Complicated Plaques Research Articles

Acute myocardial infarction and allergy, causal or casual relationship?

A 53-year-old man with a known allergy to metamizole presented for acute gonalgia, receiving metamizole by mistake. He suffers a severe allergy reaction accompanied by chest pain and signs of acute lower myocardial infarction, which subsides with treatment of anaphylactic shock and fibrinolysis, without observing intracoronary thrombus or signs of complication of atherosclerotic plaque. Keywords: Kounis syndrome; Allergic myocardial infarction; Myocardial infarction with normal coronary arteries.

Carotid endarterectomy and carotid artery stenting in advanced age patients

The manuscript is devoted to world experience of carotid endarterectomy and carotid artery stenting in advanced age patients. Some authors report the advantages of endovascular surgery in elderly patients while the others prefer carotid endarterectomy. Senile patients (75-80 years old) with asymptomatic internal carotid artery stenosis is one of the most difficult group for the management. This is due to a more complex assessment of perioperative surgical risk, high incidence of complicated atherosclerotic plaques in carotid arteries and dubious benefits of surgery considering short life expectancy and severe comorbidities. Accumulation of experience in the management of advanced age patients should be valuable for either optimizing or individualizing surgical strategy.

The effect of TEE on treatment change in patients with acute ischemic stroke.

Background and purposeIschemic stroke is a widespread disease carrying high morbidity and mortality. Transesophageal echocardiography (TEE) is considered an important tool in the work-up of patients with acute ischemic stroke (AIS) and transient ischemic attack (TIA) patients; its utility is limited by a semi-invasive nature. The purpose of this study was to evaluate the probability of treatment change due to TEE findings (yield) in the work-up of AIS and TIA patients.MethodsRetrospective data on patients with AIS or TIA who underwent TEE examination between 2000–2013 were collected from the institutional registry.ResultsThe average age of 1284 patients who were included in the study was 57±10.4, 66% of patients were male. The most frequent TEE findings included aortic plaques in 54% and patent foramen ovale (PFO) in 15%. TEE findings led to treatment change in 135 (10.5%) patients; anticoagulant treatment was initiated in 110 of them (81%). Most common etiology for switch to anticoagulation was aortic plaques (71 patients); PFO was second most common reason (26 patients). Significant TEE findings (thrombus, endocarditis, tumor) were found in 1.9% of patients, they were more common in young patients (<55; 56% of the patients).ConclusionsThe beginning of anticoagulation treatment in patients with thick and complicated plaques was found frequently in our study. Significant TEE findings, were infrequent, constituted an absolute indication for treatment change and were more common in younger patients.

Complicated Carotid Artery Plaques as a Cause of Cryptogenic Stroke

BackgroundThe underlying etiology of ischemic stroke remains unknown in up to 30% of patients. ObjectivesThis study explored the causal role of complicated (American Heart Association−lesion type VI) nonstenosing carotid artery plaques (CAPs) in cryptogenic stroke (CS). MethodsCAPIAS (Carotid Plaque Imaging in Acute Stroke) is an observational multicenter study that prospectively recruited patients aged older than 49 years with acute ischemic stroke that was restricted to the territory of a single carotid artery on brain magnetic resonance imaging (MRI) and unilateral or bilateral CAP (≥2 mm, NASCET [North American Symptomatic Carotid Endarterectomy Trial] <70%). CAP characteristics were determined qualitatively and quantitatively by high-resolution, contrast-enhanced carotid MRI at 3T using dedicated surface coils. The pre-specified study hypotheses were that that the prevalence of complicated CAP would be higher ipsilateral to the infarct than contralateral to the infarct in CS and higher in CS compared with patients with cardioembolic or small vessel stroke (CES/SVS) as a combined reference group. Patients with large artery stroke (LAS) and NASCET 50% to 69% stenosis served as an additional comparison group. ResultsAmong 234 recruited patients, 196 had either CS (n = 104), CES/SVS (n = 79), or LAS (n = 19) and complete carotid MRI data. The prevalence of complicated CAP in patients with CS was significantly higher ipsilateral (31%) to the infarct compared with contralateral to the infarct (12%; p = 0.0005). Moreover, the prevalence of ipsilateral complicated CAP was significantly higher in CS (31%) compared with CES/SVS (15%; p = 0.02) and lower in CS compared with LAS (68%; p = 0.003). Lipid-rich and/or necrotic cores in ipsilateral CAP were significantly larger in CS compared with CES/SVS (p < 0.05). ConclusionsThese findings substantiate the role of complicated nonstenosing CAP as an under-recognized cause of stroke. (Carotid Plaque Imaging in Acute Stroke [CAPIAS]; NCT01284933)

Ischemic Heart Disease Pathophysiology Paradigms Overview: From Plaque Activation to Microvascular Dysfunction.

Ischemic heart disease still represents a large burden on individuals and health care resources worldwide. By conventions, it is equated with atherosclerotic plaque due to flow-limiting obstruction in large–medium sized coronary arteries. However, clinical, angiographic and autoptic findings suggest a multifaceted pathophysiology for ischemic heart disease and just some cases are caused by severe or complicated atherosclerotic plaques. Currently there is no well-defined assessment of ischemic heart disease pathophysiology that satisfies all the observations and sometimes the underlying mechanism to everyday ischemic heart disease ward cases is misleading. In order to better examine this complicated disease and to provide future perspectives, it is important to know and analyze the pathophysiological mechanisms that underline it, because ischemic heart disease is not always determined by atherosclerotic plaque complication. Therefore, in order to have a more complete comprehension of ischemic heart disease we propose an overview of the available pathophysiological paradigms, from plaque activation to microvascular dysfunction.

Isolation of Prunin FromBauhinia variegataand Its Antioxidant Activity in Rats Fed an Atherogenic Diet

Atherosclerosis is no longer a disease attributed mainly to high cholesterol content in the body; it has come to be regarded as a chronic inflammatory disease with an autoimmune component. The purpose of this study was to investigate the effect of the prunin fraction (PF) isolated from the ethanolic extract of Bauhinia variegata against the release of various proinflammatory mediators in rats fed an atherogenic diet. The diet was administered orally to Sprague Dawley rats for 60 days to induce atherosclerosis. The blood serum of the rats was used to estimate the levels of tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), thiobarbituric acid reactive substance, catalase, total cholesterol, triglyceride, low-density lipoprotein, and high-density lipoprotein using assay kits. Other physical parameters, such as body weight, feed intake, and systolic blood pressure, were also determined during the study. The results showed a significant protective effect of the PF against diet-induced atherosclerosis by decreasing the levels of proinflammatory mediators such as TNF-α and IL-6. Rats treated with PF (20 and 40 mg/kg) showed a change in systolic blood pressure and a reduction in oxidative stress induced by the atherogenic diet. Reduction in body weight and modulation of food intake were observed in PF-treated rats, which indicated atheroprotective, hypolipidemic, and antioxidant effects. The study concludes that the atheroprotective properties of PF are due to effects on the initial phase of plaque formation to thrombus formation. This study may help researchers to find a better alternative for selecting optimal therapies and preventing plaque formation. Future Significance: This article focuses on the molecular mechanisms involved in the evolution of atherosclerotic plaques and different targets that act at the starting stage of the plaque to thrombus formation. This may pave the way for selecting optimal therapies and preventing plaque complications.

Atherosclerosis and carcinoma: Two facets of dysfunctional cholesterol homeostasis.

Althoughcholesterol is an essential and necessarycomponent for biological systems; inappropriate accumulation of cholesterol in blood vessels and intracellular territory is also detrimental to living things. On one hand, cholesterol is the acting precursor of many metabolic regulators, a component of the structural veracity and scaffold fluidity of biomembranes, an insulator of electrical transmission in nerves and many more; on the other hand, its deposition in blood vessels induces atherosclerotic plaque and cardiovascular complications with the consequences of heart attack and stroke. It is also an emerging fact that cholesterol is a prelate in the cell nucleus for cell proliferation and any oddity in this venture may be the cause of tumorigenesis. Hence, cholesterol homeostasis is a very crucial element in issues of health management. Cholesterol is now a global target for maintaining quality health, particularly to control the two giants of the present world health tragedy: atherosclerosis and carcinoma, which appearto be the two facets of dysfunctional cholesterol homeostasis.

Angioplasty and carotid artery stenting: clinical and morphological factors affecting long-term outcomes

Aim. To identify clinical and morphological factors affecting the longterm outcomes of endovascular angioplasty and carotid artery stenting.Material and methods. The analysis included 198 patients after carotid artery stenting between 03.2014 and 05.2018. There were following inclusion criteria: (1) 50% of symptomatic or 70% of asymptomatic carotid artery stenosis of according to NASCET (North American Symptomatic Carotid Endarterectomy Trial) criteria; (2) follow-up for each patient for at least 1 year. Using the univariate and multivariate logistic regression, risk factors associated with adverse events were determined.Results. The incidence of major adverse events during the 12-month follow-up was 9,6% (n=19), including 4 (2%) major and 6 (3%) minor strokes, 7 (3,5%) cases of transient ischemic attack; one (0,5%) patient had transient blindness and one (0,5%) died in the long-term follow-up period due to acute cerebrovascular accident in the target arterial territory. Also, 11 (5,6%) patients had restenosis &gt;50% after 12-month follow-up. Multivariate analysis showed that long-term outcomes were significantly affected by: age &gt;70 years (odds ratio (OR)=1,27, 95% confidence interval (CI): 1,07-1,61 (p=0,01); using of open-cell stents (OR=1,02, 95% CI: 1,01-1,03 (p=0,034)); contralateral stenosis (OR=1,28, 95% CI: 1,05-1,57 (p=0,01); lesion length &gt;15 mm (OR=1,46, 95% CI: 1,12-1,89 (p=0,01)); residual stenosis &lt;30% (OR=1,38, 95% CI: 1,09-1,49 (p=0,012)); complicated atherosclerotic plaque (OR=1,78, 95% CI: 1,21- 2,34 (p=0,007)). The development of in-stent restenosis was significantly influenced by factors such as the residual stenosis &gt;&lt;30% (OR=1,26, 95% CI: 1,1-1,65; p=0,017) and severe plaque calcification (OR=1,24, 95% CI: 1,04-1,31; p=0,02). Conclusion. The results obtained indicate the need for more careful preparation for endovascular intervention. Such factors as the use of open-cell stents, contralateral stenosis, lesion length &gt;&lt; 30% (OR=1,38, 95% CI: 1,09-1,49 (p=0,012)); complicated atherosclerotic plaque (OR=1,78, 95% CI: 1,21- 2,34 (p=0,007)). The development of in-stent restenosis was significantly influenced by factors such as the residual stenosis &lt;30% (OR=1,26, 95% CI: 1,1-1,65; p=0,017) and severe plaque calcification (OR=1,24, 95% CI: 1,04-1,31; p=0,02).Conclusion. The results obtained indicate the need for more careful preparation for endovascular intervention. Such factors as the use of open-cell stents, contralateral stenosis, lesion length &gt;15 mm, and residual stenosis &lt; 30% may be associated with an increased risk of adverse events.

Detection of cholesterol crystals by optical coherence tomography.

The aim of this study was to determine the ability of optical frequency domain imaging (OFDI)/optical coherence tomography (OCT) imaging systems to visualise the presence of cholesterol crystals (CCR) in human atherosclerotic coronary arteries. We performed ex vivo imaging of human coronary arteries by OFDI/OCT. A total of 559 cross-sectional images from 45 autopsy cases were co-registered with histology; 117 histologic sections showed presence of necrotic core with cholesterol clefts (CC). We modified a previously used OFDI/OCT definition for identification of CCRs which we now define as a linear and discrete high-intensity signal (bright area) within the plaque with sharp borders between it and adjacent low-/intermediate-intensity tissue. Additionally, the high-intensity signal is not a spot but a well-defined area distinguishing it from macrophages which lack sharp borders. OFDI/OCT imaging identified the presence of CCR in 30 of the 117 histologic sections. The sensitivity and specificity of OFDI/OCT for detection of CCR was 25.6% and 100.0%, respectively. By multivariate analysis, significant predictors to visualise CCR by OCT/OFDI were 1) an overlying fibrous plaque, and 2) the presence of stacked CC, defined as CC arranged one on top of another with >3 layers of CC. The prevalence of complicated plaques (i.e., plaque haemorrhage and late necrotic core) was significantly higher in detectable CCR by OFDI/OCT as compared to undetectable CCR. The presence of stacked CCs is required to detect CCR by OFDI/OCT. Detection of CCR by OCT/OFDI may help us to identify the late stages of atherosclerotic coronary plaque progression and improve risk stratification.

Coronary inflammation: why searching, how to identify and treat it.

Inflammation plays an important role in the development of atherosclerotic lesions. A variety of stimuli promote atherosclerosis, including increased LDL cholesterol in blood, exposure to tobacco, diabetes mellitus, hypertension, or rheological stress. Inflammatory cells have an established role in the growth of atherosclerotic lesions. Macrophages recognize and internalise ox-LDL to eventually become lipid-laden foam cells, the hallmark cellular component of atheroma. Infiltrating CD4-T cells have a role too, by interacting with ox-LDL and other antigens. Cytokines secreted by inflammatory cells stimulate smooth muscle cells migration whilst macrophages produce metalloprotease that lead to fibrous cap rupture. The necrotic debris of died macrophages and smooth muscle cells help to continue the inflammatory process. The inflammatory response can also directly activate platelets and promote thrombus formation at the surface of complicated coronary plaques. The CANTOS trial can be waived as an innovative study promoting a novel approach of personalized medicine. In patients with previous myocardial infarction, high-sensitivity C-reactive protein level of 2 mg and normal LDL level (<70 mg/dL), canakinumab a therapeutic monoclonal antibody targeting interleukin-1β, at a dose of 150 mg every 3 months, led to a significant reduction of the primary efficacy end point: nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death at 48 months. Based on the CANTOS results, patients on statins and residual inflammatory risk as assessed by means of a high-sensitivity CRP >2 mg/l at baseline have a high risk of future cardiac events, comparable to that of statin-treated patients with suboptimal cholesterol LDL level. The inhibition of interleukin-1β by means of canakinumab, which is only one of many potential anti-inflammatory pathways, open new perspectives, showing that a selective inhibition of the inflammatory pathway may be beneficial in reducing cardiovascular risk. In a process of personalized medicine, there is need to accurately identify patients at high risk of events, to be treated with potent statins or anti-inflammatory drugs. Perhaps in the near future a more specific assessment of coronary inflammations, possibly obtained with imaging modalities (either invasive or non-invasive), will better select patients at risk of events. In this scenario, in the setting of secondary prevention, OCT may serve the scope of identifying vulnerable plaques with local aggregates of inflammatory cells. Future studies are needed to understand the clinical effectiveness of strategies based on invasive coronary assessment.

Optical Coherence Tomography for In Vivo Identification, Characterization and Optimal Treatment of Spontaneous Recanalization of Coronary Thrombus.

Spontaneous recanalization of coronary thrombus (SRCT) is a rare in vivo appearance, with a nonspecific angiographic aspect. The aim of this study was to investigate the importance of optical coherence tomography (OCT) use for SRCT identification, characterization of pathogenic mechanisms and optimal treatment. We retrospectively analyzed all patients with angiographic suspicion of SRCT who underwent coronary angiography for suspected coronary artery disease and afterward investigated by OCT imaging. We identified 28 cases with angiographic suspicion of SCRT (0.41% of CA) and confirmed it in 4 patients (0.05% of CA). OCT provided insight about the underlying SRCT mechanism: possible complicated atherosclerotic plaques in two cases and, respectively, spontaneous coronary artery dissection in other two cases. OCT provided accurate lesion assessment and offered optimal PCI materials selection. Besides providing the diagnosis, OCT also improved characterization of SRCT pathogenic mechanisms, in the four confirmed SRCT cases, supporting the role of coronary wall in situ complications, namely dissection of an atherosclerotic plaque or spontaneous dissection of a normal coronary wall.

A hidden aortic rupture heralded by recurrent brain and retinal embolism

Central MessageAn unrecognized contained aortic rupture may be responsible for repeated embolism and may be detected by means of transthoracic, transesophageal 2-dimensional echocardiography and computed tomography.See Commentary on page 17. An unrecognized contained aortic rupture may be responsible for repeated embolism and may be detected by means of transthoracic, transesophageal 2-dimensional echocardiography and computed tomography. See Commentary on page 17. Atherosclerotic changes in the aortic wall of major arterial vessels represent an important risk factor of systemic embolism. Necropsy studies have demonstrated that complicated aortic plaques are variably associated with ischemic cerebral lesion that may be clinically silent.1Khatibzadeh M. Mitusch R. Stierle U. Gromoll B. Sheikhzadeh A. Aortic atherosclerotic, plaques as a source of systemic embolism.J Am Coll Cardiol. 1996; 27: 664-669Crossref PubMed Scopus (129) Google Scholar In the patient described here, the source of systemic embolism was identified in a previously undiagnosed calcific pseudoaneurysm of the noncoronary sinus. A 65-year-old man experienced recurrent strokes with areas of brain and retinal ischemia (Figure 1, A and B). After hospitalization, continuous monitoring excluded episodes of atrial fibrillation. Transthoracic and transesophageal 2-dimensional echocardiography (Figure 1, C) showed moderate aortic regurgitation and the presence of a 7 × 5 cm saccular aneurysm of the noncoronary sinus that was confirmed by a computed tomography, which also showed gross calcification of the wall (Figure 1, D). At surgery, firm adhesions between the aortic root and the right atrium raised the suspicion of a pseudoaneurysm due to undiagnosed contained rupture (Figure 1, E); fragile calcific deposits (Figure 1, F) were considered the source of embolization. Repair of the pseudoaneurysm was obtained by replacement of the noncoronary sinus using a polyethylene terephthalate patch. The patient recovered uneventfully with no further embolic episodes at 3-month follow-up.

Emerging Roles of Lysyl Oxidases in the Cardiovascular System: New Concepts and Therapeutic Challenges.

Lysyl oxidases (LOX and LOX-likes (LOXLs) isoenzymes) belong to a family of copper-dependent enzymes classically involved in the covalent cross-linking of collagen and elastin, a pivotal process that ensures extracellular matrix (ECM) stability and provides the tensile and elastic characteristics of connective tissues. Besides this structural role, in the last years, novel biological properties have been attributed to these enzymes, which can critically influence cardiovascular function. LOX and LOXLs control cell proliferation, migration, adhesion, differentiation, oxidative stress, and transcriptional regulation and, thereby, their dysregulation has been linked to a myriad of cardiovascular pathologies. Lysyl oxidase could modulate virtually all stages of the atherosclerotic process, from endothelial dysfunction and plaque progression to calcification and rupture of advanced and complicated plaques, and contributes to vascular stiffness in hypertension. The alteration of LOX/LOXLs expression underlies the development of other vascular pathologies characterized by a destructive remodeling of the ECM, such as aneurysm and artery dissections, and contributes to the adverse myocardial remodeling and dysfunction in hypertension, myocardial infarction, and obesity. This review examines the most recent advances in the study of LOX and LOXLs biology and their pathophysiological role in cardiovascular diseases with special emphasis on their potential as therapeutic targets.

Periodontal and prosthetic outcomes on teeth prepared with biologically oriented preparation technique: a 4-year follow-up prospective clinical study

PurposeTo evaluate the clinicaland biological behavior of full coverage restorations on teeth prepared without finish line during a 4-year follow-up. MethodsThis prospective study included 149 teeth treated using biologically oriented preparation technique (BOPT). The sample (149 teeth) was divided into two groups: Seventy four teeth restored with crowns, and 75 teeth supporting fixed partial dentures (FPD). Restorations were fabricated with zirconium oxide cores and ceramic coverings. Patients attended regular annual check-ups when probe depth, presence of inflammation with bleeding on probing, presence of plaque, gingival thickness, marginal stability, biological or mechanical complications, and the patient’s level of satisfaction were registered over a 4-year follow-up. ResultsAfter the 4-year follow-up, 2.1% of teeth underwent increases in probing depth; 12% of the sample presented inflammation and bleeding on probing; 20% of the restored teeth presented plaque; gingival thickening increased a 32.5%; 98.6% of teeth presented marginal stability; the restoration survival rate was 96.6%, with 2% of biological complications and 1.4% of mechanical complications. General satisfaction score was 80.73. ConclusionsRestorations placed on teeth prepared using BOPT present good periodontal behavior, increase of gingival thickening, and marginal stability over a 4-year follow-up. High survival rates after 4 years show that the technique produces predictable outcomes. Clinical significanceThe BOPT technique is a good treatment option in cases where replacement of an old restoration is required; presenting good periodontal behavior, gingival thickening, and marginal stability.

Inflammation: a common contributor to cancer, aging, and cardiovascular diseases-expanding the concept of cardio-oncology.

Inflammation participates in the pathogenesis of both cancer and cardiovascular disease. This review examines the mechanistic commonalities between these two scourges of humanity through the lens of inflammation biology. Inflammatory pathways contribute to the initiation, the progression, and the complication of both malignant tumours and atherosclerotic plaques. Modulation of inflammatory pathways have proven transformative in the treatment of cancers and have crossed the threshold of clinical reality as treatments to reduce the risk of cardiovascular events. The finding that clonal haematopoiesis drives both leukaemia and cardiovascular events provides yet another link between these two seemingly disparate diseases. The nascent specialty of cardio-oncology has initially focused on the cardiovascular complications of cancer therapies. The recognition of a more profound pathophysiologic connection between cancer and cardiovascular diseases should expand the concept of cardio-oncology. Embracing the mechanistic connection and transcending traditional barriers between disciplines offers immense opportunities for speeding innovative research that can address the growing burden of both cancer and cardiovascular disease.

Circulating IL-10 Levels in Carotid Artery Disease

Abstract Carotid atherosclerosis may be associated with neurosymptoms including cerebral infarction. IL-10 exerts atheroprotective effects, but its role in carotid disease is not fully defined. We aimed to investigate serum IL-10 levels in patients undergoing endarterectomy and their relation to the degree of carotid stenosis, plaque types and neurosymptoms. Two hundred consecutive patients with atherosclerotic carotid stenosis and 29 healthy controls were enrolled in this study. Plaque types were classified according to AHA criteria. Serum IL-10 levels were determined by ELISA. Patients undergoing endarterectomy had significantly higher circulating IL-10 levels (18.7 ± 3.2 pg/ml) in comparison with healthy controls (7.2 ± 1.8pg/ml; P =0.0001) and IL- 10 has good discriminatory efficacy between these two groups (ROC curve, AUC = 0.723, P=0.0001). Patients with &lt; 70% and those with &gt; 70% of carotid stenosis did not differ in terms of age, sex, cardiovascular risk factors except hypertension, neurosymptoms and AHA plaque types. Circulating IL-10 levels differed significantly among patients with different carotid plaque types (P = 0.002). Patients with uncomplicated plaques had significantly higher serum levels of IL-10 (23.0 ± 6.1 pg/ml) compared to those with complicated plaques (13.0 ±1.4 pg/ml, P=0.035) and IL-10 can differentiate patients between these two groups (ROC curve, AUC = 0.413, P= 0.035). Our findings reveal an important role for IL-10 in carotid atherosclerosis. IL-10 might be a potential biomarker in discriminating patients with carotid disease from healthy controls. Decreased serum levels of IL-10 are related to complicated carotid plaques.

Abstract WMP39: Laser Angioscopy in Carotid Artery Disease: Imaging Findings and Histopathological Correlation

Our understanding and management of carotid artery disease has largely relied on angiography, US and MR. However, existing modalities cannot accurately identify the spectrum of thrombogenic lesions on the vascular surface or reliably detect structural markers of instability. Thus, the natural history of the different histopathological hallmarks of advanced or complicated plaques is unknown, and many patients with culprit substenotic plaques are misdiagnosed with cryptogenic stroke. An intraluminal approach to directly inspect the endovascular surfaces at unprecedented resolutions would enable detailed structural analysis of carotid plaques and the identification of the root cause of carotid-related strokes. A scanning fiber angioscope (SFA), a high-definition 1.2-mm forward-viewing camera that generates videos by spirally scanning low-power laser beams, was developed for clinical use and employed to analyze the endovascular surfaces of ex vivo human carotid arteries (n=95) and endarterectomized plaques (n=20). Specimens were then imaged with US and micro-CT, and all vascular diagnostic tests obtained in the patients undergoing carotid revascularization were accessed. Imaging findings in the vascular surfaces were then validated by histomorphological analysis of &gt;300 lesions, and an angioscopic classifier for atherosclerosis was generated. Full-color videos at 30Hz and at a resolution &gt;200,000 pixels were generated from the entire endovascular circumference in all specimens with depth-of-focus larger than 5cm in saline solution. The ability to analyze the surface anatomy with unparalleled detail allowed the identification of early, intermediate, advanced and complex atherosclerotic lesions, including ulceration of fibrotic cap, excavation of the necrotic core leading to pseudolumens, intimal flaps, exposed necrotic core to the lumen, erosions, recent and remote intimal hemorrhages, luminal thrombus, eruptive calcified nodules and calcified intimal sheaths and plates. SFA offers a direct view of the endoluminal surfaces with unparalleled resolution and has the potential to revolutionize research, diagnosis, prognosis and image-guided therapy in carotid atherosclerosis.

Abstract TP256: DWI Positive Cerebral Lesion is the Risk of Ischemic Stroke in Retinal Ischemic Patients

Background: Retinal ischemia might be mainly caused by carotid stenosis and warning sign for ischemic stroke. Retinal ischemia is rare condition, therefore it is uncertain what lead to ischemic stroke in retinal-ischemic-patient. Methods: We retrospectively identified 128 patients who diagnosed retinal ischemia at 3 hospitals using each hospital stroke database collected from April 1st 2004 to Jun 30th 2016. We extracted data as patient sex, age, comorbidities and checked medical record for detecting recurrent of ischemic stroke and retinal ischemia. Logistic regression analysis was performed to analyze the effect of various factors on the recurrent of ischemic stroke. Results: The mean age of the patients at admission was 69 years old, and 93 patients (73%) was men. Seventy nine patients were diagnosed amaurosis fugax and 49 were retinal embolism. More than one visual defect attack had seen in 25 patients. One hundred twenty three patients were done cerebral MRI and DWI positive ischemic lesion was revealed in 12patients.Carotid stenosis were detected in 38 patients, patent foramen ovale were 40 patients, atrial fibrillation were 8 patients, complicated aortic plaque were 36 patients, and cancer were 25 patients. Mean follow-up period was 645 days and 6 patients had ischemic stroke, 4 had retinal ischemia and 18 underwent surgical intervention (carotid endarterectomy 12, carotid stenting 4, extracranial to intracranial bypass 2). Multivariable analysis found that the prevalence of ischemic stroke was significantly increased in DWI positive (odds ratio 10.9, confidence interval 1.7-69.6), under treatment cancer (10.0, 1.2-85.0), more than one visual attack (2.8, 1.1-7.3). Conclusion: DWI positive ischemic lesion on cerebral MRI was risk factor for ischemic stroke in retinal ischemic patients. We should consider to do MRI on retinal ischemic patients.

Influence of the root plaque formation with different species on oxytetracycline accumulation in rice (Oryza sativa L.) and its elimination in culture solution

Hydroponic experiments were conducted to investigate the role of different root plaque formation on oxytetracycline (OTC) uptake/translocation by rice seedlings (Oryza sativa L.) and solution-OTC elimination at two initial OTC concentrations (10 and 30mgL-1). The results indicated OTC accumulation in rice was always in the order root surface > shoot > inside root whether plaques were formed or not. It demonstrated that Fe-Mn-Mt (montmorillonite) treatment was easier to promote significantly (p< 0.05) OTC accumulation in the underground part (root surface and inside root) and decrease significantly (p< 0.05) OTC translocation from the root to the shoot in rice compared to no plaque treatments (CK), especially for OTC 30mgL-1 level with the lowest shoot-OTC accumulation in Fe-Mn-Mt treatment. Plaque treatments increased half-life of solution-OTC elimination in the order Fe-Mn-Mt > Fe-Mn > Fe > CK, which was caused mainly by OTC degradation from Fe2+-binding influence in solution, not by the enhancement of OTC accumulation on the root surface and inside root. And solution-OTC elimination increased with decreasing initial OTC concentrations, the drop of Fe2+ and the increment of Fe3+ and pH during the experiment. These findings are useful for reducing OTC accumulation and translocation in rice aboveground parts and eliminating OTC contamination in agricultural environment simultaneously through complicated plaque formation under higher OTC concentration exposure (30mgL-1) in the future design.

111In-DANBIRT In Vivo Molecular Imaging of Inflammatory Cells in Atherosclerosis.

Atherosclerosis-related morbidity and mortality remain a global concern. Atherosclerotic disease follows a slow and silent progression, and the transition from early-stage lesions to vulnerable plaques remains difficult to diagnose. Inflammation is a key component of the development of atherosclerotic plaque and consequent life-threatening complications. This study assessed 111In-DANBIRT as an in vivo, noninvasive SPECT/CT imaging probe targeting an inflammatory marker, Lymphocyte Function Associated Antigen-1 (LFA-1), in atherosclerotic plaques. Methods. Selective binding of 111In-DANBIRT was assessed using Sprague-Dawley rats exposed to filtered air and ozone (1 ppm) by inhalation for 4 hours to induce a circulating leukocytosis and neutrophilia in peripheral blood. After 24 hours, whole blood was collected and incubated with radiolabeled DANBIRT (68Ga-DANBIRT and 111In-DANBIRT). Isolated cell component smeared slides using cytospin technique were stained with Wright-Giemsa stain. Apolipoprotein E-deficient (apoE−/−) mice were fed either a normal diet or a high-fat diet (HFD) for 8 weeks. Longitudinal SPECT/CT imaging was performed 3 hours after administration at baseline, 4, and 8 weeks of HFD diet, followed by tissue harvesting for biodistribution, serum lipid analysis, and histology. 3D autoradiography was performed in both groups 24 hours after administration of 111In-DANBIRT. Results. Increased specific uptake of radiolabeled DANBIRT by neutrophils in the ozone-exposed group was evidenced by the acute immune response due to 4-hour ozone exposure. Molecular imaging performed at 3 hours using SPECT/CT imaging evidenced an exponential longitudinal increase in 111In-DANBIRT uptake in atherosclerosis lesions in HFD-fed mice compared to normal-diet-fed mice. Such results were consistent with increased immune response to vascular injury in cardiovascular and also immune tissues, correlated by 24 hours after administration of 3D autoradiography. Histologic analysis confirmed atherosclerotic disease progression with an increased vascular lesion area in HFD-fed mice compared to normal-diet-fed mice. Conclusion. 111In-DANBIRT is a promising molecular imaging probe to assess inflammation in evolving atheroma and atherosclerotic plaque.