ST-segment elevation myocardial infarction without culprit lesion-a case report picturing the challenging interplay of epicardial atherosclerosis and coronary artery spasm.

BACKGROUND

Approximately 5-15% of patients with acute coronary syndrome have myocardial infarction with unobstructed coronary arteries (MINOCA). Guidelines recommend invasive assessments to identify underlying causes for MINOCA such as coronary artery spasm (CAS), spontaneous coronary dissection, or microvascular disease as well as non-invasive assessments in search of myocarditis, takotsubo syndrome, or cardiomyopathies.

CASE SUMMARY

A 54-year-old male patient presented with ST-segment elevation myocardial infarction (STEMI). Upon arrival, ST-segment elevation and symptoms had ceased. Emergency coronary angiography showed diffuse epicardial atherosclerosis with stenoses in the distal left anterior descending coronary artery (LAD) and second diagonal branch (D2); however, no epicardial occlusion was seen. Left ventriculography showed no clear wall motion abnormalities. Based on these findings, intracoronary acetylcholine (ACh) testing in search of CAS was performed. At 200 µg ACh intracoronary ST-segment elevation and chest pain recurred. Angiography showed occlusive epicardial spasm in the LAD and D2. Based on studies where the tendency of epicardial CAS was linked with the presence of epicardial atherosclerosis, the decision was made to perform PCI in the LAD and D2. ACh re-challenge after intracoronary nitroglycerine revealed only very mild symptoms, no demonstrable epicardial CAS, and no ST-segment elevation anymore. Cardiac enzymes reached their peak on day one [creatine kinase max 262 U/L (norm < 190 U/L), maximum of high-sensitivity troponin T 269 pg/mL ( < 14 pg/mL)].

DISCUSSION

There is a broad spectrum of patients with STEMI without culprit lesion regarding the extent of epicardial disease. In cases with an unclear culprit lesion, other causes for the acute presentation such as CAS should be investigated in an ad hoc fashion. The interplay of epicardial atherosclerosis and CAS should receive more attention in future trials.