Rob Hurks1, Aryan Vink2, Imo E Hoefer3, Jean-Paul P M de Vries4, Arjan H Schoneveld3, Marc L Schermerhorn5, Hester M den Ruijter6, Gerard Pasterkamp3, Frans L Moll7. 1. Vascular Surgery, University Medical Center Utrecht, Utrecht, The Netherlands; Experimental Cardiology, University Medical Center Utrecht, Utrecht, The Netherlands. 2. Pathology, University Medical Center Utrecht, Room H04.312, Heidelberglaan 100, 3584 CX, Utrecht, The Netherlands. Electronic address: a.vink@umcutrecht.nl. 3. Experimental Cardiology, University Medical Center Utrecht, Utrecht, The Netherlands. 4. Vascular Surgery, St Antonius Hospital, Nieuwegein, The Netherlands. 5. Vascular and Endovascular Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA. 6. Experimental Cardiology, University Medical Center Utrecht, Utrecht, The Netherlands; Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, The Netherlands. 7. Vascular Surgery, University Medical Center Utrecht, Utrecht, The Netherlands.
Abstract
OBJECTIVE: Evidence is emerging that abdominal aortic aneurysm (AAA) formation cannot completely be explained by systemic atherosclerosis and is in part due to other pathophysiological mechanisms such as local immune reactions. The aim of the present study was to study variance in AAA wall inflammation, and relate that to clinical patient characteristics. METHODS: Ventral walls from 201 patients with intact AAAs undergoing open repair were prospectively collected and processed for histology and protein measurements. Patients were monitored for 3 years postoperatively. RESULTS: The amount of lymphocytic infiltrate was used to distinguish 96 lymphocyte-poor AAAs from 105 lymphocyte-rich AAAs. The walls of lymphocyte-rich AAAs had higher concentrations of various inflammatory markers, including interleukin (IL) 6, IL8, matrix metalloproteinase (MMP) 8; however, MMP9 levels were comparable. Patients with lymphocyte-poor AAAs had more atherosclerotic risk factors: type 2 diabetes (22% vs. 9%, P = .008), hypertension (81% vs 66%, P = .019), and serum cholesterol levels (mean[SD] 5.2[2.5] vs. 4.2[1.0] mmol/L, P = .023). Intimal lesions in the AAAs revealed more frequently an extracellular lipid pool in lymphocyte-poor AAAs (66% vs. 52%, P = .026). Lymphocyte poor AAAs were associated with a worse survival during 3 years of follow-up, although this association did not reach statistical significance when correcting for other cardiovascular predictors (24% vs. 14%; HR 1.9-2.3). CONCLUSION: Low amount of inflammation in AAAs is associated with more atherosclerotic risk factors, more advanced local atherosclerotic lesions and more postoperative atherosclerotic adverse events. This observation supports the view that AAA development is a multi-factorial process in which part of the patient population has a closer relation with systemic atherosclerotic disease, while in other patients local inflammatory reactions might play a larger role.
OBJECTIVE: Evidence is emerging that abdominal aortic aneurysm (AAA) formation cannot completely be explained by systemic atherosclerosis and is in part due to other pathophysiological mechanisms such as local immune reactions. The aim of the present study was to study variance in AAA wall inflammation, and relate that to clinical patient characteristics. METHODS: Ventral walls from 201 patients with intact AAAs undergoing open repair were prospectively collected and processed for histology and protein measurements. Patients were monitored for 3 years postoperatively. RESULTS: The amount of lymphocytic infiltrate was used to distinguish 96 lymphocyte-poor AAAs from 105 lymphocyte-rich AAAs. The walls of lymphocyte-rich AAAs had higher concentrations of various inflammatory markers, including interleukin (IL) 6, IL8, matrix metalloproteinase (MMP) 8; however, MMP9 levels were comparable. Patients with lymphocyte-poor AAAs had more atherosclerotic risk factors: type 2 diabetes (22% vs. 9%, P = .008), hypertension (81% vs 66%, P = .019), and serum cholesterol levels (mean[SD] 5.2[2.5] vs. 4.2[1.0] mmol/L, P = .023). Intimal lesions in the AAAs revealed more frequently an extracellular lipid pool in lymphocyte-poor AAAs (66% vs. 52%, P = .026). Lymphocyte poor AAAs were associated with a worse survival during 3 years of follow-up, although this association did not reach statistical significance when correcting for other cardiovascular predictors (24% vs. 14%; HR 1.9-2.3). CONCLUSION: Low amount of inflammation in AAAs is associated with more atherosclerotic risk factors, more advanced local atherosclerotic lesions and more postoperative atherosclerotic adverse events. This observation supports the view that AAA development is a multi-factorial process in which part of the patient population has a closer relation with systemic atherosclerotic disease, while in other patients local inflammatory reactions might play a larger role.
Authors: Gregory T Jones; L Victoria Phillips; Michael J A Williams; Andre M van Rij; Tasnuva D Kabir Journal: J Am Heart Assoc Date: 2016-04-28 Impact factor: 5.501