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Case Report

Spontaneous Coronary Artery Perforation Secondary to a Sirolimus-Eluting Stent Infection

Ravi K. Garg, MD, James E. Sear, MD, Eric S. Hockstad, MD From the Section of Cardiology, Research Medical Center, Kansas City Cardiology, Kansas City, Missouri. The authors report no conflicts of interest regarding the content herein. Manuscript submitted February 28, 2007, provisional acceptance given May 2, 2007, manuscript accepted June 6, 2007. Address for correspondence: Ravi K. Garg, MD, Section of Cardiology, Research Medical Center, Kansas City Cardiology, 6420 Prospect Avenue, T-509, Kansas City, MO 64132. E-mail: ravi.garg@kchf.org
October 2007

ABSTRACT: Coronary stent infection is exceedingly rare despite the widespread use of percutaneous coronary intervention (PCI). The utilization of drug-eluting stents (DES) may have a higher theoretical risk of infection due to their local immunosuppressant effect. Vigilance in suspecting stent infection is important, as the associated mortality rate is approximately 50%. We discuss the case of a patient who presented with an infected DES 2 weeks after implantation which led to spontaneous Type II coronary perforation. The perforation was sealed with prolonged balloon inflation, and the patient was treated with intravenous antibiotics. This is the first reported case of a patient with a stent infection who presented with a spontaneous coronary perforation. J INVASIVE CARDIOL 2007;19:E303–E306 Key Words: coronary interventions; stenting; complications
Coronary stent implantation is one of the most common medical procedures, with nearly 1 million patients in the United States undergoing this intervention annually.1 The incidence of stent infection is unknown, but appears to be quite rare, given the limited number of cases reported since the introduction of intracoronary stenting in 1986.2 Theoretically, drug-eluting stents (DES) may present an increased risk of infection due to the localized immunosuppressant effect, the impairment of local host defense mechanisms and delayed stent endothelialization. There are no previous reports of coronary perforation associated with stent infection. We present the case of a patient with a coronary perforation associated with a DES infection and discuss previously reported cases of coronary stent infection. Case Report. An 86-year-old female presented to an outside emergency room with a non-ST-elevation myocardial infarction. She was transferred to our institution for catheterization with initial antiplatelet and anticoagulant therapy consisting of aspirin, heparin and eptifibatide. Angiography demonstrated a 95% stenosis in the mid-left anterior descending (LAD) artery (Figure 1A) and 2 sequential 80% stenoses in the mid-right coronary artery (RCA). The LAD lesion was treated with a 2.5 mm x 13 mm Cypher™ sirolimus-eluting stent (Cordis Corp., Miami Lakes, Florida) (Figure 1B). The RCA was also treated with 2 Cypher stents. The interventions were uncomplicated. The patient received a loading dose of 600 mg of clopidogrel and was initiated on a maintenance dose of 75 mg daily. Echocardiography revealed normal left ventricular function with no evidence of pericardial fluid (Figure 2A). The patient was discharged home on hospital day 3 in stable condition. She returned to the emergency room 6 days later complaining of chest discomfort similar to her initial presentation. An electrocardiogram (ECG) revealed new T-wave inversions inferiorly. Angiography demonstrated widely patent stents in the LAD and RCA. Six days later, the patient suffered recurrent chest pain. Her ECG was unchanged, but a repeat catheterization was requested because of the severity of the patient’s symptoms. A mycotic aneurysm was noted in the stented portion of the LAD, and immediately distal to the stented segment, a Type II coronary perforation was evident (Figures 3A, 3B). A 2.5 x 12 mm Maverick® balloon catheter (Boston Scientific Corp., Natick, Massachusetts) was placed across the perforated segment and inflated to 7 atm for a total of 6 minutes. Subsequent angiography confirmed that the perforation was sealed (Figure 4). The patient’s chest pain resolved. An echocardiogram demonstrated moderate-sized pericardial effusion. The patient was hemodynamically stable and there was no echocardiographic evidence of tamponade. A decision was made not to proceed with pericardiocentesis. Serial blood cultures grew methicillin resistant Staphylococcus aureus (MRSA). Because of her advanced age and her desire to avoid surgical intervention, she was treated medically with intravenous (IV) vancomycin and oral rifampin. Blood cultures remained positive for 5 days. She was monitored for an additional week in the hospital after her cultures were sterile and was subsequently transferred to a skilled nursing facility to continue antibiotic therapy. The patient died suddenly 2 weeks post-hospital discharge. Discussion. Percutaneous coronary stent implantation is a widely employed procedure, with an estimated 1.4 million stents implanted annually in the United States.1 The development of stent infection is exceedingly rare, but represents a very severe complication with an associated mortality of ~50%.3 There have been only 11 reported cases in the literature since the introduction of coronary stents over 20 years ago (Table).4–14 These patients have presented with fever and bacteremia within several days after stent implantation, and diagnostic evaluations have revealed coronary aneurysms or abscess formation. In addition, stent infections have been related to Staphylococcus or Pseudomonas species. Our case was consistent with this pattern, in that the culprit organism was identified as Staphylococcus aureus (methicillin-resistant), and a peri-stent mycotic aneurysm was demonstrated on angiography. The occurrence of coronary perforation, however, was unique to our patient. This represents the first reported case of stent infection presenting with spontaneous coronary artery perforation. Our patient was treated with balloon angioplasty to seal the perforation and IV antibiotics. However, she died suddenly 2 weeks after hospital discharge. DES may have an increased theoretical risk of infection due to the localized immunosuppressant effect. Impairment of local host defense mechanisms and delayed endothelialization of the stent might also increase a patient’s susceptibility to infection. There have been 2 previously reported cases of DES infection, both involving the use of sirolimus-eluting stents.12,14 The first case involved a 56-year-old male who presented with fevers and Staphylococcus aureus bacteremia 4 days post-implantation of a sirolimus DES in the LAD.12 Angiography demonstrated a mycotic aneurysm. The patient was treated with IV antibiotics and survived. The second case involved a 47-year-old male treated with 2 sirolimus DES for in-stent restenosis of a bare-metal stent.14 He presented 2 days later with fevers and Staphylococcus aureus bacteremia. He was initially treated with IV antibiotics. Transesophageal echocardiography (TEE) demonstrated a new, large pericardial effusion without evidence of valvular vegetations. Pericardiocentesis was performed, and the fluid cultivated Staphylococcal aureus. The patient died before completing the full course of IV antibiotics. The ideal management for stent infection has not been elucidated. Six of the reported stent infection cases were treated with IV antibiotics followed by surgical intervention, and 3 of these patients died.4–6,9–11 Four cases were treated with IV antibiotics alone, and only 1 patient died.8,12–14 An additional patient died before any treatment was initiated.7 Surgical intervention was discussed with our patient and her family, but because of her advanced age, they opted for medical management alone. Treatment of the spontaneous perforation with a covered stent was considered, but not undertaken, because of the obvious risk of exacerbating the infection. Despite the early initiation of IV antibiotics, our patient died 2 weeks post-hospital discharge. The excessive mortality rate with coronary stent infection highlights the importance of preventive measures and early diagnosis. This very severe complication should be considered in the differential of all patients presenting with fever within the first few weeks following stent implantation. Fortunately, there is a low occurrence of clinically significant bacteremia during nonsurgical cardiology procedures, and this likely limits the incidence of coronary stent infection. In a prospective study assessing the incidence of bacteremia among 960 cardiac catheterization procedures, the incidence of clinically significant procedure-related bacteremia was zero.15 Of interest was the development of positive blood cultures in 5.8% of all cultures taken. Only 0.16% of these were concluded to be clinically significant, and all were due to an IV line and none to the actual cardiac procedure. Risk factors for the development of clinically nonsignificant bacteremia from cardiac catheterization included procedure duration, multiple skin punctures, use of multiple balloons and obesity. Preventive measures during cardiac catheterization may limit the development of bacteremia and the potential risk of coronary stent infection. Conclusion. In summary, we report the first patient with a stent infection who presented with a spontaneous coronary artery perforation. The perforation was sealed with prolonged angioplasty balloon inflations, and the patient was treated with antibiotics. The patient died suddenly 2 weeks post-hospital discharge. The occurrence of stent infection is exceedingly rare, but should be suspected in patients presenting within several days of stent implantation with fever and bacteremia. Despite the identification of this rare condition, treatment strategies have yielded poor outcomes, and the associated mortality rate approaches 50%. References 1. Bank of America Securities LLC Estimates. U.S. Stent Model, 2002–2010. Equity Research 2005. 2. Sigwart U, Puel J, Mirkovitch V, et al. Intravascular stents to prevent occlusion and restenosis after transluminal angioplasty. N Engl J Med 1987;316:701–706. 3. Kaufman BA, Kaiser C, Pfisterer ME, et al. Coronary stent infection: A rare but severe complication of percutaneous coronary intervention. Swiss Med Wkly 2005;135:483–487. 4. Gunther HU, Strupp G, Volmar J, et al. Coronary stent implantation: Infection and abscess with fatal outcome. Z Kardiol 1993;82:521–525. 5. Leroy O, Martin E, Prat A, et al. Fatal infection of coronary stent implantation. Cathet Cardiovasc Diagn 1996;39:168–170. 6. Bouchart F, Dubar A, Bessou JP, et al. Pseudomonas aeruginosa coronary stent infection. Ann Thorac Surg 1997;64:1810–1813. 7. Grewe PH, Machraoui A, Deneke T, et al. Suppurative pancarditis: A lethal complication of coronary stent implantation. Heart 1999;81:559. 8. Rensing BJ, van Geuns RJ, Janssen M, et al. Stentocarditis. Circulation 2000;101:E188–E190. 9. Liu JC, Cziperle DJ, Kleinman B, et al. Coronary abscess: A complication of stenting. Catheter Cardiovasc Interv 2003;58:69–71. 10. Bangher M, Liva P, Baccaro J. Coronary stent infection: Case report and definition. Rev Esp Cardiol 2003;56:325–326. 11. Golubev N, Schwammenthal E, Di Segni E, et al. Echocardiographic imaging of coronary artery abscess following stent implantation. Echocardiography 2004;21:87–88. 12. Singh H, Singh C, Aggarwal N, et al. Mycotic aneurysm of left anterior descending artery after sirolimus-eluting stent implantation: A case report. Catheter Cardiovasc Interv 2005;65:282–285. 13. Hoffman M, Baruch R, Kaplan E, et al. Coronary stent bacterial infection with multiple organ septic emboli. Eur J Intern Med 2005;16:123–125. 14. Alfonso F, Moreno R, Vergas J. Fatal infection after rapamycin eluting coronary stent implantation. Heart 2005;91:E51. 15. Banai S, Selitser V, Keren A, et al. Prospective study of bacteremia after cardiac catheterization. Am J Cardiol 2003;92:1004–1007.

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