The American Journal of Cardiology

2001

DOI: 10.1016/s0002-9149(01)01870-7

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Going from immutable to mutable atherosclerotic plaques

Michael J. Davies

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Introduction3

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Conclusion -The Pathobiological Substrate For Coronary Even1

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Cited by 43 publications

(22 citation statements)

References 66 publications

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“…Given current concepts on the pathophysiology of ACS, an elevated CEC count may be considered as a marker of endothelial injury associated with plaque rupture and/or erosion. 19 The likelihood that the CECs originate from plaque lesions remains speculative but is supported by analysis of atherosclerotic plaques in coronary arteries. 19,20 Once plaque formation is established, endothelial cells are lost in focal areas, thus exposing the subendothelial matrix and allowing adherence of platelets.…”

Section: Discussionmentioning

confidence: 99%

Circulating Endothelial Cell Count as a Diagnostic Marker for Non–ST-Elevation Acute Coronary Syndromes

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et al. 2004

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Background-Shedding of endothelial cells from damaged endothelium into the blood occurs in a variety of vascular disorders. The purpose of this study was to evaluate the utility of circulating endothelial cell (CEC) count as a diagnostic marker of non-ST-elevation acute coronary syndromes (ACSs). Methods and Results-CEC counts were determined immediately (H0), 4 hours (H4), and 8 hours (H8) after admission in 60 patients with documented non-ST-elevation ACS and 40 control patients with no evidence of coronary artery disease. A total of 32 patients in the ACS group had elevated CEC counts (Ͼ3 cells/mL) in relation to early admission and single-episode chest pain. Patients from the control group had normal CEC counts. The interval between the chest pain episode and elevation was significantly shorter for CEC than troponin I. No correlation was found between the 2 markers. Interestingly, a subgroup of ACS patients with initially normal troponin I levels had high CEC counts, thus allowing early diagnosis in 30% more cases. At H0, the mean area under the receiver operating characteristic curve was significantly higher with the CEC count than with the troponin I level. At H4 and H8, the combined use of CEC and troponin was significantly better as a marker of ACS than CEC alone or troponin I alone. Conclusions-This study demonstrates that CEC count can be used as an early, specific, independent diagnostic marker for non-ST-elevation ACS. A combined strategy using CEC count and troponin I level could provide an effective diagnostic tool.

“…Given current concepts on the pathophysiology of ACS, an elevated CEC count may be considered as a marker of endothelial injury associated with plaque rupture and/or erosion. 19 The likelihood that the CECs originate from plaque lesions remains speculative but is supported by analysis of atherosclerotic plaques in coronary arteries. 19,20 Once plaque formation is established, endothelial cells are lost in focal areas, thus exposing the subendothelial matrix and allowing adherence of platelets.…”

Section: Discussionmentioning

confidence: 99%

Circulating Endothelial Cell Count as a Diagnostic Marker for Non–ST-Elevation Acute Coronary Syndromes

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,

²

,

³

et al. 2004

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Background-Shedding of endothelial cells from damaged endothelium into the blood occurs in a variety of vascular disorders. The purpose of this study was to evaluate the utility of circulating endothelial cell (CEC) count as a diagnostic marker of non-ST-elevation acute coronary syndromes (ACSs). Methods and Results-CEC counts were determined immediately (H0), 4 hours (H4), and 8 hours (H8) after admission in 60 patients with documented non-ST-elevation ACS and 40 control patients with no evidence of coronary artery disease. A total of 32 patients in the ACS group had elevated CEC counts (Ͼ3 cells/mL) in relation to early admission and single-episode chest pain. Patients from the control group had normal CEC counts. The interval between the chest pain episode and elevation was significantly shorter for CEC than troponin I. No correlation was found between the 2 markers. Interestingly, a subgroup of ACS patients with initially normal troponin I levels had high CEC counts, thus allowing early diagnosis in 30% more cases. At H0, the mean area under the receiver operating characteristic curve was significantly higher with the CEC count than with the troponin I level. At H4 and H8, the combined use of CEC and troponin was significantly better as a marker of ACS than CEC alone or troponin I alone. Conclusions-This study demonstrates that CEC count can be used as an early, specific, independent diagnostic marker for non-ST-elevation ACS. A combined strategy using CEC count and troponin I level could provide an effective diagnostic tool.

“…In recent years, it has been revealed that plaque disruption is the proximate cause of the greater proportion of coronary events (17)(18)(19). The propensity of plaques to rupture is not related to the extent of luminal narrowing, but instead appears to be related more to the specific features of plaque composition (20).…”

Section: Conclusion -The Pathobiological Substrate For Coronary Evenmentioning

confidence: 99%

Value of Coronary Artery Calcium Scanning by Computed Tomography for Predicting Coronary Heart Disease in Diabetic Subjects

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et al. 2003

Diabetes Care

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OBJECTIVE -The South Bay Heart Watch is a cohort study designed to determine the significance of coronary calcium in high-risk asymptomatic patients. This is a report of the relative risk (RR) for outcomes of coronary artery calcium in diabetic and nondiabetic subjects.RESEARCH DESIGN AND METHODS -A total of 1,312 diabetic and nondiabetic subjects underwent risk factor screening and computed tomography testing for coronary calcium at baseline and were followed clinically for 6.3 Ϯ 1.4 years. End points were either 1) hard events of nonfatal myocardial infarction (MI) or coronary death or 2) any cardiovascular event (nonfatal MI, coronary death, coronary revascularization, or stroke).RESULTS -The incidence rates of a hard event and any cardiovascular event for diabetic and nondiabetic subjects were 14.5 and 6.1% and 23.8 and 12.2%, respectively (P Ͻ 0.001). Cox regression analyses of the combined risk relationship of diabetes status and calcium score demonstrated that relative to nondiabetic subjects with low calcium scores (Ͻ2.8), diabetic subjects with calcium scores Ն2.8 exhibited at least a fourfold increase in the risk of either a hard or any cardiovascular event (P Ͻ 0.001). Cox regression analyses conducted separately for nondiabetic and diabetic subjects revealed that coronary calcium score risk groups were significantly associated with events in nondiabetic subjects (RR Ն 2.6, P Յ 0.01), but not in diabetic subjects (RR Յ 1.7, P Ͼ 0.05).CONCLUSIONS -The risk of coronary heart disease increases with increasing calcium scores and diabetes status. Calcium scores have less prognostic value in diabetic subjects. Diabetes Care 26:905-910, 2003

“…Increased systemic markers of inflammation, such as C-reactive protein and fibrinogen, act as prognostic markers in subjects with coronary disease with a 3-fold increase in risk for future myocardial infarction. Elevation of systemic markers may act as both cause and effect of plaque activity and therefore may have an impact on future events (7,8).…”

Section: Introductionmentioning

confidence: 99%

MRI of atherosclerosis in clinical trials

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et al. 2006

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Magnetic resonance imaging (MRI) of the arterial wall has emerged as a viable technology for characterizing atherosclerotic lesions in vivo, especially within carotid arteries and other large vessels. This capability has facilitated the use of carotid MRI in clinical trials to evaluate therapeutic effects on atherosclerotic lesions themselves. MRI is specifically able to characterize three important aspects of the lesion: size, composition and biological activity. Lesion size, expressed as a total wall volume, may be more sensitive than maximal vessel narrowing (stenosis) as a measure of therapeutic effects, as it reflects changes along the entire length of the lesion and accounts for vessel remodeling. Lesion composition (e.g. lipid, fibrous and calcified content) may reflect therapeutic effects that do not alter lesion size or stenosis, but cause a transition from a vulnerable plaque composition to a more stable one. Biological activity, most notably inflammation, is an emerging target for imaging that is thought to destabilize plaque and which may be a systemic marker of vulnerability. The ability of MRI to characterize each of these features in carotid atherosclerotic lesions gives it the potential, under certain circumstances, to replace traditional trials involving large numbers of subjects and hard end-points -heart attacks and strokes -with smaller, shorter trials involving imaging end-points. In this review, the state of the art in MRI of atherosclerosis is presented in terms of hardware, image acquisition protocols and post-processing. Also, the results of validation studies for measuring lesion size, composition and inflammation will be summarized. Finally, the status of several clinical trials involving MRI of atherosclerosis will be reviewed.

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