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High yellow color intensity (HYCI) regions of atherosclerotic plaque, determined by angioscopy with quantitative colorimetry, are associated with lipid cores underneath thin fibrous caps in ex vivo tissue samples. To determine whether HYCI regions of coronary plaque are associated with disruption or thrombus in living patients, quantitative colorimetry was applied to angioscopy, and the color of culprit lesions was measured in patients with acute coronary syndromes. In 46 patients with acute coronary syndromes (acute myocardial infarction, n = 14; unstable angina pectoris [UAP] with culprit thrombus, n = 16; and UAP without culprit thrombus, n = 16), the recorded angioscopic images of culprit lesions were analyzed using a quantitative colorimetric method based on the L*a*b* color space applied to angioscopy (positive b* = yellow color intensity). HYCI was defined as b* value >23. Plaque disruption was significantly more prevalent in 19 of 24 HYCI regions (79%) than in 9 of 22 non-HYCI regions (41%) (p = 0.007). Culprit HYCI regions were prevalent in patients with myocardial infarction (11 of 14 [79%]), followed by those with UAP with thrombus (9 of 16 [56%]) and UAP without thrombus (4 of 16 [25%]) (p = 0.01 for trend), and were significantly more prevalent in 66% of patients with myocardial infarction and UAP with thrombus compared with 25% of those with UAP without thrombus (p = 0.007). In conclusion, HYCI regions of coronary plaque may be indicative of high-risk lesions vulnerable to thrombosis. Coronary angioscopy with quantitative colorimetry could be used to study the association between high-risk coronary lesions and future cardiovascular events.

To perform intravascular imaging of atherosclerotic human coronary conduits in an animal model under conditions of flow and cardiac motion that approximate those encountered in vivo. Given the lack of animal models of vulnerable plaque, a model which would allow imaging of human disease and simulate coronary motion and blood flow could advance the development of emerging technologies to detect vulnerable plaques. Human coronary segments from adult cadaver hearts were prepared as xenografts. In anesthetized Yorkshire pigs (45–50 kg) the chest was opened and the exposed aorta and right atrium were cannulated and attached in an end-to-end fashion to the human coronary xenograft, forming an aorto-atrial conduit. The xenograft was fixed to the anterior wall of the heart to simulate motion. Angiography and intravascular ultrasound (IVUS) of each graft were performed. Twelve human coronary grafts (10 from right coronary segments) were prepared and implanted successfully in seven animals. All animals tolerated the procedure. The average graft length was 39 ± 2.3 mm. Blood flow rates distal to the graft were >100 ml/min in nine grafts. IVUS was performed in all 12 grafts and documented expansion of arterial (6.9%) and luminal (9.3%) dimensions during the cardiac cycle (P

Yellow plaques seen during angioscopy are thought to represent lipid cores underneath thin fibrous caps (LCTCs) and may be indicative of vulnerable sites. However, plaque color assessment during angioscopy has been criticized because of its qualitative nature. The purpose of the present study was to test the ability of a quantitative colorimetric system to measure yellow color intensity of atherosclerotic plaques during angioscopy and to characterize the color of LCTCs. Using angioscopy and a quantitative colorimetry system based on the L*a*b* color space [L* describes brightness (−100 to +100), b* describes blue to yellow (−100 to +100)], the optimal conditions for measuring plaque color were determined in three flat standard color samples and five artificial plaque models in cylinder porcine carotid arteries. In 88 human tissue samples, the colorimetric characteristics of LCTCs were then evaluated. In in-vitro samples and ex-vivo plaque models, brightness L* between 40 and 80 was determined to be optimal for acquiring b* values, and the variables unique to angioscopy in color perception did not impact b* values after adjusting for brightness L* by manipulating light or distance. In ex-vivo human tissue samples, b* value ≥23 (35.91 ± 8.13) with L* between 40 and 80 was associated with LCTCs (fibrous caps

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.

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; P =0.0046). Conclusions— Using angioscopy, the elevated troponin T levels in NSTE-ACS were confirmed to be strongly associated with the presence of coronary thrombus.

We 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.

Because large thrombus is a limitation for revascularization in acute myocardial infarction (AMI), the present study evaluated the effectiveness of pulse infusion thrombolysis (PIT) in patients with an AMI with a large (>15 mm) coronary thrombus, focusing on the occurrence of the `no flow' phenomenon. The retrospective study compared patients treated before (1988-95; Group A, n=74) and after (1996-99; Group B, n=40) the use of PIT, using the following parameters: lesion success (

Objective Our objective was to determine whether autologous endothelial progenitor cells (EPCs) delivered into the pericardial space will migrate to and incorporate into ischemic myocardium in a porcine model. Background Use of EPCs to enhance neovascularization and preserve myocardial function in ischemic tissue is undergoing intense scrutiny as a potential therapy. Delivery into the pericardial sac may overcome some of the limitations of currently employed cell delivery techniques. Methods EPCs were immunopurified from peripheral blood of Yorkshire pigs by selecting for the CD31 surface antigen, and adherent cells were cultured for 3–5 days. After myocardial ischemia was induced in the left anterior descending (LAD) artery, either autologous DiI (1,1′-dioctadecyl-1-3,3,3′,3′-tetramethylindocarbocyanine perchlorate)-labeled EPCs ( n =10) or serum-free medium (SFM; n =8) was delivered into the pericardial space using a percutaneous transatrial approach. Animals were sacrificed on Day 7 or 21. Echocardiography was performed at baseline, during ischemia, and on Day 7 in six SFM group animals and six EPC group animals. Results On Day 7, EPCs were identified in the left ventricular (LV) anterior wall or anterior septum in all six EPC-treated animals (cell density of 626±122/mm 2 ). On Day 21, EPCs were identified in the LV anterior wall or anterior septum in three of four EPC-treated animals (cell density of 267±167/mm 2 ). These cells showed dual staining for DiI and Bandeiraea simplicifolia lectin I (a marker of both native and exogenous endothelial cells). At the Day 7 follow-up, echocardiography demonstrated that fractional shortening in the EPC-treated group was 30.6±3.4, compared with 22.6±2.8 in SFM controls ( P =.05). Conclusions EPCs can migrate from the pericardial space to incorporate exclusively into areas of ischemic myocardium and may have favorable effects on LV function.

Background Multiple angioscopic yellow plaques are associated with diffuse atherosclerotic plaque, and may be prevalent in patients with myocardial infarction (MI), so in the present study the yellow plaques in the coronary arteries of patients with MI was evaluated using quantitative colorimetry, and compared with those of patients with stable angina (SA). Methods and Results In the recorded angioscopic images of 3 coronary vessels in 29 patients (15 patients with MI, 14 with SA), yellow plaques were determined as visually yellow regions with b* value >0 (yellow color intensity) measured by the quantitative colorimetric method. A total of 90 yellow plaques were identified (b* =19.35±8.3, 3.05-45.35). Yellow plaques were significantly more prevalent in 14 (93%) of 15 culprit lesions of MI as compared with 8 (57%) of 14 of SA (p=0.03). In non-culprit segments, yellow plaques were similarly prevalent in 13 (87%) patients with MI and 11 (79%) with SA (p=0.65). Overall, multiple (≥2) yellow plaques were prevalent in 13 (87%) patients with MI, similar to the 10 (71%) with SA (p=0.38). The number of yellow plaques was significantly higher in patients with MI (3.8±1.9) than in those with SA (2.4±1.6, p=0.03). Conclusion The present study suggests that patients with MI tend to have diffuse atherosclerotic plaque in their coronary arteries. (Circ J 2008; 72: 399 - 403)

Yellow plaques seen during coronary angioscopy are thought to be the surrogates for superficial intimal lipids in coronary plaque. Given diffuse and heterogeneous nature of atherosclerosis, yellow plaques in coronaries may be seen as several yellow spots on diffuse coronary plaque. We examined the topographic association of yellow plaques with coronary plaque. In 40 non-severely stenotic ex-vivo coronary segments (average length: 52.2 +/- 3.1 mm), yellow plaques were examined by angioscopy with quantitative colorimetry. The segments were cut perpendicular to the long axis of the vessel at 2 mm intervals, and 1045 slides with 5 microm thick tissue for whole segments were prepared. To construct the plaque surface, each tissue slice was considered to be representative of the adjacent 2 mm. The circumference of the lumen and the lumen border of plaque were measured in each slide, and the plaque surface region was constructed. Coronary plaque was in 37 (93%) of 40 segments, and consisted of a single mass [39.9 +/- 3.9 (0-100) mm, 311.3 +/- 47.4 (0.0-1336.2) mm2]. In 30 (75%) segments, multiple (2-9) yellow plaques were detected on a mass of coronary plaque. The number of yellow plaques correlated positively with coronary plaque surface area (r = 0.77, P < 0.0001). Yellow plaques in coronaries detected by angioscopy with quantitative colorimetry, some of them are associated with lipid cores underneath thin fibrous caps, may be used to assess the extent of coronary plaque. Further research using angioscopy could be of value to study the association of high-risk coronaries with acute coronary syndromes.

There is growing interest in the possibility that identification and treatment of vulnerable plaques and vulnerable patients can enhance the progress made against coronary artery disease. Innovations in medical therapy—statins and other agents—and novel interventional cardiology techniques—eg, drug-eluting stents—have significantly decreased the morbidity and mortality caused by coronary atherosclerosis. However, coronary events continue to be the leading cause of death in the United States, accounting for >479 000 deaths (1 in 5) in 2003.1 Improved preventive measures are needed because, for many individuals, sudden coronary death is the first sign of the disorder. And even those who survive an acute coronary syndrome remain at high risk. After successful treatment of the initial culprit lesion by a percutaneous coronary intervention (PCI), the risk of a coronary event from a new lesion is ≈10% in the following year and 5% in each of the subsequent 4 years2,3 (Figure 1). Figure 1. Occurrence of coronary events (revascularization, death, MI, acute coronary syndromes, or congestive heart failure) after PCI in 4 studies of bare-metal stents. In addition to events resulting from stented lesions (solid line), many events are caused by nontarget (vulnerable) plaques (dashed line). Modified from Cutlip et al2 with permission from the American Heart Association. Copyright 2004. These substantial levels of ongoing morbidity and mortality have led to heightened interest in new methods to prevent coronary events. For primary prevention, the effort has focused on plasma markers and noninvasive testing to identify vulnerable individuals. For secondary prevention, interest has focused on vulnerable patients and the vulnerable plaques they may possess that might be identified and treated during the catheterization for their initial event. ### Definitions of the Vulnerable Plaque and the Vulnerable Patient The terminology to describe vulnerability has become relatively standardized.4–10 The term “vulnerable plaque” is used to designate a plaque at high risk of disruption leading …

A 69-year-old man presented with chronic deep vein thrombosis due to massive thrombi extending from the inferior vena cava to both femoral veins. He had undergone surgery for prostatic cancer in 1991, and since then he had been taking an artificial estrogen agent. He was successfully treated by pulse infusion thrombolysis using a unique pump system, which we have developed, without complication.

Thrombus in the infarct-related artery is one of the limitations for flow restoration in primary percutaneous transluminal coronary angioplasty (PTCA) treatment for acute myocardial infarction (AMI). The present study investigated the benefit of preceding intracoronary thrombolysis (ICT) by retrospectively analyzing acute phase flow restoration in 80 AMI patients with intracoronary thrombus: 40 undergoing primary PTCA alone (primary PTCA group) and 40 treated with preceding ICT plus PTCA (combined group). Acute phase Thrombolysis in Myocardial Infarction (TIMI) grade flow was as follows: TIMI 0/1: 35.0% vs 12.5% for the primary PTCA group and the combined group, p=0.06; TIMI 2: 7.5% vs 15.0%, p=NS; TIMI 3: 57.5% vs 72.5%, p=NS). In the subgroup analysis, it was also less in the combined group among 33 patients with a left anterior descending coronary artery (LAD) lesion (42.1 % vs 7.1%, p=0.08), but not among the remaining 47 with either a right coronary artery or left circumflex artery lesion. The combined therapy may potentially provide better acute phase flow restoration in AMI patients with an intracoronary thrombus in a LAD lesion.

Monocyte chemoattractant protein-1 (MCP-1) plays an important role in the progression of atherosclerosis in coronary arteries. To examine whether or not plasma antigen levels of MCP-1 are related to restenosis after percutaneous transluminal coronary angioplasty (PTCA), the plasma antigen levels of MCP-1 were measured by enzyme-linked immunosorbent assay (pg/ml) before, 24 and 48 h, and 3 months after elective PTCA for stable exertional angina performed between June 1997 and March 1998. Restenosis was defined as recurrence of stenosis greater than 50% of the diameter in the dilated segment at 3-month follow-up angiography. There were no differences in plasma MCP-1 antigen levels before and at 24 h after PTCA between restenosis (R; n=27) and no-restenosis (N; n=43) groups (R vs N: 633+/-35 vs 589+/-34, and 669+/-41 vs 575+/-36 pg/ml before and at 24 h after PTCA, respectively), but plasma MCP-1 antigen levels were higher at 48 h and 3 months after PTCA in the R than in N group (R vs N: 678+/-41 vs 558+/-35, and 735+/-35 vs 571+/-32 pg/ml at 48 h and 3 months after PTCA, respectively). These data suggest that the MCP-1 production and macrophage accumulation in the balloon-injured site is partially associated with restenosis after PTCA.

No flow is an unsolved issue in primary percutaneous transluminal coronary angioplasty (PTCA) for patients with acute myocardial infarction (AMI), and the pathophysiology of no-flow is undetermined. To evaluate the potential participation of coronary thromboembolism in no-flow during primary PTCA, the present study reviewed cinefilms of 256 consecutive patients who underwent primary PTCA for AMI within 24 h after the onset of chest pain between January 1992 and June 1998, focusing on the thrombus size. Angiographic no-flow was defined as the cessation of flow into the distal coronary circulation of the treated vessel with a to-and-fro contrast movement, not attributable to high-grade stenosis or spasm of the original target lesion. The coronary thrombus size was determined by using the 2-cm balloon catheter as a reference after crossing the infarct-related occluded artery with a guide wire. Angiographic no-flow was observed in 37 patients (37/256, 14%): 14 of 29 cases (48%) with a large thrombus (≥2 cm) versus 23 of 227 cases (9%) with a small thrombus (

This study examined the fate of target sites that escaped high-grade restenosis (or = 70% diameter narrowing) after percutaneous transluminal coronary angioplasty. Although favorable long-term prognosis after successful percutaneous transluminal coronary angioplasty is well documented, little is known about the stability of target sites. Long-term follow-up (mean 6.5 years, range 1.0 to 12.0) was performed in 693 patients with 948 narrowings (stenosis70% in diameter at follow-up coronary angiography). Among them, 249 patients (36%) with 303 target sites received late follow-up coronary angiography. The relation of target sites to the culprit lesions for coronary events or newly developed angina was angiographically reviewed and progression/regression was also examined, focusing on the target sites. Regression was observed in 16 of 255 target sites in subjects with50% stenosis and in 21 of 48 sites in the group with midgrade stenosis of 50% to 69% luminal narrowing (16 of 255, 6.3% vs 21 of 48, 43.8%, p0.001). Progression was observed in 33 and 4 sites (33 of 255, 12.9% vs 4 of 48, 8.3%; p = NS) in each group, respectively. The rest remained within the same range of stenosis. Culprit lesions for 2 acute myocardial infarctions, 7 unstable anginas, and 17 newly developed anginas were related to the original target sites. Three lesions developed in the midgrade stenosis group. Those 26 lesions were a component of 8.6% of 303 angiographically confirmed sites and 2.7% of total target sites. Target sites that escape high-grade restenosis frequently regress and become stable plaques and rarely trigger coronary events.