CLINICAL RESEARCH: CORONARY ARTERY DISEASE
Angioscopic follow-up study of coronary ruptured plaques in nonculprit lesions
Masamichi Takano, MD,
Shigenobu Inami, MD,
Fumiyuki Ishibashi, MD,
Kentaro Okamatsu, MD,
Koji Seimiya, MD,
Takayoshi Ohba, MD,
Shunta Sakai, MD and
Kyoichi Mizuno, MD, PhD, FACC*
Department of Internal Medicine, Chiba-Hokusoh Hospital, Nippon Medical School, Chiba, Japan
Manuscript received June 3, 2004;
revised manuscript received September 8, 2004,
accepted September 13, 2004.
* Reprint requests and correspondence: Dr. Kyoichi Mizuno, Department of Internal Medicine, Chiba-Hokusoh Hospital, Nippon Medical School, 1715 Kamakari, Imba, Chiba, Japan 270-1694
(Email: mizunok{at}nms.ac.jp).
 |
Abstract
|
|---|
OBJECTIVES: Changes of ruptured plaques in nonculprit lesions were evaluated using coronary angioscopy.
BACKGROUND: The concept of multiple coronary plaque ruptures has been established. However, no detailed follow-up studies of ruptured plaques in nonculprit lesions have yet been reported.
METHODS: Forty-eight thrombi in 50 ruptured coronary plaques in nonculprit lesions in 30 patients were identified by angioscopy. The percent diameter stenosis (%DS) at the target plaques on quantitative coronary angiographic analysis and the serum C-reactive protein (CRP) level were measured.
RESULTS: The mean angioscopic follow-up period was 13 ± 9 months. Thirty-five superimposed thrombi still remained at follow-up, and the predominant thrombus color changed from red (56%) at baseline to pinkish-white (83%) at follow-up. The healing rate increased according to the angioscopic follow-up period (23% at  12 months vs. 55% at >12 months, p = 0.044). The %DS at the healed plaque increased from baseline to follow-up (12.3 ± 5.8% vs. 22.7 ± 11.6%, respectively; p = 0.0004). The serum CRP level in patients with healed plaques (n = 10) was lower than that in those without healed plaques (n = 19; 0.07 ± 0.03 mg/dl vs. 0.15 ± 0.11 mg/dl, respectively; p = 0.007).
CONCLUSIONS: 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.
|
Abbreviations and Acronyms
| | ACS = acute coronary syndrome | | CRP = C-reactive protein | | %DS = percent diameter stenosis | | IVUS = intravascular ultrasound | | LAD = left anterior descending coronary artery | | LCx = left circumflex artery | | MI = myocardial infarction | | PCI = percutaneous coronary intervention | | QCA = quantitative coronary angiogram | | RCA = right coronary artery | | SAP = stable angina pectoris | | UAP = unstable angina pectoris |
|
Atherosclerotic coronary plaque rupture (or erosion) and subsequent thrombus formation in the culprit lesion are recognized to be the major motivating factors in acute coronary syndrome (ACS) (1–5). Intravascular ultrasound (IVUS) studies recently reported that a plaque rupture occurs not only in culprit lesions but also in other atherosclerotic plaques in patients with ACS, stable angina pectoris (SAP), and silent myocardial ischemia (6–9). The concept of "pancoronaritis" or "multifocal plaque rupture" has been established. In the clinical setting, ruptured plaque in the culprit lesion is usually treated with percutaneous coronary intervention (PCI), and the natural course of ruptured plaque without PCI has not yet been reported. Previous pathologic studies have shown that healed plaques after a subclinical rupture tend to result in increased narrowing of the coronary lumen (10,11). Nevertheless, ruptured plaques in nonculprit lesions have not been well described as to whether they heal uneventfully with (or without) luminal narrowing or lead to an occurrence of acute coronary events in living patients.
Serum C-reactive protein (CRP), a predictor of acute myocardial infarction (MI), is expressed in human atherosclerotic lesions, and most CRPs show an increased expression at sites of plaque rupture (12–14). The serial changes in the serum CRP level in patients with multiple plaque ruptures have also not yet been elucidated.
Coronary angioscopy can provide direct images of the endoluminal surface and detailed information on plaque rupture (or healing), as well as on the existence and age of a thrombus. The purpose of this study was to investigate the natural course of ruptured plaques in nonculprit lesions in living patients.
|
Methods
|
|---|
Patient population.
Between September 1998 and December 2003, 327 patients were analyzed by coronary angioscopy. Thirty consecutive patients in whom two or three de novo native coronary arteries were evaluated by repeat angioscopic procedures and who had ruptured plaque(s) at nonculprit lesions were enrolled in this study. Written, informed consent approved by our institutional review boards was obtained from all study patients before catheterization.
Clinical demographics.
The patient demographics were obtained by a hospital chart review. Stable angina pectoris was defined as a positive stress test and no change in the frequency, duration, or intensity of symptoms lasting <4 weeks. Unstable angina pectoris (UAP) was new-onset severe angina, accelerated angina, or rest angina. Acute or recent MI occurred within 6 weeks, and a previous MI >6 weeks. Patients with UAP, acute MI, and recent MI were categorized as ACS. Blood sampling was collected in the fasting state, immediately before each angioscopic procedure, except for CRP in patients with ACS. In ACS, the serum CRP level four weeks after onset was selected as the baseline level because of exclusion of the effects of myocardial necrosis.
A culprit lesion was identified by the combination of the electrocardiographic findings, left ventricle wall motion abnormalities (left ventriculography or echocardiography), scintigraphic defects, and angiographic lesion morphology.
Angiographic analysis.
All angiograms were analyzed with a computer-assisted, automated edge-detection algorithm (CMS, MEDIS, Nuenen, The Netherlands) by an angiographer blinded to the clinical and angioscopic findings, using a standard qualitative definition and quantitative coronary angiographic (QCA) measurements. The variability of the QCA measurements was analyzed repeat measurements of the target plaques. The variation in minimal lumen diameter was 0.09 ± 0.09 mm and that in %DS was 2.8 ± 2.1%. A follow-up angiogram was obtained at the same angle as that in the baseline study.
Angioscopic imaging.
The coronary angioscopic procedure has been previously reported (15). The proximal segments to the culprit lesion were observed by angioscopy before PCI for avoidance of mechanical damage due to the PCI procedure. The distal segments to the culprit lesion and the other coronary arteries were examined after PCI. The angioscopic and fluoroscopic images during the angioscopic observations were recorded on digital videotape for later analysis. The exact position of the angioscopic catheter at the site of the target plaque was recorded on an angiogram to ensure a reliable comparison.
Definition and analysis of angioscopic findings.
A ruptured plaque was defined as a complex plaque and/or a superimposed thrombus. A complex plaque was considered to be present when the surface of the lesion had an irregular appearance, including a fissure, flap, and ulceration. Based on the surface color, the plaque was classified as either yellow or white. A fissure was defined as a torn intima without floating into the lumen; a flap was a disrupted fragment floating into the lumen; and ulceration was a crater-like lesion suggesting a gap in the vessel wall (Fig. 1). A thrombus was defined as a coalescent red or pinkish-white, superficial, or protruding mass adhering to the vessel surface, but clearly a separate structure that remained despite being flushed with saline solution. Complete plaque healing was defined as a covering by the neointima and the disappearance of thrombus and complex plaque.
View larger version (32K):
[in this window]
[in a new window]
|
Figure 1 Angioscopic images of nonculprit ruptured plaques. (A) Yellow plaque with a fissure (arrow) and red thrombus. (B) Yellow plaque with a flap (arrow). (C) Yellow plaque with an ulceration (arrow) and red thrombus. (D) Yellow plaque with a pinkish-white thrombus (arrow).
|
|
The intra-observer agreement on angioscopic images was measured by having an observer repeat assessment of 20 images (presented in random order) after one week. The inter-observer agreement was measured by comparing the assessment of 100 images by the two observers blinded to the clinical background. The intra-observer agreements for the evaluated angioscopic items (complex plaque, yellow plaque, and thrombus) were 95%, 95%, and 100%, respectively. The inter-observer agreements of those items were 93%, 98%, and 97%, respectively. The kappa values for intra-observer agreement of them were 0.94, 0.99, and 0.95, respectively. The kappa values for inter-observer agreement of them were 0.95, 0.96, and 0.94, respectively. When there was any discordance between the two observers, a third investigator read the images, and a consensus was obtained.
Percutaneous coronary intervention and clinical follow-up.
The PCI was performed for only the culprit lesions using a stent. Two kinds of antiplatelet agents—ticlopidine (200 mg/day) or cilostazole (200 mg/day), added to aspirin (81 to 200 mg/day)—were administered for at least six months. Glycoprotein IIb/IIIa inhibitors have not been approved for clinical use in Japan. Repeat PCI, bypass surgery, ACS, and death were all considered to be major outcome events.
Statistical analysis.
Statistical analysis was performed with StatView 5.0 (SAS Institute, Cary, North Carolina). Categorical variables are presented as frequencies and compared by the Fisher exact test. Continuous quantitative data are presented as the mean value ± SD. Continuous data were compared by the unpaired Student t test between the different categories and by the paired Student t test between the baseline and follow-up. Univariate logistic regression analysis was tested to determine clinical predictors for the healing of nonculprit ruptured plaques. Variables that achieved a significance of levels in a univariate logistic regression analysis were then selected for testing in a multivariate logistic regression analysis. A p value of <0.05 was considered to be statistically significant.
|
Results
|
|---|
Clinical characteristics at baseline.
The clinical characteristics of 30 patients at baseline are summarized in Table 1. Coronary angioscopy was performed in 73 arteries (2.4 arteries/patient): 25 right coronary arteries (RCA), 26 left anterior descending coronary arteries (LAD), and 22 left circumflex arteries (LCx).
Lesion characteristics at baseline.
A total of 50 ruptured plaques were found in 36 arteries (19 in RCA, 8 in LAD, 9 in LCx). The lesion characteristics of the ruptured plaques are summarized in Table 2. The number of ruptured plaques in nonculprit lesions ranged from one to four per patient (1.67/patient) and 0.68/artery. The %DS of ruptured plaques was 16.3 ± 9.7%. Twenty-five (50%) of 50 plaques were recognized as complex lesions on the angiograms. Forty-eight ruptured plaques (96%) were accompanied by superimposed thrombi, and 56% were red thrombi. No superimposed thrombi could be detected in each plaque with a fissure and flap. There were 13 plaques in which the underlying ruptures were not visualized due to the superimposed thrombi. Forty-six ruptured plaques (92%) were diagnosed to be yellow plaques.
Lesion characteristics at follow-up.
Follow-up angioscopy was performed 13 ± 9 months after the baseline studies to document the changes in the nonculprit ruptured plaques that had been previously identified. At follow-up, 35 thrombi still remained on the same plaques at baseline (Table 3). The frequency of red thrombi decreased to 17%, and pinkish-white thrombi became predominant. Fifteen ruptured plaques in 11 patients healed completely (Fig. 2), and the overall healing rate of the plaque was 30%. The frequency of yellow plaques in the healed plaques was 47%. The healing rate of the plaque increased according to the follow-up period (23% [9 of 39] at 12 months vs. 55% [6 of 11] at >12 months, p = 0.044) (Fig. 3).
View larger version (79K):
[in this window]
[in a new window]
|
Figure 2 Healing of nonculprit plaque in acute coronary syndrome (ACS). (A) Coronary angiogram of the left circumflex artery (LCx) in a patient with ACS. (B) A pinkish-white thrombus on the yellow plaque was observed in the mid-portion of the LCx at baseline (white arrowhead in A). (C) A 12-month follow-up coronary angiogram in the same patient. (D) The thrombus disappeared and a smooth white intima was found (white arrowhead in C). In the quantitative coronary angiogram measurements, %DS at the angioscopic image site (white arrowhead in A and C) increased from 34.5% at baseline to 43.1% at follow-up.
|
|
View larger version (10K):
[in this window]
[in a new window]
|
Figure 3 Relationship between the angioscopic follow-up period and healing rate of the nonculprit ruptured plaques. The healing rate of ruptured plaques of 12 months and >12 months were 23% and 55%, respectively. The healing rate increased according to the angioscopic follow-up period.
|
|
On QCA analysis, the %DS of the healed plaques at follow-up was greater than that at baseline (22.7 ± 11.6% vs. 12.3 ± 5.8%; p = 0.0004), whereas that of nonhealed plaque was not significantly different between that at follow-up and baseline (19.1 ± 12.0% vs. 18.0 ± 10.6%; p = 0.6).
Clinical characteristics at follow-up.
In 29 patients, all plaques in the same patient could be categorized as either healed or not. One patient who had both two healed plaques and one residual ruptured plaque was excluded from the following analysis. The clinical characteristics at follow-up in patients with healed plaques (n = 10) and in those without healed plaques (n = 19) are summarized in Table 4. The frequency of statin use in patients with healed plaques was higher than that in those without healed plaques (p = 0.009). In patients with healed plaques, the serum CRP level did not change significantly from 0.24 ± 0.34 mg/dl at baseline to 0.07 ± 0.03 mg/dl at follow-up (p = 0.16). The serum CRP level in patients with healed plaque was lower than that in those without healed plaques (0.07 ± 0.03 mg/dl vs. 0.15 ± 0.11 mg/dl; p = 0.007).
The results of univariate logistic regression analyses indicated that the serum CRP level at follow-up and statin use were predictors for plaque healing in nonculprit lesions (Table 5). Multivariate logistic regression analysis was performed, in which the serum CRP level at follow-up and statin use were the independent variables. Two clinical variables were not statistically significant (serum CRP level at follow-up: p = 0.12, odds ratio 1.21, 95% confidence interval 0.99 to 1.62; statin use: p = 0.19, odds ratio 0.27, 95% confidence interval 0.04 to 1.83).
Clinical events.
All patients underwent successful PCI for culprit lesions at baseline. The clinical follow-up period was 38 ± 16 months. Five patients underwent repeat PCI for restenosis at three to six months after baseline. A new onset of effort angina (SAP) occurred in one patient 25 months after baseline. In this patient, a healed plaque confirmed by angioscopy showed progression on an angiogram, and PCI was performed. All patients were free from bypass surgery, ACS, and death during the clinical follow-up period.
|
Discussion
|
|---|
Multiple coronary plaque ruptures, including culprit plaque and other plaques, can occur in patients with various ischemic heart disease (6–10). At the present time, ruptured plaque in the culprit lesion is commonly treated by PCI. This follow-up study clarified the changes in ruptured plaques in nonculprit lesions.
Change of thrombus color and plaque healing.
A previous IVUS study reported the frequencies of thrombus in nonculprit ruptured plaques in ACS and in non-ACS to be 32% and 8%, respectively (8). In this angioscopic study, 48 (96%) of 50 ruptured plaques were associated with superimposed thrombi. Coronary angioscopy might be superior to IVUS regarding its ability to differentiate plaque from thrombus. Moreover, angioscopy can show the thrombus color, which allows us to estimate the age and components of the thrombus. In this study, the predominant thrombus color changed from red at baseline to pinkish-white at follow-up. A red thrombus on angioscopy is considered to be a fresh one and is mainly composed of red blood cells and fibrin. In the process of thrombus organization, a red thrombus changes into a pinkish-white one with platelets and fibrin formation (3,16). Our observations on the changes in thrombus color might show the process of thrombus organization.
In our study, the angioscopic follow-up period varied. However, the frequency of disappearance of thrombus and healed plaque increased gradually according to the follow-up period. The frequency of yellow plaques in the healed plaques was lower than that at baseline. In several cases, the plaque color changed from yellow to white during the healing process. Similar to the healing of culprit plaques after PCI, a white neointima on angioscopy may cover the nonculprit ruptured plaques and also play a role in the repair process (17). Surprisingly, several thrombi were still found on the ruptured plaque after 12 months of follow-up. These results may suggest that ruptured plaques heal very slowly. A previous pathologic study demonstrated that repetitive ruptures occur in the healed plaques (10). Perhaps part of the thrombi form after recurrent ruptures, and repetitive ruptures could not be excluded in our study.
Change in angiographic stenosis.
The %DS of the healed plaques increased significantly from baseline to follow-up. A postmortem study in patients with sudden cardiac death reported that the area within the internal elastic lamina is less in healed plaque after a subclinical rupture than in acute ruptured plaque (10). Furthermore, a cellular proliferation of smooth muscle cells is higher at healed plaque than at ruptured plaque (10). These facts suggest that plaque healing results in an increased plaque burden and negative remodeling.
Our past combination study using angioscopy and IVUS revealed that nondisrupted white plaque and negative remodeling are often found in the culprit lesions of SAP (18). Probably, in several cases of SAP, stenosis of the coronary lumens developed, and clinical symptoms have appeared in the process of plaque healing after previous ruptures. The precise mechanism of angiographic progression was not clarified in this angioscopic study, although progression of the healed plaques might have resulted from negative remodeling and cell infiltration into the plaques.
Serum CRP level.
The serum CRP level predicts the risk of MI or stroke better than total and low-density lipoprotein cholesterol levels (12). A previous angiographic study revealed the presence of multiple complex stenosis in ACS patients, and such stenosis was found to correlate with elevated CRP levels (19). In our study, the serum CRP level in patients with healed plaques did not significantly decrease from baseline to follow-up. The serum CRP level in patients with healed plaques was lower than that in those without healed plaques, thus suggesting that the serum CRP level should reflect the disease activity of the plaque ruptures.
Pharmacologic intervention with statin therapy has been shown to reduce the serum CRP level. We previously reported that statin therapy reduces the serum CRP level and angioscopic complexity of the plaques (the existence of the thrombus and the irregularity of the plaque) in nonculprit lesions (20). Our present data show that frequency of administration of a statin in patients with healed plaques was significantly higher than that in those without healed plaques. Moreover, the serum CRP level in patients with healed plaques was lower than that in those without healed plaques. Our results from univariate logistic regression analyses indicated that both statin therapy and serum CRP level at follow-up are considered predictors of healing in nonculprit ruptured plaques. However, a multivariate logistic regression analysis showed that neither statin therapy nor serum CRP level at follow-up is an independent predictor of plaque healing. These results should be explained so that these two factors correlate to each other.
Clinical events.
In this study, no patients had any ACS events during the 38-month follow-up without PCI for nonculprit ruptured plaques. A previous angiographic study in ACS patients with complex coronary lesions demonstrated a poor clinical prognosis, particularly in terms of recurrent ACS episodes (21). On the other hand, an IVUS study of multiple coronary ruptures revealed no recurrence of ACS during 10-month clinical follow-up (6). In the same study, the stenosis of ruptured plaques in nonculprit lesions was less severe than that in culprit lesions (39% vs. 70%, respectively). In our study, the %DS was only 16.3% in ruptured plaques of baseline and 19.1% in nonhealed plaques of follow-up. A quantitative cross-sectional analysis by IVUS revealed that ruptured plaques at nonculprit lesions have larger lumens than do culprit lesions (6,8). Such evidence indicates that a plaque rupture itself does not always result in acute ischemic events. Our follow-up study suggests that even though there are residual ruptured plaques and thrombi, the associated lesions do not lead to the development of ACS in cases with large coronary lumens.
However, an important question remains. Angiographic studies have shown that preexisting stenoses of the culprit lesions were previously mild to moderate (22,23). It is impossible to explain that the degree of stenosis on the angiogram can help determine whether the patient develops ACS or the plaque ruptures remain asymptomatic. When patients have a systemic or local increased potential of thrombogenicity, ruptured plaques in lesions with mild to moderate stenosis may lead to ACS (24). Several IVUS studies have demonstrated that culprit lesions of ACS have a greater plaque burden than do ruptured plaques in nonculprit lesions (6–8). In the event of a plaque rupture, a large plaque is considered to contribute to accelerated local thrombogenicity and the development of thrombosis because of the exposure of a large amount of its contents, such as tissue factor and collagen (25). Conversely, at the nonculprit plaques in smaller sized plaques, even though thrombi still remain, growth of the thrombi may be limited. Therefore, both the degree of stenosis and plaque size, which are unable to be validated by an angiogram, may thus be determinant factors in the clinical course of ruptured plaques.
Atherosclerosis is a progressive disease. Repetitive coronary plaque ruptures on the healed plaques can occur, and then the degree of luminal narrowing should progress (10). A significant degree of stenosis thus appears to be associated with the cause acute thrombotic events (26). Further follow-up studies are needed to examine the development of severe stenosis and acute coronary events.
Study limitations.
The number of analyzed plaques and patients represent a limitation of this study. Coronary angioscopy was not performed in all segments of coronary arteries in all patients. Some selection bias is therefore inevitable, beginning with the selection of patients to undergo cardiac catheterization and angioscopy. The follow-up angioscopic examination, which was performed at a single time point, also has some limitations.
Conclusions.
This follow-up study documented that plaque ruptures in nonculprit lesions tend to heal slowly with a progression of luminal stenosis, and the serum CRP level might reflect the disease activity of the plaque ruptures.
|
Acknowledgments
|
|---|
The authors thank Koji Harada, Masayuki Mizuno, Yoshiko Kasahara, and Mizue Yoshitomi for their excellent assistance in our catheter laboratory. Finally, we thank Shinji Hirosaki for his statistical advice.
|
References
|
|---|
1. Fuster V, Badimon L, Badimon JJ, et al. The pathogenesis of coronary artery disease and the acute coronary syndromes N Engl J Med 1992;326:242-250, 310–8.[Web of Science][Medline]
2. Mizuno K, Miyamoto A, Satomura K, et al. Angioscopic macromorphology in patients with acute coronary disorders Lancet 1991;337:809-812.[CrossRef][Web of Science][Medline]
3. Mizuno K, Satomura K, Miyamoto A, et al. Angioscopic evaluation of coronary-artery thrombi in acute coronary syndromes N Engl J Med 1992;326:287-291.[Abstract]
4. Falk E, Shah PK, Fuster V. Coronary plaque disruption Circulation 1995;92:657-671.[Free Full Text]
5. Farb A, Burke AP, Tang A, et al. Coronary plaque erosion without rupture into a lipid core: a frequent cause of coronary thrombosis in sudden coronary death Circulation 1996;93:1354-1363.[Abstract/Free Full Text]
6. Rioufol G, Finet G, Ginon I, et al. Multiple atherosclerotic plaque rupture in acute coronary syndrome: a three-vessel intravascular ultrasound study Circulation 2002;106:804-808.[Abstract/Free Full Text]
7. Kotani J, Mintz GS, Castagna T, et al. Intravascular ultrasound analysis of infarct-related and non-infarct-related arteries in patients who presented with an acute myocardial infarction Circulation 2003;107:2889-2893.[Abstract/Free Full Text]
8. Fujii K, Kobayashi Y, Mintz GS, et al. Intravascular ultrasound assessment of ulcerated ruptured plaques: a comparison of culprit and nonculprit lesions of patients with acute coronary syndromes and lesions in patients without acute coronary syndromes Circulation 2003;108:2473-2478.[Abstract/Free Full Text]
9. Schoenhagen P, Stone GW, Nissen SE, et al. Coronary plaque morphology and frequency of ulceration distant from culprit lesions in patients with unstable and stable presentation Atheroscler Thromb Vasc Biol 2003;23:1895-1900.[Abstract/Free Full Text]
10. Burke AP, Kolodgie FD, Farb A, et al. Healed plaque ruptures and sudden coronary death: evidence that subclinical rupture has a role in plaque progression Circulation 2001;103:934-940.[Abstract/Free Full Text]
11. Mann J, Davies MJ. Mechanisms of progression in native coronary artery disease: role of healed plaque disruption Heart 1999;82:265-268.[Abstract/Free Full Text]
12. Ridker PM, Rifai N, Rose L, et al. Comparison of C-reactive protein and low-density lipoprotein cholesterol levels in the prediction of first cardiovascular events N Engl J Med 2002;347:1557-1565.[Abstract/Free Full Text]
13. Glass CK, Witztum JL. Atherosclerosis: the road ahead Cell 2001;104:503-516.[CrossRef][Web of Science][Medline]
14. Vainas T, Lubbers T, Stassen FR, et al. Serum C-reactive protein level is associated with abdominal aortic aneurysm size and may be produced by aneurismal tissue Circulation 2003;107:1103-1105.[Abstract/Free Full Text]
15. Okamatsu K, Takano M, Sakai S, et al. Elevated troponin T levels and lesion characteristics in non-ST-elevation acute coronary syndromes Circulation 2004;109:465-470.[Abstract/Free Full Text]
16. Pearson TA, Dillman J, Solez K, et al. Monoclonal characteristics of organizing arterial thrombi: significance in the origin and growth of human atherosclerotic plaques Lancet 1979;1:7-11.[Medline]
17. Sakai S, Mizuno K, Yokoyama S, et al. Morphologic changes in infarct-related plaque after coronary stent placement: a serial angioscopy study J Am Coll Cardiol 2003;42:1558-1565.[Abstract/Free Full Text]
18. Takano M, Mizuno K, Okamatsu K, et al. Mechanical and structural characteristics of vulnerable plaques: analysis by coronary angioscopy and intravascular ultrasound J Am Coll Cardiol 2001;38:99-104.[Abstract/Free Full Text]
19. Zairis M, Papadaki O, Manousakis S, et al. Multiple complex coronary plaques in patients with primary unstable angina Atherosclerosis 2000;164:355-359.
20. Takano M, Mizuno K, Yokoyama S, et al. Changes in coronary plaque color and morphology by lipid-lowering therapy with atorvastatin: serial evaluation by coronary angioscopy J Am Coll Cardiol 2003;42:680-686.[Abstract/Free Full Text]
21. Goldstein JA, Demetriou D, Grines CL, et al. Multiple complex coronary plaques in patients with acute myocardial infarction N Engl J Med 2000;343:915-920.[Abstract/Free Full Text]
22. Little WC, Constantinescu M, Applegate RJ, et al. Can coronary angiography predict the site of a subsequent infarction in patients with mild-to-moderate coronary artery disease? Circulation 1988;78:1157-1166.[Abstract/Free Full Text]
23. Fishbein MC, Siegel RJ. How big are coronary atherosclerotic plaques that rupture? Circulation 1996;94:2662-2666.[Free Full Text]
24. Naghavi M, Libby P, Falk E, et al. From vulnerable plaque to vulnerable patient: a call for new definitions and risk assessment strategies: part I Circulation 2003;108:1664-1672.[Abstract/Free Full Text]
25. Barstad RM, Hamers MJ, Kierulf P, et al. Procoagulant human monocytes mediated tissue factor/factor VIIa-dependent platelet-thrombus formation when exposed to flowing nonanticoagulated human blood Atheroscler Thromb Vasc Biol 1995;15:11-16.[Abstract/Free Full Text]
26. Qiao JH, Fishbein MC. The severity of coronary atherosclerosis at sites of plaque rupture with occlusive thrombosis J Am Coll Cardiol 1991;17:1138-1142.[Abstract]
Related Article
-
Plaque rupture and intracoronary thrombus in nonculprit vessels: An eyewitness account
- John A. Ambrose and David J. D’Agate
J. Am. Coll. Cardiol. 2005 45: 659-660.
[Full Text]
[PDF]
This article has been cited by other articles:
|
|
|
|
 
A. Maehara, G. S. Mintz, and N. J. Weissman
Advances in Intravascular Imaging
Circ Cardiovasc Interv,
October 1, 2009;
2(5):
482 - 490.
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. Yokoyama, M. Takano, M. Yamamoto, S. Inami, S. Sakai, K. Okamatsu, S. Okuni, K. Seimiya, D. Murakami, T. Ohba, et al.
Extended Follow-Up by Serial Angioscopic Observation for Bare-Metal Stents in Native Coronary Arteries: From Healing Response to Atherosclerotic Transformation of Neointima
Circ Cardiovasc Interv,
June 1, 2009;
2(3):
205 - 212.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
T. J. Bunch, C. S. Rihal, R. J. Gumina, L. Cooper, and N. M. Caplice
Progression of Nonculprit Plaque Stenosis Following Successful Percutaneous Intervention
Angiology,
May 1, 2008;
59(2):
236 - 239.
[Abstract]
[PDF]
|
|
|
|
|
|
|
C. L. Jackson, M. R. Bennett, E. A.L. Biessen, J. L. Johnson, and R. Krams
Assessment of Unstable Atherosclerosis in Mice
Arterioscler Thromb Vasc Biol,
April 1, 2007;
27(4):
714 - 720.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. Waxman, F. Ishibashi, and J. E. Muller
Detection and Treatment of Vulnerable Plaques and Vulnerable Patients: Novel Approaches to Prevention of Coronary Events
Circulation,
November 28, 2006;
114(22):
2390 - 2411.
[Full Text]
[PDF]
|
|
|
|
|
|
|
G. H. Tofler and J. E. Muller
Triggering of Acute Cardiovascular Disease and Potential Preventive Strategies
Circulation,
October 24, 2006;
114(17):
1863 - 1872.
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Takano, T. Ohba, S. Inami, K. Seimiya, S. Sakai, and K. Mizuno
Angioscopic differences in neointimal coverage and in persistence of thrombus between sirolimus-eluting stents and bare metal stents after a 6-month implantation
Eur. Heart J.,
September 2, 2006;
27(18):
2189 - 2195.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. N. DeMaria, J. Narula, E. Mahmud, and S. Tsimikas
Imaging vulnerable plaque by ultrasound.
J. Am. Coll. Cardiol.,
April 18, 2006;
47(8 Suppl):
C32 - C39.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
H. W. Strauss, C. Mari, B. E. Patt, and V. Ghazarossian
Intravascular radiation detectors for the detection of vulnerable atheroma.
J. Am. Coll. Cardiol.,
April 18, 2006;
47(8 Suppl):
C97 - C100.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
Top
Abstract
Methods