Understanding, Posterior Myocardial Infarction: The Hidden STEMI.

Dr. Zayed | Published : 28, April 2025.

Introduction

Myocardial infarction (MI), commonly referred to as a heart attack, is a life-threatening condition caused by the interruption of blood flow to the heart muscle, resulting in tissue necrosis. Inferoposterior myocardial infarction, a subtype of MI, involves the inferior (lower) and posterior (back) walls of the left ventricle. This condition poses unique diagnostic challenges due to the limitations of standard electrocardiographic (ECG) techniques and the potential for atypical clinical presentations. This blog provides an in-depth exploration of posterior MI and its spreading variants (Lateral and posterior wall), covering its anatomy, pathophysiology, clinical presentation, diagnostic approaches, prognosis and management strategies.

Anatomy and Pathophysiology

The left ventricle of the heart is anatomically divided into anterior, inferior, lateral, and posterior walls, each playing a critical role in cardiac function. The inferior wall forms the lower surface of the heart, while the posterior wall is located at the back, adjacent to the diaphragm. These regions are primarily supplied by the right coronary artery (RCA) or the left circumflex artery (LCx), depending on 'coronary dominance'. In approximately 70% of individuals, the RCA gives rise to the posterior descending artery (PDA), which perfuses the posterior wall. In 10%, the LCx supplies the PDA, and in 20%, both arteries contribute in a codominant pattern/mixed coming from both left circumflex and right coronary artery.

Posterior MI occurs when an occlusion, typically due to atherosclerotic plaque rupture or thrombosis, disrupts blood flow in the RCA or LCx, leading to ischemia and infarction of posterior walls, and can also involve inferior surface. This dual involvement often results from a proximal occlusion, affecting a larger myocardial territory and increasing the risk of complications compared to isolated posterior MI.

The pathophysiology involves a cascade of events: reduced oxygen delivery leads to myocardial ischemia, followed by necrosis if blood flow is not restored. This can impair the ventricle’s ability to pump effectively reducing the cardiac output, potentially causing heart failure or arrhythmias. The involvement of the posterior wall, which is less directly monitored by standard diagnostic tools, adds complexity to timely diagnosis.

Clinical Presentation

The clinical presentation of inferoposterior MI can vary widely. Classic symptoms include chest pain or pressure, but atypical presentations are common, particularly in older adults, women, and individuals with diabetes. For instance, patients may experience epigastric pain, nausea, diaphoresis, or fatigue without chest pain, as noted in a case where a patient presented with these symptoms alongside coronary disease risk factors. Such atypical symptoms necessitate a high index of suspicion, especially in patients with risk factors for coronary artery disease (CAD), including hypertension, hyperlipidemia, smoking, or diabetes.

The presence of these risk factors, combined with any symptoms suggestive of acute coronary syndrome (ACS), warrants immediate investigation. Failure to recognize atypical presentations can delay diagnosis and treatment, increasing morbidity and mortality.

Electrocardiographic Diagnosis

Diagnosing inferoposterior MI is challenging because the standard 12-lead ECG does not directly visualize the posterior wall of the left ventricle. Instead, indirect signs in the anterior precordial leads (V1-V3) are used to infer posterior wall involvement.

ECG diagnostic criteria to Diagnose Posterior MI Include:

NSTEMI denoting posterior infarction in V2

Horizontal ST-segment depression in leads V1-V3: These are reciprocal changes reflecting ST-segment elevation in the posterior wall, which would be visible in posterior leads (V7-V9).
Tall, broad & dominant R waves in leads V1-V3: These represent reciprocal changes to Q waves in the posterior wall, indicating myocardial necrosis.
Upright T-wave which is the mirror image of T-wave inversion of infarcted myocardium.

To make this better understand this relationship, we inverted the ecg to show you how it looks in extended leads (if taken)

Reciprocal relationship between the ECG changes seen in STEMI and those seen with posterior infarction

Isolated posterior MI, which is rare (5-10% of all MIs), standard ECGs may only show anterior lead changes without inferior or lateral involvement. To confirm the diagnosis, additional posterior leads (V7, V8, V9) placed on the patient’s back are recommended. These leads can reveal ST-segment elevation for >0.5mm or Q waves, providing direct evidence of posterior wall infarction. The use of posterior leads is particularly crucial because isolated posterior MI is frequently missed, contributing to delayed treatment which resulted in spreading of infarct in lateral, inferior and medial superior wall's. a patient exhibited ST-segment depression in V1-V3 with tall R waves in V2 and V3, alongside subtle ST-segment changes in leads III and aVF, consistent with inferoposterior MI. A critical diagnostic clue is that prominent R waves and ST-segment depression in the septal and anterior precordial leads (V1, V2, and/or V3) strongly suggest acute posterior MI.

Table: ECG Findings in Inferoposterior MI

Lead	Finding	Significance
V1-V3	ST-segment depression	Reciprocal change to posterior wall ST elevation
V1-V3	Tall R waves	Reciprocal change to posterior wall Q waves, indicating necrosis
II, III, aVF	ST-segment elevation	Indicates inferior wall infarction, often due to RCA occlusion
V7-V9 (posterior)	ST-segment elevation, Q waves	Direct evidence of posterior wall infarction with ST-segemnt elevation, used for confirmation.

Posterior Left Lead placement

Leads V7-9 are placed on the posterior chest wall in the following positions (see diagram Above):
V7 – Left posterior axillary line, in the same horizontal plane as V6
V8 – Tip of the left scapula, in the same horizontal plane as V6
V9 – Left paraspinal region, in the same horizontal plane as V6

Management

The management of inferoposterior MI aligns with evidence-based guidelines for acute coronary syndromes, as outlined in the 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes. Key therapeutic strategies include:

Antiplatelet Therapy: Aspirin (loading dose of 162-325 mg) and a P2Y12 inhibitor (e.g., clopidogrel, ticagrelor) to prevent further thrombus formation.
Anticoagulation: Heparin or enoxaparin to reduce the risk of additional clotting.
Beta-Blockers: To decrease myocardial oxygen demand, provided there are no contraindications like bradycardia or hypotension.
Nitrates: For symptom relief and preload reduction, but used cautiously in cases of suspected right ventricular infarction due to the risk of hypotension.
Percutaneous Coronary Intervention (PCI): The preferred method for revascularization, aiming to restore blood flow within 90 minutes of first medical contact for ST-elevation MI (STEMI).

In cases of right ventricular infarction, which is common in RCA-related inferoposterior MI, volume expansion with intravenous fluids may be necessary to maintain cardiac output, while inotropic agents are considered for persistent hypotension.

Prognosis and Complications

Inferoposterior MI is associated with a higher risk of complications due to the involvement of multiple myocardial regions. Research indicates that posterior MI accompanies 15-20% of ST-elevation myocardial infarctions (STEMIs), often with inferior or lateral infarction, while isolated posterior MI accounts for 5-10% of cases. The larger myocardial territory involved increases the risk of:

Right Ventricular Infarction: Occurs in up to 50% of inferoposterior MI cases, particularly with RCA occlusion, leading to elevated jugular venous pressure, hypotension, or shock.
Left Ventricular Dysfunction: Due to extensive myocardial damage, increasing the risk of heart failure.
Arrhythmias: Including atrioventricular block, ventricular tachycardia, or fibrillation. Inferior MI scars may be more arrhythmogenic than anterior ones due to preserved sympathetic nerve endings in the anterior wall, which can trigger catecholamine-mediated ventricular arrhythmias.

The prognosis for inferoposterior MI is generally worse than for isolated inferior MI but may be less severe than extensive anterior MI. However, the risk of complications, such as right ventricular dysfunction or arrhythmias, underscores the need for vigilant monitoring and long-term management. Early revascularization and adherence to guideline-directed medical therapy significantly improve outcomes.

Conclusion:

Posterior myocardial infarctions (MIs) present a diagnostic challenge, as the characteristic ST-segment elevations typically associated with acute infarction may be absent from the standard 12-lead electrocardiogram (ECG) and often misclassified as Anterior wall NSTEMI delaying reperfusion procedures. Instead, these infarctions often manifest as tall R waves and horizontal ST-segment depressions in leads V1 and V2, which represent reciprocal changes to the primary Q waves and ST elevations that would be recorded directly over the posterior myocardium. During the evolution of posterior MIs, deep T wave inversions may develop in the posterior leads, while the anterior precordial leads (particularly V1–V2) may exhibit reciprocal findings such as tall, upright T waves. In most cases, posterior infarction is accompanied by involvement of adjacent myocardial territories. Extension into the lateral wall of the left ventricle results in corresponding changes in lead V6, whereas extension into the inferior wall results in abnormalities in leads II, III, and aVF. Due to the frequent overlap of inferior and posterior infarction patterns, the term "inferoposterior infarction" is often employed when the ECG exhibits features suggestive of involvement of either or both regions.

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