Intravascular Ultrasound Assessment of Ulcerated Ruptured Plaques

Fujii, Kenichi; Kobayashi, Yoshio; Mintz, Gary S.; Takebayashi, Hideo; Dangas, George; Moussa, Issam; Mehran, Roxana; Lansky, Alexandra J.; Kreps, Edward M.; Collins, Michael B.; Colombo, Antonio; Stone, Gregg W.; Leon, Martin B.; Moses, Jeffrey W.

doi:10.1161/01.cir.0000097121.95451.39

Cited by 214 publications

(24 citation statements)

References 46 publications

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“…Atherosclerotic plaque rupture is considered to be a key event in the pathogenesis of ACS [31]. The severity of the culprit lesion or thrombus formation after plaque rupture may be responsible for the development of ACS [32]. Results obtained using ECG and serum biomarkers often failed to identify the disease in outpatients and high-risk patients.…”

Section: Discussionmentioning

confidence: 99%

The serum protein fetuin-B is involved in the development of acute myocardial infarction

et al. 2015

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The rupture of an atherosclerotic plaque is one of the main causes of coronary artery thrombotic occlusion, leading to myocardial infarction. However, the exact mechanism and causal risk factors for plaque rupture remain unclear. To identify a potential molecule that can influence atherosclerotic plaque rupture, we investigated protein expression in serum from patients with acute myocardial infarction (AMI) and stable angina (SA), using proteomic analysis. The expression of six proteins, including fibrinogen, fetuin-B, keratin 9, proapolipoprotein and fibrinogen, were altered in serum from patients with AMI compared with serum from those with SA. Of these, fetuin-B, proapolipoprotein, fibrinogen γ-B-chain precursors and fibrinogen expression were greater in serum from patients with AMI than from patients with SA. Increased fetuin-B expression in serum from AMI patients was also confirmed by Western blot analysis. Treatment with recombinant human fetuin-B increased the migration in monocytes and macrophages in a concentration-dependent manner. Fetuin-B also affected vascular plaque-stabilizing factors, including lipid deposition and cytokine production in macrophages, the activation of matrix metalloproteinase (MMP)-2 in monocytes, and the activation of apoptosis and MMP-2 in vascular smooth muscle cells. Moreover, in vivo administration of fetuin-B decreased the collagen accumulation and smooth muscle cell content and showed an increased number of macrophages in the vascular plaque. From these results, we suggest that fetuin-B may act as a modulator in the development of AMI. This study may provide a therapeutic advantage for patients at high risk of AMI.

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Section: Discussionmentioning

confidence: 99%

The serum protein fetuin-B is involved in the development of acute myocardial infarction

et al. 2015

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“…Culprit-lesion, infarct-related plaque rupture is found in 66% of culprit lesions of patients with acute myocardial infarction versus 27% of target lesions in patients with SA [17]. Symptoms develop when plaque rupture leads to thrombus formation and lumen obstruction or when plaque rupture is superimposed on a larger prerupture plaque burden [18]. …”

Section: Discussionmentioning

confidence: 99%

Pregnancy-Associated Plasma Protein-A as a Marker of Culprit Lesion Instability in Unstable Angina Patients: An Intravascular Ultrasound Study

Liu²,

Dong³

et al. 2013

Cardiology

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Background: We evaluated the relationship between pregnancy-associated plasma protein-A (PAPP-A) and coronary plaque instability as assessed by intravascular ultrasound (IVUS). Methods: We performed greyscale IVUS analysis in culprit lesions of 93 patients with unstable angina (UA) and 72 with stable angina (SA). A sandwich enzyme-linked immunosorbent assay technique was used to assay circulating PAPP-A. Results: Patients with UA had higher PAPP-A levels than those with SA 10.8 mIU/l [interquartile range (IQR) 8.3-14.4] vs. 5.4 (IQR 2.9-9.8) mIU/l, p < 0.001]. Lesions in patients with higher PAPP-A levels were associated with larger plaque burden than lesions in patients with lower PAPP-A levels. IVUS attenuated plaque, positive remodeling and plaque rupture. Thrombus and angiographic Ambrose type-II eccentric lesions or multiple irregularities were more common in patients with higher PAPP-A levels than in those with lower PAPP-A levels. They were also more common in patients with UA and higher PAPP-A levels than in patients with (1) SA and higher PAPP-A levels, (2) UA and lower PAPP-A levels or (3) SA and lower PAPP-A levels. Conclusions: Higher PAPP-A levels were associated with coronary plaque instability in vivo and unstable symptoms in patients with coronary artery disease.

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“…20, 21 In an analysis of 51 ruptures plaques, the size of the emptied cavity was on average larger in lesions with positive remodeling and showed a linear relation with lesion plaque and vessel size but not with the degree of narrowing. 22 It also has been reported that ruptured plaques have more varied distribution, and the presence of thrombus is more common in culprit lesions in patients with unstable angina or acute myocardial infarction (AMI) and in multiple ruptures. 22 Ruptured plaques in culprit lesions in acute coronary syndromes (ACS) also have smaller lumen, greater plaque burden, area stenosis, and positive remodeling.…”

Section: Can We Predict Plaque Vulnerability By Non-invasive and Imentioning

confidence: 99%

“…22 It also has been reported that ruptured plaques have more varied distribution, and the presence of thrombus is more common in culprit lesions in patients with unstable angina or acute myocardial infarction (AMI) and in multiple ruptures. 22 Ruptured plaques in culprit lesions in acute coronary syndromes (ACS) also have smaller lumen, greater plaque burden, area stenosis, and positive remodeling. 21 …”

Section: Can We Predict Plaque Vulnerability By Non-invasive and Imentioning

confidence: 99%

Imaging Plaques to Predict and Better Manage Patients With Acute Coronary Events

García‐García

Jang

Serruys

et al. 2014

Circulation Research

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Culprit lesions of patients who have had an acute coronary syndrome commonly are ruptured coronary plaques with superimposed thrombus. The precursor of such lesions is an inflamed thin-capped fibroatheroma. These plaques can be imaged by means of invasive techniques such as intravascular ultrasound (and derived techniques), optical coherence tomography and near-infrared spectroscopy. Very often these patients exhibit similar (multiple) plaques beyond the culprit lesion. These remote plaques can be assessed non invasively by computed tomography angiography and magnetic resonance imaging and also using invasive imaging. The detection of these remote plaques is not only feasible, but also in natural history studies have been associated with clinical coronary events. Different systemic pharmacological treatments have been studied (mostly statins) with modest success and therefore newer approaches are being tested. Local treatment for such lesions is in its infancy and larger, prospective and randomized trials are needed. This review will describe the pathological and imaging findings in culprit lesions of patients with acute coronary syndrome and as well as the assessment of remote plaques. In addition, the pharmacological and local treatment options will be reviewed.

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Intravascular Ultrasound Assessment of Ulcerated Ruptured Plaques

Cited by 214 publications

References 46 publications

The serum protein fetuin-B is involved in the development of acute myocardial infarction

The serum protein fetuin-B is involved in the development of acute myocardial infarction

Pregnancy-Associated Plasma Protein-A as a Marker of Culprit Lesion Instability in Unstable Angina Patients: An Intravascular Ultrasound Study

Imaging Plaques to Predict and Better Manage Patients With Acute Coronary Events

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