An infarct, or myocardial infarction (MI), occurs when a lack of blood flow causes the death of heart muscle tissue. This blockage starves the affected area of necessary oxygen and nutrients. The term “inferior infarct” specifically identifies this injury as occurring in the lower wall of the heart. This location dictates the unique symptoms, risks, and recovery path associated with this common type of heart attack.
Location and Anatomical Significance
The inferior wall of the heart is its lower surface, resting directly upon the diaphragm. This surface is primarily formed by the muscular wall of the left ventricle, the heart’s main pumping chamber, with a smaller contribution from the right ventricle.
The integrity of the left ventricle’s inferior wall is important for overall function, as damage can reduce the heart’s ability to pump efficiently. This area also contains structures like the posteromedial papillary muscle, which helps secure the mitral valve and maintain proper blood flow direction.
The inferior wall is distant from the heart’s main electrical center, the SA node, but it is adjacent to the Atrioventricular (AV) node. The AV node coordinates the electrical signal between the upper and lower chambers of the heart.
The Artery Responsible for the Blockage
An inferior infarct results from a sudden and complete blockage in a specific coronary artery supplying the inferior wall. In the majority of individuals (about 80%), the blood supply to this region comes from the Right Coronary Artery (RCA).
The RCA gives rise to the Posterior Descending Artery (PDA), which directly feeds the inferior wall. The blockage usually begins when a cholesterol-rich plaque ruptures and triggers a blood clot, obstructing the artery and halting blood flow.
In a smaller portion of the population, the inferior wall is supplied by a branch of the Left Circumflex Artery (LCx), a variation known as left dominance. The RCA being the most frequent culprit explains the unique complications seen in inferior infarcts, as the RCA often supplies the heart’s electrical nodes.
Acute Symptoms and Diagnostic Confirmation
While intense chest pain is a common symptom of any heart attack, inferior infarcts often present with less classic symptoms that can be mistaken for a gastrointestinal issue. Patients frequently experience significant nausea, vomiting, or pain localized to the upper abdomen (epigastric pain). This atypical presentation is thought to be due to the inferior wall’s close proximity to the diaphragm, which can irritate the vagus nerve.
Doctors rely on two primary methods for acute diagnosis. The first is an Electrocardiogram (ECG), which measures the heart’s electrical activity. A characteristic finding is ST-segment elevation in leads II, III, and aVF, which electrically monitor the inferior surface of the heart.
The second method involves blood tests that check for elevated cardiac biomarkers, specifically troponin. Troponin is a protein released into the bloodstream when heart muscle cells are damaged or die, confirming that a heart attack has occurred.
Specific Risks and Recovery Outlook
The proximity of the inferior wall to the heart’s electrical wiring system creates unique immediate risks. The AV node, which controls the pace of electrical signals, often receives its blood supply from the RCA.
When the RCA is blocked, damage to the AV node can cause the electrical signal to slow down or stop, resulting in heart block or bradycardia (slow heart rate). A high-degree heart block is observed in up to 19% of patients with an acute inferior infarct.
Another concern is that in approximately 40% of cases, the damage extends to involve the right ventricle, making the patient sensitive to blood pressure drops.
Despite these immediate complications, the overall recovery outlook for an isolated inferior infarct is generally more favorable than for an infarct in the heart’s anterior wall. The mortality rate is typically low, ranging between 2% and 9% with timely intervention.