Plaque Morphology Research Articles

Revascularization methods in patients with carotid stenosis and concomitant coronary heart disease

A major feature of the atherosclerotic process is its systemic and progressive character. The plaque pathogenetic mechanisms, morphology, evolution, and predilection site (bifurcation zones) determine the frequent coincidence of carotid and coronary atherosclerosis in the same patient.The present overview chronologically traces the history, effectiveness, and benefit of surgical and continuously improving interventional carotid revascularization. It thereby analyzes the indications, results, and complications based on a number of randomized clinical trials, industry-sponsored registries, and large single-center series in the last 3 decades. Carotid endarterectomy (CEA) and percutaneous carotid angioplasty (CAS) have evolved from 'dubious' procedures to a modern strategy resulting in a significantly lower incidence of stroke and death compared to medical treatment only. Although almost every second patient with carotid stenosis and indications for CAS has coronary atherosclerosis, studies on therapeutic modeling in such a combination are few, showing controversial results. Having both CHD and CS doubles the risk of myocardial infarction, stroke, HF, and death. An isolated revascularization approach compromises the results of therapeutic strategies and worsens patient survival. The high risk associated with coronary heart disease in CAS and CEA is a fact and minimization requires both an individualized and uniform stepwise revascularization strategy.

On the nonlinear relationship between wall shear stress topology and multi-directionality in coronary atherosclerosis

Background and ObjectiveIn this paper we investigate twelve multi-directional/topological wall shear stress (WSS) derived metrics and their relationships with the formation of coronary plaques in both computational fluid dynamics (CFD) and dynamic fluid-structure interaction (FSI) frameworks. While low WSS is one of the most established biomechanical markers associated with coronary atherosclerosis progression, alone it is limited. Multi-directional and topological WSS derived metrics have been shown to be important in atherosclerosis related mechanotransduction and near-wall transport processes. However, the relationships between these twelve WSS metrics and the influence of both FSI simulations and coronary dynamics is understudied. MethodsWe first investigate the relationships between these twelve WSS derived metrics, stenosis percentage and lesion length through a parametric, transient CFD study. Secondly, we extend the parametric study to FSI, both with and without the addition of coronary dynamics, and assess their correlations. Finally, we present the case of a patient who underwent invasive coronary angiography and optical coherence tomography imaging at two time points 18 months apart. Associations between each of the twelve WSS derived metrics in CFD, static FSI and dynamic FSI simulations were assessed against areas of positive/negative vessel remodelling, and changes in plaque morphology. Results22–32% stenosis was the threshold beyond which adverse multi-directional/topological WSS results. Each metric produced a different relationship with changing stenoses and lesion length. Transient haemodynamics was impacted by coronary dynamics, with the topological shear variation index suppressed by up to 94%. These changes appear more critical at smaller stenosis levels, suggesting coronary dynamics could play a role in the earlier stages of atherosclerosis development. In the patient case, both dynamics and FSI vs CFD changes altered associations with measured changes in plaque morphology. An appendix of the linear fits between the various FSI- and CFD-based simulations is provided to assist in scaling CFD-based results to resemble the compliant walled characteristics of FSI more accurately. ConclusionsThese results highlight the potential for coronary dynamics to alter multi-directional/topological WSS metrics which could impact associations with changes in coronary atherosclerosis over time. These results warrant further investigation in a wider range of morphological settings and longitudinal cohort studies in the future.

Phenotypic and Genotypic Characterization of Newly Isolated Xanthomonas euvesicatoria-Specific Bacteriophages and Evaluation of Their Biocontrol Potential

Bacteriophages have greatly engaged the attention of scientists worldwide due to the continuously increasing resistance of phytopathogenic bacteria to commercially used chemical pesticides. However, the knowledge regarding phages is still very insufficient and must be continuously expanded. This paper presents the results of the isolation, characterization, and evaluation of the potential of 11 phage isolates as natural predators of a severe phytopathogenic bacterium-Xanthomonas euvesicatoria. Phages were isolated from the rhizosphere of tomato plants with symptoms of bacterial spot. The plaque morphology of all isolates was determined on a X. euvesicatoria lawn via a plaque assay. Three of the isolates were attributed to the family Myoviridae based on TEM micrographs. All phages showed good long-term viability when stored at 4 °C and -20 °C. Three of the phage isolates possessed high stability at very low pH values. Fifty-five-day persistence in a soil sample without the presence of the specific host and a lack of lytic activity on beneficial rhizosphere bacteria were found for the phage isolate BsXeu269p/3. The complete genome of the same isolate was sequenced and analyzed, and, for the first time in this paper, we report a circular representation of a linear but circularly permuted phage genome among known X. euvesicatoria phage genomes.

The possibility of visualizing TGF-β1 expression in ApoE-/- mice atherosclerosis using MR targeted imaging.

Endothelial TGF-β1 signaling is a primary driver of atherosclerosis-associated vascular inflammation. Targeted imaging and inhibition of the expression of TGF-β1 may reduce the atherosclerotic vessel wall inflammation and stop the progression of atherosclerotic plaque. To investigate the possibility of the anti-TGF-β1-ultrasmall superparamagnetic iron oxide (USPIO) specific probe as an imaging marker for the expression of TGF-β1 in ApoE-/- mice atherosclerosis detected with 7.0-T magnetic resonance imaging (MRI). Here, 70 ApoE-/- mice on a high-fat diet served as the experimental group and 30 C57BL/6 mice on a normal diet served as the control group. The morphology of plaques was viewed by H&E staining, and the expression and distribution of TNC and TGF-β1 were detected by immunohistochemical staining. Another 40 mice in the experimental group were classified into a targeted group, which was administrated an anti-TGF-β1-USPIO probe, and the pure group, which was injected with pure USPIO. The 7.0-T MRI showed that the relative signal intensity (rSI) changes of the targeted group decreased more than those of the pure group (-19.34 ± 0.68% vs. -5.61 ± 0.57%; P < 0.05). Histopathological analyses demonstrated expression of TGF-β1 in atherosclerotic plaque formation progression from 10 to 28 weeks. The MR images of the expression of TGF-β1 in atherosclerosis correlated well with the pathological progression of atherosclerotic plaque formation. Anti-TGF-β1-USPIO could provide a useful molecular imaging tool for detecting and monitoring the expression of TGF-β1 in atherosclerotic plaques by MRI.

Atherosclerotic carotid plaque characteristics vary with time from ischemic event: A multicenter, prospective magnetic resonance vessel wall imaging registry study

Recent studies report that the rate of recurrent stroke is highest in the stages immediately following cerebral infarction and decreases over time in patients with atherosclerotic carotid stenosis. The purpose of this study was to identify temporal differences in early stage carotid plaque components from acute cerebrovascular ischemic events using carotid MRI. Carotid plaque images were obtained on 3 T MRI from 128 patients enrolled in MR-CAS. Among the 128 subjects, 53 were symptomatic and 75 asymptomatic. The symptomatic patients were classified into three groups based on interval from onset of symptoms to the date of the carotid MRI (Group <14 days; 15-30 days; and > 30 days). The volume of each plaque component was identified and quantified from MR images. The presence of juxtaluminal loose matrix/inflammation (LM/I) was identified as a possible indicator of inflammation on the luminal side. Plaque components were compared between groups using the Wilcoxon rank-sum or the Chi-square test. Patient characteristics and carotid plaque morphology were similar among all four groups. The median volume of LM/I in Group >30 days was significantly lower than in other groups (0 mm3 vs 12.3 mm3 and 18.1 mm3; p = 0.003). In addition, the prevalence of juxtaluminal LM/I decreased over time (ptrend = 0.002). There were no statistically significant differences in other plaque components between the symptomatic groups. The volume of LM/I was significantly smaller in Group >30 days and prevalence of juxtaluminal LM/I in the atherosclerotic carotid plaque was high in the early stages after events. This suggests that carotid plaques undergo rapid evolution after an acute cerebrovascular ischemic event.

Abstract WMP84: Symptomatic Intracranial Atherosclerotic Plaques: Different Morphological Features In The Anterior Versus Posterior Circulation

Introduction: We compared the morphology of intracranial atherosclerotic plaques in the anterior versus posterior circulation, using three-dimensional rotational angiography (3DRA). Methods: We prospectively recruited adult patients with acute ischemic stroke or transient ischemic attack attributed to high-grade (60-99%), atherosclerotic intracranial stenosis as confirmed by 3DRA. We assessed the plaque morphology in 3DRA, including the percentage of luminal stenosis, smooth/irregular/ulcerative plaque surface contour, plaque thickness, length, eccentricity, upstream plaque shoulder angulation, longitudinal distribution of the maximal stenosis, and adjoining branch atheromatous disease (BAD). We compared characteristics of patients with middle cerebral artery-M1 (MCA-M1) and basilar artery (BA) plaques, and the plaque morphology in the two subgroups. Results: Overall, 164 and 17 patients respectively with MCA-M1 and BA plaques were analyzed, with similar age (medians 60 versus 62 years), sex (male 64.6 versus 52.9%) and history of common vascular risk factors. The percentage of luminal stenosis (medians 77 versus 81%), proportion of smooth/irregular/ulcerative plaque surface contour, upstream plaque shoulder angulation (32.1 versus 25.8 °), longitudinal distribution of the maximal stenosis, and presence of adjoining BAD (56.7 versus 64.7%) were similar between MCA-M1 and BA plaques. However, BA plaques were thicker (1.5 versus 1.3mm; p=0.03) and longer (16.4 versus 8.4mm; p&lt;0.001), but less likely eccentric (70.6 versus 88.4%; p=0.039). Conclusions: There were differences in the morphology of symptomatic atherosclerotic plaques in anterior and posterior circulations, independent of demographics and common vascular risk factors. Different artery geometry and the hemodynamics may underlie such differences.

CRT-400.03 Lipoprotein(a) and Plaque Morphology by OCT After High-Dose Statin Treatment

CRT-400.03 Lipoprotein(a) and Plaque Morphology by OCT After High-Dose Statin Treatment

Relationship between coronary high-intensity plaques on T1-weighted imaging by cardiovascular magnetic resonance and vulnerable plaque features by near-infrared spectroscopy and intravascular ultrasound: a prospective cohort study

BackgroundThis study aimed to compare the coronary plaque characterization by cardiovascular magnetic resonance (CMR) and near-infrared spectroscopy (NIRS)-intravascular ultrasound (IVUS) (NIRS-IVUS), and to determine whether pre–percutaneous coronary intervention (PCI) evaluation using CMR identifies high-intensity plaques (HIPs) at risk of peri-procedural myocardial infarction (pMI). Although there is little evidence in comparison with NIRS-IVUS findings, which have recently been shown to identify vulnerable plaques, we inferred that CMR-derived HIPs would be associated with vulnerable plaque features identified on NIRS-IVUS. Methods52 patients with stable coronary artery disease who underwent CMR with non-contrast T1-weighted imaging and PCI using NIRS-IVUS were studied. HIP was defined as a signal intensity of the coronary plaque-to-myocardial signal intensity ratio (PMR) ≥ 1.4, which was measured from the data of CMR images. We evaluated whether HIPs were associated with the NIRS-derived maximum 4-mm lipid-core burden index (maxLCBI4mm) and plaque morphology on IVUS, and assessed the incidence and predictor of pMI defined by the current Universal Definition using high-sensitive cardiac troponin-T. ResultsOf 62 lesions, HIPs were observed in 30 lesions (48%). The HIP group had a significantly higher remodeling index, plaque burden, and proportion of echo-lucent plaque and maxLCBI4mm ≥ 400 (known as large lipid-rich plaque [LRP]) than the non-HIP group. The correlation between the maxLCBI4mm and PMR was significantly positive (r = 0.51). In multivariable logistic regression analysis for prediction of HIP, NIRS-derived large LRP (odds ratio [OR] = 5.41; 95% confidence intervals [CIs] 1.65–17.8, p = 0.005) and IVUS-derived echo-lucent plaque (OR = 5.12; 95% CIs 1.11–23.6, p = 0.036) were strong independent predictors. Furthermore, pMI occurred in 14 of 30 lesions (47%) with HIP, compared to only 5 of 32 lesions (16%) without HIP (p = 0.005). In multivariable logistic regression analysis for prediction of incidence of pMI, CMR-derived HIP (OR = 5.68; 95% CIs 1.53–21.1, p = 0.009) was a strong independent predictor, but not NIRS-derived large LRP and IVUS-derived echo-lucent plaque. ConclusionsThere is an important relationship between CMR-derived HIP and NIRS-derived large LRP. We also confirmed that non-contrast T1-weighted CMR imaging is useful for characterization of vulnerable plaque features as well as for pre-PCI risk stratification.Trial registration The ethics committee of Juntendo Clinical Research and Trial Center approved this study on January 26, 2021 (Reference Number 20-313).

Risk assessment of the newly emerged H7N9 avian influenza viruses

ABSTRACT Since the first human case in 2013, H7N9 avian influenza viruses (AIVs) have caused more than 1500 human infections with a mortality rate of approximately 40%. Despite large-scale poultry vaccination regimes across China, the H7N9 AIVs continue to persist and evolve rapidly in poultry. Recently, several strains of H7N9 AIVs have been isolated and shown the ability to escape vaccine-induced immunity. To assess the zoonotic risk of the recent H7N9 AIV isolates, we rescued viruses with hemagglutinin (HA) and neuraminidase (NA) from these H7N9 AIVs and six internal segments from PR8 virus and characterized their receptor binding, pH of fusion, thermal stability, plaque morphology and in ovo virus replication. We also assessed the cross-reactivity of the viruses with human monoclonal antibodies (mAbs) against H7N9 HA and ferret antisera against H7N9 AIV candidate vaccines. The H7N9 AIVs from the early epidemic waves had dual sialic acid receptor binding characteristics, whereas the more recent H7N9 AIVs completely lost or retained only weak human sialic acid receptor binding. Compared with the H7N9 AIVs from the first epidemic wave, the 2020/21 viruses formed larger plaques in Madin-Darby canine kidney (MDCK) cells and replicated to higher titres in ovo, demonstrating increased acid stability but reduced thermal stability. Further analysis showed that these recent H7N9 AIVs had poor cross-reactivity with the human mAbs and ferret antisera, highlighting the need to update the vaccine candidates. To conclude, the newly emerged H7N9 AIVs showed characteristics of typical AIVs, posing reduced zoonotic risk but a heightened threat for poultry.

Optical Coherence Tomography (OCT) evaluation of culprit lesions in patients with Non-ST Elevation Acute Coronary Syndromes (NSTE-ACS)

Abstract Funding Acknowledgements Type of funding sources: None. Background OCT is an excellent tool to determine plaque morphology in Acute Coronary Syndromes. While plaque rupture has been determined to be the dominant morphology in ST Elevation Myocardial Infarction, there is paucity of literature in NSTE-ACS, which includes Non–ST Segment Elevation Myocardial Infarction (NSTEMI) and Unstable angina (UA). Purpose To characterize culprit lesion morphology by OCT in NSTE-ACS and to evaluate the frequency of each type of lesion in patients presenting with NSTEMI and UA. Methods In this single-centre observational study, OCT imaging of culprit lesion was acquired during coronary angioplasty of culprit lesions of 50 patients presenting with NSTE-ACS between August 2020 to July 2021. A comparison of the frequency of each type of lesion between NSTEMI and UA was performed. Results OCT of culprit vessel in the entire cohort of NSTE-ACS showed plaque erosion in 32% (n=16), plaque rupture in 32% (n=16), tight stenosis in 26% (n=13) and calcific nodule in 10% (n= 5) patients. Lipid plaque was seen in a higher number of patients with plaque erosion and plaque rupture (93.8% and 87.5% respectively). Comparison of the frequency of these lesions in NSTEMI and UA, revealed that among NSTEMI patients (n=25), 48% had plaque erosion, 36% had plaque rupture, 12% had tight stenosis and 4% had calcific nodule whereas, among UA patients (n=25), 16% had plaque erosion, 28% had plaque rupture, 40% had tight stenosis and 16% had calcific nodule. There was a statistically significant increase in plaque erosion in NSTEMI compared to UA (p=0.015) while tight stenosis was significantly more common in UA (p=0.024). Similarly, red thrombus and spotty calcium (p=0.002 and 0.008 respectively) were higher in NSTEMI compared to UA. There was no significant difference in frequency of thin cap fibroatheroma, macrophages, cholesterol crystals, white thrombus, and neovascularization among the two groups. Conclusions OCT provides unique insights into the mechanisms of NSTE-ACS. In our study plaque erosion and plaque rupture were both equally seen in patients presenting with NSTE- ACS. However, NSTEMI patients had a higher frequency of plaque erosion, red thrombus, and spotty calcium when compared to UA. While UA patients had a higher incidence of tight stenosis.

Immature neutrophil is associated with coronary plaque vulnerability based on optical coherence tomography analysis

IntroductionHigh neutrophil to lymphocyte ratio is considered to predict poor prognosis of acute coronary syndrome (ACS). However, the association of neutrophil subpopulation with plaque vulnerability and the incidence of ACS remains unknown. Methods and resultsBlood samples from 48 patients with unstable angina (UA), 31 with ST-segment elevation myocardial infarction (STEMI) and 33 healthy controls were collected at admission. The morphology of coronary plaques in 48 UA patients were further evaluated by optical coherence tomography (OCT). According to maturation stages of neutrophils and the expression of CD10 and CD101, circulating neutrophils could be divided into pre-neutrophils (CD101−CD10−), immature neutrophils (CD101+CD10−) and mature neutrophils (CD101+CD10+). While the number of pre-neutrophil was quite low in blood and comparable among three groups, the absolute counts and percentage of CD10− immature neutrophils were higher in peripheral bloods of UA and STEMI patients compared with those in healthy controls. The concentration of plasma myeloperoxidase was positively associated with the percentage of CD10− immature neutrophils. Furthermore, UA patients with thin-cap fibroatheroma (TCFA) observed by OCT had a higher proportion and larger number of immature neutrophils as compared to those without TCFA. The percentage of immature neutrophils also closely correlated with plaque rupture and the feature of vulnerable plaque, including thinner fibrous cap and larger lipid core, but did not associate with percent lumen stenosis. ConclusionOur findings emphasize that the abnormally increased level of CD10− immature neutrophils may sever as a promising marker of the incidence of ACS and plaque vulnerability.

Combining IVUS + OCT Data, Biomechanical Models and Machine Learning Method for Accurate Coronary Plaque Morphology Quantification and Cap Thickness and Stress/Strain Index Predictions

Assessment and prediction of vulnerable plaque progression and rupture risk are of utmost importance for diagnosis, management and treatment of cardiovascular diseases and possible prevention of acute cardiovascular events such as heart attack and stroke. However, accurate assessment of plaque vulnerability assessment and prediction of its future changes require accurate plaque cap thickness, tissue component and structure quantifications and mechanical stress/strain calculations. Multi-modality intravascular ultrasound (IVUS), optical coherence tomography (OCT) and angiography image data with follow-up were acquired from ten patients to obtain accurate and reliable plaque morphology for model construction. Three-dimensional thin-slice finite element models were constructed for 228 matched IVUS + OCT slices to obtain plaque stress/strain data for analysis. Quantitative plaque cap thickness and stress/strain indices were introduced as substitute quantitative plaque vulnerability indices (PVIs) and a machine learning method (random forest) was employed to predict PVI changes with actual patient IVUS + OCT follow-up data as the gold standard. Our prediction results showed that optimal prediction accuracies for changes in cap-PVI (C-PVI), mean cap stress PVI (meanS-PVI) and mean cap strain PVI (meanSn-PVI) were 90.3% (AUC = 0.877), 85.6% (AUC = 0.867) and 83.3% (AUC = 0.809), respectively. The improvements in prediction accuracy by the best combination predictor over the best single predictor were 6.6% for C-PVI, 10.0% for mean S-PVI and 8.0% for mean Sn-PVI. Our results demonstrated the potential using multi-modality IVUS + OCT image to accurately and efficiently predict plaque cap thickness and stress/strain index changes. Combining mechanical and morphological predictors may lead to better prediction accuracies.

Are acute type A aortic dissections atherosclerotic?

Type A aortic dissections (TAAD) are devastating aortic complications. Patients with Marfan syndrome, a bicuspid aortic valve or a thoracic aortic aneurysm have an increased risk to develop a TAAD. These predisposing conditions are characterized by a histologically thin intimal layer and hardly any atherosclerosis. Little is known about the susceptibility for atherosclerosis in patients with a type A aortic dissection. We aim to systematically describe atherosclerotic lesions in TAAD patients. A total of 51 patients with a TAAD (mean age 62.5 ± 10.8 years, 49% females) and 17 control patients (mean age 63 ± 5.5 years, 53% females) were included in this study. Cardiovascular risk factors were assessed clinically. All sections were stained with Movat pentachrome and hematoxylin eosin. Plaque morphology was classified according to the modified AHA classification scheme proposed by Virmani et al. In the TAAD group thirty-seven percent were overweight (BMI > 25). Diabetes and peripheral arterial disease were not present in any of the patients. Fifty-nine percent of the patients had a history of hypertension. The intima in TAAD patients was significantly thinner as compared to the control group (mean thickness 143 ± 126.5 μm versus 193 ± 132 μm, p < 0.023). Seven TAAD patients had a normal intima without any form of adaptive or pathological thickening. Twenty-three TAAD patients demonstrated adaptive intimal thickening. Fourteen had an intimal xanthoma, also known as fatty streaks. A minority of 7 TAAD patients had progressive atherosclerotic lesions, 4 of which demonstrated pathological intimal thickening, 3 patients showed early fibroatheroma, late fibroatheroma and thin cap fibroatheroma. In the control group the majority of the patients exhibited progressive atherosclerotic lesions: three pathologic intimal thickening, two early fibroatheroma, six late fibroatheroma, one healed rupture and two fibrotic calcified plaque. This study shows that TAAD patients hardly exhibit any form of progressive atherosclerosis. The majority of TAAD patients showcase non-progressive intimal lesions, whereas the control group mostly demonstrated progressive intimal atherosclerotic lesions. Findings are independent of age, sex, or the presence of (a history of) hypertension.

Cardiovascular Disease Among Persons Living With HIV: New Insights Into Pathogenesis and Clinical Manifestations in a Global Context

Widespread use of contemporary antiretroviral therapy globally has transformed HIV disease into a chronic illness associated with excess risk for disorders of the heart and circulatory system. Current clinical care and research has focused on improving HIV-related cardiovascular disease outcomes, survival, and quality of life. In high-income countries, emphasis on prevention of atherosclerotic coronary artery disease over the past decade, including aggressive management of traditional risk factors and earlier initiation of antiretroviral therapy, has reduced risk for myocardial infarction among persons living with human immunodeficiency virus-1 infection. Still, across the globe, persons living with human immunodeficiency virus-1 infection on effective antiretroviral therapy treatment remain at increased risk for ischemic outcomes such as myocardial infarction and stroke relative to the persons without HIV. Unique features of HIV-related cardiovascular disease, in part, include the pathogenesis of coronary disease characterized by remodeling ectasia and unusual plaque morphology, the relative high proportion of type 2 myocardial infarction events, abnormalities of the aorta such as aneurysms and diffuse aortic inflammation, and HIV cerebrovasculopathy as a contributor to stroke risk. Literature over the past decade has also reflected a shift in the profile and prevalence of HIV-associated heart failure, with a reduced but persistent risk of heart failure with reduced ejection fraction and a growing risk of heart failure with preserved ejection fraction. Cardiac magnetic resonance imaging and autopsy data have emphasized the central importance of intramyocardial fibrosis for the pathogenesis of both heart failure with preserved ejection fraction and the increase in risk of sudden cardiac death. Still, more research is needed to better characterize the underlying mechanisms and clinical phenotype of HIV-associated myocardial disease in the current era. Across the different cardiovascular disease manifestations, a common pathogenic feature is that HIV-associated inflammation working through different mechanisms may amplify underlying pathology because of traditional risk and other host factors. The prevalence and phenotype of individual cardiovascular disease manifestations is ultimately influenced by the degree of injury from HIV disease combined with the profile of underlying cardiometabolic factors, both of which may differ substantially by region globally.

Evaluation of Carotid Arteries in Stroke Patients using Colour Doppler Sonography: A Cross-sectional Study

Introduction: Cerebral ischaemic stroke is a neurological condition that can be fatal and debilitating and is one of the leading causes of morbidity and mortality. The major benefit of sonography is its capacity to describe plaque and identify plaques with increased risk of embolisation, in addition, to evaluate the degree of stenosis. Aim: To diagnose and characterise the plaque morphology in extracranial portion of carotid arteries using colour Doppler sonography in patients with stroke. Materials and Methods: A time-bound, hospital-based cross-sectional study was conducted in the Department of Radiodiagnosis, MGM Medical College and MY Hospital, Indore, Madhya Pradesh, India from August 2021 to July 2022. There were 80 stroke patients in the study. Risk factors like smoking, diabetes, hypertension, and family history were recorded. B- mode ultrasonography was used to assess carotid arteries and various Doppler parameters like Peak Systolic Velocity (PSV). Plaque characteristics and morphology like smooth margin, irregular margin, ulceration and haemorrhage were evaluated. Statistical parameters such as Student’s t-test were used for association between ICA PSV and ICA/CCA PSV with degree of stenosis. Results: Hypertension was the most common risk factor 57 (71.1%). A total of 54 (67%) stroke patients were found to have plaque in their carotid vasculature. A total of 21 (38.8%) of patients had type-3 plaque followed by type-1 plaque 14 (25.9%). Out of 67% of patients who had plaque, majority of patients 38 (47.5%) had &lt;50% stenosis and 16 (29.6%) of patients had significant stenosis (&gt;50%). Conclusion: It was shown that carotid Doppler ultrasonography can be used as a screening tool for patients, who have risk factors for stroke to find asymptomatic carotid disease.

Coronary Physiology-Based Approaches for Plaque Vulnerability: Implications for Risk Prediction and Treatment Strategies.

In the catheterization laboratory, the measurement of physiological indexes can help identify functionally significant lesions and has become one of the standard methods to guide treatment decision-making. Plaque vulnerability refers to a coronary plaque susceptible to rupture, enabling risk prediction before coronary events, and it can be detected by defining a certain type of plaque morphology on coronary imaging modalities. Although coronary physiology and plaque vulnerability have been considered different attributes of coronary artery disease, the underlying pathophysiological basis and clinical data indicate a strong correlation between coronary hemodynamic properties and vulnerable plaque. In prediction of coronary events, emerging data have suggested independent and additional implications of a physiology-based approach to a plaque-based approach. This review covers the fundamental interplay between coronary physiology and plaque morphology during disease progression with clinical data supporting this relationship and examines the clinical relevance of physiological indexes in prediction of clinical outcomes and therapeutic decision-making along with plaque vulnerability.

Sex Differences Define the Vulnerability to Atherosclerosis.

For several decades, atherosclerosis has attracted the attention of researchers around the world. Even being a major cause of serious cardiovascular disease and events, atherosclerosis is still not fully understood. Despite the fact that the main players in the pathogenesis of atherosclerosis are well known, many mechanisms of their implementation and interactions remain unknown. The same can be said about the risk factors for atherosclerosis. Many of them are known, but exactly how they work remains to be seen. The main objective of this review is to summarize the latest data on sex as a biological variable in atherosclerosis in humans and animals; to determine what we do not still know about how sex affects the process of growth and complications of atherosclerosis. In this review, we summarized data on sex differences at 3 atherosclerotic aspects: inflammation, vascular remodeling, and plaque morphology. With all overviewed data, we came to the conclusion on the atheroprotective role of female sex.

Increased Epicardial Adipose Tissue (EAT), Left Coronary Artery Plaque Morphology, and Valvular Atherosclerosis as Risks Factors for Sudden Cardiac Death from a Forensic Perspective.

Background: In sudden cardiac deaths (SCD), visceral adipose tissue has begun to manifest interest as a standalone cardiovascular risk factor. Studies have shown that epicardial adipose tissue can be seen as a viable marker of coronary atherosclerosis. This study aimed to evaluate, from a forensic perspective, the correlation between body mass index (BMI), heart weight, coronary and valvular atherosclerosis, left ventricular morphology, and the thickness of the epicardial adipose tissue (EAT) in sudden cardiac deaths, establishing an increased thickness of EAT as a novel risk factor. Methods: This is a retrospective case-control descriptive study that included 80 deaths that were autopsied, 40 sudden cardiac deaths, and 40 control cases who hanged themselves and had unknown pathologies prior to their death. In all the autopsies performed, the thickness of the epicardial adipose tissue was measured in two regions of the left coronary artery, and the left ventricular morphology, macro/microscopically quantified coronary and valvular atherosclerosis, and weight of the heart were evaluated. Results: This study revealed a higher age in the SCD group (58.82 ± 9.67 vs. 53.4 ± 13.00; p = 0.03), as well as a higher incidence in females (p = 0.03). In terms of heart and coronary artery characteristics, there were higher values of BMI (p = 0.0009), heart weight (p &lt; 0.0001), EAT of the left circumflex artery (LCx) (p &lt; 0.0001), and EAT of the left anterior descending artery (LAD) (p &lt; 0.0001). In the multivariate analysis, a high baseline value of BMI (OR: 4.05; p = 0.004), heart weight (OR: 5.47; p &lt; 0.001), EAT LCx (OR: 23.72; p &lt; 0.001), and EAT LAD (OR: 21.07; p &lt; 0.001) were strong independent predictors of SCD. Moreover, age over 55 years (OR: 2.53; p = 0.045), type Vb plaque (OR: 17.19; p &lt; 0.001), mild valvular atherosclerosis (OR: 4.88; p = 0.002), and moderate left ventricle dilatation (OR: 16.71; p = 0.008) all act as predictors of SCD. Conclusions: The data of this research revealed that higher baseline values of BMI, heart weight, EAT LCx, and EAT LAD highly predict SCD. Furthermore, age above 55 years, type Vb plaque, mild valvular atherosclerosis, and left ventricle dilatation were all risk factors for SCD.

S-07-3: THE TESTOSTERONE-ANDROGEN RECEPTOR PATHWAY IS ASSOCIATED WITH CAROTID ATHEROSCLEROTIC PLAQUE INSTABILITY IN MEN WITH SEVERE CAROTID ATHEROSCLEROSIS

Objective: Carotid atherosclerotic plaques can be stable or unstable; the latter more likely to rupture resulting in strokes. Sex differences exist in carotid plaque morphology and composition: carotid plaques of men tend to be more unstable than of women, who tend to have more fibrous and stable plaques. Yet, women experience greater morbidity and mortality rates post-stroke. Given that sex hormones exert pleiotropic effects on the cell types involved in the atherosclerotic process, and given that estradiol is largely atheroprotective in women, we hypothesize that sex hormones and their receptors may affect plaque instability. Design and Methods: In this cross-sectional study, we measured sex hormones in the circulation and their receptors in the plaque of older men and postmenopausal women undergoing a carotid endarterectomy (n = 160). Using liquid chromatography mass spectrometry, circulating estradiol, testosterone, dehydroepiandrosterone (DHEA), and androstenedione were measured in blood samples. Plaques collected post-operatively were classified into 4 groups (n = 40/group): women with stable, women with unstable plaques, men with stable, and men with unstable plaques. Protein expression of estrogen receptor α (ER-α), estrogen receptor β (ER-β), G protein-coupled estrogen receptor (GPER), and androgen receptor (AR) was quantified using immunohistochemistry and western blot analysis. Plaque sex hormone receptor mRNA expression was assessed using qRT-PCR. Results: Men with unstable plaques demonstrated greater circulating concentrations of testosterone and androstenedione compared to men with stable plaques (P = 0.02 and P = 0.047, respectively). Unstable plaques in men demonstrated significantly less AR and ER-α mRNA expression compared to stable plaques from men (P = 0.0003 and P = 0.042, respectively) and compared to unstable plaques from women (P = 0.0088 and P = 0.002). Yet, AR, ER-α, ER-β, and GPER protein expression was significantly greater in unstable plaques from men compared to stable plaques from men (P = 0.039, P = 0.006, P &lt; 0.0001, and P = 0.0002, respectively) and compared to unstable plaques from women (P = 0.005, P = 0.041, P = 0.028, and P = 0.002, respectively). Expression was observed in macrophages, foam cells, endothelial cells, and smooth muscle cells. Moreover, unstable plaques from men demonstrated greater features of plaque instability compared to unstable plaques from women, including hemorrhage, large lipid core, abundance of inflammatory cells, and fibrous cap infiltration by inflammatory cells (P &lt; 0.05 for all). Conclusion: Our preliminary findings indicate a possible association between androgens and the androgen receptor pathway and plaque instability. With further investigations, our ongoing work will unravel the underlying mechanisms, and may ultimately lead to hormone-specific therapies aimed at stabilizing plaques and reducing the incidence of stroke for men and women.

Association between carotid and coronary atherosclerotic plaque morphology: a virtual histology intravascular ultrasound study

Association between carotid and coronary atherosclerotic plaque morphology: a virtual histology intravascular ultrasound study