From the Guidelines
ST segment elevation in acute myocardial infarction occurs due to transmural myocardial injury caused by occlusion of a coronary artery, typically by a thrombus forming on a ruptured atherosclerotic plaque, leading to ischemia, injury, and necrosis of cardiac cells, and resulting in altered repolarization patterns and a current of injury that elevates the ST segment on the ECG. This process is supported by the pathogenesis of ST-segment elevation acute myocardial infarction, as described in the European Society of Cardiology's guidelines 1. The guidelines explain that most cases of STEMI are caused by an occlusion of a major coronary artery, usually due to physical disruption of an atherosclerotic plaque with subsequent formation of an occluding thrombus.
The mechanism of ST segment elevation can be further understood by considering the effects of coronary occlusion on the heart muscle. When a coronary artery becomes occluded, the heart muscle supplied by that artery loses its blood supply and oxygen, leading to ischemia and eventually necrosis of cardiac cells 1. The injured myocardial cells cannot maintain normal electrical activity, resulting in altered repolarization patterns. Specifically, the damaged cells develop a current of injury that flows between the injured and healthy myocardium. During electrical diastole (when the heart is at rest), this current flows toward the recording electrode, causing elevation of the ST segment on the ECG.
The location of the ST elevation on the ECG can also provide valuable information about the location of the occluded coronary artery. For example, ST elevation in leads II, III, and aVF suggests an inferior wall MI, typically from right coronary artery occlusion, while elevation in V1-V4 suggests an anterior wall MI from left anterior descending artery occlusion. This is consistent with the guidelines, which emphasize the importance of rapid and accurate diagnosis of STEMI to guide treatment decisions 1.
In contrast to the guidelines for management of acute coronary syndromes without persistent ST-segment elevation 1, the management of STEMI requires rapid and complete recanalization of the occluded coronary artery, either through fibrinolytic treatment or primary angioplasty. The guidelines for STEMI management are based on evidence from clinical trials and reflect the current understanding of the pathogenesis and treatment of this condition 1.
Overall, the ST segment elevation in acute myocardial infarction is a critical diagnostic sign that requires prompt attention and treatment to minimize morbidity and mortality. The guidelines provide a framework for understanding the pathogenesis of STEMI and guiding treatment decisions, and emphasize the importance of rapid and accurate diagnosis to improve patient outcomes 1.
From the Research
ST Segment Elevation in Acute Myocardial Infarction
The ST segment is elevated in acute myocardial infarction (AMI) due to the interruption of blood flow to the heart muscle, leading to ischemia and damage.
- The elevation of the ST segment is a key diagnostic feature of AMI, particularly in ST-segment elevation myocardial infarction (STEMI) 2.
- STEMI is caused by a complete thrombotic occlusion of an epicardial coronary vessel, resulting in significant morbidity and mortality 2.
- The American College of Chest Physicians recommends rapid evaluation for reperfusion therapy in patients with STEMI, including primary percutaneous coronary intervention (PCI) or fibrinolytic therapy 3.
Pathophysiology and Treatment
The pathophysiology of STEMI involves the formation of a thrombus in a coronary artery, leading to complete occlusion and subsequent ischemia and infarction of the heart muscle.
- Fibrinolytic agents, such as streptokinase, alteplase, reteplase, and tenecteplase, are used to dissolve the occluding thrombus and restore blood flow to the affected area 4, 5.
- Primary PCI is the preferred reperfusion strategy for STEMI, but fibrinolytic therapy is an important alternative when timely PCI is not possible 5.
- The initiation of reperfusion therapy, either through PCI or fibrinolysis, is critical in limiting myocardial ischemia and infarct size, and reducing the risk of post-STEMI complications and heart failure 2.