Aorta is one of the great arteries of the heart arising from the outflow tract of the left ventricle to supply oxygenated blood to the body (see figure 105b and figure 25).

Figure 105b

Four-chamber view showing mitral (MV) and tricuspid (TV) valves. The annulus of the tricuspid valve is more spiral than the annulus of the mitral valve (MV). LA= left atrium; LV= left ventricle; RA= right atrium; RV= right ventricle; VS= ventricular septum.
BF Waller et al: Tomographic views of normal and abnormal hearts: The anatomic basis for various cardiac imaging techniques. Clin Cardiol 13:804(pt 1), 877(pt II), 1990.

Figure 25

Morphology of the normal aortic valve. AMBL= anterior mitral valve leaflet; Ao= aorta; AV= aortic valve; LV= left main; N= noncoronary cusp; LA= left atrium; R= right; RC= right coronary artery. Arrows point to line of closure. Portion of aortic cusp above the line of closure is called the lunula.

From BF Waller: Morphologic aspects of valvular heart disease: Part I. Curr Prob Cardiol IX:13, 1985.


Figure 29

Pericarditis secondary to the fungus, nocardia, with multiple lung nodules and small left pleural effision in CXR

Drapkin,M.S. and Mark,E.J.,A -69-Old -Renal- Transplant Recipient with Low-Grade F ever and Multiple Pulmonary Nodules, New England Journal of Medicine September 21,2000,pp.870-879,Vol.343,No.12

Diagnosis and Treatment of Diseases of the Aorta

Structurally a simple conduit, the aorta can manifest disease in only a limited number of ways. When weakened by disease, its wall may dilate, producing an aneurysm, or it may split in its long axis, producing dissection. In either case, fatal rupture may result. Moreover, like all pipes, it may become obstructed. More often than narrowing of the main trunk, however, obstruction at the origin of a main branch is encountered. In contrast to these relatively few clinical manifestations, an array of disease processes can involve the aorta. Not surprisingly, there is considerable overlap in the clinical presentation of these disorders.
This chapter will first discuss the various diseases that involve the aorta together with their pathogenetic mechanisms, characteristic pathologic features, and typical clinical findings. A description of the common clinical manifestations of aortic disease for which there may be several etiologies or for which the etiology is unknown will follow.


Etiologic And Pathogenetic Considerations In Aortic Disease

Medial Changes of Aging

Circumferential plates or lamellae of elastin fibers constitute the most conspicuous feature of the aortic media when it is examined histologically. Dispersed between the circular elastic fibers are longitudinally oriented smooth muscle cells, collagen fibers, microfibrils, and ground substance.
Clinicians have long recognized dilatation and elongation of the aorta in the elderly. Characteristic alterations in the structure of the aortic wall accompany these changes. Schlatmann and Beckeridentified these as fragmentation of elastic fibers and loss of smooth muscle cell nuclei, so-called medionecrosis. Moreover, collagenous tissue and basophilic ground substance deposits are a feature of the aging aorta.

Aortic Atherosclerosis

Pathologic Anatomy

By middle life, aortic atherosclerosis is nearly universal in the Western world. ts severity varies from individual to individual.

Diabetes, hypercholesterolemia, smoking, and hypertension are among the factors promoting it. The pathology of atherosclerosis is discussed in elsewhere.

Advanced atherosclerotic changes display a characteristic distribution, and involvement is most severe below the renal arteries in the abdominal aorta, is common but less severe in the descending thoracic segment, and is least severe in the ascending segment. With diabetes mellitus, however, disease is frequently severe throughout. Individuals with familial hypercholesterolemia are a second exception to the rule that the ascending aorta is spared. Also, the aortic root and aortic valve may be severely involved in familial cholesterolemia. Both supravalvular and valvular aortic stenosis may develop. Finally, syphilitic ascending aortitis promotes severe atherosclerosis.



Aortic atherosclerosis is manifest as aneurysm, obstruction of the infrarenal aorta, embolization from atheromatous plaques to distal arterial beds, and medial dissection initiated by penetration of a plaque into the media.


Aneurysm of the abdominal aorta has long been presumed to result from penetration into and weakening of the media by atherosclerosis. Thus abdominal aortic aneurysms characteristically appear in individuals with the most severe aortic atherosclerosis in nonaneurysmal segments.
Recent recognition of familial clustering of patients with abdominal aortic aneurysm, the identification of genetic defects in collagen in a family with multiple aneurysms' and the detection of abnormal collagenase and elastase in tissue from aortic aneurysms resected at operation have led some to the assumption that atherosclerosis is invariably the underlying pathophysiologic mechanism. These findings suggest that atherosclerosis represents a secondary response to dilatation of the aorta resulting from medial weakness.Aneurysm of the descending thoracic aorta also traditionally has been attributed to atherosclerosis, since such lesions are commonly accompanied by an infrarenal aneurysm.

Obstruction of the Terminal Aorta

Obstruction of the main aortic channel most often develops in the infrarenal aorta and may extend into the proximal iliac arteries. Obstruction of branch arteries is more common than aortic obstruction.


The luminal surface of a severely diseased aortic segment is often rough and covered with thrombus. Embolization of plaque material and thrombus from these surfaces now appears to he far more common than was once appreciated. Emboli to the brain, the lower extremities, and the coronary, renal, or visceral circulations have been reported.
Transesophageal echocardiography now provides rather startling views of pedunculated thrombus or other atherosclerotic material waving in the aortic blood flow ( Fig. 105d ). Aortas with ulcerated plaques, pedunculated or mobile thrombi, or spontaneous echo contrast are more apt to embolize than are those with flat, layered atherosclerosis. Anticoagulant therapy may be protective against future events.
A variation on the theme, the clinical syndrome labeled cholesterol embolization, with small atherosclerotic particles obstructing small arteries, is a rare complication of severe aortic atherosclerosis. Clinical signs include mottled skin and "purple toes" in the lower extremities together with renal insufficiency and visceral ischemia in more severe cases.this rarely recognized condition may he spontaneous but is more commonly encountered as a complication of intraaortic catheter manipulation. Because eosinophilia is frequent in the initial phases of this event, an immune reaction to the free particles has been suggested.

Penetrating Atherosclerotic Ulcers

Atherosclerotic plaque penetration into the media predisposes to formation of an intramural hematoma. Extension circumferentially and in the long axis of the media may produce a limited medial dissection ( Fig. 105e ). Radial extension results in pseudoaneurysm or rupture. Penetrating ulcers are most commonly recognized in the descending thoracic aorta.
The clinical picture resembles that of aortic dissection or of expansion/rupture of a preexisting aneurysm. Sudden onset of severe back pain in a hypertensive patient or one known to have atherosclerosis is typical. Many are identified in the course of imaging for suspected aortic dissection. Since they are more limited in axial length than typical dissection, and since they arc located in the descending thoracic aorta, aortic regurgitation and altered pulses are not characteristic features. Surgical treatment is often indicated, although some patients survive without operation.


Figure 38b

Pericarditis secondary to nocardia with bilateral pleural fluid, pericardial effusion (see arrow) and lung nodules in CATscan

Drapkin,M.S. and Mark,E.J.,A 69year old renal transplant recipient with low grade fever and multiple pulmonary nodules,New England Journal of Medicine,September 21,2000,pp.870-879,Vol.343,No.12