A myocardial infarction, commonly known as a heart attack, occurs when blood flow to a section of the heart muscle is severely reduced or stopped, causing tissue death, or necrosis. This tissue death is referred to as an infarct. The location of this damage heavily influences the severity of the event and the immediate prognosis. An anterior infarct refers to a heart attack specifically impacting the front wall of the heart.
Defining the Anterior Infarct
An anterior infarct, or anterior wall myocardial infarction (AWMI), is defined by the location of the heart muscle damage, which is the front wall of the left ventricle. The left ventricle is the heart’s strongest and largest chamber, responsible for pumping oxygenated blood out to the rest of the body. Damage to this wall significantly compromises the heart’s overall pumping function, or its contractility.
Because the left ventricle performs the majority of the heart’s work, the death of tissue in this area can lead to severe consequences. The resulting reduced ability to pump blood, known as left ventricular dysfunction, is a main reason why anterior heart attacks are associated with a higher rate of complications and mortality compared to heart attacks in other locations. The area of the heart involved can be extensive, affecting the front wall and the muscular wall separating the two lower chambers, known as the interventricular septum.
The Specific Cause: Blockage of the Left Anterior Descending Artery
The cause of an anterior infarct is almost always a blockage in the Left Anterior Descending (LAD) coronary artery. The LAD is a major branch of the left main coronary artery and is the largest of the coronary vessels. It supplies blood to the anterior, lateral, and apical walls of the left ventricle, as well as the anterior two-thirds of the interventricular septum.
Because of the extensive territory supplied by the LAD, its sudden occlusion can deprive a massive amount of heart muscle of oxygen. This leads to an extensive infarction and severe impairment of the heart’s ability to function, putting the patient at high risk for major complications.
The blockage typically forms when an atherosclerotic plaque, a fatty deposit, ruptures within the artery wall. The rupture exposes material that triggers the body’s clotting mechanism, causing a thrombus, or blood clot, to rapidly form and completely obstruct the vessel. This sudden stop of blood flow leads to the rapid onset of tissue necrosis characteristic of an anterior infarct. The severity of the damage is proportional to how close the blockage occurs to the start of the LAD artery, with more proximal occlusions affecting a larger area of the heart.
Recognizing the Signs and Symptoms
While many heart attacks present with classic symptoms, an anterior infarct often features a severe presentation due to the large amount of heart muscle involved. The most common symptom is a deep, crushing chest pressure or pain, known as angina, which can last for 30 minutes or more. This pain frequently radiates to the jaw, neck, left arm, or back.
Patients with an extensive anterior infarct often experience symptoms that reflect immediate heart failure. This includes profound and sudden shortness of breath, or dyspnea, as the damaged left ventricle struggles to pump blood effectively, causing fluid to back up into the lungs. Another common sign is marked diaphoresis, or intense sweating, often described as a cold sweat, along with pale skin.
The extensive damage to the left ventricle can also lead to cardiogenic shock, a life-threatening condition where the heart cannot pump enough blood to meet the body’s needs. Symptoms of shock include a rapid, weak pulse, a significant drop in blood pressure, and signs of poor tissue perfusion such as altered mental status. Cardiogenic shock is a complication frequently seen with large anterior infarcts, often associated with the loss of over 40% of the left ventricular muscle mass. Any suspicion of these symptoms warrants an immediate call for emergency medical services.
Diagnosis and Immediate Medical Response
The diagnosis of an anterior infarct begins immediately upon arrival at the hospital with two primary tools: the Electrocardiogram (ECG) and blood tests. An ECG should be performed within 10 minutes of a patient presenting with symptoms of a heart attack. The ECG measures the heart’s electrical activity and is used to identify a specific type of heart attack called an ST-segment elevation myocardial infarction (STEMI).
An anterior STEMI is characterized by changes in the electrical tracing, specifically an elevation of the ST segment in the chest leads, such as V1 through V6, which correspond to the anterior and septal walls of the heart. This finding confirms a complete, or nearly complete, blockage of a coronary artery, most often the LAD, requiring immediate intervention. Blood tests are simultaneously drawn to measure levels of cardiac biomarkers, such as Troponin.
Troponin is a protein released into the bloodstream when heart muscle cells are damaged or die. An elevated Troponin level confirms that myocardial injury has occurred, providing biochemical confirmation of the infarct. Once an anterior STEMI is diagnosed, the immediate medical response is focused on reperfusion therapy, which means restoring blood flow to the blocked artery as quickly as possible.
The preferred method of reperfusion is Primary Percutaneous Coronary Intervention (PCI), which involves a procedure like angioplasty to physically open the blocked vessel and often place a stent. The time from the patient’s arrival at the emergency department to the opening of the artery with a balloon or stent is tracked as the “door-to-balloon” (DTB) time. Current guidelines emphasize the need for this DTB time to be as short as possible, ideally 90 minutes or less, to minimize the extent of heart muscle damage. Following the successful opening of the artery, patients are monitored closely due to the high risk of severe complications, including dangerous heart rhythm disturbances, or arrhythmias.