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

Glaser, Ruchira; Selzer, Faith; Faxon, David P.; Laskey, Warren K.; Cohen, Howard A.; Slater, James; Detre, Katherine M.; Wilensky, Robert L.

doi:10.1161/01.cir.0000150335.01285.12

Cited by 250 publications

(161 citation statements)

References 43 publications

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“…The PROSPECT study16 of coronary atherosclerosis demonstrated that cardiac events were related to high atherosclerotic burden rather than the severity of coronary artery stenosis. It is now accepted that atherosclerotic burden in coronary arteries is more important than stenosis in predicting subsequent cardiovascular events17, 18, 19, 20, 21.…”

Section: Introductionmentioning

confidence: 99%

Carotid plaque volume in patients undergoing carotid endarterectomy

Ball

Rogers

Kanesalingam

et al. 2018

British Journal of Surgery

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BackgroundThe main indication for carotid endarterectomy (CEA) is severity of carotid artery stenosis, even though most strokes in carotid disease are embolic. The relationship between carotid plaque volume (CPV) and symptoms of cerebral ischaemia, and the measurement of CPV by minimally invasive tomographic ultrasound imaging, were investigated.MethodsThe volume of the endarterectomy specimen was measured using a validated saline suspension technique in patients undergoing CEA. Time from last symptom and severity of stenosis measured by duplex ultrasonography were recorded. Middle cerebral artery emboli were counted using transcranial Doppler imaging (TCD) in a subset of patients.ResultsSome 339 patients were included, 270 with symptomatic and 69 with asymptomatic carotid stenosis. Mean(s.d.) CPV was higher in symptomatic than in asymptomatic patients (0·97(0·43) versus 0.74(0·41) cm3; P < 0·001). CPV did not correlate with severity of carotid stenosis (P = 0·770). Mean CPV was highest at 1·03(0·46) cm3 in the 4 weeks following cerebral symptoms, declining to 0·78(0·36) cm3 beyond 8 weeks. Among 33 patients who had TCD, mean CPV was 1·00(0·48) cm3 in the 27 patients with ipsilateral cerebral emboli compared with 0·67(0·16) cm3 in those without (P = 0·142). There was excellent correlation between CPV measured by tomographic ultrasound imaging and the endarterectomy specimen in 34 patients (r = 0·93, P < 0·001).ConclusionCPV correlated with symptoms of cerebral ischaemia, but not carotid stenosis. It could be a potential indicator for CEA.

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Section: Introductionmentioning

confidence: 99%

Carotid plaque volume in patients undergoing carotid endarterectomy

Ball

Rogers

Kanesalingam

et al. 2018

British Journal of Surgery

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“…Natural history studies have revealed that most coronary events were preceded by rapid plaque expansion that was unusual and unrelated to baseline plaque burden [22][23][24]. IPH, with the capability to induce changes in plaque behavior [25], may play a critical role in the pathogenesis of coronary events.…”

Section: Discussionmentioning

confidence: 99%

Incremental value of carotid intraplaque hemorrhage for discriminating prior coronary events

et al. 2015

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Background: The value of noninvasive assessment of carotid plaque composition in identifying patients with high coronary risk remains elusive. We sought to determine whether and which carotid plaque components are associated with prior coronary events independent of traditional risk factors and plaque burden. Methods: Asymptomatic subjects with 50-79 % carotid stenosis by ultrasound were imaged with a multi-contrast carotid MRI protocol at 1.5 T. The independent associations between plaque components (fibrous tissue, calcification, lipid-rich necrotic core [LRNC] and intraplaque hemorrhage [IPH]) and prior coronary events, including myocardial infarction and coronary revascularization, were evaluated by controlling for traditional risk factors and plaque burden metrics. Results: A total of 159 subjects (69.7 ± 9.0 years, 84 % males) were included. Prior coronary events were documented in 66 (42 %) subjects, and were associated with a larger carotid plaque burden consisting of more LRNC and calcification. Additionally, a higher prevalence of IPH was observed in subjects with prior coronary events (32 % vs. 15 %, p = 0.019). In multivariate analysis, the percent wall volume was an independent discriminator among plaque burden metrics after accounting for traditional risk factors (odds ratio per 1-SD increase: 1.7 [1.2, 2.6]); the presence of IPH remained as a significant discriminator after accounting for traditional risk factors and percent wall volume (odds ratio: 2.9 [1.1, 7.6]) while other compositional metrics did not. Conclusions: IPH in the carotid artery was independently associated with prior coronary events. IPH imaging may provide incremental information on patients' coronary risk beyond traditional risk factors and carotid plaque burden assessment.

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“…[20][21][22][23][24] More recent studies have demonstrated that plaques progress from mild at baseline to obstructive at the time of MI and clarified that plaque progression occurs before actual plaque rupture. 16,[31][32][33] In addition, as described later, angiography often substantially underestimates plaque severity, as revealed by intravascular ultrasound imaging, contributing to the misconception of the mild vulnerable plaque.…”

Section: Circulation Research June 19 2015mentioning

confidence: 95%

“…In the Dynamic Registry of the National Heart, Lung, and Blood Institute, 31 3747 patients undergoing percutaneous coronary intervention were retrospectively studied. In this cohort, 216 patients required an additional percutaneous coronary intervention of a nonculprit lesion within 1 year.…”

Section: Circulation Research June 19 2015mentioning

confidence: 99%

Do Plaques Rapidly Progress Prior to Myocardial Infarction?

Ahmadi

Leipsic

Blankstein

et al. 2015

Circulation Research

155

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Pathological and anatomic features of high-risk or vulnerable plaques have been reviewed extensively in the literature.1 Briefly, high-risk plaques are characterized by the presence of large plaque burden and necrotic cores that are covered by intensely inflamed, thin fibrous caps; these lesions are typically positively (or outwardly) remodeled.1 Most of the anatomic features of high-risk plaques are identifiable in vivo using invasive and noninvasive imaging modalities, such as intravascular ultrasound, optical coherence tomography, and coronary computed tomography angiography. Although difficult, inflammation has been identified by intravascular demonstration of thermal heterogeneity and targeting of macrophages by positron emission tomography. [2][3][4][5][6][7][8][9][10][11][12][13] Studies over the past 2 decades have demonstrated that high-risk plaques are usually responsible for most acute coronary syndromes (ACS).1,14-17 However, despite extensive interest and excitement regarding the potential of identifying high-risk lesions, plaque characteristics that have been shown to be associated with high-risk plaques have demonstrated a poor positive predictive value for identifying future events. 18For more than a decade, the cardiology community has believed that most ACS arise from ruptures of mildly stenotic plaques and that most major adverse events occur independent of the plaque size and the degree of luminal stenosis. 19This belief emanated from retrospective studies of patients in whom coronary angiography had been performed months to years before myocardial infarction (MI); the lesions responsible for the subsequent infarct were angiographically mild in most cases, that is, at baseline <50% diameter stenosis compared with the adjacent reference vessel lumen. [20][21][22][23][24] Pathologically, although some coronary events may be caused by rupture of plaques with a mild degree of luminal narrowing, 17 most culprit lesions at the time of the acute event are critically occlusive.

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

Cited by 250 publications

References 43 publications

Carotid plaque volume in patients undergoing carotid endarterectomy

Carotid plaque volume in patients undergoing carotid endarterectomy

Incremental value of carotid intraplaque hemorrhage for discriminating prior coronary events

Do Plaques Rapidly Progress Prior to Myocardial Infarction?

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