ECG is a cornerstone in the diagnosis and management of cardiovascular diseases. Among its many features, the elevation of the ST segment is most famously associated with ST-segment elevation myocardial infarction (STEMI), a life-threatening event requiring swift intervention. However, a myriad of other conditions can also lead to ST segment elevation, making accurate diagnosis a challenging endeavor. Clinicians must be vigilant in discerning between STEMI and its mimics to ensure appropriate and timely management.
Left Bundle Branch Block (LBBB):
LBBB can cause secondary ST-T changes, with ST-segment elevations in V1-V2 and ST-segment depressions and T-wave inversions in leads V5, V6, aVL, and limb lead 1. This can make recognition of an acute STEMI challenging. In LBBB, the modified Sgarbossa criteria can be used to increase the predictive value for or against myocardial infarction.
Benign Early Repolarization (BER):
Benign early repolarization is a common variant which causes ST elevation on an ECG, typically with a concave upward ST segment and absence of reciprocal changes suggestive of ischemia.
Left Ventricular Hypertrophy (LVH):
Left ventricular hypertrophy can cause ST elevation on an ECG, particularly in leads V1-V3. This is due to repolarization abnormalities caused by the thickening of the left ventricle.
Hyperkalemia can cause ST elevation due to depolarization of the resting membrane potential and activation of inward rectifier potassium channels, leading to changes in the myocardial action potential.
Brugada syndrome is a genetic disorder that can cause ST-segment elevation, particularly in leads V1-V3. The ST-segment elevation is thought to be due to an imbalance of currents in the heart caused by mutations in genes that encode for ion channels.
Pericarditis can cause ST-segment elevation on an ECG due to inflammation of the pericardium. The ST-segment elevation is typically diffuse and concave upward and must be distinguished from myocardial infarction.
The Osborn wave, also known as the J wave, is a positive deflection seen at the junction between the QRS complex and the ST segment. It is most commonly associated with hypothermia, but it can also be seen in other conditions, such as subarachnoid hemorrhage, brain injury, and ischemia. The Osborn wave is thought to be caused by an increase in the outward potassium current and a decrease in the inward calcium current, leading to delayed repolarization of the epicardial cells. This delayed repolarization causes a transmural voltage gradient that produces the ST-segment elevation seen on the ECG.
Hypercalcemia can cause ST elevation due to its effects on myocardial cell membrane potentials and increased myocardial contractility. The mechanism of hypercalcemia-induced ST-segment elevation is not fully understood, it can mimic acute coronary syndrome, leading to potential misdiagnosis.
Takotsubo cardiomyopathy can cause ST-segment elevation particularly in the anterior precordial leads. The ST-segment elevation is thought to be due to an increase in catecholamines, which can lead to myocardial stunning and microvascular dysfunction. Takotsubo cardiomyopathy is often referred to as "broken heart syndrome," it mirrors a STEMI but arises from emotional or physical stressors.
Aortic dissection can cause ST-segment elevation due to the involvement of the coronary arteries or the myocardium. The ST-segment elevation is typically seen in the leads corresponding to the affected coronary artery or myocardial segment.
Traumatic Brain Injury:
Traumatic Brain Injury can cause ST-segment elevation due to the release of catecholamines and increased sympathetic activity. Neurogenic stunned myocardium can mimic STEMI, leading to potential misdiagnosis.
Prinzmetal's angina, also known as variant angina, is caused by transient spasms of the coronary arteries, which can lead to ischemia in the heart muscle. The spasm of the coronary arteries can also cause ST-segment elevation. The ST-segment elevation in Prinzmetal's angina is typically seen in the leads corresponding to the affected coronary artery and is associated with multiple spasms involving different segments of the coronary arteries. The ST-segment elevation in Prinzmetal's angina is transient and reversible with vasodilators. Unlike acute STEMI, the ECG changes in Prinzmetal's angina are not usually associated with myocardial necrosis. It may be impossible to differentiate Prinzmetal's angina from acute STEMI based on the ECG alone.
Take Home Message:
In summary, ST segment elevation is not exclusive to STEMI; various conditions can trigger this ECG pattern. Accurate differentiation is vital for patient outcomes and resource use. Mistakes could lead to delayed STEMI treatment or unnecessary interventions with serious consequences.