Comparison of quantitative atherosclerotic plaque burden from coronary CT angiography in patients with first acute coronary syndrome and stable coronary artery disease

2014 ◽  
Vol 8 (5) ◽  
pp. 368-374 ◽  
Author(s):  
Damini Dey ◽  
Stephan Achenbach ◽  
Annika Schuhbaeck ◽  
Tobias Pflederer ◽  
Ryo Nakazato ◽  
...  
Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Gudrun Feuchtner ◽  
Daniel Jodocy ◽  
Ricardo C Cury ◽  
Guy Friedrich ◽  
Roger S Blumenthal ◽  
...  

Coronary CT angiography (CCTA) has emerged as a promising non-invasive tool to rule out significant coronary artery disease (CAD) as well provides additional information about atherosclerotic plaque composition. In this study we aim to assess the whether differences in plaque composition exist across patients with varying degree of stenotic CAD disease. The study population consisted of 548 subjects (58±11 years, 45% women) referred for 64-slice multi-detector CCTA for assessment of underlying degree of coronary artery disease. We analyzed plaque characteristics on a per-segment basis according to the modified AHA classification. Plaques types were classified as non-calcified, calcified, mixed type 1 (predominantly non-calcified) or mixed type 2 (predominantly non-calcified). Overall 194 (35%) had normal coronaries without evidence of plaque. In the remaining 354 patients, 187 (34%) and 167 (31%) were found to have luminal narrowing of <50% and ≥70% in at-least one coronary artery segment, respectively. Those with a higher degree of stenotic CAD demonstrated significantly more coronary segments with exclusively calcified and mixed plaques (table ). Among those with significant CAD, the overall proportion of plaque burden was more likely to be mixed predominantly calcified (18% vs. 38% vs. 44%) as well as mixed predominantly non-calcified in nature; whereas were less likely to be exclusively non-calcified (39% vs. 20% vs. 16%). Only 3/208 (1.3%) patients without any underlying calcification had significant CAD (stenosis ≥50%). In summary, significant differences in plaque composition according to severity of CAD were observed in our study with a higher mixed plaque and lesser non-calcified plaque burden among those with stenotic CAD. These findings should stimulate further investigations to assess the prognostic value of plaque according to their underlying composition.


Author(s):  
Elizabeth K. Fletcher ◽  
Yanling Wang ◽  
Laura K. Flynn ◽  
Susan E. Turner ◽  
Jeffrey J. Rade ◽  
...  

Objective: Destruction of arterial collagen allows monocyte and macrophage infiltration leading to atherosclerotic plaque formation, but it is not clear what role the MMP1 (matrix metalloprotease 1) collagenase plays in this process in vivo. To define the specific contribution of MMP1 to atherosclerotic plaque burden and pathogenesis, we generated ApoE −/− mice deficient in the human MMP1 ortholog, MMP1a. Approach and Results: After 12 to 16 weeks of Western diet, genetic loss of MMP1a resulted in a significant 50% reduction in total aortic plaque burden compared with control ApoE −/− mice. MMP1a deficiency led to significant reductions in plaque monocytes/macrophages, SMCs, and necrosis, with increases in collagen content. Collagen invasion of oxidized-LDL (low-density lipoprotein) activated peripheral blood mononuclear cells from MMP1a-deficient mice was markedly attenuated and was similar to suppressive effects with pharmacological inhibitors of MMP1 and its receptor, PAR1 (protease-activated receptor 1). Patients with coronary artery disease and acute coronary syndrome undergoing cardiac catheterization in the TRIP-PCI trial were evaluated for circulating levels of all 3 major secreted collagenases, MMP1, MMP8, and MMP13 and total number of coronary lesions with ≥50% stenosis (coronary artery disease burden). MMP1 was significantly ( P <0.001) higher by 19-fold and 5.7-fold relative to MMP13 and MMP8, respectively. MMP1 correlated with stenotic coronary artery disease burden, TNFα (tumor necrosis factor alpha) levels, and was co-expressed with PAR1 on monocytes. Treatment of patients with the PAR1 inhibitor, PZ-128, prevented a drop in monocytes following coronary catheterization, an acute protective effect that was reproduced in mice undergoing cardiac ischemia reperfusion. Conclusions: These data provide evidence for an important role for the MMP1a collagenase in atherosclerotic lesion development and leukocyte behavior and validate MMP1 as a compelling target in patients with coronary artery disease/acute coronary syndrome. REGISTRATION: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT02561000.


Author(s):  
Peter J. Meikle ◽  
Melissa F. Formosa ◽  
Natalie A. Mellett ◽  
Kaushala S. Jayawardana ◽  
Corey Giles ◽  
...  

ESC CardioMed ◽  
2018 ◽  
pp. 1209-1209 ◽  
Author(s):  
Stefan James ◽  
Marco Roffi

Coronary artery disease may develop slowly and create symptoms only in late stages due to marked narrowing of one or more coronary arteries. However, the disease progression can also be rapid and be triggered by disruption of a coronary arterial plaque, complicated by thrombosis, embolization, and varying degrees of obstruction to myocardial perfusion. The term acute coronary syndrome is used to denote the acute phases of ischaemic coronary artery disease with or without myocardial cell necrosis. This term is preferred to earlier symptom-related terminology because it encompasses the common underlying pathophysiology. The clinical features depend upon the extent and severity of myocardial ischaemia. Acute coronary syndrome describes the spectrum of clinical manifestations from worsening of stable coronary artery disease to large myocardial infarction with shock or sudden cardiac death.


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