclerosis with occluding thrombus.

Occlusion is typically seen in the proximal 2 cm of the left anterior descending and left circumflex arteries and in the proximal and distal thirds of the right coronary artery.

Vasospasm, platelet aggression or both may cause myocardial infarct without atheroslerosis.

 

Complete vessel occlusion may not cause myocardial infarct due to collateral blood flow.

 

In the absence of sudden death, thrombi may be lysed spontaneously or with fibrinolytic treatment, or vasospasm may relax, thereby reestablishing blood flow and thus spare some myocardium from necrosis.

 

The time interval between onset of complete myocardial ischemia and the initiation of irreversible injury is 20 to 40 minutes.

Sequence of changes:

Gross:

Before 6 to 12 hours: No visible lesion is seen.

By 18 to 24 hours: Infarct area becomes pale to cyanotic.

In the first week: The infarct area becomes progressively more sharply defined, yellow and softened.

By the 7 to 10 days, circumference of the infarct area becomes hyperemic, and progressively expands.

By the 6 weeks, fibrous scar is well established.

Microscopic features: 

 

Within 1 hour, of ischemic injury, there is intercellular  edema and “wavy fibers” may be present at the periphery  of the infarct. These are noncontrctile dead fibers, stretched by the adjacent viable contracting myocytes

 

Electron microscopy shows reversible changes (swelling of mitochondria & endoplasmic reticulum and relaxation of myofibrils). 

 

Histochemically, there is loss of oxidative enzyme & fall of glycogen.

 

In 12 to 72 hours, there is infiltration of neutrophils with progressive coagulative necrosis of myocytes. Dead myocytes become hypereosinophilic with loss of nuclei.

 

Between 3 and 7 days, after onset, dead myocytes begin to disintegrate and are removed by macrophages and enzyme proteolysis. There is proliferation of fibroblasts with formation of granulation tissue, which progressively replaces necrotic tissue.

 

After 6 weeks, healing is complete by fibrosis:

 

Contraction band necrosis:  Contraction band necrosis, characterized by hypereosinophilic transverse bands of precipitated myofibrils in dead myocytes is usually seen at the edge of an infarct or with reperfusion (Example: with thrombolytic therapy).

 

Reperfusion of an infarct: Reperfusion of an infarct is also associated with more hemorrhage, less acute inflammation, less limitation of the acute inflammation to the periphery in the first few days, reactive stromal cells, more macrophage infiltration earlier and a more patchy distribution of necrosis, especially around the periphery.

 

 

Complications:

 

It depends on the size and location of the lesion.

Within minutes to 3 days of onset:

1. Arrythmias :  i) ventricular fibrillation ; ii) block of A-V  bundles and its branches causing acute heart failure.

2. Cardiogenic shock (usually in large infarct) causing acute heart failure.

3. Thrombotic complication- mural thrombus over infarct area or atrial thrombus, causing embolism to brain, kidney etc.

4. Rupture of heart.

3-14 days:

Large infarct:  There is softening of dead muscle (myomalacia cordis) leading to rupture & death.

Site of rupture is ventricular wall, papillary muscle & interventricular septum.

5. Acute fibrinous or hemorrhagic pericarditis - over infarct area.

After weeks or months:

6. Chronic heart failure

7. Cardiac aneurysm, which may rupture producing hemopericardium and death.

Clinical features:

1. Chest pain- 20-30% does not cause chest pain, common in patients with diabetes mellitus, hypertension, & in elderly patients.

2. Nausea, diaphoresis and dyspnea.

Fate of the patient:

In hospitalized patients (where angiography, echocardiography and perfusion scintigraphy are available) usual fate are:

i) About 25 % of patients dye of cardiogenic shock or fatal arrythmia.

ii) Patients who survive the acute phase may develop:

 

- Congestive heart failure

- Cardiac arrythmia 

- Left ventricular failure with pulmonary edema.

- Rupture of ventricular wall, interventricular septum and papillary muscle

- Thromboembolism.

 

iii) 10-20%  patients recover with no complication.

 

iv) Early restoration of blood flow by thrombolysis or balloon angioplasty provides better prognosis.

                                                         

Diagnosis:

 

It is based on symptoms, electrocardiographic change and serum elevation of myocardial enzymes (creatine kinase-MB isoenzyme) or other proteins (troponin I, troponin T or myoglobin), that leak out of dead cells.

The classic electrocardiogram findings: ST segment elevation, followed by T wave inversion and Q waves, are associated with transmural infarction.  ST segment depression and T wave inversion are associated with subendocardial infarction.

The laboratory diagnosis of myocardial infarction:

1) This has been based on elevation of creatine phosphokinase (CPK), with an MB fraction >5% of the total CPK or a relative index >3 (if the MB fraction is measured  in mass units instead of activity units). 

The elevation of CPK begins around 8 hours after the onset of infarction, peaks around 18 hours and ends around 48 hours.

2) The late diagnosis of myocardial infarction can be based on elevation of lactate dehydrogenase (LDH), with an LDH-1 fraction >40% of the total LDH or LDH-1/LDH-2 ratio >1, because this peaks around 5 days.

3) Recently, the early and late diagnosis of acute  myocardial infarction has been based on elevated serum levels of cardiac troponin.

This elevation begins around 4 hours after the onset of infarction and lasts longer than LDH; this test has a sensitivity similar to CPK-MB fraction and better than LDH.

For the diagnosis of acute myocardial infarction even earlier than detectable by troponin levels, myoglobin can be tested.

Elevated levels of myoglobin can be detected around 2 hours after the onset of infarction, but this has only about 60% specificity for the heart.

A new type of test being evaluated for the diagnosis of acute myocardial infarction is CPK MB isoform assay, which has a 96% sensitivity and 93% specificity for infarction within 6 hours of onset of chest pain.

The combination of CPK MB and troponin testing can have even higher sensitivity and is used for the purpose of  "ruling out" myocardial infarction.

Summary of pathologic findings:

The anatomic pathologic diagnosis of acute myocardial infarction at autopsy is based on gross and microscopic features.

Acute myocardial infarction up to 12 hours old is associated with minimal gross pathologic findings. 

Over the period of 12-24 hours following infarction the myocardium manifests progressive pallor.

During the period of 2-4 days following infarction, the dead muscle becomes yellow and softened.

 4-10 days following infarction it develops a hyperemic border and a softened yellow shrunken depressed center.

Thin wavy myocytes are the earliest light microscopic finding of acute myocardial infarction.

It is visible one hour following the onset of infarction.

Coagulation necrosis, characterized by hypereosinophilia  and nuclear pyknosis, followed by karyorrhexis, karyolysis, total loss of nuclei and loss of cytoplasmic cross-striations, is generally first visible in the period from 4-12 hours following infarction.

Necrotic myocytes may retain their striations for a long time.

Neutrophilic infiltration (acute inflammation), edema and hemorrhage are also first visible at 4-12 hours but generally closer to 12 hours.

Acute inflammation is generally present in a narrow band of the periphery at 24 hours, in a broad band of the periphery at 48 hours and tends to be maximal around 72 hours, with extensive basophilic debris from degenerating neutrophils.

Infiltration by macrophages, lymphocytes, eosinophils, fibroblasts and capillaries begins around the periphery at 3-10 days.

 

                                   

Further reading:

Thrombus age, clinical presentation, and reperfusion grade in myocardial infarction.

Endocardial tears and rupture tracts of left ventricular ruptures during acute myocardial infarction: An autopsy study of 50 out-of-hospital sudden death cases.

Postmortem unenhanced magnetic resonance imaging of myocardial infarction in correlation to histological infarction age characterization.

Cardiotrophin-1 predicts death or heart failure following acute myocardial infarction.

Cardiac markers and their point-of-care testing for diagnosis of acute myocardial infarction.

Cardiogenic shock continues to be the most serious complication of the acute myocardial infarction.

Cardiac S100A1 protein levels determine contractile performance and propensity toward heart failure after myocardial infarction.

Oxidative stress as the leading cause of acute myocardial infarction in diabetics.

Absolute neutrophil counts and fibrinogen levels as an aid in the early diagnosis of acute myocardial infarction.

Serum markers in the emergency department diagnosis of acute myocardial infarction.

Early diagnostic efficiency of cardiac troponin I and Troponin T for acute myocardial infarction.

Leukocytosis: a new look at an old marker for acute myocardial infarction

The pathology of acute myocardial infarction: definition, location, pathogenesis, effects of reperfusion, complications, and sequelae.

June 2014

Dr Sampurna Roy  MD

Consultant  Histopathologist (Kolkata - India)

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