BACKGROUND: Risk factor profiles for the different vascular beds (i.e. coronary, carotid, peripheral and aortic) are remarkably different, suggesting that atherosclerosis is a heterogeneous disorder. Little is known about the morphologic progression of atherosclerosis in the peri-renal aorta, one of the primary predilection sites of atherosclerosis. METHODS: A systematic analysis was performed in 260 consecutive peri-renal aortic patches (stained with Movat Pentachrome and H&E) collected during organ transplantation (mean donor age 46.5 (range 5-76) years; 54% male symbol; mean BMI 24.9; 40% smokers; 20% hypertensive). Plaque morphology was classified according to the modified AHA classification scheme proposed by Virmani et al. [4]. Immunostaining against CD68 was used to identify the distribution of intimal macrophages and monocytes in several predefined locations among various plaque types and fibrous cap thickness. RESULTS: There was significant intimal thickening (p<0.013) and medial thinning (p<0.032) with advancing age. The incidence of atherosclerotic plaques in the abdominal aorta correlated with age (r=0.640, p=0.01). During the first three decades of life adaptive intimal thickening and intimal xanthomas were the predominant lesions. In contrast, the fourth, fifth and sixth decades hallmarked more complicated plaques of pathological intimal thickening, early and late fibroatheromas (EFAs and LFAs), thin-cap FAs (TCFAs; cap thickness <155 microm), ruptured plaques (PRs), healed rupture and fibrotic calcified plaques. The mean percentage of lesional macrophages increased significantly from LFAs to TCFAs (5-17%; p<0.001). Macrophage infiltration of the fibrous cap was negatively correlated with fibrous cap thickness (p<0.0004); TCFAs and PRs (caps<100 microm) contained significantly more macrophages (19%) compared with caps 101-300 microm (6%) and >300 microm (2%). Macrophages in shoulder regions were highest in early and late FAs ( approximately 45%) followed by TCFAs (27%) and PR (20%). Further, intimal vasa vasorum were mostly seen adjacent to the necrotic core of advanced atherosclerotic plaques and remained confined to the intimo-medial border despite marked thickening of the intima. CONCLUSION: This study shows that peri-renal aortic atherosclerosis starts early in life. Gross plaque morphologies of the peri-renal abdominal aorta are similar to coronary atherosclerosis yet indications were found for site specific differences in macrophage content and neovascularization. Copyright 2009 Elsevier Ireland Ltd. All rights reserved.
BACKGROUND: Risk factor profiles for the different vascular beds (i.e. coronary, carotid, peripheral and aortic) are remarkably different, suggesting that atherosclerosis is a heterogeneous disorder. Little is known about the morphologic progression of atherosclerosis in the peri-renal aorta, one of the primary predilection sites of atherosclerosis. METHODS: A systematic analysis was performed in 260 consecutive peri-renal aortic patches (stained with Movat Pentachrome and H&E) collected during organ transplantation (mean donor age 46.5 (range 5-76) years; 54% male symbol; mean BMI 24.9; 40% smokers; 20% hypertensive). Plaque morphology was classified according to the modified AHA classification scheme proposed by Virmani et al. [4]. Immunostaining against CD68 was used to identify the distribution of intimal macrophages and monocytes in several predefined locations among various plaque types and fibrous cap thickness. RESULTS: There was significant intimal thickening (p<0.013) and medial thinning (p<0.032) with advancing age. The incidence of atherosclerotic plaques in the abdominal aorta correlated with age (r=0.640, p=0.01). During the first three decades of life adaptive intimal thickening and intimal xanthomas were the predominant lesions. In contrast, the fourth, fifth and sixth decades hallmarked more complicated plaques of pathological intimal thickening, early and late fibroatheromas (EFAs and LFAs), thin-cap FAs (TCFAs; cap thickness <155 microm), ruptured plaques (PRs), healed rupture and fibrotic calcified plaques. The mean percentage of lesional macrophages increased significantly from LFAs to TCFAs (5-17%; p<0.001). Macrophage infiltration of the fibrous cap was negatively correlated with fibrous cap thickness (p<0.0004); TCFAs and PRs (caps<100 microm) contained significantly more macrophages (19%) compared with caps 101-300 microm (6%) and >300 microm (2%). Macrophages in shoulder regions were highest in early and late FAs ( approximately 45%) followed by TCFAs (27%) and PR (20%). Further, intimal vasa vasorum were mostly seen adjacent to the necrotic core of advanced atherosclerotic plaques and remained confined to the intimo-medial border despite marked thickening of the intima. CONCLUSION: This study shows that peri-renal aortic atherosclerosis starts early in life. Gross plaque morphologies of the peri-renal abdominal aorta are similar to coronary atherosclerosis yet indications were found for site specific differences in macrophage content and neovascularization. Copyright 2009 Elsevier Ireland Ltd. All rights reserved.
Authors: Ljubica Perisic Matic; Urszula Rykaczewska; Anton Razuvaev; Maria Sabater-Lleal; Mariette Lengquist; Clint L Miller; Ida Ericsson; Samuel Röhl; Malin Kronqvist; Silvia Aldi; Joelle Magné; Valentina Paloschi; Mattias Vesterlund; Yuhuang Li; Hong Jin; Maria Gonzalez Diez; Joy Roy; Damiano Baldassarre; Fabrizio Veglia; Steve E Humphries; Ulf de Faire; Elena Tremoli; Jacob Odeberg; Vladana Vukojević; Janne Lehtiö; Lars Maegdefessel; Ewa Ehrenborg; Gabrielle Paulsson-Berne; Göran K Hansson; Jan H N Lindeman; Per Eriksson; Thomas Quertermous; Anders Hamsten; Ulf Hedin Journal: Arterioscler Thromb Vasc Biol Date: 2016-07-28 Impact factor: 8.311
Authors: C Arnoud Meijer; Pum A A Le Haen; Rogier A van Dijk; Mitsuhisa Hira; Jaap F Hamming; J Hajo van Bockel; Jan H Lindeman Journal: Clin Sci (Lond) Date: 2012-05 Impact factor: 6.124
Authors: R A van Dijk; A J F Duinisveld; A F Schaapherder; A Mulder-Stapel; J F Hamming; J Kuiper; O J de Boer; A C van der Wal; F D Kolodgie; R Virmani; J H N Lindeman Journal: J Am Heart Assoc Date: 2015-03-26 Impact factor: 5.501
Authors: Rogier A van Dijk; Kevin Rijs; Anouk Wezel; Jaap F Hamming; Frank D Kolodgie; Renu Virmani; Alexander F Schaapherder; Jan H N Lindeman Journal: J Am Heart Assoc Date: 2016-06-16 Impact factor: 5.501
Authors: D Verzola; S Milanesi; M Bertolotto; S Garibaldi; B Villaggio; C Brunelli; M Balbi; P Ameri; F Montecucco; D Palombo; G Ghigliotti; G Garibotto; J H Lindeman; C Barisione Journal: Sci Rep Date: 2017-04-13 Impact factor: 4.379
Authors: Timo Rademakers; Emiel P C van der Vorst; Isabelle T M N Daissormont; Jeroen J T Otten; Kosta Theodorou; Thomas L Theelen; Marion Gijbels; Andrey Anisimov; Harri Nurmi; Jan H N Lindeman; Andreas Schober; Sylvia Heeneman; Kari Alitalo; Erik A L Biessen Journal: Sci Rep Date: 2017-03-28 Impact factor: 4.379
Authors: Gonzalo Sánchez-Duffhues; Amaya García de Vinuesa; Vera van de Pol; Marlieke E Geerts; Margreet R de Vries; Stef Gt Janson; Hans van Dam; Jan H Lindeman; Marie-José Goumans; Peter Ten Dijke Journal: J Pathol Date: 2019-01-16 Impact factor: 7.996
Authors: Till Seime; Asim Cengiz Akbulut; Moritz Lindquist Liljeqvist; Antti Siika; Hong Jin; Greg Winski; Rick H van Gorp; Eva Karlöf; Mariette Lengquist; Andrew J Buckler; Malin Kronqvist; Olivia J Waring; Jan H N Lindeman; Erik A L Biessen; Lars Maegdefessel; Anton Razuvaev; Leon J Schurgers; Ulf Hedin; Ljubica Matic Journal: Cells Date: 2021-05-21 Impact factor: 6.600