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Coronary Artery Disease
Acute coronary syndrome due to early multiple and complete fractures in sirolimus-eluting stent: A case report and brief literature review†
Article first published online: 2 MAY 2012
Copyright © 2012 Wiley Periodicals, Inc.
Catheterization and Cardiovascular Interventions
Volume 81, Issue 1, pages 52–56, 1 January 2013
How to Cite
Amico, F., Geraci, S. and Tamburino, C. (2013), Acute coronary syndrome due to early multiple and complete fractures in sirolimus-eluting stent: A case report and brief literature review. Cathet. Cardiovasc. Intervent., 81: 52–56. doi: 10.1002/ccd.24414
- Issue published online: 21 DEC 2012
- Article first published online: 2 MAY 2012
- Accepted manuscript online: 19 MAR 2012 11:35AM EST
- Manuscript Accepted: 14 MAR 2012
- Manuscript Received: 12 NOV 2011
- acute coronary syndrome;
- coronary, stent structure;
- complications adult cath/intervention
Despite drug eluting stents (DES), as compared to bare metal stents, have reduced in-stent restenosis, complex and long lesions remains a challenge for interventional cardiologist. Their treatment is often associated with an unfavorable outcome, related to in-stent restenosis, stent thrombosis, and target lesion revascularization. These complications may derive from the contact between metallic structures and coronary artery endothelium, and consequent overexpression of platelet activating factors, growth factors, and inflammatory cytokines. Recently, an additional mechanism has emerged as new cause of these complications: “stent fracture.” Several factors are involved in this phenomenon including material and stent platform, target vessel features, stent implantation technique, and implant duration. We reported a case of 69 years old man with rare early and complex DES fractures on right coronary that caused acute coronary syndrome 36 hr after a previous percutaneous coronary intervention.© 2012 Wiley Periodicals, Inc.
Drug-eluting stents (DES), as compared to bare metal stents (BMS), have reduced the risk of in-stent restenosis (ISR) due to inhibition of neointimal growth and have attenuated the relationship between stent length and rate of restenosis . Nevertheless, the treatment of complex and long lesions remains a challenge for interventional cardiologist and it is often associated with an unfavorable outcome.
Poor outcome derives from ISR, stent thrombosis (ST), and target lesion revascularization (TLR). These complications could be related with the contact between metallic structures and coronary artery endothelium, and consequent overexpression of platelet activating factors, growth factors, and inflammatory cytokines. Recently “stent fracture” (SF) has been reported to be an additional mechanism of these complications.
SF was defined as angiographically visible interruption of the connection between stent struts . It may lead to insufficient drug elution, resulting in decreased inhibition of neointimal growth and ISR; moreover, the mechanical stress induced on the endothelium, by the fractured stent, may result in ST.
A 69-year-old male, hypercolesterolemic, hypertensive, and smoker, was admitted to our emergency department for acute myocardial infarction with ST elevation in infero-lateral leads at electrocardiogram (EKG), typical chest pain at rest, and hypotension (arterial blood pressure was 82/44 mm Hg and heart rate 88 bpm). Creatine kinase (CK) was 365 UI/L, CK-MB 78 UI/L, and high sensitivity T-Troponin 234 ng/L. The patient had undergone percutaneous coronary intervention (PCI) only 36 hr earlier in another cath lab where he was admitted for stable angina, following a positive ergometric test. Two overlapped Sirolimus eluting stent (SES) (Cypher stents, Cordis Corporation, Bridgewater, NJ), 3.0/33 mm and 2.75/33 mm, were implanted at proximal and middle segments of right coronary artery (RCA), with final high pressure postdilation (3.0/20 mm non-compliant balloon, inflation pressure 24 atm). The patient was discharged 33 hr after PCI with medical therapy: acetylsalicylic acid (ASA) 100 mg, Clopidogrel 75 mg, Enalapril 20 mg, Bisoprolol 1.25 mg, and Rosuvastatin 10 mg.
Just 2 hr and 30 min after discharge, the patient complained of severe chest pain, so he was conducted at emergency room and transferred to our cath lab 20 min later. Coronary artery angiography showed a very unusual finding: a double and circumferential SF. Close to the overlap we observed a clear separation of the distal stent in three segments, with dislocation of the middle one and misalignment of all three (Fig. 3). Contrast injection showed haziness suggestive of thrombosis into the context of the fracture (Fig. 4) and thrombolysis in myocardial infarction (TIMI) 2 flow (see Supporting Information movie). Moreover, RCA appeared very mobile with large systo-diastolic variations. Left anterior descending artery was free from significant stenosis and left circumflex artery had chronic total occlusion starting after the origin of second obtuse marginal artery (Figs. 1 and 2).
We decided to perform PCI on RCA. The procedure started with administration of 7,000 UI of unfractionate heparin (UFH) and thromboaspiration through Eliminate catheter (Terumo Corporation, Tokyo, Japan) with extraction of small amount of white thrombus. Subsequently, stent implantation was performed with Biomatrix Flex stent 3.0/24 mm (Biosensors Interventional Technologies Pte, Singapore) followed by final postdilation with Quantum Maverick non-compliant balloon 3.0/20 mm (Boston Scientific Corporation, Natick, MA) inflated at 12 atm. Final injection showed optimal angiographic result, absence of residual thrombus inside the stent (Fig. 5), and TIMI 3 flow. After PCI patient's condition improved, with chest pain discontinuance and restoration of normal hemodynamic parameters (arterial blood pressure 135/86 mm Hg, heart rate 82 bpm).
The patient was discharged three days later with the following medical therapy: aspirin 100 mg, prasugrel 10 mg, bisoprolol 5 mg, rosuvastatin 20 mg, and enalapril 20 mg. At 1- and 6-month clinical follow-up he was asymptomatic for chest pain and dyspnea, had good hemodynamic condition, and rest EKG showed no signs of myocardial ischemia.
In BMS-era SF was a rare event without big clinical weight, possibly because early formation of neointima protected the struts by mechanical stress and fracture; furthermore, ISR was more frequent rather than DES, so interventional cardiologist not consider it as a possible cause of restenosis [3, 4].
Nakazawa et al. in post-mortem analysis observed DES fractures in 29% of stented lesion , however, not all SF have a clinical implication and various studies have reported a rate of DES fracture ranging between 0.84% and 7.7% [6–8]. We should pay attention to the percentage of SF reported in the study of Nakazawa et al. It is much higher than in other studies, and even higher than what has been clinically reported, probably due to the high resolution method used, a contrast film-based radiography (80 micron), which detect also very small fractures not related to clinical event.
In literature, SF have been reported mostly in SES [1, 9]. SES has closed-cell design which improves drug elution, but result in more rigidity and higher straightening of the vessel after implantation as compared to open-cell design stents, more flexible, and adaptable to the vessel wall [10, 11]. Moreover, fractures of SES is easier to detect, as compared to other DES, thanks to its greater radiopacity related to the strut thickness (140 μm) greater than other stents. It was observed that the most frequent site of rupture in SES is the flexible N-shaped, undulating longitudinal intersinusoidal-ring linker segment . However, there is no enough data concerning the period between SES implantation and SF.
Native coronary artery more frequently affected by SF is RCA. This complication can be related to angulation of this vessel and its change after stent implantation, tortuosity, and large vessel movements with cardiac cycle, that cause flexion, torsion and stretching phenomena .
All these factors can lead to high mechanical stress and consequent SF. Furthermore, other risk factor for SF are reported in literature: stent length, venous graft, severe calcification, coronary aneurysm, long implant duration, and small stent diameter [4, 5, 12–14]. These factors are related only to anatomical and structural features; but also important procedure-related factors are linked to SF, especially high pressure balloon dilation  and stent overlapping [4, 8]. Indeed rigid hinge points, created in overlapping sites, acting like a fulcrum for stent deformation increase the risk of fracture, like reported by Chung et al. that observed a higher rate of SF (54%) in overlapping sites [10, 16].
Several classifications have been proposed for SF, according to angiographic, fluoroscopic, and intravascular ultrasound (IVUS) parameters [3–5, 17, 18]. We chose to refer to Nakazawa et al.  and Lee et al.  classifications because they are more simple and clear.
Nakazawa et al. proposed a classification of SF, refers to a post-mortem study with high-contrast film-based radiography that includes Grades I–V:
- I:involving a single-strut fracture;
- II:two or more strut fractures without deformation;
- III:two or more strut fractures with deformation;
- IV:multiple fractures with acquired transection without gap;
- V:multiple fractures with acquired transection with gap in the stent body
Lee et al. proposed a classification of SF in vivo that includes Grades A, B, and C, according to fluoroscopic and IVUS criteria :
- A:Avulsion type with more fractured stent segments completely separated and displaced on the fluoroscopic images. On IVUS, no stent struts are observed at SF site.
- B:Partial type, defined as the absence of stent struts in >1/3 of the vessel wall on IVUS; partial fracture with minimal strut damage on fluoroscopy.
- C:Collapse type, defined as a folded and compacted inner and outer wall of the stent found in a bended segment with >45° on fluoroscopy.
Clinical implication of SF is different and includes recurrent angina, myocardial infarction, and sudden death. Nakazawa et al. observed that Grade V fractures were associated with significantly higher rate of adverse pathological findings as compared to non-fracture and Grades I–IV fracture groups, therefore in this study only Grade V fractures had significant impact on clinical outcome .
Our case report describes a fracture in long SES, occurred in hypermobile and angulated RCA, at site of long overlap, after high-pressure postdilation. But the real peculiarities of our case are the early fracture, as evidenced by the onset of symptoms at 36 hr after stent implantation, and the feature of fracture: “double Grade V” according to Nakazawa et al, “Avulsion type” according to Lee et al. classification, with separation of the stent in “three segments,” dislocation of the middle one and consequent misalignment of all three. This condition led to ST resulting in ST elevation myocardial infarction (STEMI).
The choice of implanting open-cell new generation DES was triggered by the need for a more flexible device, not predisposed to fracture again.
Other cases of SF have already been described in medical literature. Nevertheless is extremely rare to observe with standard angiography a “double Grade V SF in vivo,” causing a STEMI, with the same features of this.
With this case report we want to emphasize the concrete possibility of SF, not only at the time of stent implantation or after long time, but also early after PCI. Therefore we would like to highlight the need to consider all risk factors for SF, avoiding the actions that could lead to SF during or immediately after PCI and reducing the risk for thrombosis and ISR.
- 18Ninitol stent fractures in the SFA: the biomechanical forces exerted on the SFA provide a “stiff” challenge to endovascular stenting. Endovasc Today 2004; July/August 22–34., , .
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