Plaque erosion causing ST-segment elevation myocardial infarction: report of an optical coherence tomography-documented case and concise literature review

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A 61-year-old man presented to the Emergency Room of a referring hospital with anterior ST-segment elevation myocardial infarction (STEMI) and was immediately treated by antiplatelet therapy (intravenous aspirin and oral clopidogrel loading), and transferred to our hospital to perform a primary percutaneous coronary intervention (PCI).
On arrival, the patient reported resolution of symptoms and the ECG showed a marked reduction of anterior ST-segment elevation with negative T waves. Coronary angiography indicated normal flow through all the main epicardial vessels and an angiographically smooth lesion on the mid left anterior descending (Fig. 1). Frequency-domain optical coherence tomography (FD-OCT) was performed to characterize such stenosis. FD-OCT imaging documented the presence of white, platelet-rich thrombus overlying a fibroatheroma without any sign of rupture, indicative of coronary plaque erosion (Fig. 1). On the basis of these observations, we proceeded with primary PCI with everolimus-eluting stent implantation (Fig. 2). Post-PCI FD-OCT imaging confirmed optimal stent expansion and strut apposition (Fig. 2). The patient had an uneventful clinical course after PCI.
The present case report is interesting for two main reasons:
OCT currently represents the most accurate imaging modality for in-vivo characterization of coronary plaque morphology, but the possible clinical impact of an enhanced assessment of plaque morphology by OCT is actually unknown.
Plaque rupture and plaque erosion represent the two most frequent pathophysiological mechanisms responsible for acute coronary syndrome (ACS) and OCT enables to differentiate, in vivo, these two features 1,2. In particular, previous studies have shown that plaque erosion is responsible for about one-quarter of STEMI and that baseline TIMI flow grade is 2 or 3 in about one-quarter of these patients 3. Similar findings were observed in the recent EROSION trial 4.
At OCT, erosion appears as a plaque covered by thrombus without signs of fibrous cap disruption, whereas plaque rupture is identified by the presence of fibrous cap discontinuity, creating a communication between a cavity within the plaque and the coronary lumen. Clinically, plaque rupture is typically encountered in STEMI patients, with TIMI flow grades 0–1 and with greater frequency of multiple thin-cap fibroatheroma in other locations of the coronary tree 1,5–7. In contrast, plaque erosion typically occurs in the setting of a fibrous plaque; it is associated with smaller thrombotic burden (typically white, platelet-rich thrombus), generally occurs in younger patients, causes less severe stenosis, and is typically encountered in the setting of non-STEMI 1,3–6. Recent observations suggest that such different features may also translate into different clinical outcomes. In particular, among patients with ACS undergoing PCI, those with plaque erosion, compared with plaque rupture, had lower rates of target vessel revascularization, stent failure, and disease progression 2. In addition, patients with ACS and OCT-plaque rupture had more frequently thin-cap fibroatheroma in the entire coronary tree, suggesting the presence of a pancoronary vulnerability in these patients 7.
In conclusion, the present case shows how OCT enables characterization of the culprit lesion in the setting of an atypical STEMI angiographic presentation by documenting plaque erosion. OCT can differentiate, in vivo, plaque rupture from plaque erosion and this diagnostic differentiation could be useful in the choice of therapeutic strategy. Importantly, the recent EROSION trial suggested that patients with ACS caused by plaque erosion may be stabilized by antithrombotic therapy alone, without stenting 4. Further large-scale, randomized studies are needed to evaluate the long-term outcome of this conservative treatment strategy.

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