Severe chest pain with ST elevations and negative troponins is most consistent with which condition?

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Multiple Choice

Severe chest pain with ST elevations and negative troponins is most consistent with which condition?

Coronary vasospasm causing transient ischemia is the pattern here. When a coronary artery spasm abruptly narrows a vessel, it can produce acute chest pain and ST-segment elevations on the ECG during the episode, but because there isn’t sustained myocardial necrosis, troponin remains normal. This combination—transient ST elevations with a normal troponin—fits Prinzmetal angina (vasospastic angina) best. Think how this differs from other possibilities. In an acute STEMI, the injury is ongoing and a prolonged occlusion leads to myocardial cell death, so troponin rises and ST elevations tend to be persistent or evolve as the infarction progresses. In pericarditis, ST elevations can occur as well, but they’re typically diffuse across many leads (often with PR-segment depression) and the chest pain has a character and positional quality that differ from angina. Aortic dissection presents with sudden, severe, tearing chest pain often radiating to the back and hemodynamic clues; ECG changes aren’t the defining feature and troponin isn’t diagnostic. Managing a vasospasm episode with calcium-channel blockers and nitrates helps prevent recurrence, and avoiding triggers such as smoking or illicit stimulants is important. If symptoms persist or ACS cannot be ruled out, further evaluation is warranted.

Coronary vasospasm causing transient ischemia is the pattern here. When a coronary artery spasm abruptly narrows a vessel, it can produce acute chest pain and ST-segment elevations on the ECG during the episode, but because there isn’t sustained myocardial necrosis, troponin remains normal. This combination—transient ST elevations with a normal troponin—fits Prinzmetal angina (vasospastic angina) best.

Think how this differs from other possibilities. In an acute STEMI, the injury is ongoing and a prolonged occlusion leads to myocardial cell death, so troponin rises and ST elevations tend to be persistent or evolve as the infarction progresses. In pericarditis, ST elevations can occur as well, but they’re typically diffuse across many leads (often with PR-segment depression) and the chest pain has a character and positional quality that differ from angina. Aortic dissection presents with sudden, severe, tearing chest pain often radiating to the back and hemodynamic clues; ECG changes aren’t the defining feature and troponin isn’t diagnostic.

Managing a vasospasm episode with calcium-channel blockers and nitrates helps prevent recurrence, and avoiding triggers such as smoking or illicit stimulants is important. If symptoms persist or ACS cannot be ruled out, further evaluation is warranted.

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