Changes in monocyte subsets are associated with an increased risk of AAA and are surrogate markers for AAA morphology in patients with late-stage disease

Bianca Hamann¹Anna Klimova²Marvin Kapalla¹David M Poitz³Albert Busch¹Henning Morawietz⁴Christian Reeps¹Anja Hofmann^1*

• ¹Division of Vascular and Endovascular Surgery, Department of Visceral, Thoracic and Vascular Surgery, University Hospital and Medical Faculty Carl Gustav Carus, Dresden, Germany
• ²Institute for Medical Informatics and Biometry, Faculty of Medicine, TUD Dresden University of Technology, Dresden, Germany
• ³Institute for Clinical Chemistry and Laboratory Medicine; University Hospital and Medical Faculty Carl Gustav Carus, TUD Dresden University of Technology, Dresden, Germany
• ⁴Division of Vascular Endothelium and Microcirculation, Department of Medicine III, University Hospital and Medical Faculty Carl Gustav Carus, TUD Dresden University of Technology, Dresden, Germany

Introduction: Monocytes play a role in pathology of abdominal aortic aneurysm (AAA) and can display an immunophenotypic heterogeneity. Alterations in monocyte subsets are associated with cardiovascular risk, but their profile in AAA is poorly understood. Aim: We aimed to comprehensively define associations of monocyte phenotypes with AAA risk and AAA morphology. Methods: Monocyte subsets (CD14++CD16-; CD14++/CD16+; CD14+/CD16++) were analyzed in an observational study in patients with AAA (n=33) and varicose veins (n=33) using flow cytometry. Results: Classical monocytes were 3 % lower (P=0.001) in AAA, while intermediate and non-classical monocytes were 1.8 (P=0.019) and 1.9-fold (P=0.025) higher in AAA, respectively. The differences remained significant after adjusting for age, sex and peripheral artery disease. A lowering of classical monocytes (OR: 0.73, P=0.002) and increases in intermediate (OR: 1.41, P=0.006) and non-classical monocytes (OR: 1.54, P=0.030) were associated with a higher risk of AAA. Non-classical monocytes showed an inverse correlation with AAA diameter (rP =-0.64, P=0.001) and AAA volume (rP =-0.50, P=0.003). Conclusion: The present study revealed age-and sex-independent shifts in monocytes, all of which were associated with risk of AAA disease. Non-classical monocytes were inversely correlated with AAA diameter and volume and thus may be surrogate markers for AAA morphology. Non-standard abbreviations and acronyms AAA, abdominal aortic aneurysm; ACE, angiotensin-converting enzyme; ARBs, angiotensin receptor blocker; ASA, acetylsalicylic acid; BMI, body mass index; CAD, coronary artery disease; CAS, carotid artery stenosis; CCB, calcium channel blocker; CVD, cardiovascular disease; Hb, hemoglobin; HDL, high-density lipoprotein cholesterol; HF, heart failure; LDL, low-density lipoprotein cholesterol; PAD, peripheral artery disease; T2D, Type 2 diabetes mellitus; TC, total cholesterol