Journal articles: 'Atheromatous plaque'

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Hayashi, Junichi, Takashi Saito, and Katsuo Aizawa. "Photodynamic Diagnosis and Treatment for Atherosclerosis by an Endoscopic Approach." Diagnostic and Therapeutic Endoscopy 5, no. 3 (January 1, 1999): 191–95. http://dx.doi.org/10.1155/dte.5.191.

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The photosensitizer, mono-L-aspartyl chlorin e6 (NPe6), specifically accumulates in the atheromatous plaque. We detected the fluorescence spectra of NPe6 emitted from atheromatous plaques on the descending thoracic aorta by an angioscopic approach using the animal model of atherosclerosis. We also showed that a fluorescence spectrum peak at 675 nm was obtained laparoscopically only in parts of the abdominal aorta with an atheromatous plaque. By a fluorescence endoscope, atheromatous plaques on the carotid artery were recognized as reddish spots from outside the artery. In addition, we visualized specifically at the beating heart surface small coronary atherosclerosis using an epifluorescence stereoscope system.We examined the effects of photodynamic treatment with NPe6 on the atheromatous plaque. The change in the elastic framework in the atheromatous plaque after photodynamic treatment was evaluated using scanning electron microscopy. The destruction of the architecture of the elastic fiber network in the atheromatous plaque was revealed. We also studied the change in the lipid components of the atheromatous plaque using Fourier transform infrared (FTIR) microspectroscopy. FTIR microspectroscopic analysis showed a dissociation of ester bonds of cholesterol esters in the atheromatous plaque after photodynamic treatment. The framework of the atheromatous plaque and the lipids accumulated in the plaque could be destroyed following such treatment.

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Rath, SarojK, Manish Mukherjee, R. Kaushik, Sourav Sen, and Mukesh Kumar. "Periodontal pathogens in atheromatous plaque." Indian Journal of Pathology and Microbiology 57, no. 2 (2014): 259. http://dx.doi.org/10.4103/0377-4929.134704.

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UENO, Yuji, and Takao URABE. "Diagnosis for atheromatous aortic plaque." Neurosonology 27, no. 1 (2014): 1–2. http://dx.doi.org/10.2301/neurosonology.27.1.

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Gong, Hai-Ying, Xiao-Ke Shi, Heng-Quan Zhu, Xian-Zhong Chen, Jiang Zhu, and Bo-Wen Zhao. "Evaluation of carotid atherosclerosis and related risk factors using ultrasonic B-Flow technology in elderly patients." Journal of International Medical Research 48, no. 10 (October 2020): 030006052096122. http://dx.doi.org/10.1177/0300060520961224.

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Objective This study was performed to identify the risk factors for carotid atherosclerotic plaque formation using B-Flow ultrasound. Methods In total, 120 patients who underwent bilateral carotid ultrasound examination were enrolled in this cross-sectional study. The intima–media thickness was measured, and the risk factors for carotid atheromatous plaque formation were investigated. Results Age, sex, medical history of hypertension, coronary heart disease, and diabetes were risk factors for carotid atheromatous plaque formation. Multivariate logistic regression analysis revealed that the main risk factors for carotid atheromatous plaque formation were male sex, advanced age, a high hemoglobin concentration, a high red cell distribution width, and a high low-density lipoprotein cholesterol concentration. Conclusion The risk factors for carotid atheromatous plaque formation were basically the same as those for stroke. Early ultrasound examination of the carotid artery enables the identification of risk factors associated with stroke.

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Orzan, Marius, Roxana Hodas, Mihaela Dobra, Nora Rat, Monica Chitu, and Imre Benedek. "Original Research. Transluminal Contrast Attenuation Gradient Is Associated with Coronary Plaque Vulnerability — a Computed Tomography Angiography-based Study." Journal Of Cardiovascular Emergencies 3, no. 3 (September 26, 2017): 121–27. http://dx.doi.org/10.1515/jce-2017-0016.

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Abstract The aim of this study was to demonstrate that the transluminal contrast attenuation gradient (TAG), a new CT imaging-derived marker of functional significance of a coronary stenosis, is directly associated with the vulnerability degree of atheromatous coronary plaques. Material and methods: This is a prospective study on 21 patients with 30 atheromatous plaques in the coronary arteries, who underwent cardiac computed tomography angiography (CCTA) for assessment of coronary plaques. Results: Twelve plaques were classified as vulnerable (40%) and 18 plaques (60%) as non-vulnerable. Plaques associated with a TAG value above 10 HU exhibited in a significantly higher proportion CCTA markers of plaque vulnerability, as compared to plaques in which the attenuation gradient was below 10 HU. TAG values >10 HU were associated with a higher amount of plaque volume (107.4 ± 91.2 mm3 vs. 56.0 ± 37.5 mm3, p = 0.009), necrotic core (32.5 ± 36.9 mm3 vs. 3.1 ± 3.2 mm3, p = 0.0003), and fibro-fatty tissue (17.7 ± 16.3 mm3 vs. 4.0 ± 2.6 mm3, p = 0.0002), as compared to those lesions with TAG values below 10 HU. Linear regression analysis revealed a significant correlation between TAG values and CCTA features of plaque instability: necrotic core (r = −0.73, p <0.0001), fibrofatty tissue (r = −0.63, p = 0.0002), and plaque volume (r = −0.48, p = 0.006). Conclusions: In patients with coronary artery disease, contrast attenuation gradient along the coronary plaques, determined by CCTA, correlates with CT markers of plaque vulnerability. Vulnerable coronary plaques are associated with a higher functional significance than the stable ones with a similar anatomic profile.

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Lamberti, Giuseppe, Francesco Gelsomino, Stefano Brocchi, Antonio Poerio, Barbara Melotti, Francesca Sperandi, Mauro Gargiulo, Claudio Borghi, Michelangelo Fiorentino, and Andrea Ardizzoni. "New disappearance of complicated atheromatous plaques on rechallenge with PD-1/PD-L1 axis blockade in non-small cell lung cancer patient: follow up of an unexpected event." Therapeutic Advances in Medical Oncology 12 (January 2020): 175883592091380. http://dx.doi.org/10.1177/1758835920913801.

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Atherosclerosis is considered an irreversible process, with crucial contribution of inflammation and immune cells. Impact of cancer immunotherapy on a partly immune-driven disease, such as atherosclerosis, is poorly understood, but preclinical models suggest its worsening on programmed death/ligand-1 (PD-1/PD-L1) inhibitors. In a previously reported cohort of 11 patients with non-small cell lung cancer (NSCLC) treated with nivolumab and pre-existing complicated atheromatous plaques, 3 patients had a dramatic radiologic reduction of aortic plaques while on nivolumab; of these 3, 2 died receiving no further treatment. The remaining patient was an 83-year-old woman with history of arterial hypertension and hypothyroidism who was diagnosed with locally advanced squamous NSCLC. At relapse, complicated aortic atheromatous plaques were demonstrated on scans. The patient was then treated with nivolumab obtaining stable disease at radiological assessment, which also demonstrated almost complete vanishing of aortic plaques. After relapse and interval treatment with chemotherapy, she experienced new development of aortic atheromatous plaques. At further relapse she received atezolizumab, which yielded disease response and new reduction in aortic plaques, until nearly complete resolution. The observation of a repeated improvement of atheromatous plaques on treatment with PD-1/PD-L1 inhibitors favors the protective role of T cells on atheromatous plaques that is impaired by PD-L1 expression by plaque-associated macrophages. Validation by independent and prospective observation is needed.

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Mureebe, Leila, and James F. McKinsey. "Infrainguinal Arterial Intervention: Is There a Role for an Atherectomy Device?" Vascular 14, no. 5 (September 2006): 313–18. http://dx.doi.org/10.2310/6670.2006.00053.

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Excision of atheromatous plaque is an attractive option for the minimally invasive treatment of peripheral arterial disease. Approved for use in 2003, the SilverHawk Plaque Exicison System (FoxHollow Technologies, Redwood City, CA) is a catheter-based plaque excision device allowing percutaneous removal of atheromatous material. This device represents the most recent generation of atherectomy tools. Overall experience with plaque debulking in the peripheral arteries spans almost two decades, and understanding of the technique continues to evolve. This article reviews the technology, current practices, and data on plaque excision.

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Uno, J., M. Kawashima, M. Miyazono, T. Nakamura, and H. Gi. "Intravascular Ultrasound with Percutaneous Transluminal Angioplasty for Supra-Aortic Arteries." Interventional Neuroradiology 4, no. 1_suppl (November 1998): 27–30. http://dx.doi.org/10.1177/15910199980040s103.

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One of the major complications during or after percutaneous transluminal angioplasty (PTA) is distal embolism. We performed intravascular ultrasound (IVUS) to assess the morphological characteristics of atheromatous plaques which caused stenosis of arteries. In 7 cases of ICA stenosis, IVUS demonstrated hyperechoic plaques which were considered to be fibrous. Mixed type of plaque was observed in one case of ICA stenosis and another one case of ICA stenosis had plaque which was hyperechoic with acoustic shadowing. In all cases of SCA stenosis, plaques were hypoechoic, indicating fatty plaque. Distal embolism occurred after PTA in the case of ICA stenosis which had a mixed type of plaque. It is important to evaluate plaque morphology to prevent distal embolism. PTA is considered to he contraindicated in cases of ICA stenosis having hypoechoic plaques or ulceration.

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Novikova, Olga A., Pavel P. Laktionov, and Andrey A. Karpenko. "The roles of mechanotransduction, vascular wall cells, and blood cells in atheroma induction." Vascular 27, no. 1 (August 29, 2018): 98–109. http://dx.doi.org/10.1177/1708538118796063.

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Background This paper describes and analyzes the cellular and molecular mechanisms underlying atherosclerosis development. In particular, the roles of monocytes/macrophages, smooth muscle cells, and vascular endothelium in the formation of stable/unstable atheromatous plaques, and the contributions of some processes to atheroma formation. Methods and results In this study we analyzed endothelium: function, dysfunction, and involvement into atherogenesis; cell proteins mediating mechanotransduction; proatherogenic role of monocytes; the role of macrophages in the development of unstable atheromatous plaques and smooth muscle cell origin in atherosclerosis. Smooth muscle cell phenotypic switching; their functioning; the ability to retain cholesterol and lipoproteins as well as secretion of pro- and anti-inflammatory molecules and extracellular matrix proteins, their response to extracellular stimuli secreted by other cells, and the effect of smooth muscle cells on the cells surrounding atheromatous plaques are fundamentally important for the insight into atherosclerosis molecular basis. Conclusion Atheromatous plaque transcriptome studies will be helpful in the identification of the key genes involved in atheroma transformation and development as well as discovery of the new targets for diagnosis and therapy.

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Sargolzaie, Naser, Nava Naghibi, Amin Khajavi, Amir Moeintaghavi, Mohammad Abbasi Tashnizi, Kiarash Ghazvini, and Farid Shiezadeh. "Quantitative Detection of Periodontopathogenic Bacteria in Atherosclerotic Plaques from Coronary Arteries by Real-Time PCR." Open Dentistry Journal 14, no. 1 (December 31, 2020): 724–30. http://dx.doi.org/10.2174/1874210602014010724.

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Objectives: Epidemiologic studies have suggested periodontitis as a risk factor for Coronary Artery Diseas (CAD). Detection of periopathogens in atheromatous plaque provides some evidence for the causal relationship between these two conditions. The aim of this study was to determine the presence and quantity of periopathogens in coronary atherosclerotic plaques in patients undergoing Coronary Artery Bypass Graft (CABG) surgery. Methods: 20 patients who were candidates for endarterectomy were enrolled in this study for the periodontal examination. Subgingival and coronary atherosclerotic plaque samples were then collected. Thereafter, quantitative detection of Aggregatibacter actinomycetemcomitans (A.a), Porphyromonas gingivali (P.g), and all bacteria detected by Real-Time PCR (RT-PCR) were measured. The correlation analysis was also used to evaluate the relationship between quantities of periopathogens in atherosclerotic and subgingival plaque samples. Results: A.a was detected in 13 patients (65%) with subgingival plaques and 4 patients (20%) with atherosclerotic plaques. In addition, P.g was found in 15 patients (75%) with subgingival and 10 patients (50%) with atherosclerotic plaques. A.a represented means of 2.7% and 10.04% of detected bacteria in both atherosclerotic and subgingival plaque samples, respectively. The mean of quantity of P.g was 10.85% and 12.87% of the detected bacteria obtained from atherosclerotic and subginigival samples, respectively. Correlation analysis showed a significant correlation between the quantities of A.a in the atherosclerotic and subgingival plaques, but such a significant relationship was not found for P.g. Conclusion: This study confirmed the detection of A.a and P.g in atheromatous plaque. The quantitative data suggested that periopathogens comprise a significant proportion of atherosclerotic plaque microbiome, which may consequently contribute to the development of CAD.

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Toutouzas, Konstantinos, Andreas Synetos, Charalampia Nikolaou, Eleutherios Tsiamis, Dimitris Tousoulis, and Christodoulos Stefanadis. "Matrix Metalloproteinases and Vulnerable Atheromatous Plaque." Current Topics in Medicinal Chemistry 12, no. 10 (April 1, 2012): 1166–80. http://dx.doi.org/10.2174/1568026611208011166.

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Imanishi, Toshio, and Takashi Akasaka. "Biomarkers Associated with Vulnerable Atheromatous Plaque." Current Medicinal Chemistry 19, no. 16 (April 1, 2012): 2588–96. http://dx.doi.org/10.2174/092986712800492922.

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Kaski, J. "Atheromatous plaque location and arterial remodelling." European Heart Journal 24, no. 4 (February 2003): 291–93. http://dx.doi.org/10.1016/s0195-668x(02)00876-x.

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Agius, L. M. "Complicated atheromatous plaque as integral atherogenesis." Journal of Clinical Pathology 60, no. 6 (June 1, 2007): 589–92. http://dx.doi.org/10.1136/jcp.2006.044107.

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Nyulas, Tiberiu, Emese Marton, Victoria Ancuta Rus, Nora Rat, Mihaela Ratiu, Theodora Benedek, and Imre Benedek. "Morphological Features and Plaque Composition in Culprit Atheromatous Plaques of Patients with Acute Coronary Syndromes." Journal Of Cardiovascular Emergencies 4, no. 2 (June 1, 2018): 84–94. http://dx.doi.org/10.2478/jce-2018-0012.

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Abstract Background: The independent role of each plaque feature in relation to plaque vulnerability is still the subject of ongoing research. This study aimed to compare the morphologic characteristics of vulnerable atheromatous coronary plaques with the ones of stable, non-vulnerable plaques, and in plaques with different locations in the coronary tree, in order to identify the most relevant imaging-based biomarkers associated with coronary plaque vulnerability. Material and methods: This was a prospective observational, non-randomized study that included 50 patients with unstable angina who underwent computed tomography angiography for assessment of the entire coronary artery tree followed by complex morphologic analysis of all lesions, divided into two groups: group 1 – 25 patients with vulnerable plaque (VP) and group 2 – 25 age- and gender-matched patients with non-vulnerable plaque (NVP). Results: Lesions with a stenosis degree >70% were significantly longer than those with a stenosis degree <70% (8.27 ± 2.74 mm vs. 5.56 ± 4.11 mm, p = 0.04). VP presented significantly higher values of plaque thickness (p = 0.0005), plaque burden (p = 0.0004), and higher total plaque volume (p = 0.0005) than NVP. The remodeling index was not significantly different between the groups (p = 0.6), but the eccentricity index was (0.24 ± 0.14 compared to 0.14 ± 0.17, p = 0.023). Linear regression analysis revealed a significant correlation between plaque burden and plaque components in VP (r = 0.76, p <0.0001 for necrotic core; r = 0.62, p = 0.0008 for fibro-fatty tissue; and r = 0.5, p = 0.01 for fibrotic tissue volume). Culprit plaques located in the right coronary artery presented significantly larger plaque burden volumes (91.17 ± 4.88 mm3 vs. 83.35 ± 8.47 mm3, p = 0.04), larger volumes of necrotic core (82.03 ± 47.85 mm3 vs. 45.84 ± 43.72 mm3, p = 0.02) and fibrofatty tissue (53.23 ± 31.92 mm3 vs. 23.76 ± 20.90 mm3, p = 0.02) than the ones situated in the left coronary artery. Conclusions: VPs from the culprit lesions exhibit a different phenotype than non-vulnerable ones, and vulnerability features are present in a significantly larger extent in VPs from the right coronary artery as compared to those from the left coronary artery.

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Reininger, Armin J., Richard Brandl, Sandra Penz, Pankaj Goyal, Tamer Rabie, Enno Rother, Christine Goetz, et al. "Human Atheromatous Plaques Stimulate Thrombus Formation by Activating Platelet Glycoprotein VI." Blood 104, no. 11 (November 16, 2004): 2623. http://dx.doi.org/10.1182/blood.v104.11.2623.2623.

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Abstract Lipid-rich atherosclerotic plaques are vulnerable, and upon disruption trigger intraarterial thrombus formation. Tissue factor activating blood coagulation is viewed as the major prothrombotic stimulus within the plaque. We isolated lipid-rich atheromatous plaques from 50 patients with carotid artery stenosis and identified morphologically diverse collagenous structures within in the plaques. They stimulated platelet adhesion, dense granule secretion and aggregation, and triggered thrombus formation in hirudin-anticoagulated blood under arterial flow conditions. Even in fully anticoagulated flowing blood, i.e. in the absence of tissue factor-mediated coagulation, plaques were able to activate platelets. Thrombus formation was more rapid and stable when blood was anticoagulated with a low concentration of heparin, but, although fibrin was detectable within the thrombus, the initial step was always single platelet adhesion and not fibrin formation. In contrast, absence or inhibition of the platelet collagen receptor glycoprotein VI prevented platelet adhesion to atheromatous plaques and thrombus formation. We thus identified platelet glycoprotein VI as being essential and sufficient to mediate plaque-induced thrombus formation. Our study suggests a novel anti-thrombotic strategy to prevent and treat atherothrombosis in patients with vulnerable atherosclerotic plaques. Figure Figure

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Alvarez, Chikezie, Hafiz Muhammad Aslam, Sara Wallach, and Muhammad U. Mustafa. "A Large Grade 5 Mobile Aortic Arch Atheromatous Plaque: Cause of Cerebrovascular Accident." Case Reports in Medicine 2018 (2018): 1–4. http://dx.doi.org/10.1155/2018/5134309.

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Aortic atheromas (aortic atheromatous plaques) are defined by an irregular thickening of the intima ≥2 mm, and a complex plaque is defined as a protruding atheroma ≥4 mm with or without an attached mobile component. Stroke incidence is approximately 25% in patients with mobile plaques of the aortic arch and 2% in patients with quiescent nonmobile plaques. Antiplatelet agents, oral anticoagulants, and statins have been suggested in the management of atheromas. We present an 80-year-old male, with non-ST-segment elevation myocardial infarction (NSTEMI) and chronic dysarthria, found to have an acute cerebrovascular accident (CVA) secondary to embolism from a large 12 mm aortic arch plaque, treated medically with oral antiplatelet therapy, anticoagulation, and statin therapy.

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Teodorescu, Victoria, Jacob Rand, Alan Rosman, Julian Niemetz, and Thomas Muhlfelder. "Human Atheromatous Plaque Extracts Induce Tissue Factor Activity (TFa) in Monocytes and also Express Constitutive TFa." Thrombosis and Haemostasis 81, no. 01 (1999): 146–50. http://dx.doi.org/10.1055/s-0037-1614432.

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SummaryTissue factor activity (TFa) is a major activator of the coagulation cascade and may play a role in atheroma-induced thrombosis. Mono-cyte-macrophages (MO-MF) generate considerable quantities of TFa when stimulated by a variety of inducers. To test the hypothesis that MO could be induced by atheromatous plaque to generate TFa, plaque extracts obtained from patients with obstructive atheromatous disease were used. These extracts were also assayed for constitutive TFa. The constitutive activity was variable from extract to extract but could be very high, up to 250 U TFa. The TFa induced in MO could be also very high, up to 200 U (i.e. 1/5 of the TFa of full strength rabbit brain thromboplastin). These findings point to a major role for MO-MF TFa in the induction or thrombosis by atheromatous plaque.

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Simonetti, L., R. Agati, and M. Leonardi. "Carotid Atherosclerosis from Pathology to Neuroradiology." Rivista di Neuroradiologia 16, no. 1 (February 2003): 15–26. http://dx.doi.org/10.1177/197140090301600102.

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We describe the correlations between the pathological anatomy of atheromatous plaque and neuroradiological findings, discussing the morphological features of plaque surface and location, the histopathological and structural characteristics of the plaque and why intramural haemorrhage occurs.

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Tavora, Fabio, Ling Li, Mary Ripple, David Fowler, and Allen Burke. "Morphologic Characteristic of Coronary Artery Disease, with Emphasis on Thromboses, in Patients Younger Than 40 Years of Age." Pathology Research International 2010 (November 5, 2010): 1–7. http://dx.doi.org/10.4061/2010/628247.

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There are few pathologic descriptions of fatal coronary artery disease in the young. The morphologic characteristics of sudden coronary deaths in 47 hearts from patients younger than 40 years were studied. Numbers of plaques with necrotic cores were quantitated in each heart. Compared to 194 sudden coronary deaths >40 years, heart weight was lower, acute plaque erosions more frequent, and extent of disease less in the 40 years group. Plaque burden was less in hearts with erosions, and healed infarcts more common in hearts with stable plaque. The numbers of fibroatheromas increased with age until the 6th decade () as well as the proportion of total plaques that were atheromatous. Plaques in younger patients have fewer lipid-rich cores. Most thrombi show areas of organization, with layering frequent in erosions, suggesting a possible method of plaque enlargement in the absence of necrotic core formation.

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Biocic, Stanko, Diana Rudan, Zeljko Djurasevic, and Josip Vincelj. "Fibroelastoma or atheromatous plaque: a case report." Cardiologia Croatica 8, no. 5-6 (May 14, 2013): 209. http://dx.doi.org/10.15836/ccar.2013.209.

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Van-Assche, Tim, Veronique Huygelen, Mark J. Crabtree, and Charalambos Antoniades. "Gene Delivery Strategies Targeting Stable Atheromatous Plaque." Current Pharmaceutical Design 19, no. 9 (January 1, 2013): 1626–37. http://dx.doi.org/10.2174/1381612811319090010.

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Charakida, Marietta, and Dimitris Tousoulis. "Infections and Atheromatous Plaque: Current Therapeutic Implications." Current Pharmaceutical Design 19, no. 9 (January 1, 2013): 1638–50. http://dx.doi.org/10.2174/1381612811319090011.

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Van-Assche, Tim, Veronique Huygelen, Mark J. Crabtree, and Charalambos Antoniades. "Gene Delivery Strategies Targeting Stable Atheromatous Plaque." Current Pharmaceutical Design 19, no. 9 (March 1, 2013): 1626–37. http://dx.doi.org/10.2174/138161213805219603.

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Charakida, Marietta, and Dimitris Tousoulis. "Infections and Atheromatous Plaque: Current Therapeutic Implications." Current Pharmaceutical Design 19, no. 9 (March 1, 2013): 1638–50. http://dx.doi.org/10.2174/138161213805219658.

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AbdullGaffar, Badr, and Krysztof Waslewski. "Myxoid Emboli." International Journal of Surgical Pathology 26, no. 7 (April 6, 2018): 609–16. http://dx.doi.org/10.1177/1066896918768029.

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Emboli are common clinicopathologic findings. Recognition of the type of arterial emboli could be the first clue to the original source. Emboli with myxomatous changes are rare. Myxoma-like features in mural organizing thrombi have been reported. The most challenging differential diagnosis is between embolic cardiac myxomas and myxomatous thromboemboli. Emboli from sarcomas and arteriosclerotic plaques with myxoid features are also potential pitfalls. There is scarcity of studies focusing on myxoid emboli and their clinical and pathologic importance. We performed a retrospective study over 12 years. We retrieved all of the embolectomy specimens. We histologically screened the emboli for myxoid stroma, myxomatous changes, and mucinous degeneration. We retrieved 12 cases (3%) of myxoid emboli out of 391 embolectomy specimens. We found 4 cases of thromboemboli, 5 cases of atrial myxomas, 2 cases of atheromatous plaques, and a myxoid liposarcoma. The age range was between 35 and 71 years, with a mean age of 51 years. The male-to-female ratio was 3:2. Myxoid thromboemboli and myxomas were large, while atheromatous plaque emboli were small. Myxoid emboli arising from organizing mural thrombi can be histologically confused with cardiac myxomas and vice versa. Myxoid emboli from atheromatous plaque and myxoid sarcomas can mimic embolizing myxomas. Certain histologic features are helpful hints to differentiate between myxoid emboli. In doubtful cases, immunohistochemistry is helpful. Correct histologic recognition of the different types of myxoid emboli helps guide the clinicians to the most likely etiology and appropriate management in occlusive peripheral vascular diseases with clinically unrecognized lesions.

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Péter, Levente. "Letter to the Editor. Atheromatous Plaque Vulnerability — the Neglected Vulnerable Carotid Plaques." Journal Of Cardiovascular Emergencies 3, no. 3 (September 26, 2017): 144–45. http://dx.doi.org/10.1515/jce-2017-0020.

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Felici, C., B. Porcelli, I. Ciari, C. Setacci, R. Guerranti, R. Pagani, and L. Terzuoli. "Th-P17:435 Virtual gel of atheromatous plaque." Atherosclerosis Supplements 7, no. 3 (January 2006): 589. http://dx.doi.org/10.1016/s1567-5688(06)82393-7.

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Nishida, Satoru, Takeshi Takagi, and Kenichi Muramatsu. "Large mobile atheromatous plaque of the ascending aorta." Asian Cardiovascular and Thoracic Annals 24, no. 5 (January 16, 2015): 491. http://dx.doi.org/10.1177/0218492314568107.

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WOODBURN, K. W., Q. FAN, D. KESSEL, M. WRIGHT, T. D. MODY, G. HEMMI, D. MAGDA, et al. "Phototherapy of Cancer and Atheromatous Plaque with Texaphyrins." Journal of Clinical Laser Medicine & Surgery 14, no. 5 (October 1996): 343–48. http://dx.doi.org/10.1089/clm.1996.14.343.

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SHIOMI, MASASHI, TAKASHI ITO, YASUHIKO HIROUCHI, and MAKOTO ENOMOTO. "Stability of Atheromatous Plaque Affected by Lesional Composition." Annals of the New York Academy of Sciences 947, no. 1 (January 25, 2006): 419–23. http://dx.doi.org/10.1111/j.1749-6632.2001.tb03977.x.

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Olcott, Cornelius. "Percutaneous removal of atheromatous plaque in peripheral arteries." Journal of Vascular Surgery 10, no. 1 (July 1989): 109–10. http://dx.doi.org/10.1016/0741-5214(89)90303-0.

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Capoccia, Laura, Caterina Pelonara, Cesira Imondi, Enrico Sbarigia, and Francesco Speziale. "From embolization to remodeling: the need for early carotid endarterectomy in symptomatic carotid plaques." Vascular 19, no. 2 (April 2011): 111–15. http://dx.doi.org/10.1258/vasc.2010.cr0228.

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Atheromatous plaques are dynamic structures undergoing continuous remodeling. Duplex ultrasound is now an accepted technique to classify the severity of arterial stenoses. It gives information about the ultrasonic echogenicity of tissue, the plaque surface and the velocity of blood flowing through vessels with the latest equipment. We report the case of a 59-year-old male patient with left hemispheric stroke and a 50% left carotid artery stenosis whose remodeling and reabsorption developed throughout three months from the onset of symptoms. Plaque surface and structural echomorphology assessment and standardization, along with the degree of carotid stenosis, might be helpful in identifying patients most likely to benefit from carotid endarterectomy.

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Benedek, Edvin, Alexandra Stănescu, Marius Orzan, Nora Rat, István Kovács, and Zsuzsanna Suciu. "Characteristics of Neoatherosclerosis Within Implanted Coronary Stents in Patients with Acute Coronary Syndromes." Journal Of Cardiovascular Emergencies 2, no. 1 (March 1, 2016): 19–26. http://dx.doi.org/10.1515/jce-2016-0004.

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Abstract Introduction: In-stent restenosis (ISR) is traditionally associated with neointimal hyperplasia. However, recent studies have suggested that an underlying progression of the atherosclerotic process called neoatherosclerosis, different from intimal proliferation, could be involved in ISR development. In this study the aim was to compare the characteristics of the neoatheromatous plaque evidenced by Multislice Angio Computed Tomography, Optical Coherence Tomography (OCT) and Virtual Histology Intravascular Ultrasound (VH-IVUS) with the characteristics of de-novo lesions in native coronary vessels of patients with ISR. Material and methods: This is a prospective single-center pilot study in which patients presenting with acute chest pain and having at least one symptomatic bare-metal stent (BMS) restenosis at six months to one year after BMS implantation, were enrolled. The characteristics of the neointimal tissue developed within the implanted stents using Acio CT, OCT and VH-IVUS were studied. Results: In total, 27 patients with 38 coronary BMS were included in the study, in whom 27 ISR lesions and 43 lesions in native coronary vessels were identified. Angio CT examination revealed that atheromatous plaques responsible for ISR tend to have a larger volume compared with native lesions located in the same coronary vessel (plaque volume 91.2 mm3 for ISR vs. 60.4 mm3 for native vessels, p <0.0001). Additionally, they show more low density plaques compared to native coronary lesions located in the same coronary vessel (33.9 mm3 vs. 18.2 mm3 for the volume of the plaque with density <30 HU, p <0.0001). Plaques responsible for ISR exhibit a higher lipid content than native ones (41.1% vs. 22.9%, p = 0.05). OCT analysis indicated an irregular shaped vascular lumen in 44.4% of ISR lesions compared to 25.6% of de-novo lesions (p = 0.1). Conclusions: Neoatherosclerosis within the implanted coronary stents is associated with signs of plaque vulnerability to a significantly higher extent than the atheromatous plaques in native coronary arteries in patients with ISR presenting with an acute coronary syndrome.

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HIGUCHI, Maria de Lourdes, and Jose A. F. RAMIRES. "Infectious agents in coronary atheromas: a possible role in the pathogenesis of plaque rupture and acute myocardial infarction." Revista do Instituto de Medicina Tropical de São Paulo 44, no. 4 (July 2002): 217–24. http://dx.doi.org/10.1590/s0036-46652002000400007.

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In this review we report our recent findings of histopathological features of plaque instability and the association with Mycoplasma pneumoniae (MP) and Chlamydia pneumoniae (CP) infection, studying thrombosed coronary artery segments (CAS) of patients who died due to acute myocardial infarction. Vulnerable plaques are known to be associated with fat atheromas and inflammation of the plaque. Here we demonstrated that vulnerability is also related with focal positive vessel remodeling that maintains relatively well preserved lumen even in the presence of large atheromatous plaques. This phenomena may explain why the cinecoronariography may not detect large and dangerous vulnerable plaques. Greater amount of these bacteria in vulnerable plaques is associated with adventitial inflammation and positive vessel remodeling: the mean numbers of lymphocytes were significantly higher in adventitia than in the plaque, good direct correlation was obtained between numbers of CD20 B cells and numbers of CP infected cells in adventitia, and between % area of MP-DNA in the plaque and cross sectional area of the vessel, suggesting a cause-effect relationship. Mycoplasma is a bacterium that needs cholesterol for proliferation and may increase virulence of other infectious agents. In conclusion, co-infection by Mycoplasma pneumoniae and Chlamydia pneumoniae may represent an important co-factor for plaque instability, leading to coronary plaque thrombosis and acute myocardial infarction, since larger amount of these bacteria strongly correlated with histological signs of more vulnerability of the plaque. The search of CMV and Helicobacter pilori in these tissues resulted negative.

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Pavlic, Verica, Dejan Peric, Ivana Stosovic Kalezic, Marwa Madi, Subraya G. Bhat, Zlata Brkic, and Danijela Staletovic. "Identification of Periopathogens in Atheromatous Plaques Obtained from Carotid and Coronary Arteries." BioMed Research International 2021 (June 17, 2021): 1–7. http://dx.doi.org/10.1155/2021/9986375.

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Increasing attention has been paid to the possible link between periodontal disease and atherosclerosis over the past decade. The aim of this study is to investigate the presence of five periopathogens: Porphyromonas gingivalis (P.g.), Aggregatibacter actinomycetemcomitans (A.a.), Tannerella forsythia (T.f.), Treponema denticola (T.d.), and Prevotella intermedia (P.i.) in atheromatous plaques obtained from the carotid and coronary arteries in patients who underwent coronary artery bypass graft surgery and carotid endarterectomy. Group I (carotid arteries) consisted of 30 patients (mean age: 54.5 ± 14.8 ), and group II (coronary arteries) consisted of 28 patients (mean age: 63 ± 12.1 ). Clinical periodontal examinations consisted of plaque index, gingival index, sulcus bleeding index, and periodontal probing depth and were performed on the day of vascular surgery. The presence of periopathogens in periodontal pockets and atherosclerotic vessels was detected using polymerase chain reaction. In both subgingival plaque and atherosclerotic plaque of carotid arteries, P.g., A.a., T.f., T.d., and P.i. were detected in 26.7%, 6.7%, 66.7%, 10.0%, and 20.0%, respectively, while for coronary arteries, P.g. was detected in 39.3%, A.a. in 25%, T.f. in 46.4%, T.d. in 7.1%, and P.i. in 35.7%. The presence of five periopathogens in carotid and coronary atherosclerotic vessels showed correlation in regard to the degree of periodontal inflammation. The present study suggests the relationship between periodontal pathogenic bacteria and atherogenesis. Further studies are necessary in relation to the prevention or treatment of periodontal disease that would result in reduced mortality and morbidity associated with atherosclerosis.

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Benedek, Annabella, Diana Opincariu, Imre Benedek, Ionuț Ferenț, Roxana Hodaș, Emese Marton, and Theodora Benedek. "Association of Coronary Wall Shear Stress With Atheromatous Plaque Vulnerability: A Systematic Review." Central European Journal of Clinical Research 1, no. 1 (September 1, 2018): 12–27. http://dx.doi.org/10.2478/cejcr-2018-0004.

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AbstractAcute coronary syndromes are usually triggered by the erosion or rupture of a vulnerable coronary plaque. A vulnerable plaque (VP) is an atheromatous plaque which, after suffering different transformations, is prone to rupture causing an acute coronary event. Such a VP carries inside several biomarkers considered as “signatures of vulnerability”, which, if identified, can prompt timely initiation of therapeutic measures in order to prevent the development of an acute myocardial infarction. The most freqeuntly used techniques for identification of vulnerability markers are computed tomographic angiography (CTA), intravascular ultrasound and optical coherence tomography. Endothelial shear stress (ESS) represents a new promising biomarker associated with plaque vulnerability. Determination of ESS is nowadays possible using noninvasive imaging techniques, based on complex computational post-processing of multiple datasets extracted from CTA images and advanced computational fluid dynamics technologies. The aim of this systematic review was to evaluate the role of the coronary ESS, determined using advanced computational techniques for image post-processing, as a feature associated with CTA-derived biomarkers of atheromatous plaque vulnerability, underlining the conceptual differences between high ESS and low ESS as promotors of vulnerability.

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Alkatiri, Abdul H., Doni Firman, Amir A. Alkatiri, Paskalis I. Suryajaya, and Albert Sudharsono. "The Role of Angiotensin Antagonism in Coronary Plaque Regression: Insights from the Glagovian Model." International Journal of Vascular Medicine 2021 (April 7, 2021): 1–10. http://dx.doi.org/10.1155/2021/8887248.

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The benefit of antagonizing the effect of the renin angiotensin aldosterone system (RAAS), notably by the use of angiotensin-converting enzyme inhibitor (ACEi) and angiotensin II type 1 receptor blocker (ARB) for coronary artery disease (CAD), has been demonstrated in multiple studies, which may be attributed to their ability to inhibit the deleterious effect of RAAS to the cardiovascular system. It is well known that angiotensin II (Ang II) plays a vital role in atheromatous plaque formation and progression through multiple pathways, including inflammatory and arterial remodeling aspects. Significant coronary atheromatous plaque regression has been previously demonstrated in various studies using statin agents. Similar results have been reported in different studies using angiotensin inhibitor agents, notably ARB agents. Analysis from various trials utilizing ARB showed a significant plaque regression using olmesartan and telmisartan as evaluated by IVUS studies. In contrary, the use of ACEi did not demonstrated significant plaque regression, which may be attributed to the heavy plaque calcification in respective studies. On this review, we aim to present the basic mechanism on the role of RAAS in plaque modulation and its arterial remodeling aspect, which is then integrated with the clinical evidence based on the available intravascular ultrasonography (IVUS) studies on coronary arteries.

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Delgado, Montserrat G., and Manuel Naves. "Compliance and echographic carotid plaque evolution in patients with acute ischemic stroke treated with atorvastatin according to usual care." Vascular 22, no. 3 (May 13, 2013): 218–20. http://dx.doi.org/10.1177/1708538113478751.

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The aim of the paper is to assess the compliance and efficacy of atorvastatin treatment according to usual care on carotid atheromatous plaque and lipids during follow-up for one year in patients with acute ischemic stroke. Sixty-six patients were included. Morphological plaque characteristics were described and a complete blood analysis was performed at admission and at one year. Nineteen patients stopped treatment. Lipid reduction was significant in triglycerides, cholesterol and LDL cholesterol, with an increase in HDL cholesterol. Morphological characteristics of carotid plaque were not modified. In conclusion, an irregular compliance has been seen in patients with acute ischemic stroke treated with atorvastatin according to usual care. Nearly one-third of our patients stopped the treatment before the course of a year. The effect on lipids and its pleiotropic effect on atheromatous carotid artery disease might support the long-term use of atorvastatin, regardless of the dose, in patients with acute ischemic stroke.

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Woodcock, J. P. "Characterisation of the atheromatous plaque in the carotid arteries." Clinical Physics and Physiological Measurement 10, no. 4A (November 1989): 45–49. http://dx.doi.org/10.1088/0143-0815/10/4a/006.

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Nitschke, Yvonne, Simone Hartmann, Giovanni Torsello, Rüdiger Horstmann, Harald Seifarth, Gabriele Weissen-Plenz, and Frank Rutsch. "Expression of NPP1 is regulated during atheromatous plaque calcification." Journal of Cellular and Molecular Medicine 15, no. 2 (February 2011): 220–31. http://dx.doi.org/10.1111/j.1582-4934.2009.00988.x.

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Hong, Sung-Jin, Myeong-Ki Hong, Young-Guk Ko, Geu-Ru Hong, Jae-Kwang Shim, Young-Lan Kwak, Sak Lee, Byung-Chul Chang, and Yangsoo Jang. "Migration of Calcium and Atheromatous Plaque in Computed Tomography." Journal of the American College of Cardiology 63, no. 12 (April 2014): e23. http://dx.doi.org/10.1016/j.jacc.2013.08.1664.

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Terzuoli, Lucia, Enrico Marinello, Barbara Frosi, Ilaria Ciari, and Brunetta Porcelli. "Nitric oxide levels in patients with atheromatous carotid plaque." Biomedicine & Pharmacotherapy 62, no. 5 (June 2008): 325–27. http://dx.doi.org/10.1016/j.biopha.2007.10.001.

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Horio, Eiji, Tsuyoshi Kadomatsu, Keishi Miyata, Yasumichi Arai, Kentaro Hosokawa, Yasufumi Doi, Toshiharu Ninomiya, et al. "Role of Endothelial Cell–Derived Angptl2 in Vascular Inflammation Leading to Endothelial Dysfunction and Atherosclerosis Progression." Arteriosclerosis, Thrombosis, and Vascular Biology 34, no. 4 (April 2014): 790–800. http://dx.doi.org/10.1161/atvbaha.113.303116.

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Objective— Cardiovascular disease (CVD), the most common morbidity resulting from atherosclerosis, remains a frequent cause of death. Efforts to develop effective therapeutic strategies have focused on vascular inflammation as a critical pathology driving atherosclerosis progression. Nonetheless, molecular mechanisms underlying this activity remain unclear. Here, we ask whether angiopoietin-like protein 2 (Angptl2), a proinflammatory protein, contributes to vascular inflammation that promotes atherosclerosis progression. Approach and Results— Histological analysis revealed abundant Angptl2 expression in endothelial cells and macrophages infiltrating atheromatous plaques in patients with cardiovascular disease. Angptl2 knockout in apolipoprotein E–deficient mice ( ApoE −/− / Angptl2 −/− ) attenuated atherosclerosis progression by decreasing the number of macrophages infiltrating atheromatous plaques, reducing vascular inflammation. Bone marrow transplantation experiments showed that Angptl2 deficiency in endothelial cells attenuated atherosclerosis development. Conversely, ApoE −/− mice crossed with transgenic mice expressing Angptl2 driven by the Tie2 promoter ( ApoE −/− /Tie2- Angptl2 Tg), which drives Angptl2 expression in endothelial cells but not monocytes/macrophages, showed accelerated plaque formation and vascular inflammation because of increased numbers of infiltrated macrophages in atheromatous plaques. Tie2- Angptl2 Tg mice alone did not develop plaques but exhibited endothelium-dependent vasodilatory dysfunction, likely because of decreased production of endothelial cell–derived nitric oxide. Conversely, Angptl2 −/− mice exhibited less severe endothelial dysfunction than did wild-type mice when fed a high-fat diet. In vitro, Angptl2 activated proinflammatory nuclear factor-κB signaling in endothelial cells and increased monocyte/macrophage chemotaxis. Conclusions— Endothelial cell–derived Angptl2 accelerates vascular inflammation by activating proinflammatory signaling in endothelial cells and increasing macrophage infiltration, leading to endothelial dysfunction and atherosclerosis progression.

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Rodean, Ioana-Patricia, Luminița Lazăr, Vasile-Bogdan Halațiu, Carmen Biriș, Imre Benedek, and Theodora Benedek. "Periodontal Disease Is Associated with Increased Vulnerability of Coronary Atheromatous Plaques in Patients Undergoing Coronary Computed Tomography Angiography—Results from the Atherodent Study." Journal of Clinical Medicine 10, no. 6 (March 21, 2021): 1290. http://dx.doi.org/10.3390/jcm10061290.

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The present study aimed to investigate the link between the severity of periodontal disease (PD), coronary calcifications and unstable plaque features in patients who underwent coronary computed tomography for unstable angina (UA). Fifty-two patients with UA, included in the ATHERODENT trial (NCT03395041), underwent computed tomographic coronary angiography (CCTA) and dental examination. Based on the median value of the periodontal index (PI), patients were assigned to the low periodontal index (LPI) group (PI < 22) and a high periodontal index (HPI) group (PI > 22). Patients with HPI had higher plaque volume (p = 0.013) and noncalcified plaque volume (p = 0.0003) at CCTA. In addition, the presence of vulnerability features in the atheromatous plaques was significantly correlated with PI (p = 0.001). Among periodontal indices, loss of gingival attachment (p = 0.009) and papillary bleeding index (p = 0.002) were strongly associated with high-risk plaques. PI significantly correlated with coronary calcium score (r = 0.45, p = 0.0008), but not with traditional markers of subclinical atherosclerosis. Overall, this subgroup analysis of the ATHERODENT study indicates that patients with advanced PD and UA present a higher amount of calcium in the coronary tree and have a more vulnerable phenotype of their culprit plaques.

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Tanabe, Jun, Michihiro Tanaka, Keisuke Kadooka, and Hiromu Hadeishi. "Efficacy of high-resolution cone-beam CT in the evaluation of carotid atheromatous plaque." Journal of NeuroInterventional Surgery 8, no. 3 (January 22, 2015): 305–8. http://dx.doi.org/10.1136/neurintsurg-2014-011584.

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IntroductionA major disadvantage of carotid artery stenting (CAS) is the high incidence of perioperative cerebral embolism. Cerebral embolism after CAS is associated with soft plaque. Currently, higher spatial resolution imaging can be obtained with cone-beam CT (CB-CT). The correlation between the degree of contrast enhancement of the vasa vasorum (VV) on CB-CT and the vulnerability of plaque in terms of risk factors for CAS was evaluated.Methods18 patients who underwent CAS had high-resolution CB-CT to evaluate enhancement of the VV covering carotid plaque performed intraoperatively. The appearance of the surface of the carotid plaque was classified as either enhancing (VV-positive) or non-enhancing (VV-negative). Carotid plaque vulnerability on black-blood MRI (BB-MRI) and postoperative ipsilateral ischemic lesions on diffusion-weighted imaging (DWI) were analyzed in the two groups.ResultsOf the 18 patients, 9 were VV-positive and 9 were VV-negative. The proportion of ipsilateral new ischemic lesions on DWI was significantly higher in the VV-positive group than in the VV-negative group (8/9 patients (88.9%) vs 3/9 patients (33.3%), p=0.026). BB-MRI was performed preoperatively in 15 of 18 patients. The proportion of unstable plaque on BB-MRI was significantly higher in the VV-positive group than in the VV-negative group (9/9 patients (100%) vs 1/6 patients (16.7%), p=0.002).ConclusionsEnhancement of the VV covering carotid plaque on high-resolution CB-CT was significantly associated with unstable plaque on BB-MRI and postoperative ipsilateral new ischemic lesions.

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Olszewski, Waldemar Lech, Joanna Rutkowska, Maria Moscicka-Wesolowska, Ewa Swoboda-Kopec, Ewa Stelmach, Marzanna Zaleska, and Malgorzata Zagozda. "Bacteria of leg atheromatous arteries responsible for inflammation." Vasa 45, no. 5 (September 2016): 379–85. http://dx.doi.org/10.1024/0301-1526/a000549.

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Abstract. Background: Ischaemia of the lower limbs is frequently followed by inflammation and, in advanced cases, necrosis of peripheral tissues. Whether this is caused by arterial hypoperfusion only or by the presence of bacteria in the arterial walI as well remains unclear. The aim of the study was to prove the presence and source of bacteria in arterial specimens and evaluate their chemotactic properties resulting in the formation of periarterial cellular infiltrates. Materials and methods: Bacterial culture and testing for 16sRNA were performed in fragments of popliteal artery harvested from amputated limbs. Carotid artery plaques served as controls. Fragments of arteries were transplanted into scid mice to evaluate their chemotactic activity for macrophages. Results: a) higher prevalence of isolates and 16sRNA in atherosclerotic popliteal than carotid arteries, b) high density of plaque and periarterial infiltrates and mRNA level for pro-inflammatory cytokines in popliteal arteries, c) prevalent microbes were Staphylococcus aureus, S. epidermidis and Enterococci, d) foot skin and arterial bacterial phenotypes and DNA revealed evident similarities, and e) more intensive mouse macrophage accumulation in popliteal than carotid implants into scid mice. Conclusions: The presence of bacteria in the lower limb arterial wall was documented. They may predispose to inflammation secondary to ischaemic changes.

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Nakano, Kazuhiko, Hirotoshi Nemoto, Ryota Nomura, Hiromi Homma, Hideo Yoshioka, Yasuhiro Shudo, Hiroki Hata, et al. "Serotype distribution of Streptococcus mutans a pathogen of dental caries in cardiovascular specimens from Japanese patients." Journal of Medical Microbiology 56, no. 4 (April 1, 2007): 551–56. http://dx.doi.org/10.1099/jmm.0.47051-0.

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The involvement of oral bacteria in the pathogenesis of cardiovascular disease has been studied, with Streptococcus mutans, a pathogen of dental caries, detected in cardiovascular lesions at a high frequency. However, no information is available regarding the properties of S. mutans detected in those lesions. Heart valve specimens were collected from 52 patients and atheromatous plaque specimens from 50 patients, all of whom underwent cardiovascular operations, and dental plaque specimens were taken from 41 of those subjects prior to surgery. Furthermore, saliva samples were taken from 73 sets of healthy mothers (n=73) and their healthy children (n=78). Bacterial DNA was extracted from all specimens, then analysed by PCR with S. mutans-specific and serotype-specific primer sets. The detection rates of S. mutans in the heart valve and atheromatous plaque specimens were 63 and 64 %, respectively. Non-c serotypes were identified with a significantly higher frequency in both cardiovascular and dental plaque samples from the subjects who underwent surgery as compared to serotype c, which was detected in 70–75 % of the samples from the healthy subjects. The serotype distribution in cardiovascular patients was significantly different from that in healthy subjects, suggesting that S. mutans serotype may be related to cardiovascular disease.

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Benedek, Theodora, András Mester, Annabell Benedek, Nora Rat, Diana Opincariu, and Monica Chițu. "Assessment of Coronary Plaque Vulnerability in Acute Coronary Syndromes using Optical Coherence Tomography and Intravascular Ultrasound. A Systematic Review." Journal Of Cardiovascular Emergencies 2, no. 4 (December 1, 2016): 173–84. http://dx.doi.org/10.1515/jce-2016-0028.

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Abstract The aim of this systematic review was to analyze studies characterizing vulnerable coronary plaques using optical coherence tomography (OCT) and intravascular ultrasound (IVUS), in order to identify the most efficient invasive technique permitting plaque characterization in patients with acute myocardial infarction. Method: A total number of 432 studies were identified, 420 through database searching and 12 through manual searching. Eight duplicate studies were removed, leaving a total number of 424 studies to be screened. Twenty-six studies only available in Abstract-only form were excluded, resulting in 398 studies checked for eligibility. Eleven studies fulfilled the eligibility criteria and were included in this systematic analysis. Plaque vulnerability was investigated in plaques with thin cap fibroatheroma (TCFA) versus those with thick cap fibroatheroma, in ruptured coronary plaques versus non-ruptured coronary plaques, in culprit versus non-culprit lesions and in lipid-rich versus non-lipid-rich plaques. Results: A total of 1,568 coronary plaques in 1,225 patients with acute coronary syndromes (ACS) who underwent both IVUS and OCT for analysis of plaque features were included in the final analysis. The review identified the following IVUS-derived features as significantly correlated with plaque vulnerability: plaque burden (p <0.001), remodeling index (p <0.001), external elastic membrane cross-sectional area (p <0.001), and the amount of necrotic core (p <0.001), while OCT-derived features characterizing unstable plaque were TCFA (p <0.001), lipid arch (p <0.001), accumulation of macrophages (p = 0.03), and presence of intracoronary thrombus (p <0.001). Conclusion: Both IVUS and OCT are invasive imaging techniques able to provide relevant information on the vulnerability of coronary atheromatous plaques, identifying, as they do, various plaque features significantly associated with unstable plaques. Information provided by the two techniques is complementary, and both methods can serve as a useful clinical diagnostic tool, especially in cases of ACS patients undergoing a revascularization procedure.

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Bauriedel, G., P. C. Dartsch, R. Voisard, D. Roth, J. B. Simpson, B. Höfling, and E. Betz. "Selective percutaneous “biopsy” of atheromatous plaque tissue for cell culture." Basic Research in Cardiology 84, no. 3 (May 1989): 326–31. http://dx.doi.org/10.1007/bf01907980.

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Journal articles on the topic 'Atheromatous plaque'

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