Subacute Thrombotic Occlusion and Spontaneous Recanalization of the Right Coronary Artery After Percutaneous Coronary Intervention for ST-Elevation Myocardial Infarction Visualized by Coronary Angiography and Cardiac Magnetic Resonance Imaging
A 58-year-old male was admitted to the emergency room with an acute inferior ST-elevation myocardial infarction (Figure 1). His coronary risk factors included arterial hypertension and hypercholesterolemia. Emergency percutaneous coronary intervention (PCI) was performed with stenting of the occluded right posterolateral branch with a 2.5×18 mm Zotarolimus-eluting stent (Medtronic, Minneapolis, Minn.) (Figure 1A and 1B). The left ventricular ejection fraction was 41% and the postinterventional TIMI flow was grade II with reduced flow of the entire right coronary artery (RCA) and persistent ST elevation within the inferior leads. The maximum creatine kinase level was 1863 U/L and peaked 36 hours after PCI. 99mTechnetium-sestamibi scans to assess coronary perfusion immediately before and 6 days after intervention (Figure 2) revealed no myocardial salvage subsequent to PCI within the inferior wall. Contrast-enhanced coronary magnetic resonance angiography with the use of 0.2 mmol/kg gadolinium-DTPA of the RCA 8 days after PCI revealed a signal void along the entire course of the RCA consistent with very slow flow or a proximal occlusion (Figure 3A). Delayed magnetic resonance imaging of the coronary vessel wall was normal and showed no hyperenhancement (Figure 3B), whereas hyperenhancement was visible in the inferior wall, which was in agreement with the signal void along the course of the RCA (Figure 3A) and the 6-day 99mtechnetium-sestamibi scan (Figure 2). At this point, the patient remained clinically stable, free of symptoms and creatine kinase levels were in the normal range. Despite the evidence of postinterventional vessel occlusion, the patient did not give his consent to a repeated coronary angiography and was discharged soon thereafter. Six months later, he presented with increasing shortness of breath on exertion but no angina pectoris. Left ventriculography revealed an ejection fraction of 43%, and coronary angiography showed a bizarre appearance of the entire RCA (Figure 1C) that was consistent with a spontaneous recanalization of a previous thrombotic occlusion that most likely occurred during the first days after the infarction and that could have been caused by a dissection induced by the guiding catheter during PCI. Contrast-enhanced magnetic resonance angiography of the RCA at that time revealed a normal appearance of the proximal and mid-RCA (Figure 3C), whereas delayed-enhancement magnetic resonance imaging showed distinct contrast enhancement suggestive for vessel wall or thrombus enhancement (Figure 3D). Delayed gadolinium-enhanced magnetic resonance imaging in corresponding short-axis slices 8 days (Figure 3E) and 6 months (Figure 3F) after myocardial infarction demonstrated transmural contrast enhancement that tended to be larger at the latter time point. This case demonstrates that contrast-enhanced magnetic resonance angiography needs to be interpreted with care as the vessel wall and thrombus may have similar signal intensities as the lumen. Additional delayed-enhancement imaging can help identify the sources of signal enhancement. The patient was treated conservatively and received intensified medical therapy for heart failure.