Aortic Atherosclerosis

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Atherosclerosis is a degenerative process of arteries. This disease starts early in life and develops slowly and silently. It is particularly important to detect atherosclerosis in the main large arteries, such as the aorta and the carotid. The principal onset of atherosclerosis is formation of plaque: this can be due to several factors including endothelial dysfunction, intimal hyperplasia, lipid accumulation and inflammation.[1] Other aspects to take into consideration are aortic stiffening and aneurysm.

Atherosclerosis is the leading cause of cardiovascular mortality and morbidity in the Western countries. It is also one of the main cause driving healthcare costs and shows increasing prevalence in developing nations.[2] The main consequence of atherosclerosis is stenosis (arterial narrowing) and the related effects.[2] This disease can affect different sites: among these great emphasis has been placed on large central arteries such as the carotid and the aorta.

Aortic atherosclerosis can manifest in three different principal ways: at early stage with aortic stiffening that can lead, in conjunction with other vascular alterations, to aortic aneurysm, or aortic plaque.

aortic stiffening

The ability to identify a "vulnerable" patient can be increased by the introduction of innovative biomarkers, such as those based on laboratory analysis and omics techniques, or the ones objectively measurable on biomedical signals and images. This approach, also in diagnostics and pharmacology, is particularly important when applied to implement a model for effective prevention able to detect the presence of vascular damage at the sub-clinical, asymptomatic stage preceding of decades the onset of disease (and stenosis). In this way effective screening and prevention can be obtained, that reduce the transition of the disease to deadly (for the patient) and expensive (for the National Health Service - NHS) clinical stages. Among these innovative biomarkers, great attention has been placed on arterial stiffness and in particular on central (i.e. aortic) stiffness.

Aortic stiffness is an independent predictor of cardiovascular morbidity and mortality; this biomarker is thought to have a potential crucial role in the early prevention and diagnosis of cardiovascular diseases. Currently it is widely used in clinical studies to assess the effect of either non-pharmacological or pharmacological treatment on cardiovascular risk.[3] Arterial stiffness can be evaluated by different non-invasive techniques at systemic, regional or local level.[4] The regional evaluation by carotid to femoral pulse wave velocity (PWV) provides an estimation of aortic stiffness and it is considered to be the “gold standard” method.[4] This estimation is usually obtained by applanation tonometry; briefly, the pulse wave signal is recorded at two sites (carotid and femoral), and the temporal distance between the two feet is computed (Pulse Transit Time, PTT). The ratio between the geometrical distance and the PTT, gives us the PWV: this velocity is altered (i.e. increased) in the presence of a process of stiffening that accompanies vascular atherosclerosis since its genesis.

aortic aneurysm

Structural alterations and related biomechanical changes due to atherosclerosis can cause aneurysm.[5]

Aortic aneurysms, and in particular abdominal aortic lesions (AAAs), are focal dilata- tions of the infrarenal aorta that typically have a fusiform shape and are prone to rupture. AAAs present an abnormal shape with maximum diameter over 150 per cent of healthy vessels. They are characterized by a reduction in medial elastin and smooth muscle cells, and by a decreased elasticity.[5] Biomechanics plays fundamental roles in both the enlargement and rupture of these lesions [for further details see related web-page].

aortic plaque

Atherosclerosis develops slowly and progressively and can lead to the formation of plaque. Many plaques remain asymptomatic and stable, but some of them are prone to rupture.[1] Aortic plaques, especially in the aortic arch, are among the main causes of stroke and peripheral emboli.[6] These vulnerable plaques that result in a high risk for the patient, are characterized by a large lipid core and thin fibrous cap, inflammation, plaque ulceration and stenosis >90% or fissures.[1] A classification scale for this kind of lesion was provided by the American Heart Association, and includes six types.[7]

Ultrasound technique is usually adopted to screen for aortic lesions.[8] Atheromas in the thoracic aorta can be detected by transesophageal (TEE) echocardiograms that is considered the technique of choice in the field; this method allows aortic evaluation from its root to the descending tract with the exception of a part of the distal ascending segment close to the innominate artery.[8] The adopted criteria used to diagnose this kind of lesions are the presence of increased echodensity of the aortic intima with lumen irregularity and thickening or ulceration.[8]

Also transthoracic echocardiography (TTE), that has lower resolution, but is more feasible, can be adopted for aorta screening in short- and long-axis views,[6] in particular for the aortic root and the proximal descending segment.[8] In addition, suprasternal harmonic imaging by TTE can be used for detecting arch lesions.[8] Also in this case atherosclerosis is defined as irregular intimal thickening with increased echogenicity. With this kind of approach we can discriminate simple and between complex (mobile debris, ulceration, >4mm thickness) lesion.[8]

In addition, aortic plaques, and in particular vulnerable lesions, can also be detected by other imaging modatilies.[1] Among these:


Optical Coherence Tomography is based on back- scattered light intensity obtained by infrared low coherent light source and provides images at micron scale level. This technique allow the best results in terms of resolution and permits the evaluation of fibrous cap thickness; in addition it is able to discriminate three different tissue types with high sensitivity and specificity in aortas, carotid and coronary arteries.[1]


Magnetic resonance angiography (MRA) is used to assess the level of stenotic lesions and the high-resolution MRI is able to locate the main components of the atheroma. Human in vivo plaque characterization has been achieved in the aorta and the carotid artery.[1]


Combined plaque anatomy and function can be estimated by computed tomography in conjunction with positron emission tomography based on atheroma-targeted contrast agents. However, this approacch has still to be transfer from bench to bedside.[1]

The prevalence of aortic atherosclerosis increases with age, smoking and pulse pressure.[8] Plaques in the proximal aorta play and important role in stroke and peripheral emboli.[6] In three independent works[8] including both patients with previous events and controls, the risk of stroke in patients with severe aortic lesions in one year resulted around 10%. Besides works including high-risk patients, also analysis on general population were performed. In the SPARC (Stroke Prevention Assessment of Risk in a Community) study 588 old white subjects (age = 66.9 years) randomly selected were analysed by TEE for seven years:[6] lesions were detected in 43.7% of the population. The presence of aortic lesion was found to be related with other cardiovascular risk markers and atherosclerosis manifestations[9] but not to predict future cardiovascular events. Similar results were obtained in the APRIS study (Aortic Plaques and Risk of Ischemic Stroke).[10]

Further studies to assess the predictive value of aorta atheroscleroiss for stroke in general population are needed.


  1. 1.0 1.1 1.2 1.3 1.4 1.5 1.6 J G Kips, P Segers, L M. Van Bortel. Identifying the vulnerable plaque: A review of invasive and non-invasive imaging modalities. Artery Research (2008) 2, 21-34
  2. 2.0 2.1 W. W. Nichols, M. F. O'Rourke, C. Vlachopoulos. McDonald's Blood Flow in Arteries, 6th ed: Theoretical, Experimental and Clinical Principles.
  3. Laurent S, Kingwell B, Bank A, Weber M, Struijker-Boudier H. Clinical applications of arterial stiffness: therapeutics and pharmacology. American Journal of Hypertension 2002;15:453– 458.
  4. 4.0 4.1 Laurent S, Cockcroft J, Van Bortel L, Boutouyrie P, Giannattasio C, Hayoz D, Pannier B, Vlachopoulos C, Wilkinson I, Struijker-Boudier H; European Network for Non-invasive Investigation of Large Arteries. Expert consensus document on arterial stiffness: methodological issues and clinical applications. Eur Heart J. 2006 Nov;27(21):2588-605.
  5. 5.0 5.1 D. Haskett, G. Johnson, A. Zhou, U. Utzinger, J. Vande Geest. Microstructural and biomechanical alterations of the human aorta as a function of age and location. Biomech Model Mechanobiol (2010) 9:725–736.
  6. 6.0 6.1 6.2 6.3 I Kronzon, P Tunick. Aortic Atherosclerosis disease and stroke. Circulation 2006; 114: 63-75.
  7. Stary HC, Chandler AB, Dinsmore RE, Fuster V, Glagov S, Insull Jr W, et al. A definition of advanced types of atheroscle- rotic lesions and a histological classification of atherosclerosis. A report from the Committee on Vascular Lesions of the Coun- cil on Arteriosclerosis, American Heart Association. Circulation 1995;92(5):1355e74.
  8. 8.0 8.1 8.2 8.3 8.4 8.5 8.6 8.7 A Evangelista, F A. Flachskampf, R Erbel, F Antonini-Canterin, C Vlachopoulos, G Rocchi, R Sicari, P Nihoyannopoulos, and J Zamorano on behalf of the European Association of Echocardiography. Echocardiography in aortic diseases: EAE recommendations for clinical practice. European Journal of Echocardiography (2010) 11, 645–658.
  9. Christianson, and Yoram Agmon O. Wiebers, Jack P. Whisnant, Jody L. Covalt, Tanya M. Petterson, Teresa J.H. Irene Meissner, Bijoy K. Khandheria, Sheldon G. Sheps, Gary L. Schwartz, David. Atherosclerosis of the aorta: Risk factor, risk marker, or innocent bystander?: A prospective population-based transesophageal echocardiography study. J. Am. Coll. Cardiol. 2004;44;1018-1024.
  10. Russo C, Jin Z, Rundek T, Homma S, Sacco RL, Di Tullio MR. Atherosclerotic disease of the proximal aorta and the risk of vascular events in a population-based cohort: the Aortic Plaques and Risk of Ischemic Stroke (APRIS) study. Stroke. 2009 Jul;40(7):2313-8. Epub 2009 Jun 4.

Further reading and external links section

1. Pannier BM, Avolio AP, Hoecks A, Mancia G, Takazawa K. Methods and devices for measuring arterial compliance in humans. American Journal of Hypertension 2002;15:743 – 753.

2. Oliver JJ, Webb DJ. Non invasive assessment of arterial stiffness and risk of atherosclerotic events. Arteriosclerosis, Thrombosis and Vascular Biology Apr 2003; 23:554-556.

3. Virmani R, Kolodgie FD, Burke AP, Farb A, Schwartz SM. Lessons from sudden coronary death e a comprehensive morphological classification scheme for atherosclerotic lesions. Arterioscler Thromb Vasc Biol 2000;20(5):1262e75.



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