Abstract
Aims
Expansive vessel wall remodeling has been previously reported after implantation of drug-eluting stents. These abnormal vessel wall reactions (AVWR), though uncommon may be associated with serious clinical events. We report on a series of patients in whom symptoms developed despite patent stents.
Methods and results
We report a series of 10 consecutive patients with evidence of AVWR on angiography and/or intravascular ultrasonography after implantation of sirolimus-eluting stents (age 39-90 years, 4 females) during a period of 4 years. All patients were symptomatic despite patent stents in coronary angiographies done because of persistent chest pain. Four patients subsequently developed very late stent thrombosis (VLST). These 4 patients were only on aspirin monotherapy prior to the VLST. Of the remaining 6 patients, 3 patients underwent coronary interventions (with or without stenting) while the remaining 3 patients were managed conservatively. All 6 were advised for life-long dual antiplatelet therapy.
Conclusion
Though uncommon, AVWR might precede VLST. In our series, all patients were symptomatic despite patent stents. Additional studies are required to identify patients at risk and to determine the best treatment modality for this challenging new entity. Until further data become available, these patients should stay on dual antiplatelet therapy after an AVWR has been identified.
1
Introduction
Safety concerns have been raised regarding the long term outcome of patients treated with drug-eluting stents (DES) due to the occurrence of very late stent thrombosis (VLST) . In some patients, DES have been associated with significant positive vessel wall remodeling leading to late acquired stent malapposition and even coronary artery aneurysm formation . Despite being a rare adverse event of DES implantation, these abnormal vessel wall reactions (AVWR) may be associated with stent thrombosis, myocardial infarction and even death . Whether patients with AVWR occasionally develop symptoms prior to serious clinical events remains unknown.
2
Case 1
A 61 year old dyslipidemic, active-smoking lady presented in March 2004 with unstable angina (UA). Coronary angiography (CA) revealed a proximal 80% left anterior descending (LAD) artery stenosis after the origin of the first diagonal branch (D1) ( Fig. 1 A ) that was treated with a sirolimus-eluting stent (SES) ( Fig. 1 B). Three months later, a repeated CA was performed because of recurrent chest pain and revealed a patent LAD stent with no angiographic progression of her coronary artery disease (CAD). Four years after stenting, the patient was again hospitalized because of UA. CA revealed a patent stent in the LAD, but the wall of the artery at the stented region was aneurysmally dilated ( Fig. 1 C). Conservative treatment was advised. One year later, she presented to our center with an anterior wall ST-segment elevation myocardial infarction (STEMI) ( Fig. 1 D). Emergency CA revealed VLST with an occlusive luminal thrombus at the site of the LAD aneurysm. The vessel was successfully recanalised and treated with two paclitaxel-eluting stents (PES) ( Fig. 1 E) and the patient was advised for life-long dual antiplatelet therapy.
2
Case 1
A 61 year old dyslipidemic, active-smoking lady presented in March 2004 with unstable angina (UA). Coronary angiography (CA) revealed a proximal 80% left anterior descending (LAD) artery stenosis after the origin of the first diagonal branch (D1) ( Fig. 1 A ) that was treated with a sirolimus-eluting stent (SES) ( Fig. 1 B). Three months later, a repeated CA was performed because of recurrent chest pain and revealed a patent LAD stent with no angiographic progression of her coronary artery disease (CAD). Four years after stenting, the patient was again hospitalized because of UA. CA revealed a patent stent in the LAD, but the wall of the artery at the stented region was aneurysmally dilated ( Fig. 1 C). Conservative treatment was advised. One year later, she presented to our center with an anterior wall ST-segment elevation myocardial infarction (STEMI) ( Fig. 1 D). Emergency CA revealed VLST with an occlusive luminal thrombus at the site of the LAD aneurysm. The vessel was successfully recanalised and treated with two paclitaxel-eluting stents (PES) ( Fig. 1 E) and the patient was advised for life-long dual antiplatelet therapy.
3
Case 2
A 39 year old hypertensive, dyslipidemic, obese male patient presented in January 2005 with an inferior wall STEMI that was treated with primary PCI to the right coronary artery (RCA) using a SES. Two years later, he was admitted with accelerating angina. CA showed a 90% proximal LAD stenosis and 80% proximal D1 while RCA stent was patent. The proximal LAD was hence treated with a SES and D1 with two overlapping SESs. The patient remained symptom free for 1 year, then started to complain once again of effort angina. CA revealed a small aneurysm at the site of the LAD stent, and IVUS revealed marked positive remodeling in the LAD, D1 and RCA, with a honey-comb structure behind the LAD stent and minimal stent mal-apposition ( Figs. 2 A & 2B ). A conservative treatment plan was decided, and life-long dual anti-platelet therapy (DAPT) was recommended. Planned re-angiography in April 2010 revealed similar angiographic findings in the LAD, yet there was evidence of aneurysmal formation at the site of the RCA stent.
4
Case 3
A 61 year old dyslipidemic, active-smoking lady presented in 2007 with effort angina and a pathological stress echocardiography. CA revealed a significant proximal LAD stenosis that was treated with one SES. A few months later, she presented with recurrent anginal pain, but CA revealed a patent LAD stent with no angiographic progression of her disease. Two years later, she presented with stable angina and again a stress echocardiography was positive for ischemia. CA revealed a patent LAD stent, yet with evident coronary ectasia in the stent-covered area. The patient was advised to continue on life-long DAPT and follow-up CA revealed that the ectatic segment did not progress, but intravascular ultrasound (IVUS) revealed marked expansive vessel wall remodeling ( Fig. 3 A –D).
5
Discussion
In the period between December 2006 and December 2010 we observed a series of ten consecutive symptomatic patients with evidence of AVWR on CA and/or IVUS after implantation of the first generation SES ( Table 1 ). We defined AVWR as angiographic abnormal contrast staining outside the implanted stent with or without aneurysm formation and/or positive vessel remodeling on IVUS defined as a remodeling index (RI) > 1.05. RI was calculated as the maximal vessel cross sectional area (CSA) in the stented segment divided by the proximal reference vessel CSA. Patients’ age ranged between 39 and 90 years; 4 females and 6 males. During this time period, an average of 900 patients/year was treated with DES at our institution. All patients were symptomatic despite patent stents on repeated angiographies done based on persistent anginal symptoms.
| Age | Sex | DM | HTN | Dyslipidemia | FH | Smoking | Onset of symptoms after index procedure | Positive stress test | |
|---|---|---|---|---|---|---|---|---|---|
| Case 1 | 61 | F | − | − | + | − | + | 3 months | Positive stress ECG |
| Case 2 | 39 | M | − | + | + | − | − | 12 months | NA |
| Case 3 | 61 | F | − | − | + | − | + | 1 month | Positive stress echocardiography |
| Case 4 | 57 | M | − | + | + | + | + | 22 months | Positive scintigraphy |
| Case 5 | 61 | M | + | + | + | − | + | 14 months | NA |
| Case 6 | 90 | F | − | + | + | − | − | 3 months | NA |
| Case 7 | 43 | M | − | + | − | + | + | 12 months | NA |
| Case 8 | 56 | F | − | + | + | + | + | 24 months | NA |
| Case 9 | 61 | M | + | + | − | − | − | 36 months | NA |
| Case 10 | 48 | M | − | + | + | + | + | 8 months | Positive stress ECG |
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