Myocardial Infarction (MI)

Myocardial Infarction (MI)

Myocardial infarction (MI), also familiar as heart attack, is the death of cardiac muscle due to prolonged severe Ischaemia. The most common clinical features of Myocardial Infraction (MI) is sudden, severe, central, compressive chest pain which is usually diffuse. The pain radiates to the left shoulder, left jaw or back. The discomfort may typically feel like heartburn in case of inferior MI.

In majority cases, cardiogenic shock following acute myocardial infarction (MI) is due to left ventricular dysfunction. Howbeit it may also be due to the infraction of the right ventricle, or due to variety of mechanical complications, including cardiac tamponade (due to infringement and rupture of the free wall), an acquire ventricular septal defect, and acute mitral regurgitation.

Types of Myocardial Infarction (MI)

Transmural: Infraction involving the full or nearly full thickness of the ventricular wall in the distribution of a single coronary artery.

Subendocardia (non-transmural) Infract: Constituents an area of Ischaemic necrosis limited to the inner one third to one half of the ventricular wall.

Clinical features of Myocardial infarction (MI)


  • Prolonged cardiac pain: chest, throat, arms, epigastrium or back.
  • Anxiety and fear of impeding of death.
  • Nausea and vomiting
  • Breathlessness
  • Collapse/syncope


  • Signs of sympathetic activation: pallor, sweating, tachycardia.
  • Signs of vocal activation: vomiting, bradycardia
  • Signs of impaired myocardial function:
  • Hypotension, oliguria, cold peripheries.
  • Narrow pulse pressure.
  • Patient may have Raised jugular venous pressure.
  • Third heart sound,
  • Quiet first heart sound.
  • Diffuse apical impulse.
  • Lung crepitations.


The following sequence of events is considered most likely:

  • The first event is a sudden change in an atheromatous plaque, which may consist of intraplaque haemorrhage, erosion or ulceration or rupture of fissuring.
  • Exposed to subendothelial collagen and necrotic plaque contents, platelets adhere become activated, release their granule contents, and aggregate to form microthrombi.
  • Vasospasm is stimulated by mediators released from platelets.
  • Tissue factor activates the coagulation pathway adding to the bulk of thrombus.
  • Frequently within minutes, the thrombus evolves the completely occlude the lumen of the vessels.

Characteristics of chest pain of myocardial infarction (MI)

  • Site: centre of the chest.
  • Mode of onset: Takes several minutes or even longer to develop.
  • Character: Dull, constricting, choking or oppressive and is usually described as squeezing, crushing, burning or aching.
  • Radiation: It may radiate to either or both arms, to the throat or jaw and less commonly to the back or epigastrium.
  • Associated features: the feeling of breathlessness, autonomic symptoms such as profuse sweating, nausea, vomiting, palpitation, anxiety.
  • Timing/Duration: persists for a prolonged duration
  • Aggravating/exacerbating factors: it is precipitated by conditions which temporarily increase myocardial oxygen demand such as excretion, emotional excitement, cold weather, exercise after a meal.
  • Relieving factors: Myocardial infraction (MI0 is not usually relieved by rest or talking sublingual GTN (glyceryl-tri-nitrate).
  • Severity: it is usually severe, and the patient feels fear of death.

Assessment of risk factors of acute myocardial infarction (MI)

Myocardial infarction(Mi_ may occur at any age, but the frequency rises progressively with increasing age and when predispositions to atherosclerosis are present, such as


  • Age
  • Sex
  • Smoking
  • Alcohol
  • Hypertension
  • Diabetes Mellitus
  • Hypercholesterolaemia
  • Family history of Hypertension, Diabetes mellitus, Ischemic heart disease, hypercholesteremia
  • Type-1 personality
  • Physical inactivity
  • Dietary habit (deficient fresh food, vegetables and polyunsaturated fatty acids).
  • History of ischaemic heart disease.


  • Obesity
  • Hypertension
  • Xanthelasma-for dyslipidaemia


  • Blood sugar level
  • HbA₁c
  • Fasting lipid profile


  1. ECG; St elevation, followed by T-wave inversion, then pathological Q-wave development.
  2. Plasma biochemical marker
  • released within 3-6 hours, peak at about 36 hours and remain elevated up to 2 weeks.
  • Starts to rise at 4-6 hours, peak at about 12 hours, and falls to regular within48-72 hours.
  1. Other blood tests: leucocytosis, raised ESR and C-reactive protein.
  2. Chest X-ray: features of pulmonary oedema if LVF (left ventricular failure) develops.
  3. Echocardiography: detects infract associated regional wall motion abnormalities.
  4. Coronary angiography


  1. Contractile dysfunction
  2. Myocardial rupture
  3. Right ventricular infarction
  4. Infract extension
  5. Mural thrombi
  6. Ventrical aneurism
  7. Papillary muscle dysfunction
  8. Progressive late heart failure
  9. Arrhythmias
  10. Pericarditis
  11. Infract expansion

Treatment of acute myocardial infarction (MI)

  1. Immediate hospitalization where defibrillation facility is available.
  2. High flow-oxygen
  3. Intravenous access
  4. ECG monitoring
  5. Aspirin 300mg chewed and clopidogrel 300mg oral.
  6. Sublingual glyceryl trinitrate: table or spray (if systolic BP>110mmofhg).
  7. Intravenous analgesia: opiates (Morphine or pethidine) and anti-emetics.
  8. Beta-blockers (if no contraindication): for ongoing chest pain, hypertension, tachycardia
  9. Thrombolytic or anticoagulant:
  • If ST-elevated Myocardial Infarction (MI): thrombolysis with streptokinase 1.5 million U in 100ml of saline accustomed as an intravenous infusion over 1 hour. Alteplase and reteplase are the other options.
  • If non-ST-elevated myocardial infarction (MI): low molecular weight heparin (e.g., enoxaparin).
  1. If percutaneous intervention (PCI) is available, the patient should be prepared for that.
  2. Detection and management of acute complications, e.g. arrhythmias, cardiogenic shock, heart failure.
  3. Coronary bypass surgery when indicated.

Late management of Myocardial Infraction (MI)

  1. Risk stratifications and further investigation.

2. Lifestyle modification:

  • Cessation of smoking
  • Regular exercise
  • Weight control
  • Must avoid red meat, the yolk of egg and alcohol
  • Limitations of the extra table of salts
  • Avoidance of high calorie and fatty diet
  • Plenty of green leafy vegetables, fruits
  • Sound sleep


Myocardial Infarction (MI) occurs when there is a lack of blood supply to the heart muscles. A heart muscle needs a good blood supply to keep it healthy. As we get older, the smooth arteries that supply the blood to the heart can become blemished and narrow due to building up of fatty materials, which is called plague. Myocardial infarction (MI) is something called a heart attack, acute myocardial infarction, coronary occlusion or coronary thrombosis.

Disclaimer: The information in this article is only for educational purpose, not for treatment purpose. The myocardial infarction is one of the emergency medical condition. If you feel any of these symptoms, please do visit your nearest hospital as soon as possible.


Dr Aadarsh Yadav

Dr Adarsh Yadav is a registered medical expert currently is a medical officer at the department of paediatrics at Scheer memorial Adventist hospital, kavre, Nepal. He had been a very well trained medical practitioner, and apart from his medical practice, he had been a member of different health camps organizing blood donation camps in Bangladesh just during his internship.

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