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A comprehensive evaluation of culprit coronary lesions may help to understand vulnerable plaques responsible for ST-segment elevation myocardial infarction (STEMI). We compared intravascular ultrasound (IVUS) and histological findings in culprit coronary plaques from 94 patients with STEMI (n = 54) or stable angina (n = 40). Tissue specimens were obtained by directional coronary atherectomy and IVUS was performed before percutaneous coronary intervention. IVUS and histological data were analyzed. Clinical characteristics were largely similar between the two groups. Plaque rupture and thrombi were more frequently found in the STEMI group than in the stable angina group. There were no significant differences between plaque types or proximal and distal reference measurements in the two groups. However, the site of minimal lumen area had a greater vessel area, remodeling index, and plaque burden with lesser lumen area in the STEMI group than in the stable angina group. Plaque areas immunopositive for CD68 and CD31 were significantly larger in the STEMI group, while the area immunopositive for α-smooth muscle actin was larger in the stable angina group. In conclusion, culprit lesions in STEMI patients showed a greater plaque burden, remodeling index, and more frequent thrombi with increased inflammation and neovascularization compared to the stable angina group, supporting the current concept of vulnerable plaques being responsible for STEMI.

Background: Stanniocalcin-1 (STC1) is involved in fundamental biological processes such as angiogenesis, inflammation and wound healing, but little is known about its expression in human coronary atherosclerotic plaques or its relationship to plaque instability., Objective: STC1 expression was examined in the culprit coronary plaques of 70 patients with acute myocardial infarction (AMI; n=49) or stable angina (n=21) who underwent directional coronary atherectomy., Methods: The specimens were stained with H&E, STC1-specific antibodies, and endothelial cells, macrophages and smooth muscle cell markers., Results: The baseline characteristics of the two groups of patients were largely similar. CD31-immunopositive and CD68-immunopositive areas, indicative of the presence of endothelial cells and macrophages, respectively, were proportionately larger while areas immunopositive for α-actin, as a smooth muscle cell marker, were proportionately smaller in the AMI group than in the stable angina group. The proportion of STC1-immunopositive areas was significantly greater in the AMI group than in the stable angina group (20.0% (8.2-29.0%) vs 8.8% (3.9-19.4%), p=0.022). Areas positive for STC1 were independently correlated with those immunopositive for CD31 (r=0.42, p<0.001) and CD68 (r=0.40, p<0.001). STC1 immunoreactivity co-localised with CD31-immunopositive and CD68-immunopositive cells., Conclusions: STC1 is differentially expressed in the culprit coronary plaques of patients with AMI versus those with stable angina. STC1 may play a role in plaque instability.

It remains uncertain whether the histology of culprit coronary plaques differs between ST-segment elevation myocardial infarction (STEMI) and non-STEMI (NSTEMI). We compared intravascular ultrasound (IVUS) and histologic findings in coronary culprit plaques among patients presenting with STEMI and NSTEMI. Atherectomy specimens were obtained from 96 patients, 70 with STEMI and 26 with NSTEMI, who underwent directional coronary atherectomy for de novo coronary artery lesions. IVUS examinations were performed before directional coronary atherectomy. IVUS and histologic data were analyzed. Clinical characteristics were largely similar between the 2 groups; however, normal antegrade flow before angioplasty was less frequently observed in patients with STEMI than those with NSTEMI. Plaque rupture was more common on the proximal side of the minimal lumen site. There were no differences in vessel area, lumen area, calcification, plaque burden, or remodelling index at the reference and culprit sites. However, the arc of the ruptured cavity was significantly greater in patients with STEMI than those with NSTEMI (69.4 ± 27.9° vs 51.8 ± 20.0°, respectively, p = 0.008). The proportion of atheroma, fibrocellular, and thrombus areas was not different between the 2 groups. Similarly, the relative areas immunopositive for CD31, smooth muscle α-actin, and CD68 were similar in the 2 groups. In conclusion, coronary culprit lesions in patients with STEMI show more severe plaque rupture with similar histologic features than those in patients with NSTEMI, supporting the idea that a large plaque rupture is more likely in STEMI patients., (Copyright © 2013 Elsevier Inc. All rights reserved.)

We investigated the polarization states of macrophages in coronary atherectomy tissues retrieved from patients with acute myocardial infarction (AMI, n = 52) or stable angina pectoris (SAP, n = 22). The specimens were analyzed immunohistochemically using antibodies specific to CD11c (M1 marker), CD206 (M2 marker), and to markers of endothelial cells, macrophages, and smooth muscle cells. Baseline characteristics were similar in the 2 groups. The proportion of areas immunopositive for α smooth muscle actin was similar, but those positive for CD31 and CD68 were larger in the AMI group compared with the SAP group. In addition, AMI had significantly greater areas immunopositive for CD11c (P = .007) than did SAP, but CD206 (P = .102) positivity was not different in the 2 groups. In conclusion, M1 macrophage infiltration, not M2 macrophage infiltration, was increased in culprit plaques of patients with AMI. Macrophage heterogeneity may therefore be related to plaque instability.

ADAMTS (a disintegrin and metalloproteinase with thrombospondin type 1 motifs) proteases are emerging as key participants in the pathogenesis of vascular diseases. We studied the expression of ADAMTS-2, -3, -4 and -14 in the culprit plaques from patients presenting with acute myocardial infarction (AMI) versus stable angina. Tissue samples were gathered from 52 patients with AMI (n = 35) or stable angina (n = 17) who underwent directional coronary atherectomy. The specimens were stained with hematoxylin-eosin and analyzed immunohistochemically using antibodies specific to ADAMTS-2, -3, -13 and -14, and markers for endothelial cells, macrophages, and smooth muscle cells. Baseline characteristics of the groups were mostly similar. The proportion of smooth muscle α-actin-immunopositive area was smaller in the AMI group than in the stable angina group, but the areas immunopositive for CD31 or CD68 were higher in the AMI group. The relative areas immunopositive for ADAMTS-2, -3, and -13 in AMI were significantly larger than those in stable angina. However, the proportion of areas immunopositive for ADAMTS-14 did not differ between the two groups. Areas that stained for ADAMTS-2, -3, -13, and -14 largely overlapped with those positive for CD31 or CD68. The areas immunopositive for ADAMTS proteases were significantly correlated with CD31- or CD68-immunostained areas. In conclusions, ADAMTS-2, -3, and -13 expression, but not that of ADAMTS-14, are increased in plaques causing AMI compared those associated with stable angina. These results support a role for these enzymes in the pathogenesis of AMI.

We analyzed the innate immunity markers, C-reactive protein (CRP), serum amyloid P component (SAP) and pentraxin-3 (PTX-3), and metalloproteinase-9 (MMP-9) in coronary atherectomy tissues obtained from patients with acute ST elevation myocardial infarction (STEMI) (n=27) or stable angina (n=15). The relative areas immunopositive for CRP and SAP were similar in the two groups. In contrast, the proportion of areas immunopositive for PTX-3 and MMP-9 was higher in the STEMI group, compared to the stable angina group. PTX-3 or MMP-9-stained areas largely overlapped with those positive for CD68. We concluded that PTX-3 plays a role in the pathogenesis of STEMI.

P2Y₁₂ receptor antagonists may have pleiotropic benefits. Little is known, however, about the expression of P2Y₁₂ receptors in coronary atherosclerotic plaques. We investigated the expression of P2Y₁₂ receptor in coronary atherectomy tissues retrieved from patients with acute myocardial infarction (AMI) or stable angina pectoris (SAP). Tissue specimens were collected from 35 patients with AMI and 19 with SAP who underwent directional coronary atherectomy. Specimens were analyzed immunohistochemically using antibodies specific to P2Y₁₂ receptor and to markers of endothelial cells, macrophages, and smooth muscle cells. The 2 groups had similar baseline clinical characteristics. Plaque types were more likely to be cellular in the AMI group. The proportion of areas immunopositive for α-smooth muscle actin was smaller but those positive for CD31 and CD68 were larger in the AMI than in the SAP group. In addition, the relative area immunopositive for P2Y₁₂ receptor was significantly larger for AMI than SAP (1.1 ± 0.9% vs 0.5 ± 0.4%, respectively, p < 0.001). P2Y₁₂ receptor positivity coincided with areas positive for CD31 and α-smooth muscle actin. In conclusion, P2Y₁₂ receptor is present in coronary atherosclerotic plaques and is increased in culprit plaques of patients with AMI. P2Y₁₂ receptor may play a role in plaque destabilization., (Copyright © 2011 Elsevier Inc. All rights reserved.)

Background: ADAMTS (a disintegrin and metalloproteinase with thrombospondin type 1 motifs) proteases might contribute to plaque destabilisation by weakening the fibrous cap. However, little is known about the expression of ADAMTS proteases in coronary atherosclerotic plaques., Objective: To examine the expression of ADAMTS proteases in coronary atherectomy samples obtained from patients with acute myocardial infarction (AMI) or stable angina., Methods: Atherectomy specimens were obtained from 34 patients with AMI (n=23) or stable angina (n=11) who underwent directional coronary atherectomy. The specimens were stained with H&E and analysed immunohistochemically using antibodies specific to ADAMTS-1, -4 and -5; versican cleavage products; and markers for endothelial cells, macrophages and smooth muscle cells., Results: Baseline characteristics were similar between the two groups. The proportion of CD31 and CD68 immunopositive areas did not differ between the two groups, but the area immunopositive for smooth muscle α-actin was smaller in the AMI group. The relative area immunopositive for ADAMTS-1 in AMI (1.04% (IQR 0.59-2.09%)) was significantly greater than that in stable angina (0.24% (0.15-0.39%); p<0.001). In contrast, the proportion of areas immunopositive for ADAMTS-4 or -5 was similar in the two groups. Areas that stained for ADAMTS-1 largely overlapped with those positive for CD68 and versican cleavage products. The areas immunopositive for ADAMTS-1 were significantly correlated with CD68 immunostained areas (r=0.50, p=0.003)., Conclusions: ADAMTS-1, -4 and -5 were present in human coronary atherosclerotic plaques, and ADATS-1 was more strongly expressed in AMI plaques than in stable plaques. ADAMTS-1 may play a role in plaque instability.

We analyzed the innate immunity markers, C-reactive protein (CRP), serum amyloid P component (SAP) and pentraxin-3 (PTX-3), and metalloproteinase-9 (MMP-9) in coronary atherectomy tissues obtained from patients with acute ST elevation myocardial infarction (STEMI) ( n == 27) or stable angina ( n == 15). The relative areas immunopositive for CRP and SAP were similar in the two groups. In contrast, the proportion of areas immunopositive for PTX-3 and MMP-9 was higher in the STEMI group, compared to the stable angina group. PTX-3 or MMP-9-stained areas largely overlapped with those positive for CD68. We concluded that PTX-3 plays a role in the pathogenesis of STEMI. [ABSTRACT FROM AUTHOR]

P2Y12 receptor antagonists may have pleiotropic benefits. Little is known, however, about the expression of P2Y12 receptors in coronary atherosclerotic plaques. We investigated the expression of P2Y12 receptor in coronary atherectomy tissues retrieved from patients with acute myocardial infarction (AMI) or stable angina pectoris (SAP). Tissue specimens were collected from 35 patients with AMI and 19 with SAP who underwent directional coronary atherectomy. Specimens were analyzed immunohistochemically using antibodies specific to P2Y12 receptor and to markers of endothelial cells, macrophages, and smooth muscle cells. The 2 groups had similar baseline clinical characteristics. Plaque types were more likely to be cellular in the AMI group. The proportion of areas immunopositive for α-smooth muscle actin was smaller but those positive for CD31 and CD68 were larger in the AMI than in the SAP group. In addition, the relative area immunopositive for P2Y12 receptor was significantly larger for AMI than SAP (1.1 ± 0.9% vs 0.5 ± 0.4%, respectively, p <0.001). P2Y12 receptor positivity coincided with areas positive for CD31 and α-smooth muscle actin. In conclusion, P2Y12 receptor is present in coronary atherosclerotic plaques and is increased in culprit plaques of patients with AMI. P2Y12 receptor may play a role in plaque destabilization. [Copyright &y& Elsevier]