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Artery Atherosclerosis (artery + atherosclerosis)

Distribution by Scientific Domains
Medical Sciences63%

Kinds of Artery Atherosclerosis

  • carotid artery atherosclerosis
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    Selected Abstracts

    Combined Effects of Glycated Hemoglobin A1c and Blood Pressure on Carotid Artery Atherosclerosis in Nondiabetic Patients

    CLINICAL CARDIOLOGY, Issue 9 2010
    Wen Zhu MD
    Background The relationship between HbA1c, blood pressure, and carotid atherosclerosis in nondiabetic patients is not clear. Hypothesis HbA1c and blood pressure can affect carotid-artery atherosclerosis in nondiabetic patients. Methods This retrospective cross-sectional study included 216 patients without diabetes mellitus. A positive carotid ultrasonographic result was defined as intima-media thickness of the common carotid artery , 0.9 mm, or presence of carotid plaque. Results Compared with patients without carotid atherosclerosis, patients with carotid atherosclerosis had significantly higher levels of HbA1c and systolic blood pressure (SBP). Higher levels of HbA1c and SBP were found to be associated with increased carotid atherosclerosis. Given similar SBP levels, higher HbA1c (>5.6%) was also related to increased carotid atherosclerosis. In multiple logistic regression analysis, HbA1c (odds ratio: 4.1, P = 0.009) emerged as the only statistically significant modifiable factor that was associated with carotid atherosclerosis, independent of smoking, body mass index, fasting plasma glucose, 2-hour plasma glucose, SBP, diastolic blood pressure, low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol. Conclusions Our study shows that a slight increase of HbA1c may associate with carotid atherosclerosis in nondiabetic patients. Moreover, the coexistence of an elevated SBP level and a slightly increased HbA1c level may have a more significant effect on carotid atherosclerosis. Copyright © 2010 Wiley Periodicals, Inc. Dr. Zhu and Dr. Sun contributed equally to this work. The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology (Coats AJ. Ethical authorship and publishing. Int J Cardiol. 2009;131:149,150). This work was supported by a Chinese National Science Grant to Dr. Yong Li (Grant No. 30873350). The authors have no other funding, financial relationships, or conflicts of interest to disclose. [source]

    Prevalence of diabetes and/or ischaemic heart disease in classes of increasing carotid artery atherosclerosis: an ultrasonographic study

    DIABETIC MEDICINE, Issue 8 2003
    S. Inchiostro
    Abstract Aims To evaluate the prevalence of non-diabetic subjects and diabetic patients, with or without ischaemic heart disease (IHD), in different classes of increasing carotid atherosclerotic damage. Methods Using high-resolution B-mode ultrasound, we studied 598 subjects without known cardiovascular disease (CVD) or diabetes, 74 diabetic patients without CVD, 74 non-diabetic subjects with IHD and 36 patients with both diabetes and IHD. Carotid atherosclerosis was classified as: normal; thickened intima-media; non-stenotic plaque; stenotic plaque. Results Compared with subjects without diabetes or CVD, the frequency of patients with diabetes without known CVD increased significantly from ,normal' to ,stenotic plaque' (4.1%, 6.4%, 13%, 14.8% for normal, thickened intima-media, non-stenotic plaque and stenotic plaque, respectively; P = 0.0057). The same figures were 6%, 7.6%, 10.2%, 23.3% (P = 0.0007) for non-diabetic subjects with IHD, and 0%, 2%, 5.6%, 15.9% (P < 0.0001) for diabetic patients with IHD. No difference was found comparing subjects with diabetes without CVD with non-diabetic patients with IHD (P = 0.56). Using polychotomous logistic regression analysis, diabetic patients without CVD and non-diabetic subjects with IHD showed a similar association with the increasing degree of carotid atherosclerosis (P = 0.59), but significantly stronger compared with subjects without diabetes or CVD (P < 0.03 for both). Conclusions Diabetic patients without known CVD show an advanced degree of carotid atherosclerotic damage similar to non-diabetic subjects with IHD and significantly higher compared with non-diabetic subjects without CVD. Our data support the need for an aggressive early prevention of CVD in diabetic subjects. [source]

    Role of hyperlipidemia in atherosclerotic plaque formation in the internal carotid artery

    JOURNAL OF CLINICAL ULTRASOUND, Issue 6 2006
    Levente Kerenyi MD
    Abstract Purpose. The role of hyperlipidemia in atherosclerotic changes of the carotid artery is controversial. The aims of this retrospective study were to assess (1) the relationship between total serum cholesterol and triglyceride and the grade of internal carotid artery stenosis and (2) whether total serum cholesterol and triglyceride levels are independent risk factors for internal carotid artery atherosclerosis. Methods. The files of 1,934 acute ischemic stroke patients were investigated retrospectively. The atherosclerotic involvement of the internal carotid artery was assessed via duplex sonography as percent of stenosis and was graded as follows: group 1, no plaque; group 2, <30% stenosis; group 3, 30,99% stenosis; and group 4, occlusion. Results. The mean age of the patients was 66.9 ± 12.8 years. Patients without any plaque had significantly lower cholesterol levels compared with those with any degree of internal carotid artery stenosis. Univariate analysis revealed that age (p < 0.001), sex (p < 0.001), hypertension (p < 0.05), cholesterol (p < 0.01), triglycerides(p < 0.05), and smoking (p < 0.001) were significant contributors to atherosclerosis. In the ordinal logistic regression model, age (p < 0.001), sex (p < 0.001), smoking(p < 0.001), and cholesterol (p < 0.05) remained independent predictors of internal carotid artery atherosclerosis. Conclusions. Total serum cholesterol level seems to be an independent risk factor of atherosclerosis in the carotid artery. © 2006 Wiley Periodicals, Inc. J Clin Ultrasound 34:283,288, 2006 [source]

    Vertebral artery atherosclerosis: a risk factor in the use of manipulative therapy?

    PHYSIOTHERAPY RESEARCH INTERNATIONAL, Issue 3 2002
    Jeanette Mitchell BSc (Physiotherapy), MSc Senior Lecturer
    Abstract Background and Purpose Vertebrobasilar insufficiency, a direct result of compromised blood flow in the vertebrobasilar circulation, may be caused by stretching and/or compression of the vertebral arteries, particularly if superimposed on underlying atherosclerosis of the vessels. This is an important consideration when using manipulative therapy techniques. The aim of the present study was to investigate the incidence of atherosclerosis and to calculate the relative associated decrease in blood flow in the third and fourth parts of the vertebral artery, in a sample of the adult population. Method A laboratory-based experimental investigation was used to study 362 vertebral arteries from embalmed adult cadavers that were routinely processed for light microscopic study. The incidence of each grade of atherosclerosis in the vessels was recorded. Atherosclerosis was classified as grades 0,5, where Grade 0 represented no atherosclerosis and Grade 5 a fully developed plaque occluding more than 75% of the vessel lumen. From mean measurements of 188 of these arteries, the estimated decrease in luminal cross-sectional area and the relative decrease in blood flow in the atherosclerotic vessels were calculated. Results The highest incidence of atherosclerosis found was Grade 3 (third part of the vertebral artery (VA3): 42.0%; fourth part of the vertebral artery (VA4): 35.2%). An estimated decrease in artery luminal cross-sectional area to 6.2% of normal in Grade 5 atherosclerosis was found. Because blood flow is proportional to the fourth power of the vessel radius, relative decreases in blood flow in grades 1,5 atherosclerosis from 100% to 0% (with critical closing pressure in vessels), respectively, are likely to occur. Conclusions These data suggest that, as significant numbers of the sample showed marked (Grade 3+) atherosclerosis, concomitant with decreased blood flow in the vertebral arteries, this population is at risk for developing vertebrobasilar insufficiency. Because other Western populations may be similarly at risk, particular care should be taken when considering the use of rotational manipulative therapy techniques in treatments of the cervical spine. Copyright © 2002 Whurr Publishers Ltd. [source]

    The relationship between social status and atherosclerosis in male and female monkeys as revealed by meta-analysis

    AMERICAN JOURNAL OF PRIMATOLOGY, Issue 9 2009
    Jay R. Kaplan
    Abstract More than 25 years ago our laboratory reported sex-dependent relationships between social status and coronary artery atherosclerosis among cholesterol-fed cynomolgus monkeys (Macaca fascicularis) maintained in social groups of four to six animals each. Dominant males developed more atherosclerosis than subordinates, but only if housed in recurrently reorganized social groups. In contrast, dominant females developed significantly less atherosclerosis than subordinates, irrespective of social setting. Although we have continued to study these associations, no confirmatory investigations have been reported by other laboratories or using other atherosclerosis-susceptible monkey species. Accordingly, we conducted a meta-analysis of all relevant data sources developed in our laboratory since 1982 to determine whether the originally reported relationships between social status and atherosclerosis reflected robust associations. The sentinel (first) studies were composed of 16 females and 27 males. The current meta-analysis encompassed 419 animals (200 females and 219 males) derived from 11 separate investigations. The results confirmed that, among males, dominant individuals developed more extensive atherosclerosis than subordinates when housed in recurrently reorganized (unstable) social groups in which an estrogen-implanted female was also present. Dominant males in stable social groups tended to have less atherosclerosis than similarly housed subordinates, but this effect was not significant. On the contrary, we found that dominant females developed reliably less atherosclerosis than subordinates. Am. J. Primatol. 71:732,741, 2009. © 2009 Wiley-Liss, Inc. [source]

    Social stress, visceral obesity, and coronary artery atherosclerosis: product of a primate adaptation

    AMERICAN JOURNAL OF PRIMATOLOGY, Issue 9 2009
    Carol A. Shively
    Abstract Abdominal obesity is prevalent and often accompanied by an array of metabolic perturbations including elevated blood pressure, dyslipidemia, impaired glucose tolerance or insulin resistance, a prothrombotic state, and a proinflammatory state, together referred to as the metabolic syndrome. The metabolic syndrome greatly increases coronary heart disease (CHD) risk. Social stress also increases CHD although the mechanisms through which this occurs are not completely understood. Chronic stress may result in sustained glucocorticoid production, which is thought to promote visceral obesity. Thus, one hypothesis is that social stress may cause visceral fat deposition and the metabolic syndrome, which, in turn increases CHD. CHD is caused by coronary artery atherosclerosis (CAA) and its sequelae. Cynomolgus monkeys (Macaca fascicularis) are a well-established models of CAA. Social subordination may be stressful to cynomolgus monkeys and result in hypercortisolemia and exacerbated CAA in females. Herein is reviewed a body of literature which suggests that social stress increases visceral fat deposition in cynomolgus monkeys, that subordinate females are more likely than dominants to have visceral obesity, that females with visceral obesity have behavioral and physiological characteristics consistent with a stressed state, and that females with high ratios of visceral to subcutaneous abdominal fat develop more CAA. While these relationships have been most extensively studied in cynomolgus macaques, obesity-related metabolic disturbances are also observed in other primate species. Taken together, these observations support the view that the current obesity epidemic is the result of a primate adaptation involving the coevolution with encephalization of elaborate physiological systems to protect against starvation and defend stored body fat in order to feed a large and metabolically demanding brain. Social stress may be engaging these same physiological systems, increasing the visceral deposition of fat and its sequelae, which increase CHD risk. Am. J. Primatol. 71:742,751, 2009. © 2009 Wiley-Liss, Inc. [source]

    Coronary heart disease of females: lessons learned from nonhuman primates

    AMERICAN JOURNAL OF PRIMATOLOGY, Issue 9 2009
    Thomas B. Clarkson
    Abstract The cynomolgus monkey model has contributed to significant advances regarding the understanding of coronary artery atherosclerosis of females. There are currently 8 million women in the United States living with heart disease, necessitating further study and understanding of this leading cause of morbidity and mortality for postmenopausal women. Specifically, studies involving the monkey model have allowed greater understanding of the effect of the stage of reproductive life, time since menopause, and the extent of subclinical atherosclerosis as determinates of estrogen-mediated effects on arteries. Utilizing the commonalities among monkeys and human beings, these studies have shown that postmenopausal atherosclerosis is associated with the premenopausal reproductive timeframe. In addition, monkey studies have shown that estrogen deficiency during the premenopausal stage is extremely relevant regarding the progression of atherosclerosis. After several postmenopausal years, however, studies have shown that estrogen has no beneficial effects on atherosclerosis progression and may, in fact, be deleterious. Studies using the monkey model are currently underway to investigate further uses and possibilities of postmenopausal hormone therapy for treating menopausal symptoms while protecting the breast and uterus and inhibiting the progression of coronary artery atherosclerosis. These studies will hopefully clarify the role of estrogen and eliminate the need for the possibly harmful progestin effects through the use of a highly selective estrogen receptor modulator. Am. J. Primatol. 71:785,793, 2009. © 2009 Wiley-Liss, Inc. [source]

    Relationship of carotid intima-media thickness, pulse wave velocity, and ankle brachial index to the severity of coronary artery atherosclerosis

    CLINICAL CARDIOLOGY, Issue 11 2004
    Yoshihiro Matsushima M.D.
    Abstract Background: Carotid intima-media thickness (IMT), pulse wave velocity (PWV), and the ankle brachial index (ABI) are widely used noninvasive modalities for evaluating atherosclerosis. Hypothesis: The aim of this study was to determine the relationship of carotid IMT, PWV, and ABI with the severity of coronary artery disease (CAD), expressed as the Gensini score, and the presence of coronary risk factors. Methods: We examined 205 consecutive patients (mean age 65 ± 12 years) who were clinically suspected of having CAD and were scheduled to undergo coronary angiography. Carotid intima-media thickness, brachial-ankle PWV (baPWV), and ABI were measured in all subjects before they underwent coronary angiography. Results: Of the 205 patients, 124 patients were diagnosed as having CAD based on the presence of > 50% stenosis in a major coronary artery; the remaining 81 patients did not have CAD. A relatively good correlation was obtained between carotid IMT and the Gensini score (R = 0.411, p < 0.0001), whereas baPWV correlated only weakly with the Gensini score (R = 0.203, p = 0.0035), and ABI did not correlate with it. A multiple regression analysis revealed that the Gensini score correlated significantly and independently with age, male gender, and carotid IMT. Conclusions: Of the three noninvasive methods, carotid IMT may be more useful for determining coronary artery atherosclerosis than baPWV or ABI. [source]

    The GH,IGF-I axis and the cardiovascular system: clinical implications

    CLINICAL ENDOCRINOLOGY, Issue 3 2008
    Annamaria Colao
    Summary Background, GH and IGF-I affect cardiac structure and performance. In the general population, low IGF-I has been associated with higher prevalence of ischaemic heart disease and mortality. Both in GH deficiency (GHD) and excess life expectancy has been reported to be reduced because of cardiovascular disease. Objective, To review the role of the GH,IGF-I system on the cardiovascular system. Results, Recent epidemiological evidence suggests that serum IGF-I levels in the low-normal range are associated with increased risk of acute myocardial infarction, ischaemic heart disease, coronary and carotid artery atherosclerosis and stroke. This confirms previous findings in patients with acromegaly or with GH-deficiency showing cardiovascular impairment. Patients with either childhood- or adulthood-onset GHD have cardiovascular abnormalities such as reduced cardiac mass, diastolic filling and left ventricular response at peak exercise, increased intima-media thickness and endothelial dysfunction. These abnormalities can be reversed, at least partially, after GH replacement therapy. In contrast, in acromegaly chronic GH and IGF-I excess causes a specific cardiomyopathy: concentric cardiac hypertrophy (in more than two-thirds of the patients at diagnosis) associated to diastolic dysfunction is the most common finding. In later stages, impaired systolic function ending in heart failure can occur, if GH/IGF-I excess is not controlled. Abnormalities of cardiac rhythm and of cardiac valves can also occur. Successful control of acromegaly is accompanied by decrease of the left ventricular mass and improvement of cardiac function. Conclusion, The cardiovascular system is a target organ for GH and IGF-I. Subtle dysfunction in the GH,IGF-I axis are correlated with increased prevalence of ischaemic heart disease. Acromegaly and GHD are associated with several abnormalities of the cardiovascular system and control of GH/IGF-I secretion reverses (or at least stops) cardiovascular abnormalities. [source]