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Background: The aim of this study was to investigate the relationship between (i) carotid intima-media thickness (CIMT) at baseline as well as (ii) change in CIMT over 5 years (ΔCIMT) and atherosclerotically induced luminal narrowing in non-coronary arterial territories assessed by whole-body magnetic resonance angiography (WBMRA)., Methods and Results: In subgroups of the Prospective Investigation of Vasculature in Uppsala Seniors (PIVUS) study, US measurements of CIMT in the common carotid arteries were analysed at 70 and 75 years and ΔCIMT was calculated (n = 272). WBMRA, assessing arterial stenosis in five different territories by which also a total atherosclerotic score (TAS) was calculated, was performed at 70 years (n = 306)., Results: Carotid intima-media thickness in the carotid artery at baseline was correlated with TAS (P = 0.0001) when adjusted to a set of traditional risk factors for atherosclerosis, as well as to stenosis in two of the different investigated territories (aorta and lower leg, P = 0.013 and P = 0.004), but there was no significant correlation between ΔCIMT and TAS (P = 0.41)., Conclusions: In the present study, CIMT, but not ΔCIMT over 5 years, in the carotid artery was related to overall stenoses in the body, as assessed by WBMRA. These findings support CIMT as a general marker for atherosclerosis., (© 2014 The Authors. Clinical Physiology and Functional Imaging published by John Wiley & Sons Ltd on behalf of Scandinavian Society of Clinical Physiology and Nuclear Medicine.)

Adiponectin has been shown to have beneficial cardiovascular effects and to signal through the adiponectin receptors, AdipoR1 and AdipoR2. The original aim of this study was to investigate the effect of combined AdipoR1 and AdipoR2 deficiency (AdipoR1(-/-)AdipoR2(-/-)) on atherosclerosis. However, we made the interesting observation that AdipoR1(-/-) AdipoR2(-/-) leads to embryonic lethality demonstrating the critical importance of the adiponectin signalling system during development. We then investigated the effect of AdipoR2-ablation on the progression of atherosclerosis in apolipoprotein E deficient (ApoE(-/-)) mice. AdipoR2(-/-)ApoE(-/-) mice fed an atherogenic diet had decreased plaque area in the brachiocephalic artery compared with AdipoR2(+/+) ApoE(-/-) littermate controls as visualized in vivo using an ultrasound biomicroscope and confirmed by histological analyses. The decreased plaque area in the brachiocephalic artery could not be explained by plasma cholesterol levels or inflammatory status. However, accumulation of neutral lipids was decreased in peritoneal macrophages from AdipoR2(-/-)ApoE(-/-) mice after incubation with oxidized LDL. This effect was associated with lower CD36 and higher ABCA1 mRNA levels in peritoneal macrophages from AdipoR2(-/-)ApoE(-/-) mice compared with AdipoR2(+/+)ApoE(-/-) controls after incubation with oxidized LDL. In summary, we show that adiponectin receptors are crucial during embryonic development and that AdipoR2-deficiency slows down the progression of atherosclerosis in the brachiocephalic artery of ApoE-deficient mice.

Diet is a significant modifiable risk factor for cardiovascular disease and high fish intake has been associated with vascular health in population studies. However, intervention studies have been inconclusive. In this study, male low-density lipoprotein receptor-deficient mice were given 16-week high fat/high sucrose diets, supplemented with either minced herring fillets or minced beef. The diets were matched in total fat and cholesterol content; taurine content and fatty acid composition was analysed. Body weights were recorded throughout the study; plasma lipids were analysed at week 8 and 16. Body composition and adipocyte size were evaluated at study end. Atherosclerosis was evaluated at week 12 (ultrasound) and at termination (en face histology). Herring-fed mice had a higher proportion of long-chain n-3 polyunsaturated fatty acids in the hepatic triacylglycerides (TAG) and phospholipid fractions. The herring-fed mice had increased body weight (P=0.007), and reduced epididymal adipocyte size (P=0.009), despite similar food intake and body composition as the beef-fed mice. The herring-fed mice had lower plasma TAG and very-low-density lipoprotein (VLDL)-cholesterol concentrations throughout the study (TAG; P=0.0012 and 0.004, VLDL-cholesterol; P=0.006 and 0.041, week 8 and 16, respectively). At week 16, the herring-fed had higher plasma concentrations of HDL-cholesterol (P=0.004) and less atherosclerotic lesions in the aortic arch (P=0.007) compared with the beef-fed mice. In conclusion, dietary herring in comparison to beef markedly improved vascular health in this mouse model, suggesting that herring provides an added value beyond its content of macronutrients.

Objective: The principal aim of this study was to determine whether the amount of visceral adipose tissue (VAT) is more related than subcutaneous adipose tissue (SAT) to atherosclerosis assessed by whole-body MRA (WBMRA). A further objective was to investigate whether traditional risk factors, inflammation, or adipokines could explain the hypothesized relationship between VAT and atherosclerosis., Methods: Men and women aged 70 were recruited from the general population into the Prospective Investigation of The Vasculature in Uppsala Seniors (PIVUS) and 306 of them underwent WBMRA in a clinical 1.5-T scanner. The arterial tree was assessed for degree of stenosis or occlusion and a total atherosclerotic score (TAS) was established. Information on risk factors and BMI and on SAT and VAT, segmented on an axial MR scan was collected. Adiponectin, leptin, and high sensitive C-reactive protein (hsCRP) were measured in serum. HOMA index was used as a marker of insulin resistance., Results: VAT was related to TAS independently of gender, total obesity (BMI), amount of SAT, hsCRP and also to the traditional risk factors included in the Framingham risk score (FRS) in an elderly population. Adiponectin or the HOMA insulin resistance, but not leptin or VAT, together with FRS was significantly related to TAS in a multiple censored regression model., Conclusion: Adiponectin attenuated the relationship between VAT and TAS, suggesting that adiponectin and insulin resistance is an important link between visceral adiposity and atherosclerosis.

This study investigated the effects of rosuvastatin on plaque progression and in vivo coronary artery function in apolipoprotein E-knockout (ApoE-KO) mice, using noninvasive high-resolution ultrasound techniques. Eight-week-old male ApoE-KO mice (n = 20) were fed a high-fat diet with or without rosuvastatin (10 micromol.kg(-1).day(-1)) for 16 wk. When compared with control, rosuvastatin reduced total cholesterol levels (P < 0.05) and caused significant retardation of lesion progression in the brachiocephalic artery, as visualized in vivo using an ultrasound biomicroscope (P < 0.05). Histological analysis confirmed the reduction of brachiocephalic atherosclerosis and also revealed an increase in collagen content in the statin-treated group (P < 0.05). Coronary volumetric flow was measured by simultaneous recording of Doppler velocity signals and left coronary artery morphology before and during adenosine infusion. The hyperemic flow in response to adenosine was significantly greater in left coronary artery following 16 wk of rosuvastatin treatment (P < 0.001), whereas the baseline flow was similar in both groups. In conclusion, rosuvastatin reduced brachiocephalic artery atherosclerotic plaques in ApoE-KO mice. Coronary artery function assessed using recently developed in vivo ultrasound-based protocols, also improved.

The aim of this study was to create a scoring system for whole-body magnetic resonance angiography (WBMRA) that allows estimation of atherosclerotic induced luminal narrowing, and determine whether the traditional cardiovascular (CV) risk factors included in the Framingham risk score (FRS) were related to this total atherosclerotic score (TAS) in an elderly population. A group of 306 subjects, aged 70, were recruited from the general population and underwent WBMRA in a 1.5-T scanner. Three-dimensional sequences were acquired after administration of one i.v. injection of 40 ml gadodiamide. The arterial tree was divided into five territories (carotid, aorta, renal, upper and lower leg) comprising 26 vessel segments, and assessed according to its degree of stenosis or occlusion. FRS correlated to TAS (r = 0.30, P < 0.0001), as well as to the atherosclerotic score for the five individual territories. Of the parameters included in the FRS, male gender (P < 0.0001), systolic blood pressure (P = 0.0002), cigarette pack-years (P = 0.0008) and HDL cholesterol (P = 0.008) contributed to the significance. A scoring system for WBMRA was created. The significant relation towards traditional CV risk factors indicates that the proposed scoring system could be of value for assessing atherosclerotically induced luminal narrowing.

Objective: The principal aim of the present study was to explore the feasibility of using whole-body magnetic resonance angiography to assess atherosclerosis in different vascular territories in a cohort of elderly., Methods and Results: Three hundred six 70-year-old subjects (145 women, 161 men) recruited from a population-based cohort study (Prospective Investigation of the Vasculature in Uppsala Seniors, ie, the PIVUS study) underwent 1.5-T whole-body magnetic resonance angiography with gadodiamide. The arteries were divided into 26 segments. In total, 7956 vessel segments were evaluated with 7900 segments (99.3%) possible to evaluate. Of these, 7186 segments (91%) were normal. Luminal narrowing of > or = 50% was observed in 9 (1.5%) of the renal arteries, 12 (1.8%) of the carotid arteries, in 31 segments (1.1%) of the pelvic/upper leg territories, and in 136 segments (6.2%) of territories in the lower leg. Approximately one-third of the sample had no vascular abnormalities, one-third had stenoses of < 50%, and the remainder had stenoses > or = 50% or occlusions. Six subjects (2%) had aortic aneurysms. In subjects without evident vascular disease, 26% had significant vascular abnormalities., Conclusions: Whole-body magnetic resonance angiography performed with a clinical scanner can be used for quantifying atherosclerosis in different vascular territories in a single examination in an elderly population.

There are increasing needs to develop imaging techniques to study in vivo vascular morphology and function in various mouse models of atherosclerosis. Using ultrasound biomicroscopy (UBM), we developed and validated a new imaging protocol to follow lesion progression in atherosclerotic mice. ApoE and LDL receptor double knockout mice (DKO) with various degree of atherosclerosis and normal control mice were imaged at the level of the ascending aorta using UBM. Average plaque thickness, as well as plaque area were delineated in the short-axis images, and were subsequently compared with histological measurements. We showed that plaque area at this vascular site was closely correlated to total plaque burden from en face measurement (p<0.0001). UBM-measured plaque thickness and area correlated with indices for histology measures from the same vascular region (p<0.0001 respective p<0.0001). Furthermore, in 16 DKO mice aged from 32 to 35 weeks, UBM showed significantly weekly increases of IMT in the ascending aorta from 0.106+/-0.108 mm at 32 weeks of age to 0.256+/-0.345 mm at 35 weeks of age (p=0.0002). In conclusion, this novel imaging protocol provides us with a non-invasive, accurate and inexpensive way to follow lesion progression in mice in vivo.

Although in vitro model systems are useful for investigation of atherosclerosis-associated processes, they represent simplification of complex events that occur in vivo, which involve interactions between many different cell types together with their environment. The use of animal model systems is important for more in-depth insights of the molecular mechanisms underlying atherosclerosis and for identifying potential targets for agents that can prevent plaque formation and even reverse existing disease. This chapter will provide a survey of such animal models and associated techniques that are routinely used for research of atherosclerosis in vivo., (© 2022. The Author(s), under exclusive license to Springer Science+Business Media, LLC, part of Springer Nature.)

Apolipoprotein E-knockout (Apoe-/-) mice constitute the most widely employed animal model of atherosclerosis. Deletion of Apoe induces profound hypercholesterolemia and promotes the development of atherosclerosis. However, despite its widespread use, the Apoe-/- mouse model remains incompletely characterized, especially at late time points and advanced disease stages. Thus, it is unclear how late atherosclerotic plaques compare to earlier ones in terms of lipid deposition, calcification, macrophage accumulation, smooth muscle cell presence, or plaque necrosis. Additionally, it is unknown how cardiac function and hemodynamic parameters are affected at late disease stages. Here, we used a comprehensive analysis based on histology, fluorescence microscopy, and Doppler ultrasonography to show that in normal chow diet-fed Apoe-/- mice, atherosclerotic lesions at the level of the aortic valve evolve from a more cellular macrophage-rich phenotype at 26 weeks to an acellular, lipid-rich, and more necrotic phenotype at 52 weeks of age, also marked by enhanced lipid deposition and calcification. Coronary artery atherosclerotic lesions are sparse at 26 weeks but ubiquitous and extensive at 52 weeks; yet, left ventricular function was not significantly affected. These findings demonstrate that atherosclerosis in Apoe-/- mice is a highly dynamic process, with atherosclerotic plaques evolving over time. At late disease stages, histopathological characteristics of increased plaque vulnerability predominate in combination with frequent and extensive coronary artery lesions, which nevertheless may not necessarily result in impaired cardiac function. [ABSTRACT FROM AUTHOR]

Atherosclerosis remains the main cause of death worldwide. Most important issues concerning atherosclerosis are hemodynamics and how it affects plaque prevalence and distribution, as well as the symmetry and asymmetry of vasculature and plaques. To present the symmetry in the vascular system an analysis of PubMed and MEDLINE databases was performed. As of February 21, 2023, the results were as follows: for "symmetry" AND "atherosclerosis" there were 47 results; for "symmetry" AND "atherosclerotic lesions" - 20 results; for "symmetry" AND "artery stenosis" - 82 results; for "asymmetry" AND "atherosclerosis" - 87 results. Not without meaning are preventive measures. In the light of the Fourth Industrial Revolution artificial intelligence (AI) solutions help to develop new tools outperforming already existing cardiovascular risk scales. The aim of this paper is to present a current view on symmetry within vasculature and atherosclerosis as well as present a new approach to assess individuals' cardiovascular risk in accordance with precision medicine assumptions. Symmetry and asymmetry within the human vascular system play a crucial role in understanding of arterial diseases, including atherosclerosis. Moreover, it is unavoidable to use AI in cardiovascular risk stratification. [ABSTRACT FROM AUTHOR]

Purpose of Review: Atherosclerosis is a chronic disease characterized by lipid retention and inflammation in the artery wall. The retention and oxidation of low-density lipoprotein (LDL) in sub-endothelial space play a critical role in atherosclerotic plaque formation and destabilization. Oxidized LDL (ox-LDL) and other modified LDL particles are avidly taken up by endothelial cells, smooth muscle cells, and macrophages mainly through several scavenger receptors, including CD36 which is a class B scavenger receptor and membrane glycoprotein. Recent Findings: Animal studies performed on CD36-deficient mice suggest that deficiency of CD36 prevents the development of atherosclerosis, though with some debate. CD36 serves as a signaling hub protein at the crossroad of inflammation, lipid metabolism, and fatty acid metabolism. In addition, the level of soluble CD36 (unattached to cells) in the circulating blood was elevated in patients with atherosclerosis and other metabolic disorders. Summary: We performed a state-of-the-art review on the structure, ligands, functions, and regulation of CD36 in the context of atherosclerosis by focusing on the pathological role of CD36 in the dysfunction of endothelial cells, smooth muscle cells, monocytes/macrophages, and platelets. Finally, we highlight therapeutic possibilities to target CD36 expression/activity in atherosclerosis. [ABSTRACT FROM AUTHOR]

Background: 4D flow MRI shows great potential in neurovascular disorders such as stenosis, atherosclerotic disease, aneurysms, and vascular malformations. Its widespread application in the neurovascular system requires evidence of good test-retest multicenter reproducibility.Purpose: To assess the multicenter reproducibility, test-retest reliability and interobserver dependence of 4D flow MRI in measurements of cerebral blood flow/velocity in main intracranial vessels.Study Type: Prospective study.Subjects: Ten healthy subjects underwent 4D flow scans at three different centers. All subjects were scanned twice at 2 different days at each center.Field Strength/sequence: 3.0 T; 4D flow sequence.Assessment: Multicenter reproducibility, test-retest reliability and interobserver agreement for measurements of the blood flow and peak velocity from five regions of interest were assessed (bilateral internal carotid arteries, bilateral medial cerebral arteries, and sagittal sinus).Statistical Test: A Shapiro-Wilks test was conducted to assess normality of measurements in each scan. Coefficient of variances (CVs) was computed to evaluate intra- and intersite variances of all measurements. The multicenter reproducibility was assessed by two-way mixed intraclass correlation coefficient (ICC). A Bland-Altman plot and Pearson correlation were used to evaluate test-retest reliability. ICC was calculated to assess interobserver agreements.Results: All P-values for Shapiro-Wilks tests were greater than 0.05, which indicated the normality of all measurements. Both intra- and intersite CVs were lower than 12%. There was good test-retest reliability for both blood flow and peak velocity of all ROIs (r = 0.75-0.94). In addition, high multicenter reproducibility was detected (ICC = 0.77-0.96, all P < 0.001). The results of these measurements also showed great interobserver agreement (all ICC > 0.9 and all P < 0.001).Data Conclusion: High multicenter reproducibility and test-retest reliability was shown for 4D flow in the measurements of blood flow and peak velocity of intracranial vessels. In addition, these measurements showed great interobserver agreement.Level Of Evidence: 2 Technical Efficacy: Stage 1 J. Magn. Reson. Imaging 2019;49:1543-1552. [ABSTRACT FROM AUTHOR]

Background: Alcohol abuse and adherence to atherogenic diet (AD; a low‐carbohydrate–high‐protein diet) have been positively associated with cardiovascular disease. In addition, it has been demonstrated clinically that dietary intake is increased on days when alcohol is consumed. Here, the additive effects of ethanol (EtOH) and AD on atherosclerosis, a major underlying cause of cardiovascular disease, were investigated in apolipoprotein E/low‐density lipoprotein receptor double‐knockout (KO) mice. The mechanisms, especially aortic oxidative stress damage, were highlighted. Methods: Twelve‐week‐old male KO mice on AD with or without EtOH treatment were bred for 4 months. Age‐matched male C57BL/6J mice on a standard chow diet without EtOH treatment served as controls. Analyses were conducted using ultrasound biomicroscopy, histopathological and fluorescence immunohistochemical examinations, Western blots, and polymerase chain reaction. Results: KO mice on AD with EtOH treatment showed increases in aortic maximum intima media thickness, hypoechoic plaque formation, and mean Oil‐Red‐O content. These results were associated with enhanced ratio of aortic 8‐hydroxy‐2′‐deoxyguanosine (8‐OHdG)‐immunopositive area to the metallothionein (MT) immunopositive area and suppression of AD‐induced up‐regulated aortic Mt1, Mt2, and upstream stimulatory factor 1 mRNA expressions. Moreover, 8‐OHdG was expressed in the nuclei of CD31‐ and alpha smooth muscle actin‐immunopositive cells, and the up‐regulated mRNA expressions of aortic nitric oxide synthase 3 and platelet‐derived growth factors were only observed in the KO mice on AD with EtOH treatment. Conclusions: Alcohol abuse and adherence to AD may promote the shift of aortic oxidative stress and antioxidative stress balance toward oxidative stress predominance and reduced antioxidative stress, which may be partly due to the decrease in MT at the cell biological level and down‐regulation of Mt at the gene level, which in turn could play a role in the up‐regulation of endothelial dysfunction‐related and vascular smooth muscle cell proliferation‐related gene expression and the progression of atherosclerosis in mice with hyperlipidemia. Alcohol consumption in combination with atherogenic diet increased indices of atherosclerosis in apolipoprotein E/low‐density lipoprotein receptor double‐knockout mice (A‐C) via promoting the shift of aortic oxidative stress and anti‐oxidative stress balance toward oxidative‐stress predominance and reduced anti‐oxidative stress (D‐G). Yellow arrowheads in C indicate hypoechoic plaque formations, 8‐OHdG and Cybb were used as oxidative stress markers and metallothionein (MT) was used as the anti‐oxidative stress marker. The data are presented as the means ± SDs. *p < 0.05. [ABSTRACT FROM AUTHOR]

Introduction: The burden of coronary artery disease (CAD) and peripheral vascular pathologies caused by atherosclerosis is constantly increasing. There is continuous research aiming to develop new methods that can evaluate the extent of atherosclerotic disease in different vascular beds, thus estimating global risk. Similar to carotid artery thickness, which is an established marker for increased cardiovascular risk and cerebrovascular disease, femoral intima-media thickness (f-IMT) may have the same role in case of peripheral arterial involvement. The aim of the study was determine whether f-IMT, determined at the level of the superficial femoral artery, is related to traditional risk factors, markers of peripheral vascular atherosclerosis and inflammation. Material and methods: Forty-six patients with known cardiovascular disease were included in the study. Demographical data, cardiovascular history, and risk factors were assessed. We determined metabolic parameters (uric acid, fasting glucose, total cholesterol, HDL-cholesterol, LDL-cholesterol, triglycerides), renal function (creatinine and GFR), and inflammation status for all patients. Each patient underwent ultrasound examination of the superficial femoral artery, by which f-IMT was determined for right and left limbs. Ankle-brachial index was also calculated. Data from the low (f-IMT <0.75 mm) and high (f-IMT >0.75 mm) f-IMT groups were compared and correlation coefficients were determined in each groups for f-IMT in relation to the other parameters. Results: Mean age was 71.08 ± 9.78 years. 86.95% of the patients suffered from hypertension, 56.62% had coronary heart disease, and 21.73% had a history of stroke. More females had history of hypertension and CAD. The most prevalent cardiovascular risk factors were dyslipidemia (68.86%), diabetes (21.73%), and smoking (21.73%). There were significant differences between gender groups for total cholesterol levels (161.36 ± 25.04 mg/dL, 95%CI 150.26-172.47 in males vs. 201.33 ± 52.73 mg/dL, 95%CI 170.07-223.60 in females, p = 0.02), creatinine values (1.04 ± 0.22 mg/dL, 95%CI 0.94-1.14 for males vs. 0.91 ± 0.23 mg/dL, 95%CI 0.81-1.00 for females, p = 0.018), and left f-IMT (0.87 ± 0.18 mm, 95%CI 0.79-0.95 for males vs. 0.75 ± 0.10 mm, 95%CI 0.70-0.79 for females, p = 0.0049). In the group with low f-IMT, a significant, reverse correlation was established between f-IMT, uric acid (r = -0.483, p = 0.042), and right ABI (r = -730, p = 0.0006). In the group with high f-IMT, age (r = 0.408, p = 0.031), fasting glucose (r = 0.407, p = 0.034), total cholesterol (r = 0.429, p = 0.02), HDL-cholesterol (r = -0.56, p = 0.0019), triglycerides (r = 0.45, p = 0.01), hs-CRP (r = 0.45, p = 0.01), and left ABI (r = -0.71, p <0.0001) showed a significant correlation to f-IMT. Conclusions: Increased femoral intima-media thickness is related to age, cardiovascular risk factors, and markers of peripheral arterial disease. Patients with higher f-IMT have a more augmented inflammatory status. Based on these correlations, in patients with cardiovascular disease, f-IMT could become a marker for increased cardiovascular risk. [ABSTRACT FROM AUTHOR]

Regular fish/fish oil consumption is widely recommended for protection against cardiovascular diseases (CVD). Fish and other marine life are rich sources of the cardioprotective long-chain n-3 polyunsaturated fatty acids (n-3 PUFA) eicosapentaenoic acid (C20:5 n-3; EPA) and docosahexaenoic acid (C22:6 n-3; DHA). The lipid content and fatty acid profile of fish, however, vary greatly among different fish species. In addition to n-3 PUFA, certain fish, such as saury, pollock, and herring, also contain high levels of long-chain monounsaturated fatty acids (LCMUFA), with aliphatic tails longer than 18 C atoms (i.e., C20:1 and C22:1 isomers). Compared with well-studied n-3 PUFA, limited information, however, is available on the health benefits of marine-derived LCMUFA, particularly in regard to CVD. Our objective in this review is to summarize the current knowledge and provide perspective on the potential therapeutic value of dietary LCMUFA-rich marine oil for improving CVD risk factors. We will also review the possible mechanisms of LCMUFA action on target tissues. Finally, we describe the epidemiologic data and small-scaled clinical studies that have been done on marine oils enriched in LCMUFA. Although there are still many unanswered questions about LCMUFA, this appears to be promising new area of research that may lead to new insights into the health benefits of a different component of fish oils besides n-3 PUFA. [ABSTRACT FROM AUTHOR]

Low levels of vitamin D have been associated with increased cardiovascular disease risk. However, few studies have evaluated the association between vitamin D status and peripheral arterial disease (PAD). We therefore aimed to investigate whether low 25-hydroxyvitamin D (25(OH)D) levels were associated with increased risk of PAD in the Korean population. This cross-sectional study was conducted among 8,960 subjects aged 50 years or older without known myocardial infarction or stroke. PAD was defined by an ankle brachial blood pressure index ＜0.9. Multivariate logistic regression was used to evaluate the association between serum 25(OH)D levels and risk of PAD. Of the 8,960 subjects, 3.0% had PAD and the age and sex adjusted prevalence of PAD decreased with the increasing 25(OH)D quartile. After adjusting for potential confounders and parathyroid hormones, serum 25(OH)D levels were associated with a significantly decreased risk of PAD (OR for one SD increase, 0.98; 95% CI, 0.95-1.0, P for trend=0.040). Compared with the first 25(OH)D quartile, the odds of PAD were 0.86 (95% CI, 0.62-1.21), 0.67 (95% CI, 0.46-0.97), and 0.71 (95% CI, 0.49-1.04) for the second, third, and fourth quartiles, respectively. In this cross-sectional study, we found that low serum 25(OH)D levels were associated with an increased risk of PAD, independent of traditional cardiovascular risk factors and parathyroid hormone. Our findings suggest that low vitamin D levels may contribute to PAD in the Korean population. [ABSTRACT FROM AUTHOR]

ApoE/LDLR-/- mice represent a reliable model of atherosclerosis. However, it is not clear whether cardiac performance is impaired in this murine model of atherosclerosis. Here, we used MRI to characterize cardiac performance in vivo in apoE/LDLR-/- mice with advanced atherosclerosis. Six-month-old apoE/LDLR-/- mice and age-matched C57BL/6J mice (control) were examined using highly time-resolved cine-MRI [whole-chamber left ventricle (LV) imaging] and MR tagging (three slices: basal, mid-cavity and apical). Global and regional measures of cardiac function included LV volumes, kinetics, time-dependent parameters, strains and rotations. Histological analysis was performed using OMSB (orceine with Martius, Scarlet and Blue) and ORO (oil red-O) staining to demonstrate the presence of advanced coronary atherosclerosis. MR-tagging-based strain analysis in apoE/LDLR-/- mice revealed an increased frequency of radial and circumferential systolic stretch (25% and 50% of segments, respectively, p ≤ 0.012), increased radial post-systolic strain index (45% of segments, p = 0.009) and decreased LV untwisting rate (−30.3° (11.6°)/cycle, p = 0.004) when compared with control mice. Maximal strains and LV twist were unchanged. Most of the cine-MRI-based LV functional and anatomical parameters also remained unchanged in apoE/LDLR-/-mice, with only a lower filling rate, longer filling time, shorter isovolumetric contraction time and slower heart rate observed in comparison with control mice. The coronary arteries displayed severe atherosclerosis, as evidenced by histological analysis. Using comprehensive MRI methods, we have demonstrated that, despite severe coronary atherosclerosis in six-month-old apoE/LDLR-/- mice, cardiac performance including global parameters, twist and strains, was well preserved. Only subtle diastolic alterations, possibly of ischemic background, were uncovered. Copyright © 2016 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Background: The aim of this study was to use whole body cardiovascular magnetic resonance imaging (WB CVMR) to assess the heart and arterial network in a single examination, so as to describe the burden of atherosclerosis and subclinical disease in participants with symptomatic single site vascular disease. Methods: 64 patients with a history of symptomatic single site vascular disease (38 coronary artery disease (CAD), 9 cerebrovascular disease, 17 peripheral arterial disease (PAD)) underwent whole body angiogram and cardiac MR in a 3 T scanner. The arterial tree was subdivided into 31 segments and each scored according to the degree of stenosis. From this a standardised atheroma score (SAS) was calculated. Cine and late gadolinium enhancement images of the left ventricle were obtained. Results: Asymptomatic atherosclerotic disease with greater than 50% stenosis in arteries other than that responsible for their presenting complain was detected in 37% of CAD, 33% of cerebrovascular and 47% of PAD patients. Unrecognised myocardial infarcts were observed in 29% of PAD patients. SAS was significantly higher in PAD patients 24 (17.5-30.5) compared to CAD 4 (2-11.25) or cerebrovascular disease patients 6 (2-10) (ANCOVA p < 0.001). Standardised atheroma score positively correlated with age (β 0.36 p = 0.002), smoking status (β 0.34 p = 0.002), and LV mass (β -0.61 p = 0.001) on multiple linear regression. Conclusion: WB CVMR is an effective method for the stratification of cardiovascular disease. The high prevalence of asymptomatic arterial disease, and silent myocardial infarctions, particularly in the peripheral arterial disease group, demonstrates the importance of a systematic approach to the assessment of cardiovascular disease. [ABSTRACT FROM AUTHOR]

Nonalcoholic fatty liver disease (NAFLD) is a metabolic stress-induced liver disease that is closely related not only to genetic susceptibility but also to insulin resistance and highly linked with metabolic syndrome. In recent years, the prevalence of NAFLD has increased rapidly, paralleling the epidemic of type 2 diabetes mellitus and obesity leading to cardiovascular disease. It has been demonstrated that NAFLD is highly associated with atherosclerosis. With recently gained knowledge, it appears that NAFLD may induce insulin resistance, dyslipidemia, oxidative stress, inflammation, and fluctuation of adipokines associated with atherosclerosis. In this review, we aimed to summarize recent discoveries related to both NAFLD and atherosclerosis, and to identify possible mechanisms linking them. [ABSTRACT FROM AUTHOR]

Cardiovascular disease is the largest cause of morbidity and mortality among patients with chronic kidney disease (CKD) and end-stage kidney disease, with nearly half of all deaths attributed to cardiovascular disease. Hydroxychloroquine (HCQ), an anti-inflammatory drug, has been shown to have multiple pleiotropic actions relevant to atherosclerosis. We conducted a proof-of-efficacy study to evaluate the effects of hydroxychloroquine in an animal model of atherosclerosis in ApoE knockout mice with and without chronic kidney disease. Forty male, 6-week-old mice were divided into four groups in a 2 x 2 design: sham placebo group; sham treatment group; CKD placebo group; and CKD treatment group. CKD was induced by a two-step surgical procedure. All mice received a high-fat diet through the study duration and were sacrificed after 16 weeks of therapy. Mice were monitored with ante-mortem ultrasonic echography (AUE) for atherosclerosis and vascular stiffness and with post-mortem histology studies for atherosclerosis. Therapy with HCQ significantly reduced the severity of atherosclerosis in CKD mice and sham treated mice. HCQ reduced the area of aortic atherosclerosis on en face examination by approximately 60% in HCQ treated groups compared to the non-treated groups. Additionally, therapy with HCQ resulted in significant reduction in vascular endothelial dysfunction with improvement in vascular elasticity and flow patterns and better-preserved vascular wall thickness across multiple vascular beds. More importantly, we found that presence of CKD had no mitigating effect on HCQ’s anti-atherosclerotic and vasculoprotective effects. These beneficial effects were not due to any significant effect of HCQ on inflammation, renal function, or lipid profile at the end of 16 weeks of therapy. This study, which demonstrates structural and functional protection against atherosclerosis by HCQ, provides a rationale to evaluate its use in CKD patients. Further studies are needed to define the exact mechanisms through which HCQ confers these benefits. [ABSTRACT FROM AUTHOR]

Visual interpretation of the Doppler waveform in the common femoral or distal external iliac artery (EIA) was reported to be useful in screening for proximal peripheral artery occlusive disease ( PAOD) in patients with lower limb ischemia. Commonly patients with coronary artery disease ( CAD) referred for echocardiography have coexistent arterial pathology. Therefore, we decided to study whether echocardiographic evaluation of the distal EIA flow can be useful for detection of PAOD in patients with CAD. We studied 150 consecutive patients (pts) with CAD referred for echocardiography. At the end of an echocardiographic examination, evaluation of the flow in the distal EIA with an echocardiographic probe was performed. The Doppler waveform was classified as normal-with early diastolic flow reversal or abnormal-without early diastolic flow reversal. Echocardiographic findings were compared in a blinded fashion with the results of the ankle brachial index measurements ( ABI). Based on the ABI ≤ 0.9, peripheral artery disease was diagnosed in 54 pts (36%) and abnormal external iliac Doppler waveform was found in 27 pts (18%). Sensitivity of abnormal external iliac Doppler waveform in predicting PAOD was 48%, specificity 99%, positive predictive value (PPV) 96%, and negative predictive value 77%. Peripheral arterial occlusive disease is common in patients with CAD referred for echocardiographic study. Echocardiographic assessment of distal EIA Doppler waveform has low sensitivity, but high specificity and high PPV in the diagnosis of peripheral arterial occlusive disease. [ABSTRACT FROM AUTHOR]

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The article presents a research which analyzes the cardiac and vascular phenotypes, and examines the interplay of among nitric oxide, reactive oxygen species (ROS), aging and diet in the impairment of cardiovascular function in apolipoprotein E-deficient mouse. It is reported that, several signaling steps are triggered by excess production of ROS responding to internal or environmental stress.

The present study was undertaken to examine the hemodynamic state using the latest ultrasound biomicroscopy (UBM) technique and to investigate the effect of local shear stress on the development of atherosclerosis in the constrictive collar-treated carotid arteries of apolipoprotein E-deficient (apoE-/-) mice. Fifty-six male apoE-/- mice fed a high-lipid diet were divided into an interventional group (n = 48) and the control group (n = 8). Constrictive and nonconstrictive collars were placed around the carotid artery of the mice in the interventional group and the control group, respectively. The carotid lumen diameters and flow velocities were measured by UBM, and shear stress in the lesion region was calculated. Histopathology and electron microscopy were performed to observe the morphological changes in the carotid artery. in the region proximal to the constrictive collar, shear stress was significantly reduced 2 days after collar placement and remained low over time compared with the baseline level. In contrast, within the constrictive collar region, shear stress was increased significantly. Although endothelial permeability was enhanced in both regions, monocyte chemotaxis protein-1 (MCP-l) expression, macrophage infiltration, and atherosclerotic lesions were more prominent in the region proximal to the constrictive collar. Moreover, increased MCPI expression was observed as early as 2 days after constrictive collar placement, which preceded the morphological changes of the vessel wall. In conclusion, UBM offers a noninvasive and reliable technique for measuring shear stress in apoE-/- mice. Persistent low shear stress promotes endothelial permeability and enhances MCP-l expression and macrophage recruitment, which were essential in the pathogenesis of atherosclerosis in apoE-/- mice. [ABSTRACT FROM AUTHOR]

Carotid artery stenosis (CAS) is an atherosclerotic disease characterized by a narrowing of the artery lumen and a high risk of ischemic stroke. Risk factors of atherosclerosis, including smoking, hypertension, hyperglycemia, hyperlipidemia, aging, and disrupted circadian rhythm, may potentiate atherosclerosis in the carotid artery and further reduce the arterial lumen. Ischemic stroke due to severe CAS and cerebral ischemic/reperfusion (I/R) injury after the revascularization of CAS also adversely affect clinical outcomes. Melatonin is a pluripotent agent with potent anti-inflammatory, anti-oxidative, and neuroprotective properties. Although there is a shortage of direct clinical evidence demonstrating the benefits of melatonin in CAS patients, previous studies have shown that melatonin may be beneficial for patients with CAS in terms of reducing endothelial damage, stabilizing arterial plaque, mitigating the harm from CAS-related ischemic stroke and cerebral I/R injury, and alleviating the adverse effects of the related risk factors. Additional pre-clinical and clinical are required to confirm this speculation. [ABSTRACT FROM AUTHOR]