Author + information
- Received October 27, 2014
- Revision received January 28, 2015
- Accepted January 28, 2015
- Published online February 1, 2016.
- Adriano Caixeta, MD, PhDa,∗ (, )
- Philippe Généreux, MDb,c,
- Maria Eduarda M. de Siqueira, MDa,
- Antonio Baruzzi, MDa,
- Alexandre Abizaid, MD, PhDa and
- Gregg W. Stone, MDb
- aHospital Israelita Albert Einstein, São Paulo, Brazil
- bColumbia University Medical Center and Cardiovascular Research Foundation, New York, New York
- cHôpital du Sacré-Coeur de Montréal, Université de Montréal, Montréal, Québec, Canada
- ↵∗Reprint requests and correspondence:
Dr. Adriano Caixeta, Department of Cardiovascular Interventions, Hospital Israelita Albert Einstein, Av. Albert Einstein, 627 - Morumbi, São Paulo 05652-000, Brazil.
Acute myocardial infarction and sudden cardiac death are the first manifestations of coronary artery disease in most patients. Identifying patients at high risk for developing acute coronary syndromes (ACS) is a major challenge for contemporary cardiovascular imaging. Prior studies using invasive ultrasound imaging have demonstrated that angiographically mild lesions with high plaque burden and features consistent with a thin-cap fibroatheroma (TCFA) are prone to symptomatic rapid lesion progression over the course of several years (1). Noninvasive imaging with modern computed tomography angiography (CTA) scanner technology provides information regarding atherosclerotic coronary plaques beyond simple luminal narrowing and plaque type defined by calcium content. Previous studies have suggested that the presence of vulnerable plaque features as detected by CTA (positive remodeling, low attenuation, spotty calcification, and napkin-ring sign) may identify patients at increased risk for future ACS (2). Such studies, however, have not demonstrated that individual plaques with those features represent the specific lesions from which ACS events originate.
A 68-year-old asymptomatic man with dyslipidemia but no other cardiac risk factors underwent coronary CTA as part of routine risk factor management. His 10-year risk, based on 2013 American College of Cardiology/American Heart Association pooled atherosclerotic cardiovascular disease risk estimator, was 18.4%. His coronary artery calcium score of 47 placed him below the 25th percentile according to his age, sex, and ethnicity. The 320-row CTA was notable only for a noncalcific soft atherosclerotic plaque in the second obtuse marginal (OM2), which was <30% stenotic (Figure 1). Tissue and morphological plaque characterization (QAngio CT RE 2.1 model; Medis Medical Imaging Systems, Leiden, the Netherlands) showed a large lipid-rich necrotic core abutting the lumen, suggestive of a TCFA (Figure 2). The patient was given a prescription for a statin and for several years underwent annual myocardial scintigraphy, which showed no signs of ischemia. Three years later, he was admitted to our emergency department with an inferolateral and posterior ST-segment elevation acute myocardial infarction. Coronary angiography showed a severely stenotic and thrombotic ulcerated plaque in the OM2 at the site of the prior CTA lesion. After manual thrombus aspiration, optical coherence tomography (OCT) documented a disrupted TCFA. Histology demonstrated a cluster of macrophages, cholesterol crystals, and intraluminal red thrombus (Figure 3). In the present case, the presence of a large lipid-rich necrotic core detected by CTA served as the nidus for future plaque rupture and coronary thrombosis despite statin therapy.
By characterizing plaque phenotype, CTA may identify vulnerable plaque, providing guidance for intensifying medical therapy. Ongoing randomized trials (PROSPECT ABSORB [A Multicentre Prospective Natural History Study Using Multimodality Imaging in Patients With Acute Coronary Syndromes - PROSPECT II (Natural History Study), Combined With a Randomized, Controlled, Intervention Study]; NCT02171065) will determine whether preventative revascularization might be considered in select cases.
The authors have reported that they have no relationships relevant to the contents of this paper to disclose. Ami E. Iskandrian, MD, served as the Guest Editor for this paper.
- Received October 27, 2014.
- Revision received January 28, 2015.
- Accepted January 28, 2015.
- American College of Cardiology Foundation