[Regression of coronary sclerosis in familial hypercholesterolemia IIa by specific LDL apheresis].
The long-term effect of specific LDL plasma immunabsorption on the course of coronary arteriosclerosis was tested in ten patients with familial hypercholesteremia type IIa (seven females, three males; age range 15-57 years). Available were ECG, bicycle ergometry, hemodynamic and angiographic data. These tests were repeated seriatim in the course of the LDL immunabsorption. It was found that exercise tolerance markedly increased, ischemic ST-changes became less marked and the initial hemodynamic parameters remained unchanged. The morphology of the coronary arteries was influenced lastingly: among 22 stenoses only one progressed, there was no further progression in 11 stenoses and regression in ten. When there was generalized arteriosclerosis, progression occurred in two of 79 coronary artery segments, progression was arrested in 56 and regression was noted in 21 of 79 segments. These results demonstrate that specific LDL plasma immunabsorption for the elimination of LDL cholesterol favorably influences the course of coronary arteriosclerosis in patients with familial hypercholeremia type IIa. The findings support the lipid theory of atherosclerosis and coronary arteriosclerosis, at least in this special group of patients.
D000293:Adolescent; D000328:Adult; D001781:Blood Component Removal / Q000295:instrumentation / Q000379:methods; D008078:Cholesterol, LDL / Q000302:isolation & purification*; D003324:Coronary Artery Disease / Q000209:etiology / Q000503:physiopathology / Q000628:therapy*; D005069:Evaluation Studies as Topic; D005260:Female; D006439:Hemodynamics; D006801:Humans; D006938:Hyperlipoproteinemia Type II / Q000150:complications / Q000503:physiopathology / Q000628:therapy*; D007163:Immunosorbent Techniques / Q000295:instrumentation; D008297:Male; D012871:Skin Diseases / Q000209:etiology / Q000628:therapy; D014973:Xanthomatosis / Q000209:etiology / Q000628:therapy
D008078:Cholesterol, LDL
Regression der Koronarsklerose bei familiärer Hypercholesterinämie IIa durch spezifische LDL-Apherese.