DOI
https://doi.org/10.25772/RY48-MH46
Defense Date
1976
Document Type
Thesis
Degree Name
Master of Science
Department
Pathology
First Advisor
Marvin J. Allison
Abstract
Arterial disease is virtually a universal entity in man. Some cultures, such as the African Bantus have very little in the way of vascular lesions, while in the United States and other industrialized nations atherosclerosis affects a large segment of the population. With this in mind it is not hard to understand why ischemia, or arteriosclerotic heart disease, is second only to cardiovascular diseases in general as the major cause of death in the United States (4, 42).
Ruffer (112) noted the presence of arterial lesions in Egyptian mummies dating back 3,400 years. The presence of atherosclerotic lesions has also been reported in a 2100 year old Chinese mummy (36). Though atherosclerosis is an ancient disease it is seen more and more often in our culture in vascular disease.
The early sixteenth and seventeenth century anatomists were the first to make note of arterial lesions and guess at their origins. Over the centuries came theories and definitions that are at the least confusing. Virchow in 1856 (6, 7, 45 ) was the first to propose the theory of mechanical damage to the intima of the artery to account for the entry of blood plasma into the arterial wall. The lesions were attributed to chronic irritation. Marchand in 1904 coined the term atherosclerosis. At the time the dominant concept was one of arterial lesions forming after there was an increase in sub-intimal connective tissue due to irritative or mechanical forces. Today much more is understood about the processes of arteriosclerosis, but definitions still vary among authors.
Arteriosclerosis is the broad generic term which literally means "hardening of the arteries" and involves the processes of thickening and loss of elasticity to arterial walls (42, 108, 109). Three distinct morphological entities are grouped under this broad heading; (1) medial sclerosis, (2) arteriolosclerosis and (3) atherosclerosis.
The medial or Monckeberg’s sclerosis is characterized by calcifications within the media of medium to small arteries, particularly the femoral, tibial, radial and ulnar arteries.
Arteriolosclerosis is particularly common in hypertension and affects the small arteries and arterioles. It is distinguished by hyaline proliferation and fibrous and elastic hyperplasia of the media and the intima.
Atherosclerosis is the most commonly seen form of the arteriosclerotic diseases and when it occurs it has the most serious clinical consequenses. The aorta and other large elastic arteries of the extremities are the primary locations for atherosclerosis. The disease is characterized by patchy, nodular lesions due to a thickening of the intima and a degenerative process in which lipid deposition occurs. The media may also become involved.
The earliest descernible lesion is termed a fatty streak. It presumably occurs over an area of stress to the vessels. Lipid is deposited in the site and soon macrophages and myocytes become filled with the fat droplets and form "foam cells". The intima is thickened and the elastic lamina is disrupted by extracellular fat. As the pathogenesis continues the arterial tissue attempts to repair itself and a fibrous capsule is layed down over the lesion thickening the intima even more. The term fibrous or pearly plaque now differentiates the lesion. The cells in the center of this lesion die due to a lack of oxygen and a necrotic mass, termed "gruel" is formed. From the vasa vasorum large capillaries or "sinusoids" invade the gruel and at the same time calcium is being deposited and the lesion can become calcified or "hardened". Up to this point the body has been doing though the usual healing and repair processes, but now destructive changes can occur. The cracking or breaking away of a plaque can cause hemorrhage or ulceration. These degenerative changes can be a grave threat when aneurysm or thrombus formation occurs.
It appears that this sequence of lesion formation must occur in waves throughout a lifetime since lesions of various size and age can be found side by side in the aorta. In general however, there is agreement that in North America at least the fatty streaks appear during the first decade of life while pearly plaques are forming in the second and third decade. The complications and their consequences occur from the fourth decade on (16, 21, 72).
Rights
© The Author
Is Part Of
VCU University Archives
Is Part Of
VCU Theses and Dissertations
Date of Submission
7-14-2016