A Peculiar Case of Very Late Restenosis in a Drug-eluting Stent

Citation
American Heart Hospital Journal 2011;9(1):63-4
DOI
https://doi.org/10.15420/ahhj.2011.9.1.63

In 2002, a 60-year-old man suffered an inferior ST elevation myocardial infarction (STEMI), which was initially successfully treated with thrombolysis. He was then referred to our center for percutaneous coronary intervention (PCI) due to post-infarct angina. In his past history he was a very heavy smoker with an 80-pack-per-year history. He also had established hypertension, a family history of ischemic heart disease and hypercholesterolemia.

He underwent PCI to the right coronary artery (RCA) and a good result was obtained following deployment of a 3 x 28 mm TAXUS stent distally before the crux. This was overlapped proximally with a 3.5 x 32 mm TAXUS and post-dilated with a 4.0 mm non-compliant balloon. He had discontinued clopidogrel at 12 months post-procedure, as per local protocol. The patient remained well until 2004 when he underwent a further angiogram due to unexplained breathlessness. This revealed no in-stent restenosis (ISR) or new coronary lesions. The patient was then symptom-free for five years.

In April 2009 the patient presented with signs and symptoms of an infero-lateral NSTEMI with inferior T-wave changes on the electrocardiogram (ECG) and a troponin release of 0.23 μ/l. Angiography confirmed clear, multiple, lobulated filling defects within the RCA-stented area and initially some thrombus was interspersed between these lesions (see Figure 1). Following acute medical treatment with anticoagulation and standard anti-platelet drugs, repeat PCI was undertaken from the right radial approach and the vessel was imaged by intravascular ultrasound (IVUS) + Virtual HistologyTM (Volcano Corp) using a motorised pullback of 0.5 mm/sec (see Figure 2). There was evidence of severe stent under deployment in regions adjacent to heavy intimal calcification. Late stent malapposition was also identified as well as new outgrowths of plaque or intimal hyperplasia between some stent struts (see arrows, Figure 2). Some areas of this restenosis appear to have a density similar to calcification at the luminal surface. It remains undecided whether this appearance represents calcified outgrowths of neo-intimal hyperplasia, fibro-calcific changes due to plaque prolapse or late reactive tissue deposition within and around the stent. It is theoretically possible that this could be related to the long-term effects on the vessel of the drug or polymer.

The area in question was treated by further PCI using high-pressure non-compliant and cutting balloon (3.0 x 10+12 mm) pre-dilatation, as two previous compliant balloons had ruptured on the lesion. A 3.5 x 28 mm Promus stent was deployed and post-dilated to high pressure (24 atm) with a 4.0 mm non-compliant balloon. The angiographic result obtained was satisfactory with TIMI III flow (see Figure 3). However, the subsequent IVUS examination did show persistence of some areas of tissue, to a lesser degree than before, between stent struts despite two layers of stent (see Figure 4).

We welcome expert comment and discussion from readers on this appearance and any details of similar cases in other centers.