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Atheroembolism; a late complication of arteriosclerosis
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Atheroembolism; of arteriosclerosis
a late
Coronary, cerebral, and peripheral vascular diseases are well recognized as complications of arteriosclerosis. The recent literature emphasizes the frequency of an old phenomenon observed by pathologists, namely atheroembolism, characterized by the presence of small cholesterol crystals in one or multiple organs of the body in patients with a severely atherosclerotic aorta. Nowadays, there is little doubt that these cholesterol crystals come from dislodgement of atheromatous plaques located in the aorta and its main branches. This represents the late stage of arteriosclerosis involving the large arteries, in which the ulceration of an atheromatous plaque with the discharge of amorphous eosinophilic material and cholesterol crystals to various organs and tissues seems to be the explanation of the clinical features of atheroembolism. Although the symptoms may be related to any they frequently produce a recognizable organ, clinical pattern. Presenting manifestations which should arouse suspicion of this entity include (1) paroxysmal and ischemic changes of the feet and legs, livedo reticulares, and gangrene despite adequate arterial pulses; (2) hypertension and impaired renal function; (3) abdominal pain, gastrointestinal hemorrhage, and pancreatitis; (4) occasional neurologic symptoms and retinal emboli, and (5) myocardial infarction or coronary insufficiency.1-4 In a recent publication 5 cases were described, in four of which muscle biopsy from the lower extremities proved to be a valuable diagnostic aid. Leukocytosis with neutrophilia, elevated sedimentation rate, azotemia, albuminuria, and melena were frequently present. This syndrome occurs almost exclusively in the elderly. Diabetes, syphilis, and gout seem to play an important role as predisposing factors. The diversified symptomatology explains the multiple terms applied to this syndrome, “diffuse arteriopathy, ‘I6 “purple toe syndrome,“6 and cholesterol embolization, but those titles are misleading because we are not describing a primary disease of
278
complication
the arteries or pure cholesterol emboli but atheromatous embolism which happens to contain cholesterol. The unanswered question in atheroembolism is, how to treat this condition. Prevention of arteriosclerosis and its associated hypercholesterolemia and hyperglyceridemia should be the main aim, In this regard the use of diets, nicotinic acid, and estrogens leaves much to be desired. Do anticoagulants help or worsen this condition? Clinical observations and some experimental work seem to demonstrate that the latter possibility is more likely, by favoring the dislodgement of atheromatous material from the damaged and eroded arterial wall. These studies are not yet extensive enough for satisfactory interpretation and more work in this field is needed before any definitive conclusion could be reached. Jorge A. Carvajal, M.D. Veterans Administration Hospital Long Beach, Calif. REFERENCES 1. Carvajal, J. A., et al.: Atheroembolism an etiologic factor in renal insufficiency, gastrointestinal hemorrhages and peripheral vascular disease, Arch. Int. Med. 119593, 1967. 2. Eliot, R. S., Kanjuh, V. I., and Edwards, J. E.: Atheromatous embolism, Circulation 30:611, 1964. 3. Hollenhorst, R. W.: Vascular status of patients who have cholesterol emboli in retina, Am.J.Ophth. 61:1159,1966. 4. Porter, W. B., and Vaughan, E. W.: Coronary embolism. A complication of syphilitic aortitis. Report of 3 cases, Am. J. M. SC. 200:184, 1940. 5. Evans, W.: Diffuse arteriopathy, Brit. Heart J. 24~703, 1962. 6. Moldveen-Geronimus, M., and Merriam, J. C., Jr.: Cholesterol embolization from pathological curiosity to clinical entity, Circulation 35:946, 1967.
Atheroembolism; of arteriosclerosis
a late
Coronary, cerebral, and peripheral vascular diseases are well recognized as complications of arteriosclerosis. The recent literature emphasizes the frequency of an old phenomenon observed by pathologists, namely atheroembolism, characterized by the presence of small cholesterol crystals in one or multiple organs of the body in patients with a severely atherosclerotic aorta. Nowadays, there is little doubt that these cholesterol crystals come from dislodgement of atheromatous plaques located in the aorta and its main branches. This represents the late stage of arteriosclerosis involving the large arteries, in which the ulceration of an atheromatous plaque with the discharge of amorphous eosinophilic material and cholesterol crystals to various organs and tissues seems to be the explanation of the clinical features of atheroembolism. Although the symptoms may be related to any they frequently produce a recognizable organ, clinical pattern. Presenting manifestations which should arouse suspicion of this entity include (1) paroxysmal and ischemic changes of the feet and legs, livedo reticulares, and gangrene despite adequate arterial pulses; (2) hypertension and impaired renal function; (3) abdominal pain, gastrointestinal hemorrhage, and pancreatitis; (4) occasional neurologic symptoms and retinal emboli, and (5) myocardial infarction or coronary insufficiency.1-4 In a recent publication 5 cases were described, in four of which muscle biopsy from the lower extremities proved to be a valuable diagnostic aid. Leukocytosis with neutrophilia, elevated sedimentation rate, azotemia, albuminuria, and melena were frequently present. This syndrome occurs almost exclusively in the elderly. Diabetes, syphilis, and gout seem to play an important role as predisposing factors. The diversified symptomatology explains the multiple terms applied to this syndrome, “diffuse arteriopathy, ‘I6 “purple toe syndrome,“6 and cholesterol embolization, but those titles are misleading because we are not describing a primary disease of
278
complication
the arteries or pure cholesterol emboli but atheromatous embolism which happens to contain cholesterol. The unanswered question in atheroembolism is, how to treat this condition. Prevention of arteriosclerosis and its associated hypercholesterolemia and hyperglyceridemia should be the main aim, In this regard the use of diets, nicotinic acid, and estrogens leaves much to be desired. Do anticoagulants help or worsen this condition? Clinical observations and some experimental work seem to demonstrate that the latter possibility is more likely, by favoring the dislodgement of atheromatous material from the damaged and eroded arterial wall. These studies are not yet extensive enough for satisfactory interpretation and more work in this field is needed before any definitive conclusion could be reached. Jorge A. Carvajal, M.D. Veterans Administration Hospital Long Beach, Calif. REFERENCES 1. Carvajal, J. A., et al.: Atheroembolism an etiologic factor in renal insufficiency, gastrointestinal hemorrhages and peripheral vascular disease, Arch. Int. Med. 119593, 1967. 2. Eliot, R. S., Kanjuh, V. I., and Edwards, J. E.: Atheromatous embolism, Circulation 30:611, 1964. 3. Hollenhorst, R. W.: Vascular status of patients who have cholesterol emboli in retina, Am.J.Ophth. 61:1159,1966. 4. Porter, W. B., and Vaughan, E. W.: Coronary embolism. A complication of syphilitic aortitis. Report of 3 cases, Am. J. M. SC. 200:184, 1940. 5. Evans, W.: Diffuse arteriopathy, Brit. Heart J. 24~703, 1962. 6. Moldveen-Geronimus, M., and Merriam, J. C., Jr.: Cholesterol embolization from pathological curiosity to clinical entity, Circulation 35:946, 1967.