Myocardial infarction

Myocardial infarction (MI or AMI for acute myocardial infarction), commonly known as a heart attack, occurs when the blood supply to part of the heart is interrupted causing some heart cells to die. This is most commonly due to occlusion (blockage) of a coronary artery following the rupture of a vulnerable atherosclerotic plaque, which is an unstable collection of lipids (like cholesterol) and white blood cells (especially macrophages) in the wall of an artery. The resulting ischemia (restriction in blood supply) and oxygen shortage, if left untreated for a sufficient period of time, can cause damage and/or death (infarction) of heart muscle tissue (myocardium).


Volume of myocardium at risk depends on
  • Size and territory of the vessel
  • Collateral blood supply
  • Coronary perfusion pressure
  • Time from onset of occlusion

The thrombus often undergoes spontaneous lysis over the course of the next few days, although by this time irreversible myocardial damage has occurred. Without treatment the infarct-related artery remains permanently occluded in 30% of patients. The process of infarction progresses over several hours and therefore most patients present when it is still possible to salvage myocardium and improve outcome.


Chest pain is the characteristic symptom. It is usually a prolonged cardiac pain lasting more than 30 minutes over the central aspect of the chest with radiation towards the throat, arms, epigastrium or the back. The pain may be associated with nausea and vomiting, breathlessness, collapse or syncope.


MI can present with a variety of physical signs due to the cascade of changes occuring along with it.
  • Pallor, sweating and tachycardia due to sympathetic activation.
  • Vomiting and bradycardia due to vagal activation.
  • Hypotension, oliguria, cold peripheries, narrow pulse pressure, raised jugular venous pressure, third heart sound quiet first heart sound, diffuse apical impulse and lung crepitations are signs of impaired myocardial function.
  • Fever can occur due to underlying tissue damage

And complications of MI (mitral regurgitation, pericarditis etc.) if any present with their respective signs.


The earliest ECG change is usually ST segment elevation. Later on there is diminution in the size of the R wave, and in transmural (full thickness) infarction, a Q wave begins to develop. Subsequently, the T wave becomes inverted because of a change in ventricular repolarisation; this change persists after the ST segment has returned to normal. Their sequence is sufficiently reliable for the approximate age of the infarct to be deduced.


The ECG changes are best seen in the leads that 'face' the infarcted area.

  1. Anteroseptal infarction- leads from V1 to V4
  2. Anterolateral infarction- V4 to V6, in aVL and in lead I
  3. Inferior infarction- II, III and aVF, while at the same time leads I, aVL and the anterior chest leads may show 'reciprocal' changes of ST depression.
  4. Infarction of the posterior wall of the left ventricle does not cause ST elevation or Q waves in the standard leads, but can be diagnosed by the presence of reciprocal changes (ST depression and a tall R wave in leads V1-V4)

Some infarctions (especially inferior) also involve the right ventricle; this may be identified by recording from additional leads placed over the right precordium.

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