Peripheral Vascular Atherosclerosis Research Articles

Critical gene signature and immunological characterization in peripheral vascular atherosclerosis: novel insights from mendelian randomization and transcriptomics.

Peripheral vascular atherosclerosis (PVA) is a chronic inflammatory disease characterized by lipid accumulation in blood vessel walls, leading to vessel narrowing and inadequate blood supply. However, the molecular mechanisms underlying PVA remain poorly understood. In this study, we employed a combination of Mendelian randomization (MR) analysis and integrated transcriptomics to identify the critical gene signature associated with PVA. This study utilized three public datasets (GSE43292, GSE100927 and GSE28829) related to peripheral vascular atherosclerosis obtained from the Gene Expression Omnibus database. Instrumental variables (IVs) were identified through expression quantitative trait loci (eQTL) analysis, and two-sample MR analysis was performed using publicly available summary statistics. Disease critical genes were identified based on odds ratios and intersected with differentially expressed genes in the disease dataset. GSE28829 dataset was used to validate the screened disease critical genes. Functional enrichment analysis, GSEA analysis, and immune cell infiltration analysis were performed to further characterize the role of these genes in peripheral vascular atherosclerosis. A total of 26,152 gene-related SNPs were identified as IVs, and 242 disease-associated genes were identified through MR analysis. Ten disease critical genes (ARHGAP25, HCLS1, HVCN1, RBM47, LILRB1, PLAU, IFI44L, IL1B, IFI6, and CFL2) were significantly associated with peripheral vascular atherosclerosis. Functional enrichment analysis using KEGG pathways revealed enrichment in the NF-kappa B signaling pathway and osteoclast differentiation. Gene set enrichment analysis further demonstrated functional enrichment of these genes in processes related to vascular functions and immune system activation. Additionally, immune cell infiltration analysis showed differential ratios of B cells and mast cells between the disease and control groups. The correlations analysis highlights the intricate interplay between disease critical genes and immune cells associated with PVA. In conclusion, this study provides new insights into the molecular mechanisms underlying PVA by identifying ten disease critical genes associated with the disease. These findings, supported by differential expression, functional enrichment, and immune system involvement, emphasize the role of these genes in vascular function and immune cell interactions in the context of PVA. These findings contribute to a better understanding of PVA pathogenesis and offer potential targets for further mechanistic exploration and therapeutic interventions.

Cheese consumption on atherosclerosis, atherosclerotic cardiovascular diseases and its complications: A two-sample Mendelian randomization study

Background and aimEvidence from prospective cohort studies has revealed an inverse association between cheese consumption and the development of atherosclerosis (AS), atherosclerotic cardiovascular diseases (ASCVD), and their complications. However, it remains unclear whether this observed association is influenced by potential confounding factors that may arise during the long-term development process of AS, ASCVD, and its complications. Therefore, to further clarify the causal relationship between cheese consumption and AS, ASCVD, and its complications, we conducted a two-sample Mendelian randomization (MR) analysis to explore the causal association between cheese intake and the aforementioned health outcomes. Methods and resultsWe employed a two-sample MR analysis based on publicly available genome-wide association studies (GWAS) to infer the causal relationship, with no overlap between their participating populations. The effect estimates were calculated using the random-effects inverse-variance-weighted method. Sensitivity analyses were conducted using Cochran's Q statistic, funnel plot, leave-one-out analysis, and MR-Egger intercept tests. The genetically predicted cheese intake was found to be associated with lower risks of coronary AS (odds ratio [OR] = 0.72, 95 % confidence interval [CI] 0.59–0.88, P = 0.001), peripheral vascular AS (OR = 0.56, 95 % CI 0.37–0.84, P = 0.006), other vascular AS (OR = 0.66, 95 % CI 0.44–0.99, P = 0.043), coronary artery disease (OR = 0.64, 95 % CI 0.56–0.74, P = 1.57e-09), angina pectoris (OR = 0.70, 95 % CI 0.58–0.84, P = 4.92e-05), myocardial infarction (OR = 0.63, 95 % CI 0.52–0.77, P = 3.56e-06), heart failure (OR = 0.62, 0.49–0.79, P = 1.20e-04), total ischemic stroke (OR = 0.76, 95 % CI 0.63–0.91, P = 0.003), peripheral artery disease (OR = 0.64, 95 % CI 0.43–0.95, P = 0.028), and cognitive impairment (OR = 0.65, 95 % CI 0.56–0.74, P = 3.40e-10). However, no associations were observed for cerebrovascular AS, arrhythmia, cardiac death, ischemic stroke (large artery AS), ischemic stroke (small vessel), ischemic stroke (cardioembolic), and transient ischemic attack. ConclusionThis two-sample MR analysis reveals a causally inverse association between cheese intake and multi-vascular AS (including coronary AS, peripheral vascular AS, and other vascular AS), as well as multiple types of ASCVD and its complications (such as coronary artery disease, angina pectoris, myocardial infarction, heart failure, total ischemic stroke, and peripheral artery disease). The findings from this study may lay a stronger theoretical foundation and present new opportunities for the dietary management of future atherosclerotic cardiovascular diseases.

РЕГУЛЯЦИЯ СИСТЕМНОГО ВОСПАЛИТЕЛЬНОГО ОТВЕТА У ПАЦИЕНТОВ С МУЛЬТИФОКАЛЬНЫМ АТЕРОСКЛЕРОЗОМ

Introduction. Data on the role of inflammation in the progression and manifestation of multifocal atherosclerosis (MFA) are contradictory. The systemic process of multiple lesions of different vascular beds in patients with an established diagnosis of coronary heart disease (CHD) is due to several parallel pathological mechanisms. In general, in the pathogenesis of both coronary atherosclerosis and atherosclerosis of peripheral arteries, one of the factors is the variability of immune response genes and cytokines, regulators of the inflammatory response. The aim of this work was to determine the role of variability in the genes of cytokines and innate immune response receptors in the structure of mechanisms associated with the development of MFA in patients with coronary artery atherosclerosis. Materials and methods. 260 patients with CAD (mean age 58 years) were examined. Of all those included in the study, at the time of the survey, MFA was found in 180 people (69.23%), while the incidence of MFA in men and women is comparable (70.33 vs. 64.71%, respectively). There is also no significant difference in the incidence of MFA in the two age groups (up to 60 years, 45% have lesions of two or more vascular beds, and in people older than 60 years, MFA was found in 55% of cases). All patients were informed about the course of the study and voluntarily signed an informed consent. Blood was collected from the cubital vein into Vacutainer tubes with K3EDTA. DNA isolation was carried out using the phenol-chloroform extraction method. Genotyping of 47 polymorphic sites with a single nucleotide change (SNV) of 19 genes proven to be associated with the regulation of the systemic inflammatory response (cytokines, innate immunity receptors) was performed in a 96-well format using TaqMan technology (LifeTechnologies, USA) and real-time result detection with using the ViiATM 7 RealTime PCR System (LifeTechnologies, USA) for polymerase chain reaction in accordance with the instructions. Associations were analyzed using Snpstats (https://www.snpstats.net/start.htm). Odds ratio (OR) and 95% CI for OR were calculated for risk assessment. Results. One association has been established that demonstrates a negative impact and increases the risk of developing MFA in young and middle age. Carriage of the G rs11685424 IL1RL1 allele increases the risks of earlier development of peripheral arterial lesions by 2 times (OR 2.11 (95% CI 1.09-4.06), p = 0.024) according to the recessive inheritance model. At the same time, variability in three sites (rs1974675; rs6758936; rs3755276) of the IL18 receptor gene (IL18R1) reduces the risk of MFA detection by three times (p=0.12; p=0.034: p=0.026, respectively) and this pattern is also observed in patients older age group. In the carriers of the A/A rs1974675, T/T rs3755276 and A/A rs6758936 genotypes in persons over 60 years of age, MFA was diagnosed less frequently (p=0.024; p=0.037; p=0.011, respectively). Conclusion. It has been shown that in patients with significant coronary atherosclerosis, the progression of peripheral vascular atherosclerosis is more associated with the variability of the genes responsible for the regulation of the systemic inflammatory response, rather than genes and their variants that determine the severity and strength of the immune response.

[Research advances on the mechanism of circular RNA in diabetic wound healing].

In recent years, a large number of studies have shown that non-coding RNAs play an important role in wound healing process. Among them, studies on the mechanism of circular RNA (circRNA) have shown that circRNA is closely related to the proliferation of cells related to wound healing, such as endothelial progenitor cells and keratinocytes, and circRNA is also involved in the chronic wound healing process. Based on the introduction of the related concept of circRNA, this paper focuses on the possible regulatory mechanism of circRNA in different stages of diabetic wound healing and summarizes the potential role of circRNA in the process of diabetic peripheral vascular atherosclerosis, aiming to explore the in-depth molecular mechanism and clinical significance of circRNA in diabetic wound healing process, and provide reference for further research.

Study on the Diagnostic Effect of Two-dimensional Ultrasound Imaging on Peripheral Vascular Atherosclerosis

Study on the Diagnostic Effect of Two-dimensional Ultrasound Imaging on Peripheral Vascular Atherosclerosis

Excimer laser technology in percutaneous coronary interventions: Cardiovascular laser society's position paper

Excimer Laser Coronary Atherectomy (ELCA) is a well-established therapy that emerged for the treatment of peripheral vascular atherosclerosis in the late 1980s, at a time when catheters and materials were rudimentary and associated with the most serious complications. Refinements in catheter technology and the introduction of improved laser techniques have led to their effective use for the treatment of a wide spectrum of complex coronary lesions, such as thrombotic lesions, severe calcific lesions, non-crossable or non-expandable lesions, chronic occlusions, and stent under-expansion. The gradual introduction of high-energy strategies combined with the contrast infusion technique has enabled us to treat an increasing number of complex cases with a low rate of periprocedural complications. Currently, the use of the ELCA has also been demonstrated to be effective in acute coronary syndrome (ACS), especially in the context of large thrombotic lesions.

Subclinical measures of peripheral atherosclerosis and risk of new-onset atrial fibrillation in men and women from general population

Abstract Background Limited data on the link between peripheral vascular atherosclerosis measures and the risk of new-onset atrial fibrillation (AF) in the general population exists. Moreover, comprehensive assessment of the association between the two conditions among men and women is sparse. Purpose To determine the association between baseline and longitudinal measures of carotid intima-media thickness (cIMT), carotid plaque, and ankle-brachial index (ABI) with new-onset AF. Methods 12840 participants free of AF at baseline were included in this large prospective population-based cohort study. Among the 12840 included participants, 11998 had at least one available measure for cIMT and 8532 for ABI. Presence of carotid plaque was only measured at baseline (n=11766). Three repeated measurements for cIMT and two repeated measurements for ABI were available during follow-up. The association between baseline cIMT, carotid plaque, and ABI as well as longitudinal changes in cIMT and ABI with incident AF were assessed using Cox regression and joint models respectively. Models were adjusted for age and traditional cardiovascular risk factors. Results During a median follow-up of 9.1 years, 1362 incident AF occurred. Baseline cIMT (adjusted hazard ratio–HR; 95% confidence interval–CI: 3.46; 1.97–6.05) and longitudinal changes in cIMT (adjusted HR; 95% CI: 3.35; 1.89–5.95) showed strong independent associations with incident AF among women (Figure 1). Baseline ABI showed a significant association with incident AF among men (adjusted HR; 95% CI: 0.61; 0.38–0.97) and a borderline significant association among women (adjusted HR; 95% CI: 0.65; 0.41–1.02). Longitudinal changes in ABI were not associated with the risk of incident AF independent of traditional risk factors. Conclusions Carotid atherosclerosis at baseline and progression of carotid atherosclerosis during follow-up were strongly associated with new-onset AF among women. Lower extremity peripheral atherosclerosis at baseline, but not its longitudinal changes during follow-up, was significantly associated with incident AF, in particular among men. Our findings imply that screening and monitoring for carotid atherosclerosis carry a potential for prevention of AF among women. Figure 1. HR of baseline cIMT and AF Funding Acknowledgement Type of funding source: Public Institution(s). Main funding source(s): Netherlands Organization for the Health Research and Development (ZonMw); the Research Institute for Diseases in the Elderly (RIDE)

Current concepts regarding drug dosing for peripheral stents.

Drug-eluting stent (DES) are the mainstay therapy for the treatment of coronary artery disease. Stent design and drug-elution strategies have evolved over the years leading to the last generation DES which shows optimal safety and efficacy outcome. Peripheral arteries have different mechanical and biological features and the lessons learned from the coronary field have been difficult to introduce into the development of peripheral vascular technologies. First, due to its complex biomechanical behavior the use of metallic stents is limited in some vascular segments (i.e., distal superficial fermoral artery [SFA]). Also, peripheral vascular atherosclerosis is different containing higher levels of plaque burden and calcium. Finally, peripheral arterial disease tends to be more aggressive including longer lesions and higher incidence of total chronic occlusion. In general terms, restenosis in the peripheral vascular territory is more aggressive and occurs at a later time (~12 months) requiring a different pharmacokinetic profile compared to coronary technologies. Several strategies have been evaluated in the peripheral arteries raging from the bare metal stent to the drug coated balloon and drug eluting stent with outcome varying depending on the different field of application (i.e. SFA and below-the-knee). Results coming from the clinical trial are encouraging but further studies and direct comparison among the different technologies are demanded to determine the best therapy for peripheral vascular disease.

Femoral Intima-media Thickness, Risk Factors, and Markers of Inflammation in Cardiovascular Disease

Abstract 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 hyper-tension, 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.

Peripheral vascular atherosclerosis in a novel PCSK9 gain-of-function mutant Ossabaw miniature pig model

Hypercholesterolemia is a major risk factor for atherosclerosis. Remaining challenges in the management of atherosclerosis necessitate development of animal models that mimic human pathophysiology. We characterized a novel mutant pig model with DNA transposition of D374Y gain-of-function (GOF) cDNA of chimp proprotein convertase subtilisin/kexin type-9 (PCSK9), and tested the hypothesis that it would develop peripheral vascular remodeling and target organ injury in the kidney. Wild-type or PCSK9-GOF Ossabaw miniature pigs fed a standard or atherogenic diet (AD) (n = 7 each) were studied in vivo after 3 and 6 months of diet. Single-kidney hemodynamics and function were studied using multidetector computed tomography and kidney oxygenation by blood oxygen level-dependent magnetic resonance imaging. The renal artery was evaluated by intravascular ultrasound, aortic stiffness by multidetector computed tomography, and kidney stiffness by magnetic resonance elastography. Subsequent ex vivo studies included the renal artery endothelial function and morphology of abdominal aorta, renal, and femoral arteries by histology. Compared with wild type, PCSK9-GOF pigs had elevated cholesterol, triglyceride, and blood pressure levels at 3 and 6 months. Kidney stiffness increased in GOF groups, but aortic stiffness only in GOF-AD. Hypoxia, intrarenal fat deposition, oxidative stress, and fibrosis were observed in both GOF groups, whereas kidney function remained unchanged. Peripheral arteries in GOF groups showed medial thickening and development of atheromatous plaques. Renal endothelial function was impaired only in GOF-AD. Therefore, the PCSK9-GOF mutation induces rapid development of atherosclerosis in peripheral vessels of Ossabaw pigs, which is exacerbated by a high-cholesterol diet. This model may be useful for preclinical studies of atherosclerosis.

CORRELATIONS BETWEEN THE SEVERITY OF CARDIOVASCULAR AUTONOMIC NEUROPATHY AND OTHER COMPLICATIONS IN TYPE 2 DIABETES MELLITUS

Introduction. Cardiovascular Autonomic Neuropathy (CAN), also known as the “silent killer”, represents a serious complication of diabetes mellitus and is most of the times ignored. This is a highly topical issue, given the increased number of patients diagnosed with type 2 diabetes mellitus (T2DM). The purpose of this study was to determine the association between the severity of CAN and the severity of other microvascular complications, such as diabetic sensory-motor polyneuropathy (DSMP), diabetic retinopathy (DR) and macrovascular complications (carotid and peripheral vascular atherosclerosis) in patients with T2DM. Methods. A total of 149 patients with T2DM were assessed for CAN using the Ewing’s battery of cardiovascular autonomic function tests. The patients were evaluated for diabetic microvascular complications (DSMP, RD), respectively macrovascular complications (carotid atherosclerosis by intima media thickness and peripheral vascular atherosclerosis by ankle-brachial index). Results. Of the 45 patients with intermediate CAN, 35.55% were without DR, 51.11% had non-proliferative DR and 13.33% had proliferative DR. From the 13 patients with severe CAN, 76.92% had non-proliferative DR and 23.07% had proliferative DR. From the 56 patients with subclinical CAN, 26.7% had no DSMP, 48.2% had subclinical DSMP and 25% had clinical DSMP. Of the 45 patients with intermediate CAN, 11.2% had subclinical DSMP and 80% had clinical DSMP. Conclusion. In T2DM we demonstrated that an increase in the severity of cardiovascular autonomic injury is associated with an increase in the prevalence and severity of DSMP and DR, respectively carotid and peripheral atherosclerosis.

Abstract WP291: Predictors of 30-day Same Hospital Readmission After Ischemic Stroke

Background: Health systems across the US are focusing on preventable hospital readmissions. Patient care systems are often focused on shorter hospital length of stays and faster discharges, while renewed efforts to regulate this penalizes health systems for readmissions. We aimed to explore factors that predict 30-day same hospital readmission after stroke, the impact on inpatient hospital cost and if a lower length of stay increased readmissions. Methods: We included patients discharged from UC Health System with the principle diagnosis ischemic stroke (ICD: 9 433.01-9; 346) from 10/1/2011 to 4/30/2015. We excluded all patients with inhospital death, discharged to hospice or who left against medical advice (AMA). Patients are grouped in: 1) readmitted within 30 days (all cause); 2) not admitted within 30 days. We compared demographics, pre-existing/comorbid conditions and health care metrics (length of stay (LOS), direct cost for the index admission and readmission. Severity of illness adjustments for LOS and cost were made using the University HealthSystem Consortium® (UHC) algorhthm. We used unpaired t-test for comparing means continuous variables) and chi-square to compare frequencies. Results: There were a total of 770 discharges, Group 1: 91, Group 2: 679. The groups were balanced in age, sex, race, and ethnicity, direct care cost and insurance status. Patients with readmission had longer adjusted LOS (O/E), 1.15±1.16 versus 0.97±1.11 (p=0.024), more renal failure (33.0 versus 14.0%, p<0.0001), peripheral vascular disease (9.9 versus 4.4%, p=0.048) and chronic atherosclerosis (40.7 versus 24.4%, p=0.002). (Table) Direct cost for readmissions was substantial, but not higher than for the index admission (14,746±21,795 versus 11,830±14,415, NS). Conclusion: There is no evidence that lower hospital length of stay contributed to readmission. We identified unique markers for readmission risk, which requires further review in larger samples across regions and health care systems to better understand what factors lead to readmission after stroke and to identify potentially preventable causes of readmission.

Association of interleg difference of ankle brachial index with overall and cardiovascular mortality in chronic hemodialysis patients

Background: The ankle-brachial index (ABI) is associated with peripheral vascular atherosclerosis, adverse cardiovascular outcomes, and all-cause mortality. However, there were limited data available on studying the effect of interleg ABI difference. Methods: We investigated the association of the interleg ABI difference with overall and cardiovascular mortality in chronic hemodialysis in a retrospective observational cohort of 369 Taiwanese patients undergoing chronic hemodialysis. Results: An interleg ABI difference of ≥0.15 in hemodialysis patients had significant predictive power for all-cause and cardiovascular mortality in crude analysis. The hazard ratio (HR) for all-cause mortality was 3.00 [95% confidence interval (CI), 1.91–4.71]; the HR for cardiovascular mortality was 3.13 (95% CI, 1.82–5.38). After adjustment for confounding variables, this difference continued to have significant predictive power for all-cause mortality but lost its predictive power for fatal cardiac outcome. ABI <0.9 and high brachial-ankle pulse wave velocity were independently associated with an interleg ABI difference of ≥0.15 in hemodialysis patients. Moreover, in the subgroup analysis, we found that this difference was an independent factor for overall and cardiovascular mortality, particularly in elder patients, female patients, or those with ABI <0.9. Conclusion: Detection of an interleg ABI difference of ≥0.15 was an independent risk factor for overall mortality in hemodialysis patients but it may affect cardiovascular mortality through the effect of peripheral vascular disease.

Vascular Smooth Muscle Cells in Cerebral Aneurysm Pathogenesis

Vascular smooth muscle cells (SMC) maintain significant plasticity. Following environmental stimulation, SMC can alter their phenotype from one primarily concerned with contraction to a pro-inflammatory and matrix remodeling phenotype. This is a critical process behind peripheral vascular disease and atherosclerosis, a key element of cerebral aneurysm pathology. Evolving evidence demonstrates that SMCs and phenotypic modulation play a significant role in cerebral aneurysm formation and rupture. Pharmacological alteration of smooth muscle cell function and phenotypic modulation could provide a promising medical therapy to inhibit cerebral aneurysm progression. This study reviews vascular SMC function and its contribution to cerebral aneurysm pathophysiology.

Aortic sclerosis and mitral annulus calcification: a window to vascular atherosclerosis?

Several similarities exist between atherosclerosis in the vasculature and chronic degenerative changes in valvular structures. It has been suggested that aortic valve sclerosis (AVS) and mitral annulus calcification (MAC) are manifestations of a generalized atherosclerosis, have similar pathogenesis, share common risk factors and are observed with higher prevalence in patients with different forms of atherosclerotic vascular disease. Moreover, recent studies have shown a close relation of MAC and AVS with adverse cardiovascular and cerebrovascular outcomes. However, many patients with AVS or MAC do not have coexisting peripheral vascular atherosclerosis and vice versa. Lipid-reducing therapy has been uniformly unsuccessful in slowing valvular calcification. Thus, whether valve calcifications are the result of a more generalized atherosclerosis, or reflect a primary degenerative process, progressing with advancing age, still remains. From a clinical point of view, it is of great importance to identify common links between valve calcification and vascular atherosclerosis with a view to assess whether the detection of AVS, MAC or both are indicative of subclinical atherosclerosis and predicts cardiovascular or cerebrovascular events. Thus, in this article, the authors review current evidence regarding the association between AVS and MAC with vascular atherosclerosis.

Przemieszczenie stentu wieńcowego do tętnicy biodrowej – powikłanie ze szczęśliwym zakończeniem

ENWEndNote BIBJabRef, Mendeley RISPapers, Reference Manager, RefWorks, Zotero AMA Dziuba M, Lenczewski P, Chiżyński K, et al. Coronary stent deployment to the iliac artery – a complication with a successful treatment. Advances in Interventional Cardiology/Postępy w Kardiologii Interwencyjnej. 2012;8(2):146-152. doi:10.5114/pwki.2012.29656. APA Dziuba, M., Lenczewski, P., Chiżyński, K., Zielińska, M., Religa, W., & Kaszyński, M. et al. (2012). Coronary stent deployment to the iliac artery – a complication with a successful treatment. Advances in Interventional Cardiology/Postępy w Kardiologii Interwencyjnej, 8(2), 146-152. https://doi.org/10.5114/pwki.2012.29656 Chicago Dziuba, Michał, Piotr Lenczewski, Krzysztof Chiżyński, Marzenna Zielińska, Wojciech Religa, Marek Kaszyński, and Ludomir Stefańczyk et al. 2012. "Coronary stent deployment to the iliac artery – a complication with a successful treatment". Advances in Interventional Cardiology/Postępy w Kardiologii Interwencyjnej 8 (2): 146-152. doi:10.5114/pwki.2012.29656. Harvard Dziuba, M., Lenczewski, P., Chiżyński, K., Zielińska, M., Religa, W., Kaszyński, M., Stefańczyk, L., and Kidawa, M. (2012). Coronary stent deployment to the iliac artery – a complication with a successful treatment. Advances in Interventional Cardiology/Postępy w Kardiologii Interwencyjnej, 8(2), pp.146-152. https://doi.org/10.5114/pwki.2012.29656 MLA Dziuba, Michał et al. "Coronary stent deployment to the iliac artery – a complication with a successful treatment." Advances in Interventional Cardiology/Postępy w Kardiologii Interwencyjnej, vol. 8, no. 2, 2012, pp. 146-152. doi:10.5114/pwki.2012.29656. Vancouver Dziuba M, Lenczewski P, Chiżyński K, Zielińska M, Religa W, Kaszyński M et al. Coronary stent deployment to the iliac artery – a complication with a successful treatment. Advances in Interventional Cardiology/Postępy w Kardiologii Interwencyjnej. 2012;8(2):146-152. doi:10.5114/pwki.2012.29656.

SYNERGISTIC IMPACT OF CHRONIC KIDNEY DISEASE AND DIABETES MELLITUS ON PERIPHERAL VASCULAR ATHEROSCLEROTIC PLAQUE NEOVASCULARIZATION AND INFLAMMATION

Neovascularization and inflammation in peripheral vascular atherosclerosis is increased in patients with diabetes mellitus (DM). Although chronic kidney disease (CKD) augments thrombotic risk in these patients, the impact of CKD on atherosclerotic plaque progression in the setting of DM remains

New Insights About Vitamin D and Cardiovascular Disease

The worsening worldwide trend toward nutritional insufficiency and the emerging knowledge of the nonhormonal actions of vitamin D and its metabolites have increased interest in the synthesis, metabolism, and action of vitamin D. Vitamin D deficiency has been linked with hypertension, myocardial infarction, and stroke, as well as other cardiovascular-related diseases, such as diabetes, congestive heart failure, peripheral vascular disease, atherosclerosis, and endothelial dysfunction. This review discusses the physiology and definition of vitamin D deficiency, evaluates the worldwide prevalence of vitamin D deficiency, and discusses recent evidence for the association between hypovitaminosis D and cardiovascular disease. Few randomized, controlled trials have evaluated the effect of vitamin D replacement on cardiovascular outcomes, and the results have been inconclusive or contradictory. Carefully designed randomized, controlled trials are essential to evaluate the role of vitamin D supplementation in reducing cardiovascular disease.

Homocysteine, a Risk Factor for Cardiovascular Disease.

Fasting hyperhomocysteinemia is an independent risk factor for coronary artery disease, stroke, peripheral vascular atherosclerosis, and for arterial and venous thromboembolism. The risk for cardiovascular disease with homocysteine is similar to conventional risk factors. The interaction of hyperhomocysteinemia with hypertension and smoking is strong and the combined effect is more than multiplicative. The combined effect of homocysteine and cholesterol is additive. Homocysteine produces atherosclerosis, thromboembolism, and vascular endothelial cell injury. Vascular dysfunction produced by homocysteine may be due to endothelial cell damage. Homocysteinemia-induced atherosclerosis is probably due to various factors including endothelial cell injury, inability to sustain S-nitroso-homocysteine formation because of imbalance between production of nitric oxide by dysfunctional endothelium and homocysteine, smooth muscle cell proliferation, and thromboembolism. There is strong evidence that endothelial cell injury is associated with oxidative stress produced by homocysteine. Hyperhomocysteinemia is associated with numerous conditions, including coronary disease, stroke, peripheral vascular disease (carotid artery and cerebrovascular atherosclerosis), venous thrombosis, renal disease, diabetes mellitus, and organ transplant. Folic acid, vitamin B12 and B6 have been shown to be beneficial in reducing plasma homocysteine levels. Folic acid is specifically very effective, safe and inexpensive.

Molecular Pathways Involved in RAGE Mediated Attenuation of Arteriogenesis

The receptor for advanced glycation endproducts (RAGE) has been implicated in promoting vascular dysfunction through the activation of proinflammatory cascades and the induction of oxidative stress. Chronic activation of RAGE is associated with diabetes‐related vascular complications including coronary and peripheral vascular atherosclerosis and diabetic retinopathy. We have demonstrated that RAGE activation in monocytes and macrophages also regulates vascular remodeling in response to acute ischemia in a mouse model of hind‐limb ischemia. Lentiviral‐directed overexpression of RAGE in monocytes prevents the development of collateral vessels (arteriogenesis) in response to hind‐limb ischemia. To better understand the molecular mechanisms responsible for these observations, we have undertaken a cell culture approach to address the effect of monocyte ‐specific RAGE activation on the production of proarteriogenic and proangiogenic factors under hypoxic conditions and determine how chronic RAGE activation influences receptor recycling. We have generated soluble RAGE using a baculovirus system, which will provide a valuable reagent to evaluate RAGE signaling in response to hypoxic conditions. In addition, we are generating N‐terminal GFP‐tagged versions of the RAGE receptor that will allow us to evaluate RAGE receptor recycling following activation in a macrophage cell line.