Recent clinical studies have demonstrated that 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors are effective in the prevention of cardiovascular events and regression of atherosclerotic lesions evaluated by angiography. In this study, the authors investigated how lipid-lowering therapy effects on the progression of aortic atherosclerosis by using plain and enhanced computed tomography (CT) of the lower abdominal aorta. Twenty-nine hyperlipidemic patients (mean age 61.4 +/- 7.2 yr) were enrolled in a prospective open-labeled study. All patients underwent baseline CT scanning of abdominal aorta, screening for serum lipid profile and coagulation-fibrinolysis measurement, then treatment with simvastatin was begun. After 2 years, a follow-up CT scan was done and atherosclerotic lesions were compared between baseline and on-treatment scan. In spite of significant improvement of lipid and fibrinolytic profiles by simvastatin administration, mean aortic wall thickening volume (AWV) was increased during observation period. When patients were divided into subgroups by the levels of on-treatment LDL cholesterol (LDL-C), development rate of AWV was more potently suppressed in patients whose on-treatment LDL-C were below 125 mg/dL (median LDL-C). We could not find any associations of coagulation-fibrinolysis measurements with atherosclerotic lesions. In regard to aortic calcification volume (ACV), low levels of total and HDL cholesterol and higher age were associated with aortic calcification at baseline. These results suggest that aggressive treatment with LDL-C below 125 mg/dL may suppress the progression of wall thickening and factors that promote arterial calcifications and those for wall thickening may be different.

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A case is reported of a 65 year old man who suffered myocardial ischemia resulting from extensive stenosis of the intramural coronary arteries secondary to systemic vascular involvement by primary amyloidosis. In the myocardium, there were multiple fibrotic foci scattered mainly in the subendocardial region of the ventricle. Intramural coronary arteries were stenotic or occlusive due to amyloid-induced luminal narrowing, but there was no significant stenosis of the epicardial coronary arteries. Quantitative analysis of amyloid deposits in the intramural coronary arteries demonstrated that occlusive arteries were predominant in the surrounding area of myocardial fibrosis, and the extent of coronary stenosis by amyloid deposition was significantly more severe than in hearts of the five control patients who had coronary amyloidosis without myocardial fibrosis. These results indicate that myocardial fibrosis originates from coronary ischemia due to vascular amyloid deposition. This is the first time that the relationship between myocardial lesions and coronary amyloid deposition has been elucidated using histopathologic quantitative analysis.

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