Integrated backscatter with 2DE represents a useful noninvasive tool for evaluating the tissue structure of human plaque.

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Background-The process of progression in coronary artery disease is unknown. Methods and Results-The subjects were 36 patients with 36 objective vessels with clinically significant progression of coronary artery disease (Ն15% per year) in whom 4 serial coronary arteriograms (CAGs) were performed at intervals of Ϸ4 months in a 1-year period. The degree of progression of percent stenosis between each of 2 serial CAGs was classified as marked (M: Ն15%), slight (S: 5% to 14%), and no progression (N: Ͻ5%). From the pattern of progression, the 36 vessels were classified as 14 type 1 vessels with marked progression (N3 N3 M in 13 vessels and S3 S3 M in 1 vessel) and 22 type 2 vessels without marked progression (S3 S3 S in 18 vessels, N3 S3 S in 4). Percent stenosis at the first, second, third, and final CAGs was 44Ϯ14%, 46Ϯ13%, 46Ϯ13%, and 88Ϯ10% (PϽ0.05 versus first CAG) in type 1 vessels and 44Ϯ11%, 50Ϯ9%, 59Ϯ9%, and 67Ϯ9% in type 2 vessels (PϽ0.05 for second, third, and final CAGs versus first CAG). Type 1 vessels featured the sudden appearance of severe stenosis due to marked progression, angina pectoris, or myocardial infarction (71%) and Ambrose type II eccentric lesions indicating plaque rupture or thrombi (57%). Type 2 vessels featured continuous slight progression of stenosis with smooth vessel walls; angina pectoris (14%) occurred when the percent stenosis reached a severe level. An increase in serum C-reactive protein was observed only in the type 2 vessel group, which suggests a relation between continuous slight progression and inflammatory change. Conclusions-Two types of stenosis progression provide a new insight into the mechanism of coronary artery disease.(Circulation. 1999;100:903-909.)

The appearance of marked progression and Ambrose's type II eccentric lesion on coronary angiograms 3 days before AMI suggests the presence of a considerable time from the onset of plaque rupture and/or thrombi until the onset of AMI. These features may be predictors of AMI. The concept provides new insight into the mechanism and prevention of human AMIs.