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Coronary Stent Infections: A Case Series


In 2003 Liu et al. reported for the first time an infected bare-metal stent presenting as a coronary artery mycotic aneurysm [1]. Four earlier reported cases of coronary stent infection did not describe mycotic aneurysms [2]. In 2005 Kaufmann compiled 10 reported cases and reviewed the risk factors, clinical presentation, diagnosis, therapy, and prognosis of coronary stent infection [3], including the first case of a drug-eluting stent (DES) infection [4]. Here we report three cases of coronary stent infection: two with mycotic aneurysms that ruptured into an adjacent cardiac chamber (one DES, and one bare-metal), and one DES infection that resulted in purulent pericarditis.

Case 1

In December 2006, a 59-year-old man presented to an outside institution with acute anterior ST-segment elevation myocardial infarction. Emergency coronary angiography showed proximal occlusion of the left anterior descending (LAD). He underwent successful percutaneous coronary intervention (PCI) with bare-metal stent placement. The left ventricular ejection fraction was 30%. The procedure was uncomplicated, and he was discharged 48 hr after stent implantation.
Two days later he was hospitalized with fevers and chills, and blood and urine cultures grew Staphylococcus aureus. Despite appropriate antibiotic therapy, he developed shock and pulmonary edema. He was transferred in extremis to our institution and underwent cardiac catheterization and intra-aortic balloon pump placement. Coronary angiography revealed a large mycotic aneurysm of the LAD originating at the proximal stent margin, with rupture into the right ventricular outflow tract (Fig. 1).
Despite aggressive efforts, the patient died during preparation for surgical intervention.

Fig. 1.
Large mycotic aneurysm of the left anterior descending artery originating at the proximal stent margin, and rupturing into the right ventricular outflow tract.

Case 2

This 54-year-old diabetic male on chronic hemodialysis had a Cypher Bx-Velocity1 (Cordis, Warren, NJ) stent placement in the right coronary artery (RCA) in 2004. In 2006 he was hospitalized with osteomyelitis from a chronic foot ulcer and underwent transmetatarsal amputation. Blood cultures grew S. epidermidis and wound cultures grew b-hemolytic streptococci. Two months later he presented with fevers. Blood cultures grew S. aureus, but no definite source of infection was found. Despite appropriate antibiotic therapy, 1 month later he presented with fevers and inferior ST-segment elevation myocardial infarction, and underwent balloon angioplasty of an occluded RCA stent. At the time of PCI blood cultures were again positive for S. aureus of unknown origin. No coronary aneurysm was documented at that time. Thereafter, he was hospitalized several times with fevers and blood cultures positive for S. aureus. Exhaustive diagnostic evaluation failed to reveal the source of recurrent bacteremia. In August 2006 he again presented with fevers and chest pain, and coronary angiography revealed a large mycotic aneurysm of the RCA originating at the proximal stent margin, with rupture into the right atrium (Fig. 2). The patient underwent successful surgical repair with abscess drainage, stent explantation, RCA ligation, and saphenous vein bypass grafting, left internal mammary artery bypass to the LAD, and repair of the right atrium. He was discharged 5 weeks postoperatively to an extended care facility.

Fig. 2.
Large mycotic aneurysm of the right coronary artery originating at the proximal stent margin, and rupturing into the right atrium.

Case 3

In March 2007, a 68-year-old man presented to an outside institution with chest pain and dyspnea 2 weeks after suprapubic prostatectomy. A non-ST elevated myocardial infarction was diagnosed by electrocardiographic changes and serum troponin-I elevation. At the time of hospitalization, he had an E. coli urinary tract infection and cultures from the suprapubic incision grew methicillin-resistant S. aureus (MRSA). Coronary angiography, performed after several days of oral trimethoprim-sulfamethoxazole and intravenous vancomycin, showed severe coronary artery disease. PCI was performed, with two discontiguous DESs placed in the LAD artery (3.5 3 18 mm and 2.5 3 18 mm Cypher Bx-Velocity stents, Cordis) and one DES in the left circumflex artery (2.5 3 13 mm Cypher Bx- Velocity stent, Cordis). Two weeks later he presented to our institution with weakness, chest pain, and dyspnea. No fever was reported. He had new-onset atrial fibrillation and had a white blood cell count at 18,300/mm3 with a significant left shift. Echocardiogram revealed a large pericardial effusion with tamponade physiology. Pericardiocentesis yielded 700 mL of pus and was complicated by pulseless electrical activity requiring resuscitation. Pericardial fluid cultures grew MRSA. The patient was deemed too ill for contrast coronary angiography. Coronary computed tomography-angiography revealed patent coronary stents, no extravasation of contrast from the coronary arteries, and no coronary aneurysm. Despite aggressive antibiotic therapy with vancomycin, the patient died of sepsis and multiorgan failure.


Here we have presented three cases of coronary stent infection with dramatic consequences. Two cases were complicated by rupture of a coronary mycotic aneurysm into an adjacent cardiac chamber, diagnosed during coronary angiography. One of these aneurysms occurred at the site of a DES, and the other at that of a bare-metal stent. To our knowledge, there have been no previous reports of coronary mycotic aneurysm rupture following drug-eluting coronary stent placement, although the incidence of aneurysm formation has been recently reviewed [5]. In our case of DES-associated mycotic aneurysm, it is unclear whether the aneurysm was primarily a result of infection at the time of stent placement or subsequent in-stent balloon angioplasty, or of hematogenous spread from another source of bacteremia. Neither of the other two patients underwent additional coronary instrumentation after stent placement as a possible opportunity for infection. Sterile DES-related coronary aneurysms may contribute to late-stent thrombosis [6,7] and may act as a nidus for stent infection. Pericardial empyema as a consequence of stent placement has been reported [8]. Of the risk factors summarized by Kaufmann et al., age over 60 years and the presence of congestive heart failure may have played a role in two of these cases. As in previously reported cases of stent infection, myocardial infarction was present and surgical intervention was necessary for patient survival [1,9–12]. Two of our three patients died. We suggest the possibility that recent infection with S. aureus within 16 days prior to PCI may be an additional risk factor for the complication of coronary stent infection. Also, we suggest that stent-related infection be included in the differential diagnosis of fever of unknown origin, especially in the setting of S. aureus bacteremia. In our series, as in others, S. aureus was the infecting organism [1–3,9,12–14].


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Autor: Aaron B. Schoenkerman, MD and Robert J. Lundstrom, MD

Fuente: Catheterization and Cardiovascular Interventions 73:74–76 (2009)

Ultima actualizacion: 26 DE ENERO DE 2012

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