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

Fujii, Kenichi; Kobayashi, Y.; Mintz, Gary S.

doi:10.1016/j.accreview.2004.02.053

Cited by 77 publications

(113 citation statements)

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“…[22][23][24] More recently, in-vivo studies using both intravascular imaging techniques or ex-vivo autoptycal studies showed that culprit plaques causing sudden death or MI tend to have a larger plaque burden with a thinner fibrous cap and a smaller lumen area, compared with stable or non-ruptured plaques. [25][26][27] In the present study, we identified a high prevalence of TCFA in intermediate stenoses visualized in patients with ACS. This conclusion is in line with other OCT studies pointing out that TCFA is often found in nonseverely stenotic lesions.…”

Section: Discussionsupporting

confidence: 54%

Comparison between intermediate and severe coronary stenoses and clinical outcomes of an OCT-guided PCI strategy

Vito

Cattabiani

Paoletti

et al. 2016

Journal of Cardiovascular Medicine

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aAims We compared optical coherence tomography (OCT) features of intermediate and severe coronary stenoses in patients with stable angina and acute coronary syndrome (ACS), and tested the clinical impact of an OCT-based strategy for treating intermediate stenoses.Methods The study enrolled 135 consecutive patients with either ACS or stable angina and a single de-novo coronary stenosis. Patients were divided into two groups: intermediate stenosis defined as quantitative coronary angiography percentage narrowing less than 70%, or presence of angiographic vessel haziness and severe stenosis with percentage narrowing more than 70%. OCT was performed to assess features of plaque vulnerability and to measure the minimal lumen area. We also appraised the 12-month rate of major adverse event (MACE) of an OCT-guided strategy of percutaneous coronary intervention (PCI) based on the presence of thrombus and/or minimal lumen area less than 3.0 mm 2 .Results Fifty-six patients had intermediate stenoses, whilst 79 had severe stenoses. In the 'intermediate stenosis group', patients with stable angina had a lower asymmetric index (P U 0.02) and a greater calcific arc (P U 0.0001). In the 'severe stenosis group', intermediate lesions of patients with ACS exhibited a greater lipid arc as compared with patients with stable angina (P U 0.03). A higher prevalence of thin cap fibroatheroma was seen in patients with ACS of both groups. The incidence of MACE was not significantly different between patients with an intermediate stenosis who received PCI vs. optimal medical therapy on the basis of OCT findings (P U 0.26).Conclusions Intermediate coronary stenoses showed distinctive OCT-based features according to the initial clinical presentation. The adoption of an OCT-guided PCI strategy, based on the presence of coronary thrombus and significant vessel narrowing, led to encouraging results.

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Section: Discussionsupporting

confidence: 54%

Comparison between intermediate and severe coronary stenoses and clinical outcomes of an OCT-guided PCI strategy

Vito

Cattabiani

Paoletti

et al. 2016

Journal of Cardiovascular Medicine

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“…This may be secondary to the more general population studied in the present study compared with the selected MI population studied by Goldstein et al and thus may support the notion that plaque vulnerability is a dynamic process not limited to morphological plaque characteristics. [32][33][34] The present study demonstrates that small but not insignificant numbers of patients return to the cardiac catheterization laboratory requiring PCI of a newly stenotic lesion. In the great majority of cases, the lesions were hemodynamically insignificant at the time of initial angiography, with only 13.1% of patients demonstrating lesions worse than 70% on the initial angiogram that then progressed.…”

Section: Glaser Et Al Clinical Progression Of Incidental Lesionsmentioning

confidence: 92%

Clinical Progression of Incidental, Asymptomatic Lesions Discovered During Culprit Vessel Coronary Intervention

et al. 2005

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Background-With the reduction in restenosis rates by drug-eluting stents, there is new controversy concerning the optimal management of incidental, nontarget lesions identified during percutaneous coronary intervention (PCI). Such lesions have been treated conservatively because of risk of restenosis but now are being considered for PCI to prevent plaque instability. However, the impact of incidental stenoses on future cardiac events remains unknown. Methods and Results-We performed a retrospective cohort study to determine the rate and features of clinical plaque progression using the National Heart, Lung,

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“…Culprit plaques causing acute coronary syndromes in humans have been consistently shown to rupture just proximal (upstream) to the point of maximum stenosis. This is the area of most rapid flow (560). This is true even though the area of slow flow just downstream of the stenosis is where endothelium is activated and foam cells accumulate.…”

Section: Newer Insights Into the Role Of Vsmc In Atherosclerosismentioning

confidence: 99%

Molecular Biology of Atherosclerosis

Hopkins

2013

Physiological Reviews

390

344

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At least 468 individual genes have been manipulated by molecular methods to study their effects on the initiation, promotion, and progression of atherosclerosis. Most clinicians and many investigators, even in related disciplines, find many of these genes and the related pathways entirely foreign. Medical schools generally do not attempt to incorporate the relevant molecular biology into their curriculum. A number of key signaling pathways are highly relevant to atherogenesis and are presented to provide a context for the gene manipulations summarized herein. The pathways include the following: the insulin receptor (and other receptor tyrosine kinases); Ras and MAPK activation; TNF-␣ and related family members leading to activation of NF-B; effects of reactive oxygen species (ROS) on signaling; endothelial adaptations to flow including G protein-coupled receptor (GPCR) and integrin-related signaling; activation of endothelial and other cells by modified lipoproteins; purinergic signaling; control of leukocyte adhesion to endothelium, migration, and further activation; foam cell formation; and macrophage and vascular smooth muscle cell signaling related to proliferation, efferocytosis, and apoptosis. This review is intended primarily as an introduction to these key signaling pathways. They have become the focus of modern atherosclerosis research and will undoubtedly provide a rich resource for future innovation toward intervention and prevention of the number one cause of death in the modern world.

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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

Cited by 77 publications

References 0 publications

Comparison between intermediate and severe coronary stenoses and clinical outcomes of an OCT-guided PCI strategy

Comparison between intermediate and severe coronary stenoses and clinical outcomes of an OCT-guided PCI strategy

Clinical Progression of Incidental, Asymptomatic Lesions Discovered During Culprit Vessel Coronary Intervention

Molecular Biology of Atherosclerosis

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