Cardiac Path Online
Pathology of Myocardial Infarction
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.
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).
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:
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.
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.
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.
1. Chest pain- 20-30% does not cause chest pain, common in patients with diabetes mellitus, hypertension, and 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
iii) 10-20% patients recover with no complication.
iv) Early restoration of blood flow by thrombolysis or balloon angioplasty provides better prognosis.
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.
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