Vascular Aneurysms Aetiology

· Aneurysms develop at sites of medial weakness

· Susceptible points of weakness may be congenital or acquired

· The most common causes by region are medionecrosis in the ascending aorta and atherosclerosis in the arch and descending aorta

Atherosclerosis	By far the most common cause of aortic disease and therefore aneurysm Atherosclerosis generally spares the ascending aorta — usually affects arch & descending aorta
Medial degeneration	Becoming a more frequent cause — predilection for ascending aorta Includes Marfan’s syndrome - [inheritable connective tissue disease]
Aortitis: Atherosclerosis Autoimmune	Inflammation of aorta
Aortic infection Syphilitic Bacterial TB	Common in past, less common now — predilection for ascending aorta
Trauma	Resulting in traumatic aneurysms & dissections
Myxomatous degeneration	Neoplasm of connective tissue

Etiology of Aneurysms based on location in the aorta in order of frequency
Ascending
Medionecrosis	Accumulation of mucoid material in media of wall
Syphilis	Major cause before 1950
Congenital	Eg: Marfan’s
Post stenotic dilation	2° long standing aortic stenosis
Atherosclerosis	Not a major cause in ascending
Arch
Isolated	Atherosclerosis
Associated with Ascending dx	See as for ascending
Descending
Atherosclerosis	Begins as intimal dx; major cause of thoracoabdominal aneurysms
Congenital	See as for ascending
Trauma	post blunt trauma
Infection	Syphilis, TB

Mechanism relating to expansion of aneurysm

“ When the coats of the aorta, whether from inflammation or from any other morbid action, have become diseased, they lose their elasticity, a quality which resides principally in the middle tunic. As fluids press equally in every direction, the blood propelled by each contraction of the heart into the aorta, exerts not only a longitudinal, but a lateral force, which expands the vessel, and constantly tends to enlarge the caliber. The elasticity of the arterial walls enables the vessels to resist this expansive force, and to regain its previous caliber after the diastole. Consequently, when the elasticity is impaired or lost, the vessel, not being able to regain its original dimensions after each diastole, becomes permanently dilated, and this takes place to a greater or less extent, and with greater or less promptitude, in direct proportion to the predominance of the distending over the resisting force.”

James Hope, 1832

• Aneurysms develop at sites of medial weakness, Susceptible points may be acquired or congenital. Hypertension, frequently presents in patients with aneurysm, exposes weakness that may not be otherwise be manifested and may accelerate degeneration of the aortic wall. Once begun, aneurysm formation is promoted by physical laws, especially that of Laplace. Expansion and rupture frequently result.