Acute lateral myocardial infarction due to thromboembolism originating from nonocclusive ruptured plaque of the left main trunk: a case report.

A 71-year-old man was emergently admitted to our hospital with a diagnosis of lateral acute myocardial infarction. He had a history of hypertension and familial hypercholesterolemia. Emergent coronary angiography revealed abrupt occlusion (red arrows) in the distal left circumflex (LCX) and a slight filling defect (orange arrow) in left main trunk (Fig. 1a and b). Subsequent optical coherence tomography (OCT) showed an irregular luminal surface of thrombus (yellow asterisk) without significant narrowing in the left main trunk suggesting that the distal LCX occlusion might have occurred due to a coronary thromboembolism originating from erosion of the left main trunk (Fig. 1c). We decided to treat this lesion with antithrombotic therapy without stent implantation.

Fig. 1

Serial coronary angiography and optical coherence tomography for evaluating culprit lesion. Coronary angiography revealed abrupt occlusion (red arrows) in the distal left circumflex (LCX) and a slight filling defect (orange arrow) in left main trunk (a) and (b). Subsequent optical coherence tomography (OCT) showed an irregular luminal surface of thrombus (yellow asterisk) without significant narrowing in the left main trunk (c) suggesting that the distal LCX occlusion might have occurred due to a coronary thromboembolism originating from erosion of the left main trunk. Follow-up angiography and OCT revealed a cavity consistent with ruptured plaque (yellow allows) in the left main trunk (f) due to resolution of thrombus covering that lesion, and coronary recanalization of the distal LCX (blue arrows) (d) and (e).

Dual antiplatelet therapy with heparinization was continued for 10 days. Follow-up angiography and OCT revealed a cavity consistent with ruptured plaque (yellow allows) in the left main trunk (Fig. 1f) due to resolution of thrombus covering that lesion, and coronary recanalization of the distal LCX (blue arrows) (Fig. 1d and e). The patient was discharged from the hospital and then treated with single antiplatelet therapy and alirocumab, a proprotein convertase subtilisin/kexin type 9 inhibitor 75 mg subcutaneously every 2 weeks with significant improvement in LDL-C.

Acute coronary syndrome is caused by three different underlying mechanisms, including plaque rupture, plaque erosion and calcific nodules [1].

When the coronary embolism is suspected, intravascular imaging, such as OCT, is useful to detect the source of embolism in any segments proximal to the lesions. Lesions with small plaque rupture might be misdiagnosed as plaque erosion by OCT.

Acknowledgements

Conflicts of interest

There are no conflicts of interest.