Extent and Direction of Arterial Remodeling in Stable Versus Unstable Coronary Syndromes

Schoenhagen, Paul; Ziada, Khaled M.; Kapadia, Samir; Crowe, Tim; Nissen, Steven E.; Tuzcu, E. Murat

doi:10.1161/01.cir.101.6.598

Cited by 689 publications

(385 citation statements)

References 38 publications

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“…Consequently, early-stages of coronary atherosclerosis are angiographically undetectable, or underestimated when compared to postmortem pathological studies 21 . While positively remodeled lesions may have minimal stenotic effect, these plaques have been shown to be significantly associated with acute coronary syndromes 22,23 . Lumen imaging is also limited when long segments are diffusely affected by atherosclerotic changes, because the detection of angiographic stenosis relies on a comparison to a normal reference site 24 .…”

Section: Atherosclerosis Imaging and Luminal Stenosismentioning

confidence: 99%

“…Initial description of plaque morphology focused on culprit lesions in patients presenting with acute or stable coronary syndromes 93,94 . Based on these studies, a prospective intravascular ultrasound study hypothesized that certain features would be associated with the development of acute coronary syndromes during follow-up 95 .…”

Section: Plaque Composition With Ivusmentioning

confidence: 99%

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Métodos por imagem da aterosclerose em estudos de progressão/regressão: marcador substituto ou janela direta para o processo patológico da aterosclerose?

Schoenhagen¹,

Tuzcu²

2008

Arq. Bras. Cardiol.

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SummaryCAD remains a major global cause of morbidity and mortality. Comprehensive drug development programs of novel pharmacological treatment strategies frequently utilize traditional mortality/morbidity endpoints studies and additional surrogate endpoints trials. This parallel approach allows an assessment of efficacy several years in advance of the availability of data from clinical endpoint trials. Several atherosclerosis imaging markers have been introduced into these drug-development strategies, including angiography, carotid ultrasound, IVUS, MRI, and CT. This review will discuss the current status of atherosclerosis imaging as an endpoint in progression/regression trials, with an emphasis on evidence-based data. In addition to a discussion of the results of individual imaging modalities, the emerging data comparing different modalities and approaches are presented.

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Section: Atherosclerosis Imaging and Luminal Stenosismentioning

confidence: 99%

Section: Plaque Composition With Ivusmentioning

confidence: 99%

Métodos por imagem da aterosclerose em estudos de progressão/regressão: marcador substituto ou janela direta para o processo patológico da aterosclerose?

Schoenhagen¹,

Tuzcu²

2008

Arq. Bras. Cardiol.

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“…However, more recent angiographic data reveal that acute cardiovascular events do not necessarily correlate with the extent of obstructive coronary artery lesions. 1,2 Furthermore, interventions that improve outcome may have only a minimal impact on severity of obstruction yet profoundly modulate plaque echogenicity. 2,3 Such observations suggest that the atherosclerotic plaque is not merely a static repository for lipid waste but rather a dynamic lesion that can be remodeled in ways that influence the likelihood of plaque instability and acute vascular events.…”

mentioning

confidence: 99%

Angiotensin Inhibition Decreases Progression of Advanced Atherosclerosis and Stabilizes Established Atherosclerotic Plaques

Suganuma¹,

Babaev²,

Motojima³

et al. 2007

Journal of the American Society of Nephrology

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Although increased extracellular matrix (ECM) is pathogenic in a variety of chronic tissue injuries, reduced and/or disrupted ECM may be detrimental in atherosclerosis and rather destabilize existing atherosclerotic lesions. This study therefore assessed the effects of angiotensin II (AngII) antagonism on ECM components of advanced atherosclerosis. Twenty-four-week-old apolipoprotein E-deficient mice were treated with the AngII antagonist losartan for 12 wk. Controls received water or hydralazine. AngII antagonism significantly reduced progression of established atherosclerosis, whereas hydralazine showed no benefit despite similar decrease in BP. Although there was no difference in the macrophage component, AngII antagonism increased the relative collagen portion of the lesions; lessened elastin fragmentation, increased the total elastin content of the aorta; and reduced the mRNA and activity/ protein of the elastolytic proteases, cathepsin S, and metalloproteinase-9. Extracellular elastin degradation by cultured smooth muscle cells (SMC) was reduced by losartan, as was SMC invasion through an elastin gel barrier. Thus, AngII antagonism lessens progression of atherosclerosis, increases collagen, and preserves elastin components of ECM within the vascular lesions, which, at least in part, is modulated by effects on SMC. These effects not only decrease further expansion of advanced lesions but also stabilize the established atherosclerotic plaques and may underlie the decreased incidence of acute cardiovascular events that are observed in patients in whom AngII antagonism is begun after atherosclerosis is already established.

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“…However, some previous reports with multislice CTCA have shown that the whole area of noncalcified plaque and the remodeling index at the culprit lesion were greater in ACS patients than in non-ACS patients, although the lumen stenotic ratio did not differ between ACS patients and non-ACS patients. 13,21,28,29) This may be mainly explained by differences in patient backgrounds. Patients with myocardial infarction (MI) were not included in the present study, whereas the previous reports did include MI patients.…”

Section: Discussionmentioning

confidence: 99%

Coronary Artery CT Low-Density Plaque Area and Its Ratio to the Whole Area of a Non-Calcified Plaque at the Culprit Lesion in Patients With Unstable and Stable Coronary Artery Disease

et al. 2012

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SummaryIntravascular ultrasound studies have shown that patients with unstable angina pectoris (UAP) more frequently had soft plaques in the culprit coronary arteries than patients with stable angina pectoris (SAP). We evaluated coronary plaque characteristics of culprit lesions in patients with UAP by 64-slice computed tomographic coronary angiography (64-slice CTCA). 64-slice CTCA (Aquilion 64, Toshiba Medical Systems, Otawara, Japan) was performed in 30 patients (UAP = 14, SAP = 16) before percutaneous coronary intervention (PCI). Coronary plaque area was measured by manual tracing for the difference between the area within the external elastic membrane and the area of the vessel lumen at the site of maximal luminal narrowing as observed on a cross-sectional 64-slice CTCA image where PCI was performed. Within this plaque area, CT low-density plaque area (< 50 Hounsfield units) was automatically calculated. There were no differences in stenotic rate and whole plaque area of the culprit lesion between patients with UAP and SAP. However, the CT low-density plaque area was significantly greater in patients with UAP than in those with SAP. A greater area of CT low-density plaque in the culprit lesion is associated with UAP rather than SAP. Measuring CT-low density plaque area on 64-slice CTCA images could be useful for understanding the clinical setting of UAP. (Int Heart J 2012; 53: 341-346) Key words: Unstable angina pectoris, Coronary artery plaque, Computed tomography, Lipid-rich coronary plaque R ecently, 64-slice computed tomographic coronary angiography (64-slice CTCA) has been shown to detect significant coronary stenosis (> 50% luminal narrowing) with high sensitivity and specificity as compared with invasive coronary angiography.1-7) The per segment sensitivity and specificity ranged from 80% to 99% and 85% to 95%, respectively. 4,5) Moreover, 64-slice CTCA can accurately assess plaque area and remodeling index with good correlation to intravascular ultrasound (IVUS) with good image quality in selected patients. 3,8,9) Very recently, it has been shown that 64-CT is an effective way to distinguish different qualities of coronary atherosclerotic plaque and suggest that serum Hs-CRP and IL-6 levels can be considered as one of the indexes to judge the degree of CHD and may reflect the activities of plaque in CHD patients. Thus it is important for clinical diagnosis and risk evaluation of ACS patients. 10)In addition to the evaluation of coronary artery plaque area, 64-slice CTCA enabled the evaluation of the plaque composition of the culprit lesion in patients with acute coronary syndromes (ACS) and stable angina pectoris (SAP).11-13) Culprit atherosclerotic lesions in ACS patients showed complex findings such as spotty calcification, lipid-rich plaques, and positive vascular remodeling, whereas the culprit lesions in SAP patients showed these features less frequently. 14,15) Discrete lesions detected by multislice CT were found more in patients with unstable angina pectoris or a STEMI, while diffuse and ...

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Extent and Direction of Arterial Remodeling in Stable Versus Unstable Coronary Syndromes

Cited by 689 publications

References 38 publications

Métodos por imagem da aterosclerose em estudos de progressão/regressão: marcador substituto ou janela direta para o processo patológico da aterosclerose?

Métodos por imagem da aterosclerose em estudos de progressão/regressão: marcador substituto ou janela direta para o processo patológico da aterosclerose?

Angiotensin Inhibition Decreases Progression of Advanced Atherosclerosis and Stabilizes Established Atherosclerotic Plaques

Coronary Artery CT Low-Density Plaque Area and Its Ratio to the Whole Area of a Non-Calcified Plaque at the Culprit Lesion in Patients With Unstable and Stable Coronary Artery Disease

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