Seventy-Four–Month Follow-Up of Coronary Vulnerable Plaques by Serial Gray-Scale Intravascular Ultrasound
A 56-year–old male nonsmoker with high blood pressure was referred for a first acute coronary syndrome in the lateral territory. Coronarography identified the culprit lesion on the circumflex artery. The left anterior descending artery (LAD) showed diffuse atherosclerosis and was further explored by 40-MHz intravascular ultrasound (IVUS; baseline). Ten months later, angina recurred, without circumflex artery restenosis; an LAD plaque (P4, among the 5 plaques ultimately detected) was detected and managed medically (Figure 1). Because the patient developed Canadian Cardiovascular Society (CCS) class 3 angina, this single stenosing LAD lesion was treated by bare-metal stenting at 22 months of follow-up. Symptoms resolved, but 1 year later (at 33-month follow-up) there was recurrence of CCS-3 angina without enzyme elevation. No intrastent restenosis was observed. A de novo mid-LAD stenosis (P5) was again managed by bare-metal stenting. Clinical evolution included 2 episodes of unstable angina without troponin elevation, 3 (69-month follow-up) and 4 years later (74-month follow-up). The culprit lesions were both distal and could be managed medically. There was no visible restenosis at the stented plaques (P4 and P5). At the end of 6-year medical follow-up (total follow-up, 12 years), the patient presented stable CCS-2 angina under medical control, with no acute coronary syndrome. From the outset, treatment associated β-blockers, statin, and antiplatelets. Low-density lipoprotein cholesterol was consistently ≤0.85 g/L, and C-reactive protein was ≤0.2 mg/dL.
This particular case included 6 IVUS explorations of the LAD over a 6-year period, in which pullback and anatomic landmarks enabled precise identification and follow-up of 5 distinct atheromatous plaques. On indexing, 3 plaques (P1, P2, and P3) showed vulnerability criteria. P1 ruptured and healed between 33 and 69 months later. P2 and P3 presented a thin cap fibro-atheroma aspect, which remained morphologically unchanged in P2 while evolving toward resolution without stenosis in P3. None of these 3 plaques were associated with acute coronary syndrome. Two plaques (P4 and P5) progressed over follow-up toward symptomatic stenosis without acute coronary syndrome and without specific morphological features on IVUS; evolution of plaque burden and remodeling index showed considerable variation over time (Figure 2).
The present clinical case report is, to the best of our knowledge, unique, with 6 years of follow-up and 6 IVUS explorations after the evolution of 5 distinct atherosclerotic coronary plaques, 3 of which showed morphological criteria of vulnerability. Morphological criteria varied considerably over time in this single patient, with no particular association with any specific clinical events. A vulnerable plaque is an asymptomatic coronary atheromatous plaque, liable to become a culprit in acute coronary syndrome.1 This concept is founded on numerous anatomopathologic studies, and detection of specifically vulnerable plaques, notably on IVUS, is a source of great therapeutic hope.2 The natural evolution of thin cap fibro-atheroma, however, seems inconstant, reported as varying on repeat IVUSs performed at a 1-year interval.3 The present 6-year follow-up extends the concept, raising doubts as to a vulnerable plaque detection strategy even by iterative arterial wall imaging.
- © 2012 American Heart Association, Inc.