Posterior Myocardial Infarction on ECG

Mechanism of Changes: Reciprocity Phenomenon

The basic principle of topographic ECG diagnosis of infarction is the evaluation of direct and indirect (reciprocal) signs of injury. Direct, specific changes are recorded in those leads whose electrodes lie directly over the necrosis zone.

However, the posterior wall of the heart is anatomically hidden from standard precordial electrodes. This is where the reciprocity phenomenon comes to the aid. Leads reflecting the heart wall opposite to the affected one (in this case, the anterior wall) record a mirror image of the electrical processes. The main rule: if the ST segment rises (elevation) in the real necrosis zone, it naturally decreases in the opposite leads.

Key ECG Markers of Posterior Necrosis

Posterior infarction develops when blood flow is impaired in the distal bed of the circumflex branch of the left coronary artery or in the right coronary artery. On a standard ECG, one should look for changes in the right precordial leads (V1–V3):

• ST-segment depression.
• Positive T wave, which stands out particularly clearly against the background of the depressed ST segment.

Important: Detection of these signs requires the mandatory recording of additional posterior leads (V7–V9). It is in these leads that direct ST elevation can be recorded and the diagnosis definitively confirmed.

Clinical Mask: Abdominal Form

In necrosis of the posterior wall (as well as the cardiac apex), infarction can present atypically, completely mimicking acute gastrointestinal pathology. This is the abdominal (gastralgic) form, which occurs with a frequency of 2–3%.

The clinical picture includes:

• Paroxysmal pain in the upper abdomen.
• Persistent hiccups and vomiting.
• Diarrhea and false urges (tenesmus).
• Profuse cold sweat.

The patient is often misdiagnosed with food poisoning, although the electrocardiogram at that moment shows an absolutely typical picture of acute myocardial infarction.

Differentiation from NSTE-ACS

Reciprocal depression in posterior MI must be distinguished from the direct manifestation of non-ST-segment elevation acute coronary syndrome (NSTE-ACS). The latter is characterized by the following signs in at least two contiguous leads:

1. Transient ST elevation lasting less than 20 minutes.
2. ST depression (downsloping or horizontal) with a depth of 0.05 mV (0.5 mm) or more.
3. T-wave inversion with a depth greater than 0.1 mV (1 mm) in leads with a dominant R wave (R/S ratio > 1).

Pronounced symmetric negative T waves (from 0.2 mV) in precordial positions are considered a high risk for ischemia. The absence of changes on a resting ECG does not rule out NSTE-ACS, so it is crucial to compare the current tracing with previous recordings.

Confirmation of Diagnosis by Cardiac MRI

For precise visualization of the affected myocardial volume (jeopardised myocardium), cardiac MRI (CMR) with late gadolinium enhancement is used. The contrast agent distributes in the extracellular space, and its volume is maximal precisely in the necrotic tissue.

Contrast accumulation in infarction is localized subendocardially and strictly corresponds to the arterial basin. Comparing the necrosis area with the total edema area (area at risk) allows for the calculation of the Myocardial Salvage Index (Myocardial Salvage Index). If necrosis has not had time to develop (aborted myocardial infarction), contrast does not accumulate, and the index reaches 100%, which has excellent prognostic value.

Class and exam questions

What else to study on this topic

• Stages of Q-wave myocardial infarction: hyperacute, acute, subacute, and scarred.
• Signs of microvascular obstruction on ECG and cardiac MRI.
• ECG mapping (35 leads) in suspected infarction and "silent" ECG.
• Clinical features of other atypical forms: asthmatic, cerebral, painless.
• Topographic diagnosis of extensive anteroseptal-apical myocardial infarction.

Other topics in the "Additional Topics" section

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