Home About us Contact
|
Home About us Contact | ||
|
|
||
Plaque Rupture (plaque + rupture)
Selected AbstractsProteomic analysis of human vessels: Application to atherosclerotic plaquesPROTEINS: STRUCTURE, FUNCTION AND BIOINFORMATICS, Issue 6 2003Mari Carmen Duran Abstract Atherosclerosis is a chronic disease that affects medium and large arteries. This process originates from the interaction between cells of the arterial wall, lipoproteins and inflammatory cells, leading to the development of complex lesions or plaques that protrude into the arterial lumen. Plaque rupture and thrombosis result in acute clinical complications such as myocardial infarction and stroke. Owing to the heterogeneous cellular composition of the plaques, a proteomic analysis of the whole lesion is not appropriate. Therefore, we have studied the proteins secreted by human carotid atherosclerotic plaques, obtained by endarterectomy. Normal artery segments and different regions of the surgical pieces (noncomplicated plaque, complicated plaque with thrombus) were cultured in protein-free medium and the secreted proteins (supernatants) analyzed by two-dimensional gel electrophoresis. Normal artery segments secreted a moderate number of proteins (42 spots). However in the two-dimensional (2-D) gels (pH 3,10) of segments bearing a plaque, the number of spots increased markedly (154). The number of spots also increased (202) in the 2-D gels of artery segments with a ruptured plaque and thrombus. Thus, the more complicated the lesion, the higher the number of secreted proteins, suggesting the production of specific proteins relating to the complexity of the atherosclerotic lesion. [source] The pathophysiology of peri-operative myocardial infarctionANAESTHESIA, Issue 7 2010B. M. Biccard Summary It is generally believed that plaque rupture and myocardial oxygen supply-demand imbalance contribute approximately equally to the burden of peri-operative myocardial infarction. This review critically analyses data of post-mortem, pre-operative coronary angiography, troponin surveillance, other pre-operative non-invasive investigations, and peri-operative haemodynamic predictors of myocardial ischaemia and/or myocardial infarction. The current evidence suggests that myocardial oxygen supply-demand imbalance predominates in the early postoperative period. It is likely that flow stagnation and thrombus formation is an important pathway in the development of a peri-operative myocardial infarction, in addition to the more commonly recognised role of peri-operative tachycardia. Research and therapeutic interventions should be focused on the prediction and therapy of flow stagnation and thrombus formation. Plaque rupture appears to be a more random event, distributed over the entire peri-operative admission. [source] Rupture of a peripheral popliteal artery plaque documented by intravascular ultrasound: A case report,CATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS, Issue 7 2009Hiroaki Kohno MD Abstract A 58-year-old male with dyslipidemia and coronary spastic angina suddenly experienced pain in the right limb while walking on November 1, 2008. Right-ankle brachial pressure index (ABI) was decreased (0.80) and left-ABI was normal (1.24). Bilateral ABI was normal during January 2008. Ultrasonography in the right-lower limb artery revealed severe stenosis in the right-popliteal artery with extended and large echolucent plaques containing an isoechoic area. We carried out lower limb angiography: subtotal occlusion of the popliteal artery was found. By intravascular ultrasound (IVUS), right-popliteal artery plaques were echolucent and eccentric; ulceration with a thin fibrous cap was noted. Percutaneous transluminal angioplasty was done and popliteal artery blood flow was improved. Right-ABI improved to 1.13 after 4 days. To prevent the progression and rupture of the plaques, lipid-lowering therapy and antiplatelet therapy were started. Plaque rupture of the popliteal artery was diagnosed by these characteristics on IVUS. Patients with peripheral artery disease may have plaque rupture similar to those with acute coronary syndromes who have identical unstable plaques and unstable atheromas. In addition to appropriate local revascularization, systemic therapy to stabilize the unstable plaque is indicated because failure to do so may cause recurrent events. © 2009 Wiley-Liss, Inc. [source] Thiazolidinediones as anti-inflammatory and anti-atherogenic agentsDIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue 1 2008Antonio Ceriello Abstract In the last few years, there has been increasing focus on the impact of interventions on cardiovascular outcomes in patients with type 2 diabetes. Insulin resistance and hyperglycaemia often co-exist with a cluster of risk factors for coronary artery disease, but the underlying mechanisms leading to the development of such vascular complications are complex. The over-production of free radicals in patients suffering from diabetes results in a state of oxidative stress, which leads to endothelial dysfunction and a greater risk of atherosclerosis. Moreover, inflammatory factors which play a critical role in atherothrombosis and plaque rupture are often found to be at elevated levels in this patient population. Thiazolidinediones (TZDs) are now routinely used to manage glucose levels, and have been suggested to influence other cardiovascular risk factors and therefore the pathways leading to macrovascular events. Consequently, recent studies have investigated the anti-inflammatory and anti-atherogenic properties of TZDs. The data available up to the present time, in the context of the emerging cardiovascular outcome profiles of rosiglitazone and pioglitazone, will be discussed here. Copyright © 2007 John Wiley & Sons, Ltd. [source] Procoagulant and inflammatory response of virus-infected monocytesEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 10 2002J. J. M. Bouwman Abstract Background Monocytes play a prominent role in inflammation, coagulation and atherosclerosis by their ability to produce tissue factor (TF) and cytokines. The aim of the present study was to establish whether virus-infected monocytes initiate coagulation. In addition, the production of cytokines by monocytes may accelerate the chronic process of atherosclerosis and may contribute to coronary syndromes by eliciting plaque instability. Materials and methods Monocytes were isolated by Vacutainer®, BD Biosciences, Alphen aan den Rijn, Netherlands and subsequent magnetic cell sorting (MACS®, Milteny Biotec, Bergish Gladbach, Germany). Coagulation times in normal pooled plasma and Factor VII-deficient plasma were measured after infection with cytomegalovirus (CMV), Chlamydia pneumoniae (Cp) and influenza A\H1N1. Anti-TF antibodies were added to neutralize TF expressed on monocytes. Interleukins (IL) 6, 8 and 10 were measured in the supernatants. Results Chlamydia pneumoniae- and CMV-infected monocytes decreased the clotting time by 60%, and influenza-infected monocytes by 19%, as compared to uninfected monocytes. Procoagulant activity was absent when Factor VII-deficient plasma or anti-TF antibodies were used. Monocytes produced both IL-6 and IL-8 after infection with CMV (317 pg mL,1 and 250 pg mL,1) or Cp (733 pg mL,1 and 268 pg mL,1). Similar results were obtained for influenza virus-infected monocytes, but the levels of both cytokines were 3,5-fold higher (1797 pg mL,1 and 725 pg mL,1). Interleukin-10 was not produced by infected monocytes. Conclusion The procoagulant activity of virus-infected monocytes is TF-dependent. Although influenza infection did not generate a significant reduction in clotting time, the pronounced expression of IL-6 and IL-8 may induce local and/or systemic inflammatory reactions, which may be associated with plaque rupture and atherosclerosis. The lack of production of the anti-inflammatory cytokine IL-10 may even accelerate these processes. [source] Elucidation of the molecular mechanism of platelet activation: Dense granule secretion is regulated by small guanosine triphosphate-binding protein Rab27 and its effector Munc13-4GERIATRICS & GERONTOLOGY INTERNATIONAL, Issue 4 2006Hisanori Horiuchi Cardiovascular diseases such as myocardial and cerebral infarction are common critical diseases occurring more frequently in the elderly. The trigger of the diseases is platelet activation following plaque rupture or erosion. Investigation of the molecular mechanism in platelet activation has been exclusively performed pharmacologically. We have succeeded in establishing the granule secretion and aggregation assays using permeabilized platelets. These systems enabled us to examine the molecular mechanism in platelet activation with molecular biological and biochemical methods. Using these assay systems, we have been investigating the molecular mechanism of platelet activation. With a support grant from the Novartis Foundation for Gerontological Research, we found several molecules involved in the regulation. In this report, I present the progress in the research of the granule secretion mechanism in activated platelets, which was reported in the Japanese Geriatric Society Meeting in 2005. [source] Roles of oxidized low-density lipoprotein and its receptors in the pathogenesis of atherosclerotic diseasesGERIATRICS & GERONTOLOGY INTERNATIONAL, Issue 4 2002Noriaki Kume In elderly populations, atherosclerotic diseases, including ischemic heart disease and stroke, frequently impair quality of life and affect mortality. Hypercholesterolemia, especially increased plasma low-density lipoprotein (LDL), is one of the strongest risk factors for atheroscletorotic diseases. Oxidative modification of LDL appears to convert LDL particles to more atherogenic forms. Scavenger receptor class A (SR-A) and CD36 have been identified and well-characerized as receptors for Ox-LDL in macrophages. In addition to these molecules, lectin-like oxidized LDL receptor (LOX)-1 and scavenger receptor for phosphatidylserine and oxidized lipoprotein (SR-PSOX) are type II and I membrane glycoproteins, respectively, both of which can act as cell-surface endocytosis receptors for atherogenic oxidized LDL (Ox-LDL). LOX-1 expression can dynamically be induced by pro-inflammatory stimuli, and is detectable in cultured macrophages and activated vascular smooth muscle cells (VSMC), in addition to endothelial cells. LOX-1-dependent uptake of Ox-LDL induces apoptosis of cultured VSMC. In vivo, endothelial cells that cover early atherosclerotic lesions, and intimal macrophages and VSMC in advanced atherosclerotic plaques dominantly express LOX-1. LOX-1 expressed on the cell-surface can be cleaved in part and released as soluble molecules, suggesting the diagnostic value of soluble LOX-1. SR-PSOX is a newly identified receptor for Ox-LDL, which appears to be identical to CXCL16, a novel membrane-anchored chemokine directed to CXCR6-positive lymphocytes. In contrast to LOX-1, which is expressed by a variety of cell types, SR-PSOX expression appeared relatively confined to macrophages in atherogenesis. Taken together, oxidized LDL receptors, including LOX-1 and SR-PSOX, may play important roles in atherogenesis and atherosclerotic plaque rupture. [source] Pathology of the Thin-Cap Fibroatheroma:JOURNAL OF INTERVENTIONAL CARDIOLOGY, Issue 3 2003A Type of Vulnerable Plaque Thin cap atheroma is the precursor of plaque rupture, which accounts for a majority of coronary thrombi. The morphologic features of thin cap atheromas that predict rupture are unknown, but we know from studies of ruptured plaques that large necrotic cores, fibrous cap <65 microns and numerous macrophages within the cap likely indicate instability. There is some evidence that a speckled pattern of calcification is associated with vulnerability to rupture. There are usually multiple thin cap atheroma in the hearts of patients dying with acute plaque rupture, as well as multiple fibroatheromas with intraplaque hemorrhage. Targeted therapy for the purpose of stabilizing coronary lesions that are prone to rupture is a major future goal of the interventionist. (J Interven Cardiol 2003;16:267,272) [source] Vulnerable Plaque: The Pathology of Unstable Coronary LesionsJOURNAL OF INTERVENTIONAL CARDIOLOGY, Issue 6 2002RENU VIRMANI M.D. Vulnerable plagues have been defined as precursors to lesions that rupture. However, coronary thrombosis may occur from other lesions like plaque erosion and calcified nodules, although to a lesser frequency than rupture. Therefore, the definition of vulnerable plaque should be all-inclusive. Using descriptive terminology, the authors define the precursor lesion of plaque rupture as "thin-cap fibroatheroma" (TCFA). Morphologically, TCFAs have a necrotic core with an overlying thin fibrous cap (< 65 mm) consisting of collagen type I, which is infiltrated by macrophages. These lesions are most frequent in the coronary tree of patients dying with acme myocardial infarction and least common in those with plaque erosion. TCFAs are more common in patients with high serum total cholesterol (TC) and a high TC to high density cholesterol ratio, in women >50 years, and in those patients with elevated levels of high sensitivity C-reactive protein. TCFAs are mostly found in the proximal left anterior descending coronary arteries and less commonly in the proximal right or the proximal left circumflex coronary arteries. In TCFAs, necrotic core length is , 2,17 mm (mean 8 mm) and the underlying cross-sectional luminal narrowing in over 75% of cases is < 75% (< 50% diameter stenosis). The area of the necrotic core in at least 75% of cases is ,3 mm2. Clinical studies of TCFAs are limited as angiography and intravascular ultrasound (TVUS) catheters cannot precisely identify these lesions. Newer catheters and other techniques are at various stages of development and will play a significant role in the understanding of plaque progression and the development of symptomatic coronary artery disease. [source] Effect of oral melatonin on the procoagulant response to acute psychosocial stress in healthy men: a randomized placebo-controlled studyJOURNAL OF PINEAL RESEARCH, Issue 4 2008Petra H. Wirtz Abstract:, Acute mental stress is a potent trigger of acute coronary syndromes. Catecholamine-induced hypercoagulability with acute stress contributes to thrombus growth after coronary plaque rupture. Melatonin may diminish catecholamine activity. We hypothesized that melatonin mitigates the acute procoagulant stress response and that this effect is accompanied by a decrease in the stress-induced catecholamine surge. Forty-five healthy young men received a single oral dose of either 3 mg melatonin (n = 24) or placebo medication (n = 21). One hour thereafter, they underwent a standardized short-term psychosocial stressor. Plasma levels of clotting factor VII activity (FVII:C), FVIII:C, fibrinogen, D-dimer, and catecholamines were measured at rest, immediately after stress, and 20 min and 60 min post-stress. The integrated change in D-dimer levels from rest to 60 min post-stress differed between medication groups controlling for demographic and metabolic factors (P = 0.047, = 0.195). Compared with the melatonin group, the placebo group showed a greater increase in absolute D-dimer levels from rest to immediately post-stress (P = 0.13; = 0.060) and significant recovery of D-dimer levels from immediately post-stress to 60 min thereafter (P = 0.007; = 0.174). Stress-induced changes in FVII:C, FVIII:C, fibrinogen, and catecholamines did not significantly differ between groups. Oral melatonin attenuated the stress-induced elevation in the sensitive coagulation activation marker D-dimer without affecting catecholamine activity. The finding provides preliminary support for a protective effect of melatonin in reducing the atherothrombotic risk with acute mental stress. [source] Complementary roles of platelets and coagulation in thrombus formation on plaques acutely ruptured by targeted ultrasound treatment: a novel intravital modelJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 1 2009M. J. E. KUIJPERS Summary.,Background:,Atherothrombosis is a major cause of cardiovascular events. However, animal models to study this process are scarce. Objectives:,We describe the first murine model of acute thrombus formation upon plaque rupture to study atherothrombosis by intravital fluorescence microscopy. Methods:,Localized rupture of an atherosclerotic plaque in a carotid artery from Apoe,/, mice was induced in vivo using ultrasound. Rupture of the plaque and formation of localized thrombi were verified by two-photon laser scanning microscopy (TPLSM) in isolated arteries, and by immunohistochemistry. The thrombotic reaction was quantified by intravital fluorescence microscopy. Results:,Inspection of the ultrasound-treated plaques by histochemistry and TPLSM demonstrated local damage, collagen exposure, luminal thrombus formation as well as intra-plaque intrusion of erythrocytes and fibrin. Ultrasound treatment of healthy carotid arteries resulted in endothelial damage and limited platelet adhesion. Real-time intravital fluorescence microscopy demonstrated rapid platelet deposition on plaques and formation of a single thrombus that remained subocclusive. The thrombotic process was antagonized by thrombin inhibition, or by blocking of collagen or adenosine diphosphate receptor pathways. Multiple thrombi were formed in 70% of mice lacking CD40L. Conclusions:,Targeted rupture of murine plaques results in collagen exposure and non-occlusive thrombus formation. The thrombotic process relies on platelet activation as well as on thrombin generation and coagulation, and is sensitive to established and novel antithrombotic medication. This model provides new possibilities to study atherothrombosis in vivo. [source] Atorvastatin and omega-3 fatty acids protect against activation of the coagulation system in patients with combined hyperlipemiaJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 4 2003A. Nordøy Summary., Activation of factor (F)VII by tissue factor may represent a critical event during plaque rupture in acute coronary syndromes. Patients with combined hyperlipemia are at high risk for developing coronary heart disease and their tendency to thrombosis may be accelerated during postprandial hyperlipemia. In the present double-blind, placebo-controlled parallel study, 42 patients with combined hyperlipemia and serum triglycerides between 2.0 and 15.0 mmol L,1 and serum cholesterol >5.3 mmol L,1 at the end of a 3-month dietary run-in period were treated with atorvastatin at 10 mg day,1 for at least 10 weeks. During the last 5 weeks the patients were randomized into two groups receiving 1.68 g day,1 omega-3 fatty acids (,-3 FA) or placebo (corn oil). The fasting levels of FVII antigen (FVII-Ag) and FVII coagulant activity (FVII:C) were high compared with healthy males. The fasting levels of activated FVII (FVIIa) and FVII-Ag correlated both to serum triglycerides and apolipoprotein A1 (apoA1). FVIIa and FVII:C increased during postprandial hyperlipemia. This increase of FVIIa correlated to the fasting triglyceride and apoA1 levels, but not to the degree of postprandial hypertriglyceridemia. The concentrations of fasting FVIIa in these patients were reduced in parallel with a reduction of fasting triglycerides by treatment with atorvastatin + placebo. This treatment also reduced the postprandial level of FVIIa. ,-3 FA in addition to atorvastatin further reduced FVIIa concentrations, fasting and postprandially, and also significantly reduced FVII:C and FVII-Ag during postprandial hyperlipemia. Prothrombin fragment 1 + 2 (F1 + 2) increased during postprandial hyperlipemia. This increase was significantly reduced after treatment with atorvastatin plus ,-3 FA. The increase of F1 + 2 measured as incremental area under the curve (iAUC) during postprandial hyperlipemia correlated to the fasting levels of FVIIa, FVII:C and FVII-Ag and also to the levels of these factors during postprandial lipemia. In conclusion, patients with combined hyperlipemia are at risk for activation of the coagulation system, particularly during postprandial lipemia. This activation may be significantly reduced by statins and ,-3 FA. [source] Aqueous extract of rhubarb stabilizes vulnerable atherosclerotic plaques due to depression of inflammation and lipid accumulationPHYTOTHERAPY RESEARCH, Issue 7 2008Yunfang Liu Abstract The study evaluated the effect of the traditional Chinese medicine rhubarb on the stability of atherosclerotic plaque. Atherosclerotic lesions were induced in rabbits through balloon injury with a high-cholesterol diet and then were divided into a control group, a rhubarb group and a simvastatin group. At week 24 recombinant-p53 adenoviruses were locally delivered to the atherosclerotic plaques. At week 26 plaque rupture was triggered by the intra-arterial Chinese Russell's viper venom and histamine. Serological, ultrasonographic, pathologic, immunohistochemical and gene expression studies were performed. The results showed that the incidence of plaque rupture in the rhubarb group and the simvastatin group was significantly lower than that in the control group (42.86% and 35.71% versus 80.00%, both p < 0.05). Serum TC, LDL-C (p < 0.05,0.01), IMT (both p < 0.01), PA (both p < 0.01), PB (%) (both p < 0.01) and the mRNA and protein expressions of TLR2, TLR4 and NF- ,B (p < 0.05, 0.01, respectively) in the rhubarb group and the simvastatin group were significantly lower than those in the control group. In contrast, AIIc% (both p < 0.05) in the two treatment groups were significantly higher than those in the control group. These results suggest that rhubarb has antiatherosclerotic and plaque-stabilizing properties due to antiinflammation and lipid-lowering effects. Copyright © 2008 John Wiley & Sons, Ltd. [source] Local matrix metalloproteinase 2 gene knockdown in balloon-injured rabbit carotid arteries using nonviral-small interfering RNA transfectionTHE JOURNAL OF GENE MEDICINE, Issue 1 2009Hanna Hlawaty Abstract Background Small interfering RNA (siRNA) delivery is a promising approach for the treatment of cardiovascular diseases. Matrix metalloproteinase (MMP) 2 over-expression in the arterial wall has been implicated in restenosis after percutaneous coronary intervention, as well as in spontaneous atherosclerotic plaque rupture. We hypothesized that in vivo local delivery of siRNA targeted at MMP2 (MMP2-siRNA) in the balloon-injured carotid artery of hypercholesterolemic rabbits may lead to inhibition of MMP2 expression. Methods Two weeks after balloon injury, 5 µmol/l of Tamra-tagged MMP2-siRNA, scramble siRNA or saline was locally injected in the carotid artery and incubated for 1 h. Results Fluorescent microscopy studies showed the circumferential uptake of siRNA in the superficial layers of neointimal cells. MMP2 mRNA levels, measured by the real-time reverse transcriptase-polymerase chain reaction, was decreased by 79 ± 25% in MMP2-siRNA- versus scramble siRNA-transfected arteries (p < 0.05). MMP2 activity, measured by gelatin zymography performed on the conditioned media of MMP2-siRNA versus scramble siRNA transfected arteries, decreased by 53 ± 29%, 50 ± 24% and 46 ± 14% at 24, 48 and 72 h, respectively (p < 0.005 for all). No effect was observed on MMP9, pro-MMP9 and TIMP-2 levels. Conclusions The results obtained in the present study suggest that significant inhibition of gene expression can be achieved with local delivery of siRNA in the arterial wall in vivo. Copyright © 2008 John Wiley & Sons, Ltd. [source] The pathophysiology of peri-operative myocardial infarctionANAESTHESIA, Issue 7 2010B. M. Biccard Summary It is generally believed that plaque rupture and myocardial oxygen supply-demand imbalance contribute approximately equally to the burden of peri-operative myocardial infarction. This review critically analyses data of post-mortem, pre-operative coronary angiography, troponin surveillance, other pre-operative non-invasive investigations, and peri-operative haemodynamic predictors of myocardial ischaemia and/or myocardial infarction. The current evidence suggests that myocardial oxygen supply-demand imbalance predominates in the early postoperative period. It is likely that flow stagnation and thrombus formation is an important pathway in the development of a peri-operative myocardial infarction, in addition to the more commonly recognised role of peri-operative tachycardia. Research and therapeutic interventions should be focused on the prediction and therapy of flow stagnation and thrombus formation. Plaque rupture appears to be a more random event, distributed over the entire peri-operative admission. [source] Differences in the detection of cyclo-oxygenase 1 and 2 proteins in symptomatic and asymptomatic carotid plaquesBRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 7 2001S. M. Wijeyaratne Background: The expression of cyclo-oxygenase (COX) 1 and 2 has been demonstrated in atherosclerotic arteries. In the present study this was correlated with symptoms arising from a carotid plaque. Methods: Carotid plaques from 12 asymptomatic patients were compared with 11 plaques from patients who had had neurological symptoms within the preceding 30 days. Sections were stained with haematoxylin and eosin, elastin van Gieson and goat antihuman antibodies to COX-1 and COX-2. Plaque morphology was correlated with neurological symptoms. The area with positive COX-1 and COX-2 staining was measured by computerized planimetry in entire cross-sections and in specific areas of the plaque. Results: There was a significant association between cap thinning and plaque rupture with symptoms (P = 0·003). The percentage area of positive staining in entire cross-sections for both COX-1 and COX-2 was significantly greater in symptomatic plaques (P = 0·001 and 0·0004 respectively). Staining in symptomatic plaques was significantly greater in the cap (COX-1: P = 0·001; COX-2: P = 0·0001) and shoulder (COX-1: P = 0·008; COX-2: P = 0·007) regions of the plaque. COX-1 expression in the sclerotic area was not increased (P = 0·15) although COX-2 staining was significantly greater (P = 0·04). Conclusion: Both COX-1 and COX-2 detection was increased in symptomatic plaques. COX may contribute to plaque rupture and the onset of symptoms. © 2001 British Journal of Surgery Society Ltd [source] DETECTION OF PERIVASCULAR BLOOD FLOW IN VIVO BY CONTRAST-ENHANCED INTRACORONARY ULTRASONOGRAPHY AND IMAGE ANALYSIS: AN ANIMAL STUDYCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 12 2007Manolis Vavuranakis SUMMARY 1Acute coronary syndromes are mostly the result of coronary plaque rupture. Diagnostic techniques focusing on the early detection of those plaques that are prone to rupture are still limited. Increased neovascularization in the adventitia and within the atherosclerotic plaque have recently been identified as common features of inflammation and plaque vulnerability. Contrast-enhanced intravascular imaging with microbubbles can be used to trace perfusion. 2In the present study, we examined the perivascular network of the left anterior descending coronary arteries and left circumflex arteries of four domestic, clinically healthy pigs using intracoronary ultrasound after injection of microbubbles with a differential imaging technique (ACESÔ; Computational Biomedicine Laboratory, University of Houston, Houston, TX, USA). Our aim was to detect blood flow into the coronary lumen and perivascular flow in contrast-enhanced images. Eleven regions of interest (ROI), including perivascular structures, were compared with regard to their grey scale level before and after the injection of SonoVue® (0.06 mL/kg; Bracco Diagnostics, Princeton, NJ, USA). 3A statistically significant (P = 0.018) enhancement was found in the echogenicity of the total perivascular space (adventitial region and perivascular vessels), as indicated by an increase in grey level intensity from 8.33 ± 0.80 (before) to 10.11 ± 0.88 (after microbubble injection). A significant enhancement of the 11 selected ROI (perivascular structures) was also recorded after the injection of microbubbles (from 7.92 ± 2.14 to 14.03 ± 2.44; P = 0.008). 4We believe that the detection of perivascular structures with contrast-enhanced intracoronary ultrasonography combined with proper image processing may reinforce our future efforts in the detection of vasa vasorum, an active participant in the creation of acute coronary events. [source] | |||||||||||||||||||||||||