Author Affiliations: From the Interventional Cardiology Research Group, Royal Alexandra Hospital, Edmonton, Alberta, Canada. The authors report no conflicts of interest regarding the content herein. Manuscript submitted March 25, 2008, provisional acceptance given August 28, 2008, and final version accepted September 5, 2008. Address for correspondence: Keysun Alizadehranjbar, MD, FESC, CSC# 407, Royal Alexandra Hospital, 10240 Kingsway Avenue, Edmonton, Alberta, Canada T5H 3V9. E-mail: email@example.com
_______________________________________________ ABSTRACT: The drug-eluting stent (DES) era has seen an increasing number of stent fractures, which is considered one of the mechanisms of restenosis in DES. This increase in recognition could be due to various factors such as increased diagnosis compared to the bare-metal stent era, platform design and strut thickness, higher inflation pressures for DES deployment, and use of DES in more complex lesions (e.g., angulated, diffuse, calcified, bifurcated). The angiographic presentation of DES fracture has been reported as in-stent restenosis (either symptomatic or asymptomatic) in all published cases. We discuss a case of DES fracture presented as an ST-elevation myocardial infarction that was associated with a large coronary artery aneurysm.
J INVASIVE CARDIOL 2008;20:E324–E326 In the drug-eluting stent (DES) era there are increasing numbers of reports of stent fracture, which is considered one of the mechanisms of restenosis in DES.1,2 This increase in recognition could be due to several factors such as more diagnosis compared to the bare-metal stent era, different platform design and strut thickness, higher inflation pressure for DES deployment, and DES use in more complex lesions (e.g., angulated, diffuse, calcified, bifurcated).3,4 The angiographic presentation of DES fracture has been reported as in-stent restenosis (either symptomatic or asymptomatic) in all published cases. We discuss here a case of DES fracture presenting as an ST-elevation myocardial infarction (STEMI) that was associated with a large coronary artery aneurysm. Case Report. A 67-year-old male was admitted to a local rural health center because of prolonged resting chest pain and was transferred for emergency coronary angiography due to anterior STEMI. He had an extensive history of previous cardiovascular problems. In 1996, the patient suffered an acute MI (anterior STEMI) which was treated with plain-old balloon angioplasty (POBA) of the proximal left anterior descending artery (LAD). In 2004, he presented with a non-ST-elevation MI (NSTEMI), and was treated with angioplasty and stenting (sirolimus-eluting stents [SES]) of the proximal LAD (Figures 1 and 2) as follows: 1) predilatations with a 2.0 x 20 mm semicompliant balloon at 12 atm; 2) a 3.0 x 33 mm SES was deployed in the mid-part of the LAD at 18 atm; 3) a second 3.0 x 13 mm SES was deployed at 18 atm proximal to the first stent with 1–2 mm of overlap. No postdilatation was done because of perfect angiographic result. There was no evidence of coronary artery aneurysm or ectasia on the previous pre- and/or post-percutaneous coronary interventional angiograms (Figures 1 and 2). The patient was fine until this admission in January 2007. He had a history of hypertension and dyslipidemia (well controlled on medication), and has also been treated for hyperuricemia since 1997. On arrival (of his present admission with STEMI), the patient had mild chest pain with persistent ST-elevation in the anterior leads with no further evolutionary changes on electrocardiography (ECG). His peak troponin I was 30.72. Using a 5 Fr radial approach, coronary angiography showed a large coronary aneurysm in the proximal LAD with some thrombus in the distal part of the LAD stent (Figure 3). The left circumflex artery (LCx) showed severe narrowing proximally, and the right coronary artery (RCA) was diffusely diseased in mid and distal portions. Left ventriculography revealed an estimated left ventricular ejection fraction (LVEF) of 40% with apical akinesis and mild-to-moderate mitral regurgitation (MR). During angiography, stent fracture with a gap between two parts was confirmed by double magnification cine angiography without contrast injection (Figure 4). Fracture occurred at the proximal part of the LAD stent which covered an extremely angulated segment (Figure 5). By analyzing the jet flow of contrast into the aneurysm, it was also evident that the entrance site of the aneurysm was located at the same sharp angle (Figure 5). The patient underwent bypass surgery 2 weeks later without any complication and he was discharged 10 days post operation. During the operation the presence of an aneurysm in the proximal LAD was confirmed. Discussion. Recently, several cases of stent fracture were reported, particularly with SES. The incidence of stent fracture has been widely variable in different studies (2.6%, 38.4%),5,6 which are not a true incidence of stent fracture, and only report the percentage of stent fracture in a group of patients with in-stent restenosis who have undergone follow-up angiography. Stent fracture is a mechanical complication of stent deployment and its occurrence depends on the interaction between two contradictory parameters: the external forces on the stent, and the stress-strain behavior of the stent.6,7 The former is usually determined by the lesion characteristics (e.g., calcified vs. noncalcified, long lesions, saphenous vein graft lesions, lesions in angulated segments, bifurcations, lesions in a highly mobile-hinge area, and the use of overlapping stents), or sometimes by the pressure which was applied during stent deployment (high pressure or postdilatation with a larger balloon).3,6 On the other hand, the “stress-strain” behavior is determined by coronary stents’ inherent specifications (material, design, strut thickness).7 In our case, we assume that the lesion characteristic (extremely sharp angulation) was the major contributing factor for fracture, although the type of stent (SES) could have been responsible. There is no head-to-head comparison to show that stent fracture is more frequent with SES than with paclitaxel-eluting stents. However, all of the case reports on stent fracture (except for one) involved SES.8 These reports highlighted the role of platform design in stent fracture (open-cell vs. closed-cell design), but it should be kept in mind that identifying the fracture (just based on fluoroscopy) in an open-cell design platform is more difficult than with a closed-cell design. Also, recently, Lee et al revealed that the incidence of stent fracture with the Bx-Velocity stent (Cordis Corp., Miami Lakes, Florida) was much lower than with SES in patients with restenosis. Since the design of the SES platform is the same as that of the Bx-Velocity stent, stent design might be less important in stent fracture cases.5 Furthermore, no accurate data even exists on whether there is a higher risk of stent fracture with DES versus BMS. Lack of neointimal proliferation as a means of support for stent struts in DES and the weakness of struts during the DES manufacturing process (involving heat) might explain the difference between DES and BMS in the incidence of fracture,5 but this increase in the number of reports on DES fracture could be simply due to more diagnoses of DES fractures (compared to BMS), or higher usage of DES in more complex lesions, or a combination all of the above factors. The other aspect of our case involves aneurysm formation. Like stent fracture, case reports on aneurysm formation after DES deployment have been increasing. However, the mechanism, clinical implication, treatment and long-term prognosis still need to be clarified.9 Although the mechanism of restenosis in DES fracture seems logically straightforward (lack of drug delivery in the gap area and local mechanical irritation), for aneurysm formation it is more complex. Histopathologic examination of aneurysms in the setting of DES implantation revealed that inflammatory changes due to reaction to the polymers in DES might be a possible mechanism for aneurysm formation.9 While compromised repairing capabilities of the arterial wall (due to drug effects), sharp irregular edges irritating the arterial wall (inflammatory response to physical injury), and a longstanding jet effect (due to high-velocity blood flow, particularly in angulated arterial segments) are considered to be possible mechanisms. In our case, we postulate that a combination of continuous jet effect (through the angulated fracture site), local inflammatory reaction, and impaired repairing capabilities of the vessel wall were responsible for this angiographic feature. From a clinical point of view, both DES fracture and/or aneurysm formation in coronary arteries following DES implantation increase the rate of major adverse cardiac events.1,9 Clinical presentation ranges from asymptomatic patients to those with acute coronary syndrome, or even sudden cardiac death.1,10 Finally, because of the limited number of reports, the optimal treatment for DES-induced coronary artery aneurysm is unclear; in some cases, it has been treated with covered stents, while in others, the patients were sent for bypass surgery.9 Conclusion. DES fracture is an occurrence which is likely underestimated and its clinical significance needs to be elucidated by further clinical investigations. While almost all published reports have addressed restenosis as the angiographic feature of DES fracture, ours revealed that coronary aneurysm formation could be another type of angiographic presentation. Regardless of its angiographic presentation, DES fracture (with or without aneurysm formation) increases the rate of target lesion revascularization. Long-term outcomes and treatment options are still unclear and require further clinical evaluations.
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