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Interact CardioVasc Thorac Surg 2007;6:741-743. doi:10.1510/icvts.2007.157339 © 2007 European Association of Cardio-Thoracic Surgery
Systemic inflammatory response after endoluminal stenting of the descending thoracic aortaDepartment of Cardiothoracic Surgery, Department of Cardiology, Bristol Heart Institute, The Bristol Royal Infirmary, Upper Maudlin Street, Bristol, BS2 8HN, UK Received 11 April 2007; received in revised form 31 July 2007; accepted 2 August 2007
*Corresponding author. Tel.: +44-117 342 0501.
The effect of the underlying pathology on postoperative inflammation after stenting of the thoracic aorta has not been described. A retrospective review of patients undergoing thoracic aortic stents was performed. Patients with large degenerative aneurysms developed pyrexia and significantly raised CRP in the first 5 days after the procedure compared with the rest of the cohort. Endoluminal stenting of large degenerative descending thoracic aortic aneurysms is associated with post-implantation systemic inflammatory response.
Key Words: Aneurysm; Stents
A ‘post-implantation syndrome’ characterised by systemic inflammation is recognised after stenting of the abdominal aorta. The main features are pyrexia and leukocytosis. It was first described by Valazquez et al. [1] but has since been reported by other authors. Similar observations after thoracic aortic stenting have not been described despite the increase in endoluminal stenting of the thoracic aorta over recent years. The indications for thoracic aortic stenting are numerous, including traumatic aortic transection, acute and chronic type B dissections, aneurysmal disease and congenital lesions. One of the main differences in these pathologies is the amount of thrombus contained within the aorta. A large aneurysm will usually contain a large volume of thrombus as opposed to a congenital lesion, which usually contains no thrombus. A possible cause of systemic inflammation post-stent implantation is cytokine release after manipulation of endovascular thrombus. A program of thoracic aortic stenting has recently been established in our institution and in this paper we present our observations on clinical evidence of an inflammatory response after endoluminal stenting of the thoracic aorta, and the relationship between thoracic aortic pathology and a systemic inflammatory response.
All patients having endoluminal thoracic stents in a single institution over a 3-year period from October 2003 to October 2006 form the cohort for this report. The cohort was divided into two groups. Group A consisting of patients with large degenerative aneurysms (Fig. 1) and Group B, the rest of the cohort. Patients were identified from a prospective database. Intra and postoperative data were collected from a retrospective review of the case notes.
Endovascular stenting was under general anaesthesia in the cardiac catheterisation suite in all cases and performed by a cardiac surgeon and an interventional cardiologist. After the administration of a single dose of 5000 IU of intravenous heparin, the common femoral artery was dissected and an 8–10-mm sized Dacron graft was sutured to the artery to provide access to the thoracic aorta. The Talent endoprosthesis (Medtronic) was used in all cases. All patients were admitted to a high dependency unit after the procedure. Temperature was recorded twice daily. Leukocyte count was measured daily on the first five postoperative days. C-reactive protein (CRP) was measured depending on the clinical status of the patient. All patients had a post-procedure CT scan to assess the position of the stent and detect complications.
The cohort was 22 patients of mean age 53(18) years. Sixty-four percent were male. The indications for thoracic stenting were acute type B dissection (7), traumatic aortic rupture (7), degenerative aneurysm of the descending aorta (4), a saccular aneurysm of the ductus arteriosus (2), false aneurysm of the descending aorta (1) and a mycotic saccular aneurysm of the descending aorta (1). There was a technical failure of the procedure in one patient, due to inability to pass the stent through a small femoral artery. Early after the procedure, one patient with a degenerative aneurysm of the descending aorta suffered temporary lower limb paraplegia, which resolved after CSF drainage. One patient with an acute type B dissection died from mesenteric ischaemia 20 days after endoluminal stenting. There were four patients in Group A and 18 patients in Group B. The mean aortic diameter in the Group A was 7.3(1.5) cm vs. 4(1) cm in Group B, P=0.01. When the mean temperature in the first five postoperative days was compared, patients in Group A had a significant pyrexia, with a mean temperature of 38.3(0.9) vs. 36.8(0.4) °C in Group B, P=0.017. Fig. 2 shows the mean temperature in the first five postoperative days for Group A and Group B.
Similarly, when the mean CRP in the first five postoperative days was compared patients in Group B had a significantly raised CRP, 204(38) vs. 119(105) mg/ml, than patients in Group B, P=0.05. There was no difference in the mean leukocyte count during the first five postoperative days between the two groups, 11.2(2.3) in Group A vs. 8.2(2.7)x109/l, in Group B, P=0.7. There was no difference in the length of stay on the ICU [2(1) vs. 4(2) days, P=0.1 for Groups A and B, respectively], or total length of stay in hospital [10(5) vs. 13(9) P=0.1 for Groups A and B, respectively]. In all cases, extensive blood, urine, and sputum cultures were negative. So far no patient has developed a prosthesis-related infection.
A post-implantation syndrome characterised by fever and leukocytosis was first described after stenting of the abdominal aorta [1]. This has been attributed to complex immunological changes occurring in the first week after stenting mediated by TNF-  [2]. This immune response appears to be different from the more generalised immune response seen after open repair of the abdominal aorta, which is due to extensive surgical trauma and reperfusion injury [3]. The trigger for the immune response is unclear. The impact of endograft material has been extensively studied. In one study, grafts made of polyester resulted in more episodes of pyrexia compared with grafts made from expanded polytetrafluoroethylene (ePTFE) [4]. In our unit it has consistently been observed that patients with large degenerative descending thoracic aortic aneurysms usually containing thrombus, develop a systemic inflammatory response after stenting. This response is characterised by pyrexia and a raised CRP. In all cases pyrexia continued despite antibiotic therapy and no positive culture results were attained. This phenomenon has not been observed when stenting was performed for a variety of other pathologies.
It is likely that the inflammatory response was due to the large size of the aneurysm and the thrombus within the aneurysm sac. It is possible that manipulation of the endoprosthesis in the large amounts of thrombus present in the large denenerative aneurysm may explain the systemic inflammatory reaction not observed when the diameter of the stented aorta is much smaller and when no thrombus was present. The mechanism may be the release of cytokines, in particular interleukin-6, causing activation of leukocytes and promotion of TNF- In conclusion, stenting of large degenerative aneurysms of the thoracic aorta is associated with a systemic inflammatory response, which is not observed when the thoracic aorta is stented for other pathology. This is probably related to the volume of thrombus within the large aneurysm sac.
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Abstract
1. Introduction
