The Relationship Between Abdominal Aortic Aneurysm Distensibility and Serum Markers of Elastin and Collagen Metabolism

Wilson, Katie A.; Lindholt, Jes Sanddal; Hoskins, Peter; Heickendorff, Lene; Vammen, Sten; Bradbury, Andrew W.

doi:10.1053/ejvs.2001.1303

Cited by 76 publications

(44 citation statements)

References 20 publications

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“…Increased collagen neosynthesis was observed in AAA compared with control indicating an increased collagen turnover, and related positively to pressure-strain elastic modulus and stiffness in the wall of AAA [79]. These results were in agreement with previous similar studies that were performed specifically in the wall of IRAA aneurysms and control IRAAs.…”

Section: Effects Of Diseasesupporting

confidence: 92%

“…overall: , ** overall: degraded, disrupted [78,79] atherosclerosis overall: [80] rsif.royalsocietypublishing.org J R Soc Interface 10: 20121004 rsif.royalsocietypublishing.org J R Soc Interface 10: 20121004 the normal aorta, and exhibited no structural alterations either [100,101,109]. However, while this trend was consistent for the thoracic aorta as a whole in dissecting aneurysms, specifically at sites of dissection, collagen content was increased and collagen concentration was decreased [103].…”

Section: Effects Of Diseasementioning

confidence: 99%

“…Evaluating the degree of elastin degradation (elastolysis) in the wall of AAA from older (median 68 years) male patients, Wilson et al [79] measured serum elastin peptides (SEPs) and plasma elastin-alpha1-antitrypsin complex (E-AT), which are considered markers of elastin degradation. The content of SEP was increased in the wall of AAA, indicating a higher degree of degradation, and both E-AT and SEP were related inversely to the pressure-strain elastic modulus and stiffness.…”

Section: Effects Of Diseasementioning

confidence: 99%

See 2 more Smart Citations

Elastin and collagen fibre microstructure of the human aorta in ageing and disease: a review

Tsamis

Krawiec

Vorp

2013

J. R. Soc. Interface.

397

300

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Aortic disease is a significant cause of death in developed countries. The most common forms of aortic disease are aneurysm, dissection, atherosclerotic occlusion and ageing-induced stiffening. The microstructure of the aortic tissue has been studied with great interest, because alteration of the quantity and/or architecture of the connective fibres (elastin and collagen) within the aortic wall, which directly imparts elasticity and strength, can lead to the mechanical and functional changes associated with these conditions. This review article summarizes the state of the art with respect to characterization of connective fibre microstructure in the wall of the human aorta in ageing and disease, with emphasis on the ascending thoracic aorta and abdominal aorta where the most common forms of aortic disease tend to occur.

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Section: Effects Of Diseasesupporting

confidence: 92%

Section: Effects Of Diseasementioning

confidence: 99%

Section: Effects Of Diseasementioning

confidence: 99%

See 1 more Smart Citation

Elastin and collagen fibre microstructure of the human aorta in ageing and disease: a review

Tsamis

Krawiec

Vorp

2013

J. R. Soc. Interface.

397

300

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“…29 Wilson et al investigated the relationship between compliance, maximum diameter, and growth rate, and concluded that large aneurysms tended to be less compliant, or stiffer. 30 This group later investigated serum markers in AAA and concluded that increased elastolysis is associated with decreased AAA wall stiffness 31 ( Figure 1). More recently this group has shown that the female gender, higher blood pressure, a decrease in the pressure strain elastic modulus (Ep), and a larger maximum diameter have a significant influence on time to AAA rupture.…”

Section: In Vivo Mechanical Evaluationmentioning

confidence: 99%

Biomechanical Determinants of Abdominal Aortic Aneurysm Rupture

Vorp

Geest

2005

ATVB

229

172

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Abstract-Rupture of abdominal aortic aneurysm (AAA) represents a significant clinical event, having a mortality rate of 90% and being currently ranked as the 13th leading cause of death in the US. The ability to reliably evaluate the susceptibility of a particular AAA to rupture on a case-specific basis could vastly improve the clinical management of these patients. Because AAA rupture represents a mechanical failure of the degenerated aortic wall, biomechanical considerations are important to understand this process and to improve our predictions of its occurrence. Presented here is an overview of research to date related to the biomechanics of AAA rupture. This includes a summary of results related to ex vivo and in vivo mechanical testing, noninvasive AAA wall stress estimations, and potential mechanisms of AAA wall weakening. We conclude with a demonstration of a biomechanics-based approach to predicting AAA rupture on a patient-specific basis, which may ultimately prove to be superior to the widely and currently used maximum diameter criterion. Key Words: abdominal aortic aneurysm Ⅲ biomechanics Ⅲ rupture Ⅲ strength Ⅲ stress A bdominal aortic aneurysm (AAA) is a focal enlargement of the infrarenal aorta, which occurs over a time course of several years. This condition is present in Ϸ2% of the elderly population, with Ϸ150 000 new cases diagnosed each year, and the incidence is increasing. 1,2 If left untreated, AAA will gradually expand until rupture; it is an event that carries a mortality rate of 90% and that is ranked as the 13th most common cause of death in the US. 3 Current AAA repair procedures are expensive and carry significant morbidity and mortality risks.Open repair of AAA is a major surgical procedure that requires patients to be hospitalized typically for 1 week and to recuperate at home for several more weeks. The mean postoperative mortality for elective repair is Ϸ5% and for emergency operations 47% (range 27% to 69%). 4 The major drawback of open repair is the compromised quality of life after surgery because of postoperative pain, the prolonged recovery period, and the high costs associated with both the surgery and the recovery.An alternative approach that avoids the extensive tissue dissection associated with open repair is the minimally invasive endovascular repair procedure. The potential advantages of endovascular AAA repair include reductions in mortality, morbidity, blood loss, hospital stay, intensive careOriginal

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“…67 Similarly, another study in men (65-72 years) with asymptomatic AAA showed that increased AAA wall distensibility (an important predictor of growth and rupture) was associated with increased elastolysis and decreased collagen turn-over. 68 In this context it is of interest that the aortic augmentation index, a measure of arterial wave reflection and stiffness, is inversely associated with cardiorespiratory fitness in men without coronary heart disease. 69 Plasmin Plasmin is a common activator of the proteolytic systems involved in aneurysmal degradation and it has been associated with the expansion of AAA.…”

Section: Pathophysiologymentioning

confidence: 99%

Smoking and Aortic Diseases

Kakafika

Mikhailidis

2007

Circ J

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Cigarette smoking is a major cause of cardiovascular disease (CVD) and is responsible for approximately 11% of the annual total CVD deaths in the United States. 1 Smoking acts synergistically with other vascular risk factors (eg, hypertension, dyslipidaemia and diabetes) to increase vascular morbidity and mortality. 2 However, smoking has a variable magnitude of increased risk for different vascular diseases: the risk is highest for peripheral arterial disease and aortic aneurysm, and is lowest for coronary artery and cerebrovascular diseases. 2 These effects are thought to reverse after smoking cessation. The constituents of cigarette smoke with the major contribution to pathogenesis of vascular disease are nicotine, carbon monoxide, oxidant gases and polycyclic aromatic hydrocarbons. 2 Nonsmokers who are exposed to "secondhand" smoke experience on average a 30% excess risk of ischemic heart disease and nonfatal myocardial infarction. 3 Secondhand smoke exposure has been shown to activate platelets and to produce endothelial dysfunction, in both experimental animals and humans. 3 The mechanisms by which smoking causes acute cardiovascular events include endothelial dysfunction, thrombosis and inflammation.Endothelial dysfunction is an initiating event in atherogenesis, as well as a major factor in causing acute cardiovascular events. Cigarette smoking impairs flow-mediated endothelium-dependent peripheral arterial vasodilatation, an effect that is, at least partly, reversible after smoking Circulation Journal Vol.71, August 2007 cessation. 4 Smokers without atherosclerosis have coronary vasoconstrictor responses to acetylcholine that, in the presence of normal endothelium, produce vasodilatation. 5 Indeed, the oxidant chemicals of smoke degrade nitric oxide (NO) and reduce NO release, with subsequent impairment of vascular dilation and platelet function. 2 Smokers have lower than normal levels of antioxidant vitamins, reflecting their consumption in response to ongoing oxidant stress. 6 In addition, nicotine itself alters the structural and functional characteristics of vascular smooth muscle cells (VSMC) and endothelial cells. 7,8 Experimental data show that human aortic endothelial cells undergo apoptotic changes when they are exposed to cigarette smoke extracts. 9 This process may be prevented by pre-activation of NO synthase by Larginine. 9,10 Furthermore, smoking causes an increase in vascular superoxide production, which results in decreased NO bioactivity and concomitantly increases production of vasoconstrictor eicosanoids. 11 Cigarette smoke extracts, but not nicotine, also inhibit prostacyclin (PGI2: a vasodilator and inhibitor of platelet aggregation) synthesis in human, rabbit and rat vascular tissue. 12 Smoking-mediated endothelial dysfunction also results in reduced secretion of tissue plasminogen activator (tPA) 13 and increased secretion of plasminogen activator inhibitor (PAI)-1, 1 which results in impaired fibrinolysis. This acts in concert with the increased levels of tissue factor and fibrin...

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The Relationship Between Abdominal Aortic Aneurysm Distensibility and Serum Markers of Elastin and Collagen Metabolism

Abstract: increased elastolysis is associated with increased AAA wall distensibility; whereas increased collagen turn-over is associated with reduced distensibility.

Cited by 76 publications

References 20 publications

Elastin and collagen fibre microstructure of the human aorta in ageing and disease: a review

Elastin and collagen fibre microstructure of the human aorta in ageing and disease: a review

Biomechanical Determinants of Abdominal Aortic Aneurysm Rupture

Smoking and Aortic Diseases

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