scholarly journals Risk factors and pathogenesis of atherosclerotic lesion.

1999 ◽  
Vol 66 (6) ◽  
pp. 372-381
Author(s):  
Goro Asano ◽  
Ruojiao Wang ◽  
Kohji Kameyama ◽  
Nobutaka Yamada ◽  
Munehiko Onda ◽  
...  
Keyword(s):  
Risk Factors ◽  
Atherosclerotic Lesion

scholarly journals Mechanisms of aortic valve calcification: the LDL-density-radius theory: a translation from cell signaling to physiology

2010 ◽  
Vol 298 (1) ◽  
pp. H5-H15 ◽  
Author(s):  
Nalini M. Rajamannan
Keyword(s):  
Risk Factors ◽  
Severe Aortic Stenosis ◽  
Elevated Serum ◽  
Experimental Studies ◽  
Atherosclerotic Lesion ◽  
Disease Process ◽  
Prognostic Indicator ◽  
Epidemiologic Studies ◽  
Factors Associated ◽  
Early Stages

Recent epidemiologic studies have revealed the risk factors associated for vascular atherosclerosis, including the male sex, smoking, hypertension, and elevated serum cholesterol, similar to the risk factors associated with the development of AV stenosis. An increasing number of models of experimental hypercholesterolemia demonstrate features of atherosclerosis in the AV, which are similar to the early stages of vascular atherosclerotic lesions. Experimental and clinical studies demonstrate that the hypercholesterolemic AV develops an atherosclerotic lesion which is proliferative and expresses high levels of osteoblast bone markers which mineralize over time to form bone. Calcification, the end-stage process of the disease, is necessary to understand as a prognostic indicator in the modification of this cellular process before it is too late. In summary, these findings suggest that medical therapies may have a potential role in patients in the early stages of this disease process to slow the progression to severe aortic stenosis and to delay the timing of the need for surgery. The translation of these experimental studies to clinical practice will be important to understand the potential for medical therapy for this disease process.

scholarly journals Coronary arteries thrombosis in a patient with myocarditis

2020 ◽  
Vol 27 (2) ◽  
pp. 46-56
Author(s):  
O. M. Parkhomenko ◽  
Ya. M. Lutay ◽  
O. I. Irkin ◽  
A. O. Stepura ◽  
M. Yu. Sokolov ◽  
...  
Keyword(s):  
Magnetic Resonance Imaging ◽  
Risk Factors ◽  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Coronary Arteries ◽  
Coronary Thrombosis ◽  
Atherosclerotic Lesion ◽  
Resonance Imaging ◽  
Acute Thrombosis ◽  
Regular Intake

The article presents the case of the development of acute thrombosis of two coronary arteries in a 35-year-old patient without atherosclerotic lesion of the heart vessels according to optical coherence tomography. Acute myocardial infarction in a patient developed on the background of previous diffuse myocarditis, foci of which of different time were identified during magnetic resonance imaging. Smoking and chronic intoxication due to contact with paint and varnish materials and regular intake of alcohol were the only risk factors for myocarditis and coronary thrombosis that were able to be detected in this patient.

scholarly journals Level of N-terminal fragment of brain natriuretic peptide progenitor and atherosclerotic damage of brachocephalic arteries in patients with rheumatoid arthritis with inefficiency and/or injurability of basic anti - inflammatory treatment

2019 ◽  
Vol 91 (5) ◽  
pp. 34-39
Author(s):  
E V Gerasimova ◽  
T V Popkova ◽  
A V Martynova ◽  
E I Markelova ◽  
D S Novikova ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Risk Factors ◽  
Cardiovascular Diseases ◽  
Natriuretic Peptide ◽  
Prognostic Significance ◽  
Atherosclerotic Lesion ◽  
Control Group ◽  
Inflammatory Drugs ◽  
Anti Inflammatory ◽  
Traditional Risk Factors

The high prognostic significance of the concentration of the N-terminal - pro-B-type natriuretic peptide (NT-proBNP) in the development of cardiovascular diseases (CVD) was identified for rheumatoid arthritis (RA) and general populations. Aim: to investigate the significance of NT-proBNP level in patients (pts) with RA with the ineffectiveness and/or intolerance of basic anti - inflammatory therapy; compare the level of NT-proBNP with atherosclerotic lesion of the brachiocephalic arteries (BCA), traditional risk factors and inflammatory markers. Materials and methods. The investigation enrolled 28 pts (24women/4men) with the lack of efficacy/resistance and/or intolerance of basic anti - inflammatory drugs (DMARDs); median age was 55 [46; 61] years, median disease duration 114 [60; 168] month; DAS28 6,2 [5.1; 7.0]; SDAI 35.0[23.9; 51.0], CDAI 30.0[21.0; 42.0], serum positivity for rheumatoid factor (RF) (100%)/anti - cyclic citrullinated peptide antibodies (ACCP) (86%). The study did not include RA pts with congestive heart failure. High incidence of traditional risk factors was found in RA pts: arterial hypertension - in 75%, dyslipidemia - 61%, smoking - 17%, overweight - 61%, family history of cardiovascular diseases - 36%, hypodynamia - 68%. Coronary artery disease was diagnosed in 11% RA pts. Lack of efficacy of 3 or more DMARDs was found in 46% of pts, intolerance to previous therapy with DMARDs - in 54% pts. 47% were receiving methotrexate (20 [18; 25] mg/week), 11% - leflunomide, 7% - sulfasalazine, 46% - glucocorticoids, 75% - non - steroidal anti - inflammatory drugs. The control group consisted of 20 healthy donors, comparable to pts by age and sex. Serum levels of of NT-proBNP were measured using electrochemiluminescence method Elecsys proBNP II (Roche Diagnostics, Switzerland). The determination of the intima - media thickness (IMT) BCA were assessed from duplex scanning. Atherosclerotic lesion of BCA was assessed by the presence of atherosclerotic plaque (IMT ≥1.2 mm). Results. NT-proBNP concentrations in RA pts proved to be higher (78.7 [41.4; 101.3] pg/ml) than those in the control group (55.3 [36.6; 67.3] pg/ml, p100 pg/ml - 1 group (n=6) and ≤100 pg/ml - 2 group (n=22). Groups of RA pts did not differ in gender, age, activity of RA, frequency of detection of traditional risk factors. Atherosclerotic lesion of the BCA was detected in 3 (50%) pts of the 1 group and in 8 (36%) pts of the 2 group (p>0.05). In RA pts the level of NT-proBNP correlated with age (r=0.39; p

scholarly journals ULTRASOUND MARKERS OF PREMANIFEST ATHEROSCLEROSIS OF CAROTID AND FEMORAL ARTERIES IN ASSESSMENT OF CARDIOVASCULAR RISK

2018 ◽  
pp. 92-98 ◽  
Author(s):  
A. I. Ershova ◽  
S. A. Boytsov ◽  
О. M. Drapkina ◽  
Т. V. Balakhonova
Keyword(s):  
Risk Factors ◽  
Cardiovascular Risk ◽  
Ultrasound Examination ◽  
Subclinical Atherosclerosis ◽  
Atherosclerotic Lesion ◽  
Unknown Risk ◽  
High Prevalence ◽  
Risk Patients ◽  
Predictive Role ◽  
Traditional Risk Factors

More than a half of cardiovascular events occur in low to moderate cardiovascular risk patients if assessed based on the traditional risk factors. At the same time, ultrasound examination of arteries makes it possible to reveal atherosclerosis even at early stages of its development. High prevalence of subclinical atherosclerosis in low to moderate risk patients, which is a realization of traditional and “unknown” risk factors, makes ultrasound examination a useful method for risk stratification. The review is focused on ultrasound markers of atherosclerosis with association to traditional risk factors, on the possibility to improve predictive role of current scores and influence on outcomes. Predictive significance of the markers is regarded for primary prevention in general population, in high risk persons and from the perspective of quantitative indicator of atherosclerotic lesion grade or plausibility as a surrogate cardiovascular diseases marker.

Carbenoxolone treatment attenuates symptoms of metabolic syndrome and atherogenesis in obese, hyperlipidemic mice

2007 ◽  
Vol 293 (6) ◽  
pp. E1517-E1528 ◽  
Author(s):  
Alli M. Nuotio-Antar ◽  
David L. Hachey ◽  
Alyssa H. Hasty
Keyword(s):  
Risk Factors ◽  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Body Fat ◽  
Fat Mass ◽  
Severe Obesity ◽  
Plasma Lipids ◽  
Ldl Receptor ◽  
Atherosclerotic Lesion ◽  
Body Fat Mass

Glucocorticoids, which are well established to regulate body fat mass distribution, adipocyte lipolysis, hepatic gluconeogenesis, and hepatocyte VLDL secretion, are speculated to play a role in the pathology of metabolic syndrome. Recent focus has been on the activity of 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1), which is capable of regenerating, and thus amplifying, glucocorticoids in key metabolic tissues such as liver and adipose tissue. To determine the effects of global 11β-HSD1 inhibition on metabolic syndrome risk factors, we subcutaneously injected “Western”-type diet-fed hyperlipidemic mice displaying moderate or severe obesity [LDL receptor (LDLR)-deficient (LDLR−/−) mice and mice derived from heterozygous agouti ( A y /a) and homozygous LDLR−/− breeding pairs ( A y /a;LDLR−/− mice)] with the nonselective 11β-HSD inhibitor carbenoxolone for 4 wk. Body composition throughout the study, end-point fasting plasma, and extent of hepatic steatosis and atherosclerosis were assessed. This route of treatment led to detection of high levels of carbenoxolone in liver and fat and resulted in decreased weight gain due to reduced body fat mass in both mouse models. However, only A y /a;LDLR−/− mice showed an effect of 11β-HSD1 inhibition on fasting insulin and plasma lipids, coincident with a reduction in VLDL due to mildly increased VLDL clearance and dramatically decreased hepatic triglyceride production. A y /a;LDLR−/− mice also showed a greater effect of the drug on reducing atherosclerotic lesion formation. These findings indicate that subcutaneous injection of an 11β-HSD1 inhibitor allows for the targeting of the enzyme in not only liver, but also adipose tissue, and attenuates many metabolic syndrome risk factors, with more pronounced effects in cases of severe obesity and hyperlipidemia.

Precocious virulent coronary atherosclerosis in the very young

2011 ◽  
Vol 22 (2) ◽  
pp. 184-187
Author(s):  
Robert Chait ◽  
Rajesh Ramineni ◽  
Erin A. Fender
Keyword(s):  
Risk Factors ◽  
Risk Factor ◽  
Atherosclerotic Lesion ◽  
Traditional Risk Factor ◽  
Risk Factor Modification ◽  
Risk Patients ◽  
Traditional Risk Factors ◽  
Artery Disease ◽  
Cardiac Catheterizations ◽  
Angioplasty And Stenting

AbstractBackgroundThe incidence of Myocardial Infarction (MI) in patients under the age of 30 has been rarely addressed. Moreover, it is not understood why these patients develop symptomatic Coronary Artery Disease (CAD) at such an early age. Traditional risk factor assessment has not been successful in identifying these patients before they present with MI.MethodsRetrospective, single cohort, observational study of 14,704 cardiac catheterizations performed in a community hospital between January 2006–January 2010 identified 12 cases age <30 with MI secondary to a fixed atherosclerotic lesion requiring angioplasty and stenting. The angiograms and charts were reviewed to assess the incidence and frequency of traditional risk factors such as smoking, dyslipidemia and diabetes and family history.ResultsAll the patients had single vessel disease. Many of the patients were noted to have traditional CAD risk factors. 2 patients had an intervention and then months later sustained another acute MI secondary to a new culprit lesion despite aggressive risk factor modification.ConclusionEvaluating patients for premature CAD by screening for traditional risk factors has not effectively identified at risk patients prior to presentation with MI. There is a role for studies evaluating new and novel risk factors and imaging modalities so that these patients can be identified prior to experiencing MI.

scholarly journals The correlation between lipoprotein(a) and coronary atherosclerotic lesion is stronger than LDL-C, when LDL-C is less than 104 mg/dL

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Chuang Li ◽  
Qiwen Chen ◽  
Mei Zhang ◽  
Yin Liu ◽  
Yushun Chu ◽  
...  
Keyword(s):  
Risk Factors ◽  
Cardiovascular Disease ◽  
Risk Factor ◽  
Clinical Characteristics ◽  
Atherosclerotic Lesion ◽  
Atherosclerotic Cardiovascular Disease ◽  
Spearman Correlation ◽  
Gensini Score ◽  
Logistic Regressions ◽  
Coronary Atherosclerotic Lesion

Abstract Background Lp(a) and LDL-C are both risk factors of atherosclerotic cardiovascular disease (ASCVD). But there was a contradiction point in LDL-C and Lp(a) control. The appropriate level of LDL-C and Lp(a) in the prevention of ASCVD is still pending. Objective To investigate the correlation of Lp(a) and coronary atherosclerotic lesion, and find out the balance point in LDL-C and Lp(a) control. Method 3449 patients were divided to coronary atherosclerotic heart disease (CAHD) Group and Non-CAHD Group based on the result of coronary angiography. The clinical characteristics were compared, and Logistic regressions were applied to find the CAHD risk factors in total, High-LDL-C Group (LDL-C ≥ 100 mg/dL) and Low-LDL-C Group (LDL-C < 100 mg/dL) patients. Spearman correlation analysis of Lp(a), LDL-C and Gensini Score was performed in patients with different LDL-C concentration. Results Except male and diabetes, the traditional CAHD risk factors were well matched between two groups. But triglyceride, LDL-C and Lp(a) were higher, HDL-C and Apo-A1 were lower in CAHD group (2771). In the Logistic regression analysis, diabetes, LDL-C and Lp(a) are risk factors of CAHD in all patients, while in High-LDL-C Group, they were age, LDL-C, non-HDL-C and ApoB, in Low-LDL-C Group, they were age, Lp(a) and ApoB. Lp(a) correlated with Gensini with coefficient r = 0.41 in all patients, 0.67 in Low-LDL-C Group and 0.32 in High-LDL-C Group. The coefficient r for Lp(a) and Gensini decreased, while the r for LDL-C and Gensini increased with LDL-C concentration increasing. The two fitted lines of rs crossed at LDL-C = 2.7 mmol/L (104 mg/dL). Conclusion Lp(a) was the risk factor of CAHD in patients with LDL-C < 100 mg/dL. The correlation between Lp(a) and Gensini was influenced by LDL-C concentration, and the correlation was stronger than LDL-C when LDL-C < 104 mg/dl.

Administration of Low-Dose Cyclophosphamide Reduces Progression of Atherosclerosis in Mice by Controlling the Cellular Microenvironment.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 4452-4452
Author(s):  
Yayoi Sato ◽  
Yuichi Ohki ◽  
Haruyo Akiyama ◽  
Hiroyuki Daida ◽  
Beate Heissig ◽  
...  
Keyword(s):  
Risk Factors ◽  
Drinking Water ◽  
Atherosclerotic Lesion ◽  
High Cholesterol Diet ◽  
Cholesterol Diet ◽  
High Cholesterol ◽  
Lesion Formation ◽  
Apoe Ko Mice ◽  
Atherosclerotic Lesion Formation ◽  
Apoe Ko

Abstract Atherosclerosis develops as a result of multiple inflammatory-fibroproliferative responses and is the primary cause of heart disease and stroke in Western countries. Circulating BM-derived progenitor cells (CFU-Cs or EPCs) can regenerate injured vasculature by accelerating reendothelialization and limiting atherosclerotic lesion formation. Risk factors for coronary artery disease like age and diabetes reduce the number and functional activity of these cells, thus limiting the regenerative capacity. The impairment of stem/progenitor cells by risk factors may contribute to atherosclerotic disease progression. High leukocyte counts, and especially neutrophils, a marker of inflammation have been shown to be an independent risk factor and prognostic indicator of future cardiovascular outcomes. Cyclophosphamide (CY) is a synthetic antineoplastic drug, which reduces white blood cell counts (WBC), especially neutrophils, and under certain circumstances can promote hematopoietic progenitor (colony forming unit-cells, CFU-C) mobilization from the bone marrow (BM) into the circulation. We hypothesized that administration of CY limits atherosclerotic lesion formation by decreasing inflammation-associated cells, and by increasing circulating BM-derived progenitors cells. Apolipoprotein E knockout (ApoE−/ −) mice were fed a high cholesterol diet and received different doses of CY in their drinking water (37.5mg/kg/day, 18.75mg/kg/day, 9.375mg/kg/day or nothing). To control for possible effects on progenitor release a control experiment was set up in which C57/B6 received the highest CY in their drinking water (37.5mg/kg/day) or remained untreated. Peripheral blood was drawn from mice every other week. Peripheral blood mononuclear cells (PBMCs) were isolated and subjected to cultures to detect EPCs and CFU-Cs. In CY-treated mice, WBC and neutrophil counts decreased within the first 10 days after the start of the treatment as compared to non-treated controls, and stayed low over the course of the experiment (until day 70). When apoE mice receiving a high-cholesterol diet were treated with CY, the number of circulating CFU-Cs doubled, whereas no major change was found in the c57Bl/6 control group receiving only Cy. EPCs were not detectable at any time point in the CY or control apoE group. Aortic atherosclerotic tree lesion areas were approximately 50% smaller in apoE-KO mice receiving CY in their drinking water after 12 weeks on a high-cholesterol diet than control animals. Most strikingly, apoE-KO mice treated with CY showed a prolonged survival rate as compared to untreated controls. The presence of macrophage-derived foam cells is a hallmark of the atherosclerotic lesion, and an increase in their content promotes plaque instability. Immunohistochemical analysis revealed that the number of macrophages was reduced in plaques of CY-treated animals, indicating that plaques in these might be more stable. Vascular endothelial growth factor (VEGF) is expressed in atherosclerotic plaques from local macrophages and can induce metalloproteinase-9 (MMP-9). Plasma VEGF levels were lower in the CY-treatment group, coinciding with a decrease in MMP-9 plasma levels. This study demonstrates the potential clinical use of a myelosuppressive agent for the treatment of a benign, but not less “malignant” deadly disease like atherosclerosis.

Differential effects of exercise on aortic mitochondria

2005 ◽  
Vol 288 (4) ◽  
pp. H1683-H1689 ◽  
Author(s):  
Christal G. Young ◽  
Cynthia A. Knight ◽  
Kasey C. Vickers ◽  
David Westbrook ◽  
Nageswara R. Madamanchi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Risk Factors ◽  
Atherosclerotic Lesion ◽  
Mitochondrial Damage ◽  
Regular Exercise ◽  
Cvd Risk Factors ◽  
Cvd Risk ◽  
Lesion Development ◽  
Cardioprotective Effects ◽  
Atherosclerotic Lesion Development

Routine exercise is widely recognized as cardioprotective. Exercise induces a variety of effects within the cardiovasculature, including decreased mitochondrial damage and improved aerobic capacity. It has been generally thought that the transient increase in oxidative stress associated with exercise initiates cardioprotective processes. Somewhat paradoxically, increased oxidative stress associated with cardiovascular disease (CVD) risk factors is thought to play an important role in the promotion and development of CVD. Hence, it is possible that CVD risk factors that increase oxidative stress (e.g., hypercholesterolemia) may modulate the cardioprotective effects of exercise. In this regard, the interaction between CVD risk factors and exercise on atherosclerotic lesion development and basal oxidant load is less defined. To determine the influence of preexistent hypercholesterolemia on cardioprotective effects of exercise, atherosclerotic lesion formation, oxidant load, mitochondrial damage, protein nitration (3-nitrotyrosine levels), and mitochondrial enzyme activities were determined in aortic tissues from normocholesterolemic (C57 control) and hypercholesterolemic [apoliprotein E-deficient (apoE−/−)] mice after 16 wk of regular exercise. In normocholesterolemic mice, regular exercise was associated with decreased mitochondrial damage and oxidant load and increased SOD2 and adenine nucleotide translocator activities. Exercise did not decrease endogenous oxidant load and mitochondrial damage in hypercholesterolemic mice and did not reduce atherosclerotic lesion development. These data are consistent with the notion that CVD risk factors associated with increased oxidative stress can alter the benefits of exercise and that mitochondrial damage appears to be correlated with the cardiovascular effects of exercise.

Abstract 14157: Periodontal Microbiome Induces Inflammation and Atherosclerosis in Hyperlipidemic Atherogenic Apoe Null Mice

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Sasanka Chukkapalli ◽  
Irina Velsko ◽  
Mercedes Rivera-Kweh ◽  
Donghang Zheng ◽  
Alexandra Lucas ◽  
...  
Keyword(s):  
Risk Factors ◽  
Atherosclerotic Plaque ◽  
Fas Ligand ◽  
Alveolar Bone ◽  
Oxidized Ldl ◽  
Atherosclerotic Lesion ◽  
T Cell Response ◽  
Causal Association ◽  
Hematogenous Dissemination ◽  
Inflammatory Molecules

Introduction: Periodontal disease (PD) is a polymicrobial dysbiotic chronic inflammatory disease produced by a complex subgingival microbiome, and is linked to systemic inflammatory atherosclerotic vascular disease (ASVD). American Heart Association supported the association between PD and ASVD but not causal association. Prior reports investigated the associations between these two diseases PD and ASVD. But the complex signaling molecules and mechanisms establishing a causal association are not well defined. Methods: To investigate how polybacterial infections initiate atherosclerotic plaque growth, ApoE null mice were orally infected with a polybacterial consortium of 4 well-characterized periodontal pathogens Porphyromonas gingivalis, Treponema denticola, Tannerella forsythia and Fusobacterium nucleatum . We assessed PD characteristics, hematogenous dissemination of bacteria, peripheral T cell response, serum inflammatory cytokines, atherosclerosis risk factors, atherosclerotic plaque development, and alteration of aortic gene expression. Results: Polybacterial infections have enhanced gingival colonization and significantly induced alveolar bone loss ApoE null mice. Polybacterial infections were found to be invasive with hematogenous dissemination into heart and aorta. Polybacterial infection-induced significantly higher levels of serum risk factors (oxidized LDL, nitric oxide), altered lipid profiles (cholesterol, triglycerides, chylomicrons, VLDL) as well as accelerated aortic plaque formation in ApoE null mice. Polybacterial infection is associated with significant decreases in Apoa1, Apob, Birc3, Fga, FgB genes that are associated with atherosclerosis. Gingival infections after 12 weeks had modified levels of inflammatory molecules, with decreased Fas ligand, IL-13, SDF-1 and increased chemokine RANTES. At 24 weeks of chronic infection additional changes in inflammatory molecules were induced with reduced KC, MCSF, and enhanced GM-CSF, IFNγ, IL-1β, IL-13, IL-4, IL-13, lymphotactin, and RANTES. Conclusions: This is the first study demonstrating differences in the host immune response to a polybacterial infection with atherosclerotic lesion progression in a mouse model.

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