Abdominal Aortic Aneurysm, Leriche's Syndrome, Inguinal Herniation, and Smoking

The biology behind fascial defects and the use of implants in pelvic organ prolapse repair

“…Matrix metalloproteinases (MMP) that can break down extracellular matrix proteins are over-expressed in hernia patients as well, although this was first shown by Jackson et al in vaginal tissue of women with prolapse [6,7]. A subpopulation of hernia patients may be affected by other signs of connective tissue abnormalities, such as joint hypermobility or aneurysmata [8,9], and their lesions show the same molecular alterations as described above. Obviously, some genetic conditions, among which is Marfan's or Ehlers-Danlos syndrome, directly affect collagen metabolism, hence, predispose to hernia.…”

Abdominal aortic aneurysm and abdominal wall hernia as manifestations of a connective tissue disorder

“…Reported prevalences of inguinal hernias range between 19% and 41% for patients with a history of AAA repair, whereas values for nonaneurysm patients range between 5% and 27%. 11,[13][14][15][16][21][22][23] Pooled analysis of these studies demonstrated that patients treated for AAAs have a 2.3-fold increased risk of inguinal hernia development compared with aortoiliac occlusive disease reconstruction (OR, 2.30; 95% CI, 1.52-3.48; P Ͻ .0001; Fig 2). A reverse link has also been identified, constituting inguinal hernia as an independent risk factor for AAAs.…”

The pathobiology of aortic aneurysms

“…Its prevalence is estimated at 3% in individuals over the age of 50 [2], with a peak incidence in the eighth decade of life [3,4]. Although a definite etiology of this disease has not been identified, it has been associated with numerous, although nonspecific risk factors, including male gender, hypertension, smoking, coronary artery occlusive disease, concurrent peripheral aneurysms, a family history of aneurysm disease, and the presence of inguinal hernia(e) or emphysema [5][6][7][8][9][10][11]. Early studies regarding the pathobiology of aneurysms have indicated that they originate from a degenerative disorder of the arterial wall that is often found in conjunction with atherosclerotic change [12].…”