Background-The purpose of the present study was to define whether integrated backscatter (IB) combined with conventional intravascular ultrasound (IVUS) makes tissue characterization of coronary arterial plaques possible. Methods and Results-IB-IVUS was performed in coronary arteries (total 18 segments) of 9 patients at autopsy, and the findings were compared with the histology. RF signals, which were digitized at 2 GHz in 8-bit resolution, were obtained with an IVUS system with a 40-MHz catheter. IB values of the RF signal from the region of interest (ROI) (100-m depth, 1.4°per line) were calculated by use of a personal computer. IB values on the ROIs were divided into 5 categories, compared with each of the plaque histologies: category 1 (thrombus), Ϫ88 Ͻ IB Յ Ϫ80; category 2 (intimal hyperplasia or lipid core), Ϫ73 Ͻ IB Յ Ϫ63; category 3 (fibrous tissue), Ϫ63 Ͻ IB Յ Ϫ55; category 4 (mixed lesions), Ϫ55 Ͻ IB Յ Ϫ30; and category 5 (calcification), Ϫ30 Ͻ IB Յ Ϫ23. On the basis of these categories, we analyzed 5120 ROIs per segment in each ring-like arterial specimen. Color-coded maps of plaques were constructed by use of these IB data and conventional IVUS data, which reflected the plaque histology of autopsied coronary arteries well. Then, the same method was undertaken in 24 segments with plaque from 12 patients in vivo with angina pectoris. Comparisons between coronary angioscopy and IB-IVUS revealed that the surface color of plaques in angioscopy reflected the thickness of the fibrous cap rather than the size of the lipid core. Conclusions-IB-IVUS represents a new and useful tool for evaluating the tissue structure of human coronary arterial plaques.

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

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.)

Background —It has been reported that tumor necrosis factor-α (TNF-α) is expressed in the heart with viral myocarditis and that its expression aggravates the condition. The pathophysiological effects of TNF-α on viral myocarditis, however, have not been fully elucidated. Methods and Results —To investigate the role of TNF-α in the progression of viral myocarditis, we used TNF-α gene–deficient mice (TNF-α −/− ) and induced acute myocarditis by infection with encephalomyocarditis virus (EMCV). The survival rate of TNF-α −/− mice after EMCV infection was significantly lower than that of TNF-α +/+ mice (0% versus 67% on day 14). Injection of recombinant human TNF-α (0.2 to 4.0 μg/mouse IV) improved the survival of TNF-α −/− mice in a dose-dependent manner, indicating that TNF-α is essential for protection against viral myocarditis. The levels of viral titer and viral genomic RNA of EMCV in the myocardium were significantly higher in TNF-α −/− than in TNF-α +/+ mice. Histopathological examination showed that the inflammatory changes of the myocardium were less marked in TNF-α −/− than in TNF-α +/+ mice. Immunohistochemical analysis revealed that the levels of immunoreactivity of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 in the myocardium were decreased in TNF-α −/− mice compared with TNF-α +/+ mice. Conclusions —These observations suggested that TNF-α is necessary for adhesion molecule expression and to recruit leukocytes to inflammatory sites, and thus, the lack of this cytokine resulted in failure of elimination of infectious agents. We concluded that TNF-α plays a protective role in the acute stage of viral myocarditis.

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.

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Preischemic treatment with MOR-14 preserved glycogen, attenuated the accumulation of lactate, and reduced the myocardial infarct size by 69%. This cardioprotective effect was independent of changes of blood pressure and heart rate or regional blood flow. It may be associated with alpha-1,6-glucosidase inhibition, because MOR-14 markedly decreased the alpha-1,6-glucosidase activity in the heart.