Joseph V Moxon1, Rhondda E Jones2, Paul E Norman3, Paula Clancy1, Leon Flicker4, Osvaldo P Almeida5, Graeme J Hankey6, Bu B Yeap7, Jonathan Golledge8. 1. The Queensland Research Centre for Peripheral Vascular Disease, College of Medicine and Dentistry, James Cook University, Townsville, QLD, 4811, Australia. 2. The Australian Institute of Tropical Health and Medicine, James Cook University, Townsville, QLD, Australia. 3. School of Surgery, University of Western Australia, Perth, WA, Australia. 4. School of Medicine and Pharmacology, University of Western Australia, Perth, Australia; Department of Geriatric Medicine, Royal Perth Hospital, Perth, Australia; WA Centre for Health and Ageing, Centre for Medical Research, Perth, Australia. 5. School of Psychiatry and Clinical Neurosciences, University of Western Australia, Perth, Australia; WA Centre for Health and Ageing, Centre for Medical Research, Perth, Australia; Department of Psychiatry, Royal Perth Hospital, Perth, Australia. 6. School of Medicine and Pharmacology, University of Western Australia, Perth, Australia; Department of Neurology, Sir Charles Gardiner Hospital, Nedlands, Perth, Australia. 7. School of Medicine and Pharmacology, University of Western Australia, Perth, Australia; Department of Diabetes and Endocrinology, Fiona Stanley Hospital, Perth, Australia. 8. The Queensland Research Centre for Peripheral Vascular Disease, College of Medicine and Dentistry, James Cook University, Townsville, QLD, 4811, Australia; Department of Vascular and Endovascular Surgery, The Townsville Hospital, Townsville, QLD, Australia. Electronic address: jonathan.golledge@jcu.edu.au.
Abstract
BACKGROUND AND AIMS: Experimental studies using a rodent model have suggested that iron overload may contribute to abdominal aortic aneurysm (AAA) pathogenesis. METHODS: We assessed the association of total body iron, as measured by plasma ferritin, with AAA diagnosis, size and growth in 4024 community-dwelling older men screened for AAA, using logistic regression and linear mixed effects models. RESULTS: Plasma ferritin concentrations were similar in men who did (n = 293) and did not (n = 3731) have an AAA (median [inter-quartile range] concentrations 115.4 [63.0-203.1] and 128.5 [66.1-229.1] ng/mL respectively, p = 0.124). There was no association between plasma ferritin concentration and AAA diagnosis in unadjusted logistic regression (odds ratio (OR) for a 1 standard deviation increase: 0.880 [95%CI: 0.764-1.015]; p = 0.078), or when adjusting for AAA risk factors and factors known to influence circulating ferritin (OR for a 1 standard deviation increase: 0.898 [95% CI: 0.778-1.035]; p = 0.138). Iron overload prevalence (plasma ferritin concentrations >200 ng/mL) was lower in men with an AAA (25.3%) than those without (30.8%; p = 0.048), but was not associated with AAA diagnosis after adjusting as above (OR: 0.781 [95% CI:0.589-1.035]; p = 0.086). The association of iron overload with AAA growth was investigated in 265 men with small AAAs who received at least 1 repeat ultrasound scan in the 3 years following screening. We saw no difference in AAA growth between men who did and did not have iron overload (n = 65 and 185 respectively, p = 0.164). CONCLUSIONS: Our data suggest that iron overload is unlikely to be important in AAA pathogenesis. Crown
BACKGROUND AND AIMS: Experimental studies using a rodent model have suggested that iron overload may contribute to abdominal aortic aneurysm (AAA) pathogenesis. METHODS: We assessed the association of total body iron, as measured by plasma ferritin, with AAA diagnosis, size and growth in 4024 community-dwelling older men screened for AAA, using logistic regression and linear mixed effects models. RESULTS: Plasma ferritin concentrations were similar in men who did (n = 293) and did not (n = 3731) have an AAA (median [inter-quartile range] concentrations 115.4 [63.0-203.1] and 128.5 [66.1-229.1] ng/mL respectively, p = 0.124). There was no association between plasma ferritin concentration and AAA diagnosis in unadjusted logistic regression (odds ratio (OR) for a 1 standard deviation increase: 0.880 [95%CI: 0.764-1.015]; p = 0.078), or when adjusting for AAA risk factors and factors known to influence circulating ferritin (OR for a 1 standard deviation increase: 0.898 [95% CI: 0.778-1.035]; p = 0.138). Iron overload prevalence (plasma ferritin concentrations >200 ng/mL) was lower in men with an AAA (25.3%) than those without (30.8%; p = 0.048), but was not associated with AAA diagnosis after adjusting as above (OR: 0.781 [95% CI:0.589-1.035]; p = 0.086). The association of iron overload with AAA growth was investigated in 265 men with small AAAs who received at least 1 repeat ultrasound scan in the 3 years following screening. We saw no difference in AAA growth between men who did and did not have iron overload (n = 65 and 185 respectively, p = 0.164). CONCLUSIONS: Our data suggest that iron overload is unlikely to be important in AAA pathogenesis. Crown
Authors: Diana Thomas Manapurathe; Joseph Vaughan Moxon; Smriti Murali Krishna; Frank Quigley; Michael Bourke; Bernard Bourke; Rhondda E Jones; Jonathan Golledge Journal: Front Cardiovasc Med Date: 2022-05-03
Authors: Jenna L Pinchbeck; Joseph V Moxon; Sophie E Rowbotham; Michael Bourke; Sharon Lazzaroni; Susan K Morton; Evan O Matthews; Kerolos Hendy; Rhondda E Jones; Bernie Bourke; Rene Jaeggi; Danella Favot; Frank Quigley; Jason S Jenkins; Christopher M Reid; Ramesh Velu; Jonathan Golledge Journal: J Am Heart Assoc Date: 2018-10-02 Impact factor: 5.501