Acute Myocardial Infarction on ECG

Basic principles of ECG interpretation in myocardial infarction

Electrocardiographic diagnosis is based on two fundamental mechanisms: topographic localization and the phenomenon of reciprocity.

• Direct signs. Specific changes in the curve's shape are recorded strictly in the leads positioned over the developing necrosis zone. The main marker of acute injury is pathological elevation (rise) of the ST segment.
• Reverse (reciprocal) changes. Leads reflecting the heart wall opposite to the damaged one demonstrate a mirror image. If an anterior wall infarction shows elevation in the chest leads, the inferior wall leads (II, III, aVF) will predictably show ST-segment depression (reduction).

Over time, myocardial infarction undergoes a predictable evolution: the ST segment gradually returns to the isoelectric line, and the structure of the QRS ventricular complex changes irreversibly depending on the depth of tissue death.

Chronology of changes (using anterolateral infarction as an example)

The dynamics of an extensive transmural lesion are best tracked through time intervals starting from the appearance of the first symptoms.

1. Hyperacute stage (1 hour from pain onset). Early signs of acute ischemia and massive injury appear. On the ECG, this looks like pronounced ST-segment elevation. Often the elevation is so large that it merges with the T wave, forming a characteristic monophasic curve.
2. Acute and subacute stages (24 hours). The necrosis zone begins to form. ST elevation may still persist, but pathological changes in the QRS complex start to appear.
3. Scarring stage (10 days). Changes consolidate. A persistent pathological Q wave forms, indicating the replacement of muscle tissue with a connective tissue scar.

Topographic diagnostics of left ventricular lesions

By analyzing 12 standard leads during sinus rhythm (when heart rate is normal and the P wave is positive in lead II), the anatomical localization of the lesion can be determined with high precision.

• Leads V1–V3: Signs in this zone, especially the formation of a QS complex (deep Q wave with no R wave), indicate an anteroseptal lesion and transmural necrosis of the interventricular septum.
• Lead V4: The appearance of a pathological Q wave here indicates involvement of the left ventricular apex.
• Leads I, aVL, V5, V6: ST elevation in these leads indicates the spread of ischemic injury to the lateral wall.

The combination of these signs along with reciprocal ST depression in leads II, III, and aVF allows for a precise diagnosis: acute antero-extensive myocardial infarction with ST elevation (STEMI).

Cardiac MRI with gadolinium: confirmation of ECG findings

To determine the extent of the lesion more precisely, especially after endovascular procedures on coronary arteries, cardiac MRI (CMR) with late gadolinium enhancement is used.

• Pathophysiology: The contrast agent has extracellular distribution properties. In necrotic myocardium, its volume is maximized, causing a pronounced shortening of the T1 relaxation time compared to viable muscle tissue. Enhancement typically localizes subendocardially within the perfusion bed of the occluded artery.
• Microvascular obstruction: If persistent ST elevation and positive T waves remain in leads with the necrotic QS complex on the 3rd day post-stenting, it signals a lack of tissue perfusion. On MRI, this phenomenon is confirmed by the presence of dark unenhanced areas within the bright infarction zone.

Assessment of tissue viability: myocardial salvage index

For patient prognosis, it is critically important to assess what volume of ischemic tissue was successfully salvaged. To this end, the myocardial salvage index (Myocardial Salvage Index) is calculated.

The metric is calculated by mathematically comparing the area of gadolinium enhancement (actual necrosis zone) with the area of myocardial edema (initial area at risk).

If blood flow was restored as quickly as possible, an aborted myocardial infarction (Aborted myocardial infarction) may occur. In such a clinical situation, the edema zone is visualized on MRI, while contrast enhancement (necrosis) does not occur. The salvage index in this case reaches 100%, which is the best prognostic marker for the patient.

Class and exam questions

What else to study on this topic

• Characteristics of monophasic curve formation upon fusion of elevated ST and the T wave
• The association of proximal left anterior descending (LAD) occlusion with anteroapical infarction
• Diagnostic role of leads I, aVL, II, III, and aVF in identifying lateral and inferior necrosis
• Mechanism of gadolinium chelate distribution and T1 relaxation time shortening in injured myocardium

Other topics in the "Cardiovascular system" section

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.