52. Clinicopathology of acute myocardial infarction

Last updated on May 18, 2019 at 10:50

Myocardial infarct

Acute myocardial infarct (AMI) always occurs due to an imbalance between perfusion and blood demand of myocardium, meaning it’s an ischaemic heart disease. It’s also an acute coronary syndrome. In more than 90% of cases is this discrepancy due to coronary artery disease. Most commonly will an already occlusive atherosclerotic plaque rupture, which exposes its thrombogenic surface. A thrombus will grow on the plaque, which occludes the artery further.

Some factors either increase the demand of the myocardium, or reduce the oxygen supply, which can aggravate the ischaemia:

  • Hypertrophy
  • Hypotension
  • Shock
  • Hypoxaemia

For an irreversible ischaemia to occur must there be at least 2-4 hours of ischaemia. The result is necrosis, a type of anaemic infarct. Necrosis always begins in the subendocardial myocardium and extends towards the epicardium, potentially becoming transmural if the ischaemia is severe enough. This is because the arteries lie on the epicardium, so the subendocardial myocardium is the least perfused region.

Causes other than coronary artery disease include:

  • Thrombus
  • Embolus
  • Vasculitis
  • Coronary spasm
Phases of myocardial infarct

The phases of myocardial infarct are best summed up in a table.

PhaseTime-frameMacroscopical characteristicsMicroscopical characteristicsPotential complications
Hyperacute phase0 – 12 hoursOnly visible with diaphorase reactionOedema, haemorrhageAcute left ventricular failure if 80% of myocardium is affected. Lethal arrhythmias, like ventricular fibrillation.
Acute phase1 – 2 daysYellowish, greyish. Clay-likeSigns of necrosis (no nuclei, eosinophilia)
Recent phaseDay 2 – week 1Same as above, but with reddish demarcation zoneNeutrophil and macrophage infiltration.Rupture of infarct, can cause pericardial tamponade. Rupture of papillary muscle causes acute mitral valve insufficiency. Fibrinous pericarditis.
Chronic (subacute) phaseMonths, yearsScar tissueFibroblast involvementAneurysm of the scar tissue. Thrombosis inside aneurysm, potential embolization.


Chronic ischaemic heart disease.

Diaphorase reaction. Note how a part of the myocardium isn’t stained.


The complications of acute myocardial infarct can be divided into an early group and late group.

  • Early (within 48 hours)
    • Sudden cardiac death
    • Arrhythmia
    • Acute left ventricular failure
    • Cardiogenic shock
  • Late (after 48 hours and long-term)
    • Rupture of the myocardial wall -> Pericardial tamponade
    • Rupture of papillary muscles -> Mitral regurgitation
    • Aneurysm of the myocardium
      • Thrombosis and embolism
    • Reinfarction
    • Pericarditis
    • Chronic ischaemic heart disease -> Heart failure
Diagnosis and treatment

Diagnosis is based on three factors:

  • ECG changes (mostly ST-elevation)
  • Characteristic chest pain
  • Troponin levels in blood

Any infarct can occur without any of the three, so a complete clinical picture based on multiple criteria must be drawn. Prinzmetal’s angina for example causes the same ECG changes, but no changes in troponin levels.

Treatment is based on trying to restore circulation as soon as possible; the earlier reperfusion the better. For this we can use:

  • Thrombolytic drugs like streptokinase or tPA can break down the thrombus
  • Inserting an inflatable balloon that dilates the occluded artery, done in percutaneous transluminal coronary angioplasty (PTCA, also called PCI)
  • Taking the great saphenous vein or internal mammary artery and connecting it to the coronaries and aorta, called coronary bypass surgery.

The goal of treatment in acute myocardial infarction is to salvage as much of the myocardium as possible, so tissue perfusion should be restored as early as possible. However, reperfusion can sometimes cause more bad than good when reperfusion injury occurs. This occurs by multiple factors:

Mitochondrial dysfunction occurs in the ischaemic myocardial cells. The mitochondrial membrane becomes more permeable, so osmotically activate components can enter the mitochondria and cause it to swell and burst. This releases mitochondrial contents that promote apoptosis.

During ischaemia will the intracellular calcium levels increase. After reperfusion will myofibrils contract uncontrollably, which can cause cytoskeletal damage and cell death.

During reperfusion will the ischaemic cells regain oxygen supply, but they’re so damaged that they use the oxygen to produce reactive oxygen species, which damages the cell membrane.

Leukocyte aggregation can occur during reperfusion, which can occlude the microvasculature and lead to the “no-flow” phenomenon. Platelet and complement activation also contribute to this phenomenon by damaging the endothelium.

Reperfusion arrhythmia is a potential complication of reperfusion, for unknown reasons. Reperfusion could induce dangerous arrhythmias like ventricular tachycardia and ventricular fibrillation.

Myocardial stunning is a phenomenon that may occur in myocardial cells that were ischaemic but reperfused before the ischaemia could irreversible damage the cell. In this postischaemic state will the affected myocardium be in a non-contractile state.

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51. Angina pectoris, chronic ischemic heart disease, sudden cardiac death

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53. Pathology of the valvular disorders (inflammatory and degenerative ones)

5 thoughts on “52. Clinicopathology of acute myocardial infarction”

    1. Do you have a source? I would love to agree with you but I’m not sure that’s correct.

      The lecture states that no macroscopical changes can be seen the first 12 hours, so I would say that the hyperacute phase lasts until then. However the lecture doesn’t clearly provide a table of the different phases, and neither does Robbins, so I’d love if you could provide a reliable source.

      1. In the notes from my teacher he stated that in the hyperacute phase, there are no microscopical or macroscopical changes as the signs of necrosis occur after 4 hours. So in the hyperacute phase the only way to check whether it’s undergone a MI would be the Diophorase reaction.. but then the acute phase would be 24 to 48 hrs that’s when we see signs of necrosis..
        Not really got a source other than what was said in class.

        1. But then what’s between hour 4 and hour 24? In my opinion should the phases be continuous, so it doesn’t make sense if the hyperacute phase ends at hour 4 and the next phase starts at hour 24.

          I’ll ask my teacher for clarification on Monday.

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