Clinical Science: Medicine - Cardiology

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Quick Reference To MYOCARDIAL INFARCTION (MI)

Author: Musab T. Ejami, MBBS, Faculty Of medicine, University Of Al-Zaiem Al-Azhari

Epidemiology:

* The Most common cause of death in the U.K.
* There are approximately 300,000 new cases per year.

Pathophysiology:

* The underlying pathology is atherosclerosis, MI occurs when there is a sudden dramatic occlusion of a major coronary artery due to thrombosis, hemorrhage or lodging emboli.

Pathology:

* The myocardium becomes swollen & pale after 6 hours
* Deep red necrotic tissue develops afterwards.
* After few weeks inflammatory reactions develop and the infracted tissue turns gray, gradually forms a thin fibrous scar.
* Remodeling of the affected ventricle with/without formation of ventricular aneurysm may develop.

Clinical Features:
* Central Chest pain, which occurs suddenly without an obvious precipitating factor, stress & excretion, may play a role but it may occur at rest and tends to persist for hours (sometimes until diamorphine is given), the pain radiates to the same sites as anginal pain, and has the same character except that it is more severe, and the patient may suffer from the feeling of impeding death.
* The pain may be accompanied by dyspnoea and signs of sympathetic & parasympathetic activation:
- Sweating.
- Nausea.
- Vomiting.

Physical findings are minima (unless complications occur), they may include:
* Pallor, cold extremities, Hypotension, tachycardia (or bradycardia), and raised JVP and other signs of cardiogenic shock.
* A fourth heart sound.
* A modest fever (up to 38oC) due to myocardial necrosis may occur over the course of the first 5 days.

Notes:
* Not all MI attacks are symptomatic more than 20% of MI episodes occur without pain, the so-called “silent myocardial infarction”. This more common in elderly and diabetics, probably due to neuropathy.
* Cardiogenic shock develops when there is loss of more than 40% of the LV myocardium. Clinical cardiac failure results when 25% of the LV myocardium is lost.

Investigations:

1- ELECTROCARDIOGRAM (ECG):

ECG changes of MI are manifested in 3 main points:
* Development of Q-waves: Q waves are negative deflections that start the QRS complex and which are found normally in leads aVR & V1. They are broad (>1mm), deep (>2mm or more than 25% of the amplitude of the following R wave).
* Development T-waves changes: which is a transient change occurring due to myocardial strain and ischemia.
* Development of ST-segment changes: which is a transient change occurring due to myocardial strain and ischemia.

Hence these changes, individually or collectively can be caused by other conditions rather than MI (look at the following table), it should be remembered that it is the evolution of these changes not their occurrence that makes the diagnosis of MI not their presence.
 

Table 1: Conditions other than MI that cause mimicking ECG changes
Change in:	Q-waves	ST-Segment	T waves
Examples of Others conditions:	LBBB V. Tachycardia WPW	LBBB. LV hypertrophy with strain. Electrolyte imbalance. Drugs.	hyperkalemia

 
On the basis of the presence of Q-waves in the ECG, MI can be classified into:

• Q-waves infarcts

• Non-Q-waves Infarcts.
  
  It was long believed that Q-waves infracts are caused by Full-thickness myocardial infraction, while Non-Q-waves infarcts are caused by subendocardial infarcts; however studies showed that this does not always hold true.
  
  Q-waves infarcts:
  In the first few minutes after infarction, hyperacute T waves followed by an elevated S–T segment develop in the leads “looking” at the infracted area, hours afterwards Q-waves start to develop and T-waves may become inverted, and, at this time the S-T segment starts to return to baseline, but may sometimes persist, days afterwards T-waves may become terminally inverted or sometimes return to normal, and S-T segment may return usually but occasionally may remain elevated. Thus the presence of prominent Q-waves with or without inverted T-waves indicate old myocardial infarction, while an elevated S-T segment usually indicates a recent MI.
  Posterior MI has a little different pattern, they appear as reciprocal mirror image for the anterior leads, thus the normal pattern of inverted T-waves, S-T segment elevation and Q-waves appear as: tall T-waves, S-T segment depression & R waves.
  
  
  (click to enlarge)
  Figure 1: Evolving early ECG changes in acute anterior MI:

  • S-T segment elevation in V2.

  • Inverted T waves in lead V2.

  
  Non-Q Wave Infarcts:
  In this type of infarction typical Q-wave changes do not occur, S-T segment & T wave changes are the only ECG features present. Always look for:
  * S-T segment depression (that is because the infarct is subendocardial), and sometimes elevation.
  * T-wave inversion
  The changes may be widespread not confined to a specific area (i.e. seen all leads).
  
  Anatomical Classification of MI based on the ECG:
  Since the change in ECG is manifested in the leads that face the infarct, the diagnosis of inferior MI, anterior MI and so on is based on the ECG finding in the involved leads:
  * Anterior: leads V2 – V5.
  * Anteroseptal: V1 – V3.
  * Anetrolateral: V4-V6, lead I, Lead aVL.
  * Lateral: I,II and AVL
  * Inferior: II,III and aVF
  * Posterior: V1, V2 (reciprocal)
  * Subendocardial: any lead.

Done only in specialized centers equipped with the trained staff. Usually combined with PTCA, to diagnose vessel disease, it is indicated for those under 50 years and whom diagnosis is uncertain. It is also used to evaluate the patents prior to surgery.

Diagnosis of Myocardial Infarction:
The diagnosis of MI requires at least 2 of the following criteria:
* A typical history of ischemic chest pain.
* Evolving ECG changes.
* A rise and fall in cardiac enzymes.

Immediate Management of Acute MI:

Myocardial infarction is a medical emergency that needs rapid action, admission & CCU monitoring
* Oxygen by mask 60 – 100 % (unless COPD).
* Diamorphine 5- 10 mg I.V. (pain relief).
* ECG monitoring.
* Thrombolytic therapy:
When administered after less than 12 hours of the onset of MI, reduces mortality rate up to 50%, agents include:
- Streptokinase 1.5 million units/ 100ml 0.9% saline I.V. over one hour + aspirin 160 mg/day.
- Other agents include: urokinase, t-PA & anistreplase (APSAC).
- Heparin I.V. 5000 i.u at start then 1000 i.u. for 24 hours may also be added.

 

Table 2: Criteria for thrombolysis in acute MI Indication

Indications: Chest pain consistent of MI within 12hrs. ST-segment elevation (>1mm in 2 or more contiguous leads. New LBBB Contra-indication.

Contraindications: Stroke or active bleeding in last 2 months. Systolic pressure >200mmHg Proliferative diabetic retinopathy. Pregnancy.

Relative Contraindications Prolonged or traumatic CPR. Recent (>2 weeks) surgery or trauma. Known bleeding diathesis or current use of anticoagulants.

* Anti-anginal therapy:
- Aspirin (crushed) 150 - 300 mg/day.
- Isosorbide dinitrate (isordil, sorbinat) 10 mg orally, or 5mg sublingual.
- B-Blocker, e.g. Atenolol 50 – 100 mg or metoprolol 5 – 10 mg (avoid in COPD, cardiogenic shock, heart block & sever CHF).
* Primary PTCA: especially after less that 6 hours has a great effect. PTCA has become a medical procedure and many specialized centers worldwide are preferring it to thrombolytic therapy, indications for PTCA are:
1. Contraindication for thrombolytic therapy.
2. Failure of Thrombolytic Therapy (25% of patients)
3. When initial ECG changes are equivocal (because it gives the chance to confirm or reject the diagnosis based on radiographic evidence.
* Emergency CABG:
It is only indicated when both PTCA & thrombolytic therapy have failed, yet it carries a high mortality rate.
Non-emergency CABG is accepted when there is:
- Three vessel disease, with post MI angina.
- 2 vessel disease involving LAD.
- 2 vessel disease with poor LV function.

Further management & follow up of MI:
Concentrates on three goals:
* Manage the complications.
* Reduce the like hood of future infarcts.
* Prevent additional complications.

Further management and follow up involves:
* Monitoring in CCU for at least 48 hours (risk time for arrest and arrhythmia).
* Aspirin 150 - 300mg in daily bases (unless contra-indicated).
* B-Blockers (unless contraindicated, e.g. COPD): they reduce the mortality by 25%.
* ACE inhibitors for those with evidence of pulmonary edema.
* Early mobilization, Rehabilitation and risk factor modification.
* Regular follow up is very important

Complications:
* Ventricular extrasystole
* Ventricular tachycardia
* Ventricular fibrillation.
* Atrial fibrillation
* Sinus bradycardia.
* Sinus tachycardia.
* Conduction disturbance.
* Cardiogenic shock.
* Thromboembolism.
* Pericarditis.
* Post myocardial infraction syndrome (dressler’s syndrome)
* Left ventricular aneurysm.
* Cardiac failure.
* Valvular dysfunction.
* Sudden cardiac death.


References and resources:

1- A.J.Camm in: cardiovascular disease, Kumar & clarck clinical medicine 4th edition.
2- Making sense of the ECG.
3- W.Bruce Fye, MD: Acute myocardial Infarction: in ACCSAP CD-ROM 1997/1998.
4- Oxford’s Handbook of medicine.