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This is the first report clarifying detailed changes in coronary plaque by statin in humans. This study indicated that lipid-lowering therapy changes plaque color and morphology and should then lead to coronary plaque stabilization.

Background-Elevated troponin T levels in non-ST-elevation acute coronary syndromes (NSTE-ACS) have been shown to predict an adverse outcome. Furthermore, it has been reported that troponin T could help improve the effectiveness of such new antithrombotic drugs as platelet GPIIb/IIIa antagonists and low-molecular-weight heparins. We hypothesized that such elevated troponin T levels in NSTE-ACS indicate the presence of thrombus at culprit lesions, and this hypothesis was verified through the use of coronary angioscopy. Methods and Results-We studied 57 consecutive patients with NSTE-ACS who underwent preinterventional angioscopy.Before catheterization, we obtained blood samples to determine troponin positivity, and the patients were then classified as either troponin-positive or troponin-negative groups (diagnostic threshold, 0.1 ng/mL). Using angioscopy at the culprit lesions, we examined the presence of coronary thrombus, yellow plaque, and complex plaque. Moreover, we compared the preinterventional angiographic parameters (thrombus and complexity of the culprit lesion, and TIMI flow) between the two groups. Twenty-two patients were troponin-positive and 35 patients were troponin-negative. Univariate analyses indicated that the TIMI flow and the incidence of coronary thrombus detected with angioscopy correlate with the elevated troponin T levels. A multivariate logistic regression analysis showed the presence of coronary thrombus detected with angioscopy to be the only independent factor associated with elevated troponin T levels in patients with NSTE-ACS (odds ratio, 22.1; 95% CI, 2.59 to 188.42; Pϭ0.0046). Conclusions-Using angioscopy, the elevated troponin T levels in NSTE-ACS were confirmed to be strongly associated with the presence of coronary thrombus.

The present study demonstrated that: 1) ruptured plaques in nonculprit lesions tend to heal slowly with a progression of angiographic stenosis; and 2) the serum CRP level might reflect the disease activity of the plaque ruptures.

Predicting the occurrence of future acute coronary syndromes remains an important challenge of contemporary cardiology. It is thought that detecting the individual vulnerable plaques in patients can be an important step to preventing myocardial infarction and sudden cardiac death. Coronary angioscopy can provide detailed information of the luminal surface of plaque, such as color, thrombus, or disruption, and is one of a few possibly useful imaging modalities for identifying vulnerable plaques. During its 20-year history, coronary angioscopy has been used as a diagnostic tool or to guide coronary angioplasty, and has contributed to our understanding of the pathophysiology of coronary artery disease. Yellow plaques seen during angioscopy seem to have many characteristics of high risk or vulnerable plaques, most consistent with the thin-cap fibroatheroma. Moreover, differences in yellow color have been reported to reflect differences in the structure or composition of plaques. Development of quantitative methods to assess plaque color and histopathologic correlations in conjunction with prospective natural history studies may lead to advances in vulnerable plaque detection by coronary angioscopy. Although current angioscopic devices are limited by the need to displace the column of blood in order to see the vessel wall, and by the lack of quantitative colorimetric methods, advances in technology may lead to new device versions that could be practical for expanded clinical use.

Atherosclerotic plaque color can be consistently measured during angioscopy with quantitative colorimetry. High yellow color intensity, determined by this system, was associated with LCTCs. Quantitative colorimetry during angioscopy may be used for detection of LCTCs, which may be markers of vulnerability.

SUMMARYWe report an acute myocardial infarction in a patient with a single coronary artery. The right coronary artery arose from the middle portion in the left anterior descending artery through the transverse branch. This type of single coronary artery has not been previously reported. Moreover, this is the first report in which the culprit lesion in a patient with a single coronary artery was observed by intravascular ultrasound and coronary angioscopy. The patient underwent successful coronary stent deployment. (Jpn Heart J 2003; 44: 271-276) Key words: Single coronary artery, Acute myocardial infarction, Atherosclerotic plaque, Intravascular ultrasound, Coronary angioscopy, Coronary stent deployment A single coronary artery is a rare congenital anomaly, with an incidence of 0.02% in subjects who undergo coronary angiography.1) A single coronary artery is often associated with myocardial ischemia and additional cardiac congenital anomalies.2-6) We report a patient with an isolated single coronary artery and an acute myocardial infarction. This case deals with a very unusual type of single coronary artery in which the right coronary artery originated from the middle portion in the left anterior descending artery through the transverse branch. Moreover, this is the first case in which the culprit lesion in a single coronary artery was observed by intravascular ultrasound and coronary angioscopy. CASE REPORTA 35-year-old Japanese male smoker with hyperlipidemia visited a physiFrom

s compared with balloon angioplasty, intracoronary stenting has reduced rates of restenosis; 1,2 nevertheless, in-stent restenosis continues to be an important clinical issue. 3,4 Serial (post intervention and follow-up) intravascular ultrasound studies have shown that in-stent restenosis is almost exclusively caused by neointimal hyperplasia, [5][6][7] and tissue proliferation occuring inside or adjacent to the stent sites has been shown to be directly related to the aggressiveness of the stent implantation technique, 7 with histological studies confirming that neointimal hyperplasia post stent implantation is related to vessel trauma during the procedure. [8][9][10][11] In stented, nonatherosclerotic, balloon-injured rabbit iliac arteries, peak monocyte adherence was observable 3 days post stent implantation, with maximum proliferation observed at 7 days. 12 There was a linear correlation between monocyte adherence and neointimal hyperplasia. 11 Monocyte chemoattractant protein-1 (MCP-1), which has a potent chemotactic action on monocytes, 13 can amplify the inflammatory response through the recruitment of additional monocytes. 14 Macrophage activity has been demonstrated Japanese Circulation Journal Vol.65, April 2001 to play an important role in the progression of atherosclerosis; 15-17 however, the association between MCP-1 and restenosis post coronary stent implantation remains unclear.We designed this study to test the hypothesis that increased levels of MCP-1 are associated with an increased risk for restenosis post stent implantation. Methods Patient PopulationForty-one patients with stable exertional angina (SEA) (ie, proven ischemia on laboratory testing) underwent angiographically successful stent implantation of a single lesion with de novo, or one previous balloon angioplasty, in a native coronary artery between June 1997 and November 1997. Exclusion criteria were unsuccessful procedures (defined as the failure to place the stent at the desired position or to achieve a final diameter stenosis <30% by visual inspection) or the occurrence of one or more major adverse cardiac events (death, myocardial infarction, coronary bypass graft surgery, or repeat balloon angioplasty) during the first month post procedure. All the patients with SEA underwent follow-up angiography 6 months after the procedure. Nineteen patients with chest pain syndrome were selected as control subjects; their coronary angiographic findings were normal. The study protocol followed the guidelines of the ethics committee at the institution and written informed consent was obtained from each patient. Monocyte chemoattractant protein-1 (MCP-1) plays a fundamental role in monocyte recruitment and has been implicated in atherosclerosis. The present study tested the hypothesis that increased levels of MCP-1 are associated with an increased risk for restenosis post stent implantation. The plasma MCP-1 antigen levels were measured pre-stenting, and at 24 and 48 h and 6 months post stenting in 41 patients with stable exertional angina (S...