In Vivo Comparison of Optical Coherence Tomography and Angioscopy for the Evaluation of Coronary Plaque Characteristics

Takano, Masamichi; Jang, Ik–Kyung; Inami, Shigenobu; Yamamoto, Masanori; Murakami, Daisuke; Okamatsu, Kentaro; Seimiya, Koji; Ohba, Takayoshi; Mizuno, Kyoichi

doi:10.1016/j.amjcard.2007.09.106

Cited by 104 publications

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“…Intense yellow plaques upon angioscopic examination correlated with the presence of a plaque with a large lipid area on IB-IVUS display 14) . Postmortem histological assessment and in vivo studies with other coronary imaging devices, such as virtual histology IVUS and OCT, have shown that yellow color intensity is associated with a lipid core underneath a thin fibrous cap and that intense yellow plaques might be structurally vulnerable [15][16][17] . Similarly, it has been reported that nonintense yellow plaque was plaque with a thick fibrous cap 17) .…”

Section: Discussionmentioning

confidence: 99%

Intense Yellow Culprit Plaque Coloration is Closely Associated with Troponin-T Elevation and Flow Complications Following Elective Coronary Stenting

Murakami

Takano

Yamamoto

et al. 2011

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Section: Discussionmentioning

confidence: 99%

Intense Yellow Culprit Plaque Coloration is Closely Associated with Troponin-T Elevation and Flow Complications Following Elective Coronary Stenting

Murakami

Takano

Yamamoto

et al. 2011

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“…The cap of intense yellow color plaques is very thin 28) and is associated with plaque vulnerability. 29,30) In the present study, for patients with OMI and stable angina, yellow plaques had a higher incidence of silent plaque disruption compared to white plaques.…”

Section: Discussionmentioning

confidence: 99%

Angioscopic Study of Silent Plaque Disruption in Nonischemic Related Coronary Artery in Patients With Stable Ischemic Heart Disease

et al. 2010

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SummaryPlaque disruption, which may be associated with some coronary risk factors, plays a key role in the development of acute coronary syndromes and progression of atherosclerosis. However, the clinical profile of asymptomatic plaque disruption in stable ischemic heart disease has not been well evaluated. The aim of the present study was to investigate the frequency and determinants of silent plaque disruption (SPD) in patients with stable ischemic heart disease using coronary angioscopy. Forty-one patients with stable angina or old myocardial infarction (OMI) without any complaints within 3 months were included in the present study. Angioscopy was successfully performed through 49 nonischemic related coronary arteries. The presence of SPD and coronary risk factors were recorded. Silent plaque disruption was found in 12 patients with stable ischemic heart disease (12/41, 29.3%), and the frequency of SPD in nonischemic related coronary arteries was 26.5% (13/49). A significantly higher frequency of SPD was noted in yellow plaques than in white plaques (35.3% versus 6.7%, P = 0.043). Overall, the independent clinical risk factors of SPD in nonischemic related coronary arteries were diabetes mellitus (P = 0.018; OR, 18.8209; 95% CI, 1.6525 to 214.3523) and hypertension (P = 0.0313; OR, 6.6485; 95% CI, 1.1850 to 37.3019). These results suggest silent plaque disruption was commonly observed in nonischemic related coronary arteries in patients with stable ischemic heart disease and its determinants were diabetes mellitus and hypertension. (Int Heart J 2010; 51: 383-387) Key words: Plaque disruption, Angioscopy, Ischemic heart disease, Risk factors, Hypertension, Diabetes mellitus A cute coronary syndrome (ACS) is a special disease spectrum of coronary artery diseases, which includes unstable angina, acute myocardial infarction, and sudden death, and is the major cause of cardiovascular death. Atherosclerotic plaque disruption, vascular spasm and the consequent platelet adhesion, aggregation and secondary thrombosis are the major pathophysiological mechanisms of acute coronary syndrome. Among them, coronary arterial plaque disruption is considered to play the key role in the cascade of acute coronary syndrome. 1)However, the plaque disruption may also heal without any symptoms. Autopsy studies have observed plaque disruption in approximately 10% of patients who died from noncardiac causes and without cardiac symptoms.2) Although clinically silent, plaque disruption accompanied by mural thrombus formation may play a role in rapid plaque progression.3) Moreover, silent plaque disruption in nonculprit lesions may be an indicator of extensive coronary instability which is often underestimated by angiography. Intravascular ultrasound (IVUS) study of patients within 30 days of ACS showed that approximately 79% of cases had plaque disruption located on the nonculprit lesions. 4)It is well-known that coronary risk factors, such as hypertension, hyperlipidemia, smoking, and diabetes mellitus induce atherosclerosis and control...

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“…17,18) Miyamoto, et al reported that there was an inverse relationship between the grade of a yellow and fibrous cap thickness and coronary plaques were observed as white by angioscopy in case of a fibrous cap thickness > 75 μm, in spite of the presence of a lipid-rich yellow plaque. 19) Therefore, a thick white neointima over the stent struts probably makes it difficult to identify the struts using angioscopy.…”

Section: Discussionmentioning

confidence: 99%

Difference in Neointimal Proliferation Between Ruptured and Non-Ruptured Segments After Bare Metal Stent Implantation

et al. 2010

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SummaryThe difference in neointimal stent coverage (NSC) between ruptured segments and adjacent nonruptured segments in infarct-related lesions (IRL) of acute myocardial infarction after bare metal stent (BMS) implantation was evaluated using coronary angioscopy. Serial angioscopic observations were performed for 19 IRLs immediately after the implantation of a BMS and at 1-month and 6-month follow-up. Stented segments were divided into the ruptured segment and the nonruptured segment based on the presence of a thrombus. The grade of NSC was divided into 0 = complete exposure, 1 = partial coverage, or 2 = complete coverage. The grade of plaque color was classified semiquantitatively as 0 = white, 1 = light yellow, or 2 = intense yellow. The existence of a thrombus was also determined. The grade of NSC in the ruptured segment was lower than that of the nonruptured segment at each follow-up. The grade of plaque color at the 1-month follow-up was higher in the ruptured segment than in the nonruptured segment. At 6 months, the grade of plaque color was similar between the ruptured and nonruptured segments. In all cases, thrombi existed in the ruptured segments immediately after stenting. Although thrombi still remained frequently at 1-month, most had disappeared at the 6-month follow-up. Neointimal proliferation of the ruptured segment in IRL advanced slowly in comparison to the adjacent nonruptured segment. The presence of an atherosclerotic yellow plaque and a thrombus may affect the delayed neointimal coverage after BMS implantation. (Int Heart J 2010; 51: 7-12) Key words: Acute myocardial infarction, Stent, Neointima, Plaque R ecently, a late thrombosis after stent implantation has emerged as a major clinical concern regardless of the type of stent, such as a bare metal stent (BMS) or a drug-eluting stent, because it is a life-threatening complication.1-3) The principal mechanisms of the late stent thrombosis are delayed endothelialization, lack of neointimal stent coverage (NSC), and the presence of persistent uncovered stent struts. 4,5) Several follow-up studies after stent implantation using coronary angioscopy demonstrated that NSC had an effect on plaque stabilization due to the complete sealing of the stent by the neointima underlying the ruptured plaque regardless of any unstable clinical settings, such as an acute myocardial infarction (AMI). 6,7)Moreover, NSC after stent implantation has a different time course between patients with an AMI and those with stable angina pectoris. 7,8) The major causes of an AMI are understood to be the disruption of atherosclerotic vulnerable plaques and subsequent thrombus formation and a vulnerable plaque is recognized as yellow by coronary angioscopy.9-11) Although a coronary stent is deployed on the ruptured segment, the location of the stent extends to the nonruptured segment beyond the ruptured segment. Angioscopic plaque morphology between the ruptured and nonruptured segments is quite different. The ruptured segment is defined as the site of a vulnerable yellow pl...

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In Vivo Comparison of Optical Coherence Tomography and Angioscopy for the Evaluation of Coronary Plaque Characteristics

Cited by 104 publications

References 20 publications

Intense Yellow Culprit Plaque Coloration is Closely Associated with Troponin-T Elevation and Flow Complications Following Elective Coronary Stenting

Intense Yellow Culprit Plaque Coloration is Closely Associated with Troponin-T Elevation and Flow Complications Following Elective Coronary Stenting

Angioscopic Study of Silent Plaque Disruption in Nonischemic Related Coronary Artery in Patients With Stable Ischemic Heart Disease

Difference in Neointimal Proliferation Between Ruptured and Non-Ruptured Segments After Bare Metal Stent Implantation

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