Clinical diagnosis
Case 232
【Progress】
He was transported to other hospital where cardio-surgeon would serve him.
【Discussion】
Aortic wall composes of three tunicae (layer); intimal tunica, endometrial cells + collagen tissue + internal elastic plate; medial tunica, smooth muscle cells: adventitia tunica, external elastic plate + collagen. Atheroma is formed in intimal tunica, surrounded with collagen and fibrous cap. The surface of fibrous cap is covered with a single layer of endothelium.
When low density lipoprotein (LDL), carrying cholesterol, deposit into vascular wall, Macrophages adhere and intrude to vascular wall and phagocyte LDL, becoming foamy cells in intimal tunica. Each time foamy cells die, naïve macrophages phagocyte LDL again for restore. However, much volume of LDL coming from the vascular lumen, cannot be disposable by phagocytosis of macrophages, leading accumulation of lipid in intimal tunica. T cells stimulate smooth muscle cells to create fibrous cap and granulation tissue. When lipid pool is replaced with granulation with/without calcification, reparation of the vessel is completed. Much volume of LDL over reparation ability of macrophages and T cells, induces lipid pool produced by dying of foam cells and forms atheroma. Then, atheroma includes lipid pool, granulation tissue, foam cells, T cells and fibroid cells from smooth muscles (1-3).
Lipid pool volume accumulation of 1.5 times greater than vascular thickness induces vascular wall fragile and weak, leading to rupture, bleeding and migration of thrombus (1-3). It causes occlusion in middle-sized artery such as coronary artery and ulcer in large-sized artery such as aorta.
In our case, there is a protrusion of intima mimicking false lumen of dissection, and a thickened wall surrounding aortic lumen. We believe that rupture of fibrous cap induces migration of some lipid pool and fibrous cap itself mimics intimal dissection. Further, the regurgitation of arterial flow occurs into intimal space opened by migration of lipid pool, inducing thickened aortic wall. Abdominal aortic dissection occurs less than 5% of all aortic dissections (4). Most aortic dissection is thoracic aortic dissection: Stanford type A 70%, Stanford type B 27% (4).
Inflammatory aortic aneurysm is not a distinct clinical entity but an inflammatory variant of the well-known abdominal aortic aneurysm. It is defined as triads; abdominal pain or back pain; thickened aortic wall: elevation of inflammatory markers of white blood cell count and/or CRP values (5-7). Our patient suffered from abdominal pain once per three days and CT showed thickened aortic wall but no elevation of inflammatory markers that do not meet the clinical criteria of inflammatory aortic aneurysm.
【Summary】
We presented a sixty six years-old male suffering from abdominal pain once for three days. Enhanced CT showed intimal protrusion into the lumen with pouch-like ballooning mimicking pseudo-lumen. We diagnosed it atheromatous penetrating ulcer of abdominal aorta with mural hematoma or with thrombosed dissecting aneurysm. It is borne in mind that let alone aortic aneurysm, aortic lesions include aortic dissection aneurysm, penetrating aortic ulcer and inflammatory aneurysm. Atheroma begins low density lipoprotein (LDL) deposit to intima of the vessel, macrophage phagocyte LDL, becoming foam cells whose necrosis induces lipid accumulation. Further, T cells along with macrophages proceed smooth muscle cells to proliferation of granulation tissue and fibrous cap for reparation process. However, thickness of atheroma increases the vessel wall thickness of 1.5 fold to normal vessel wall which induces rupture causing ulcer in large-sized aorta and occlusion of middle-sized artery such as coronary artery. Abdominal aortic dissection occurs less than 5% of all aortic dissections. Inflammatory aortic aneurysm is defined as triads; abdominal pain or back pain; thickened aortic wall: elevation of inflammatory markers of white blood cell count and/or CRP values. Our patient had no elevation of inflammatory markers and no distinct pseudo-lumen, diagnosing penetrating atherosclerotic ulcer of aorta with mural hematoma or thrombosed dissection.
【References】
1.Nelson Camacho N, et al. Infrarenal Abdominal Penetrating Aortic Ulcer, an Atypical Location of a Rare Disease. Rev Port Cir Cardiotorac Vasc. 2017;24(3-4):176.
2.M, et al. Penetrating atherosclerotic ulcers of the infrarenal aorta: life-threatening lesions. Eur J Vasc Endovasc Surg. 2005;29(1):35-42
3.Sato M et al. Abdominal aortic disease caused by penetrating atherosclerotic ulcers. Ann Vasc Dis. 2012;5(1):8-14
4.Criado FJ . "Aortic dissection: a 250-year perspective". Tex Heart Inst J. 2011;38 : 694–700.
5.Rose AG, et al. Inflammatory variant of abdominal aortic atherosclerotic aneurysm. Arch Pathol Lab Med 1981; 105:409-413.
6.Walker DI, et al. Inflammatory aneurysms of the abdominal aorta. Br J Surg 1972; 59:609-614.
7.Rasmussen TE et al. Inflammatory aortic aneurysms Ann Surg 1997; 225: 155-164
2021.5.26