Paul T Albini1, Ana Maria Segura2, Guanghui Liu1, Charles G Minard3, Joseph S Coselli1, Dianna M Milewicz4, Ying H Shen5, Scott A LeMaire6. 1. Michael E. DeBakey Department of Surgery, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA; Department of Adult Cardiothoracic Surgery, Texas Heart Institute, PO Box 20345, Houston, TX 77225, USA. 2. Department of Cardiovascular Pathology, Texas Heart Institute, PO Box 20345, Houston, TX 77225, USA. 3. Dan L. Duncan Institute for Clinical and Translational Research, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA. 4. Division of Medical Genetics, Department of Internal Medicine, The University of Texas Health Science Center at Houston, 6431 Fannin Street, Suite 1200, Houston, TX 77030, USA. 5. Michael E. DeBakey Department of Surgery, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA; Department of Adult Cardiothoracic Surgery, Texas Heart Institute, PO Box 20345, Houston, TX 77225, USA. Electronic address: hyshen@bcm.edu. 6. Michael E. DeBakey Department of Surgery, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA; Department of Adult Cardiothoracic Surgery, Texas Heart Institute, PO Box 20345, Houston, TX 77225, USA. Electronic address: slemaire@bcm.edu.
Abstract
OBJECTIVE: The pathogenesis of non-familial, sporadic ascending aortic aneurysms (SAAA) is poorly understood, and the relationship between ascending aortic atherosclerosis and medial degeneration is unclear. We evaluated the prevalence and severity of aortic atherosclerosis and its association with medial degeneration in SAAA. METHODS AND RESULTS: Atherosclerosis was characterized in ascending aortic tissues collected from 68 SAAA patients (mean age, 62.9 ± 12.0 years) and 15 controls (mean age, 56.6 ± 11.4 years [P = 0.07]) by using a modified American Heart Association classification system. Upon histologic examination, 97% of SAAA patients and 73% of controls showed atherosclerotic changes. Most SAAA samples had intermediate (types 2 and 3, 35%) or advanced atherosclerosis (types ≥ 4; 40%), whereas most control samples showed minimal atherosclerosis (none or type 1, 80%; P < 0.001 after adjusting for age). In a separate analysis, we examined the total incidence and grade distribution of medial degenerative changes among SAAA samples according to atherosclerosis grade. Advanced atherosclerosis was associated with higher grades of smooth muscle cell depletion (P < 0.001), elastic fiber depletion (P = 0.02), elastic fiber fragmentation (P < 0.001), and mucopolysaccharide accumulation (P = 0.04). Aortic diameter was larger in SAAA patients with advanced atherosclerosis than in patients with minimal (P = 0.04) or intermediate atherosclerosis (P = 0.04). Immunostaining showed marked CD3+ T-cell and CD68+ macrophage infiltration, MMP-2 and MMP-9 production, and cryopyrin expression in the medial layer adjacent to atherosclerotic plaque. CONCLUSIONS: SAAA tissues exhibited advanced atherosclerosis that was associated with severe medial degeneration and increased aortic diameter. Our findings suggest a role for atherosclerosis in the progression of sporadic ascending aortic aneurysms.
OBJECTIVE: The pathogenesis of non-familial, sporadic ascending aortic aneurysms (SAAA) is poorly understood, and the relationship between ascending aortic atherosclerosis and medial degeneration is unclear. We evaluated the prevalence and severity of aortic atherosclerosis and its association with medial degeneration in SAAA. METHODS AND RESULTS:Atherosclerosis was characterized in ascending aortic tissues collected from 68 SAAApatients (mean age, 62.9 ± 12.0 years) and 15 controls (mean age, 56.6 ± 11.4 years [P = 0.07]) by using a modified American Heart Association classification system. Upon histologic examination, 97% of SAAApatients and 73% of controls showed atherosclerotic changes. Most SAAA samples had intermediate (types 2 and 3, 35%) or advanced atherosclerosis (types ≥ 4; 40%), whereas most control samples showed minimal atherosclerosis (none or type 1, 80%; P < 0.001 after adjusting for age). In a separate analysis, we examined the total incidence and grade distribution of medial degenerative changes among SAAA samples according to atherosclerosis grade. Advanced atherosclerosis was associated with higher grades of smooth muscle cell depletion (P < 0.001), elastic fiber depletion (P = 0.02), elastic fiber fragmentation (P < 0.001), and mucopolysaccharide accumulation (P = 0.04). Aortic diameter was larger in SAAApatients with advanced atherosclerosis than in patients with minimal (P = 0.04) or intermediate atherosclerosis (P = 0.04). Immunostaining showed marked CD3+ T-cell and CD68+ macrophage infiltration, MMP-2 and MMP-9 production, and cryopyrin expression in the medial layer adjacent to atherosclerotic plaque. CONCLUSIONS:SAAA tissues exhibited advanced atherosclerosis that was associated with severe medial degeneration and increased aortic diameter. Our findings suggest a role for atherosclerosis in the progression of sporadic ascending aortic aneurysms.
Authors: Varun K Krishnamurthy; Richard C Godby; G R Liu; J Michael Smith; Loren F Hiratzka; Daria A Narmoneva; Robert B Hinton Journal: J Cardiovasc Transl Res Date: 2014-11-20 Impact factor: 4.132
Authors: Christian Stern; Bernhard Scharinger; Adrian Tuerkcan; Clemens Nebert; Teresa Mimler; Ulrike Baranyi; Christian Doppler; Thomas Aschacher; Martin Andreas; Marie-Elisabeth Stelzmueller; Marek Ehrlich; Alexandra Graf; Guenther Laufer; David Bernhard; Barbara Messner Journal: Int J Mol Sci Date: 2019-09-26 Impact factor: 5.923