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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Atherosclerosis is a complex dynamic pathological problem. Apart from classic risk factors of atherosclerosis development (age, gender, arterial hypertension, elevated cholesterol concentration particularly LDL fraction, cigarette smoking, diabetes, hyperhomocysteinemia, low physical activity, obesity, mental stress), infectious-inflammatory factors play an important role in the onset of atherosclerotic changes. Vascular endothelium is the main target organ of their activity. Basing on recent literature the study presents pathomechanisms of the development of endothelial dysfunction caused by the risk factors of atherosclerosis, particularly by infectious-inflammatory factors and their mutual interactions which lead to the development of stable and unstable atheromatous plaque.
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PMID:[Etiopathogenesis of atherosclerosis--a clinical problem that is still relevant]. 1670 25

Accumulation of cellular damage with advancing age leads to atherothrombosis and associated cardiovascular disease. Ageing is also characterized by shortening of the DNA component of telomeres, the specialized genetic segments located at the end of eukaryotic chromosomes that protect them from end-to-end fusions. By inducing genomic instability, replicative senescence and apoptosis, shortening of the telomeric DNA is thought to contribute to organismal ageing. In this Review, we discuss experimental and human studies that have linked telomeres and associated proteins to several factors which influence cardiovascular risk (eg, estrogens, oxidative stress, hypertension, diabetes, and psychological stress), as well as to neovascularization and the pathogenesis of atherosclerosis and heart disease. Two chief questions that remain unanswered are whether telomere shortening is cause or consequence of cardiovascular disease, and whether therapies targeting the telomere may find application in treating these disorders (eg, cell "telomerization" to engineer blood vessels of clinical value for bypass surgery, and to facilitate cell-based myocardial regeneration strategies). Given that most research to date has focused on the role of telomerase, it is also of up most importance to investigate whether alterations in additional telomere-associated proteins may contribute to the pathogenesis of cardiovascular disease.
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PMID:Telomere biology and cardiovascular disease. 1712 47

Myocardial infarction is defined as coagulational necrosis of the cardiac muscle caused by ischaemia. In the majority of cases, myocardial infarction is a consequence of atherosclerosis of the coronary arteries. Excessive physical or mental effort can lead to a sudden increase in the required supply of oxygen necessary for the proper functioning of the cardiac muscle and in consequence to cardiac muscle necrosis. The objective of the present study was to analyze cases of myocardial infarctions occurring at work opinionated at the Medico-Legal Institute in the years 2000-2004. The analysis included 12 civil court cases where the plaintiffs demanded compensation for falling victim to myocardial infarction in a work setting. In the majority of cases (11), it was concluded that professional tasks performed during work-time did not meet the criteria of an occupational accident and the most prominent factor that caused cardiac muscle necrosis was internal rather than external in character. In one case, where the plaintiff's professional duties were not only associated with mental stress and a prolonged lack of rest, but were also performed in adverse weather conditions and required sustained and considerable physical effort, it was established that working conditions exerted a significant effect on the occurrence of a myocardial infarction. Opinionating in the above presented cases posed a significant problem due to the lack of legal criteria that would define the term of an "occupational accident".
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PMID:[Myocardial infarction as an occupational injury as represented in the materials collected at the Department of Forensic Medicine in Bydgoszcz in the years between 2000 and 2004]. 1713 60

This study was aimed to test the hypothesis that noninvasive assessment of carotid plaques can be achieved by high-resolution micro-ultrasound imaging in apolipoprotein-E knockout (apoE-KO) mice. Forty-two male apoE-KO mice were fed a high-fat diet and atherosclerotic lesions in the left common carotid artery were induced by perivascular placement of constrictive collars. Eight weeks after surgery, all mice were divided into interventional group (n=21) which received mental stress stimulation and intraperitoneal injection of lipopolysaccharide, and control group (n=21) which received only 0.9% sodium chloride solution for 4 weeks. Plaque morphology and flow velocities were evaluated by micro-ultrasonography. The results showed that micro-ultrasound imaging and corresponding cross-sectional histopathology data revealed positive correlations for plaque area, intima-medial thickness (IMT), eccentric index (EI) and remodeling index (RI) (all p<0.05). Ultrasound-derived IMT, EI and RI in the ruptured plaques were significantly greater than those in the nonruptured plaques (all p<0.05). Maximal flow velocity (Vmax) was higher in the ruptured plaque sites compared with nonruptured plaques sites (p<0.001). Multivariate logistic regression analysis revealed that IMT and Vmax were independent predictors of plaque rupture. In conclusion, micro-ultrasound imaging provides a reliable approach to the noninvasive and quantitative assessment of carotid plaques in apoE-KO mice.
Atherosclerosis 2008 Mar
PMID:Micro-ultrasound imaging assessment of carotid plaque characteristics in apolipoprotein-E knockout mice. 1787 80

Insulin Resistance along with endothelial dysfunction give rise to a constellation of syndromes designated as IRS/MBS metabolic syndrome. Endothelial dysfunction starts early in life much before the development of structural atherosclerosis. Recent insights into vascular biology enable us to understand the molecular mechanisms underlying endothelial dysfunction, and the scope and need for prevention of "pre-clinical" coronary atherosclerosis through lifestyle modification; diet, exercise and stress management. Diminished production of nitric oxide (NO) and/or increased inactivation of NO through oxidative stress (reactive oxygen species ROS and reactive nitrogen species (RNS) are the basis of endothelial dysfunction hence increasing the bioavailability of NO and decreasing its inactivation is the aim of prevention and reversal of endothelial dysfunction. Insulin regulates constitutive NOS gene expression in endothelial cells in vivo; vasodilation is an important component of Insulin-stimulated whole body glucose uptake. Successful strategies are: PPAR alpha and gamma agonists which increase NO production in endothelium; anti-oxidants such as vit. E and C; supplementation with L-arginine, tetrahydrobiopterin-BH4 or sepiapterin (precursor of BH4), SOD mimetic tempol, statins which apart from lowering cholesterol improve NO production, selective beta1 adrenoreceptor antagonists such as nebivolol; suppression of angiotensin-mediated endothelin production by ACE inhibitors and ATR blockers; CB1 receptor blockers, PKCb inhibitors, nitric oxide donors (glyceryl trinitrate and isosorbide dinitrate), dietary supplements of EPA/DHA and regular physical exercise and control of mental stress.
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PMID:Causation, prevention and reversal of vascular endothelial dysfunction. 1805 38

Sudden cardiac death is the leading cause of mortality, accounting for approximately 50% of all cardiovascular deaths and 12% deaths. Although sudden deaths are commonly seen in patients with structural and ischemic heart diseases, some patients lack any evidence of coronary atherosclerosis or structural heart abnormalities. In these patients mental stress and abnormal neurological conditions can produce cardiovascular autonomic disturbances leading to life-threatening arrhythmias and sudden death. Emotional, physiological and physical stress is associated with increased rates of cerebrovascular events and sudden deaths. Human studies in healthy individuals showed lateralization of cardiovascular autonomic function exists in the forebrain, particularly the insular cortex. Considerable evidence exists regarding the role of forebrain lateralization in cardiovascular autonomic regulation in patients with ischemic and hemorrhagic stroke. Particularly insular cortex involvement is associated with more pronounced autonomic imbalance leading to life threatening arrhythmias and sudden death. Left-handers may have a lower risk of sudden death compared with right-handers. Future studies should focus on the association of handedness with cardiovascular autonomic networks and sudden death in different neurological diseases. Identification of patients at risk for neurogenic sudden death by clinical characteristics and noninvasive diagnostic tools may help implement prophylactic and therapeutic interventions that may reduce the mortality rate.
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PMID:Brain lateralization and sudden death: its role in the neurogenic heart syndrome. 1818 55

There is growing evidence that the present risk assessment protocol for coronary heart disease appears to underestimate the risk in general and the presence and progression of atherosclerosis in particular. Little or no correlation has been found between the 10-year risk based on the Framingham model and the extent or progression of coronary calcification. In addition, a number of studies find the protocol based on current guidelines leads to an under appreciation of the risk of symptomatic coronary heart disease or the associated fatal and non-fatal events, especially in younger asymptomatic individuals and women. Furthermore, the current guidelines give secondary importance to insulin resistance and inflammation and do not include psychosocial stress and depression, both of which are established and important risk factors for coronary heart disease. An alternative approach to risk assessment is proposed which emphasizes insulin resistance and psychological stress and depression and gives much greater recognition to inflammation as a root cause and target for intervention than is found in current guidelines. Consistent with this view, a revised assessment protocol is suggested which is still appropriate to the primary care setting and which might provide a different and perhaps more effective and relevant approach to primary prevention and risk reduction.
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PMID:Psychological stress, insulin resistance, inflammation and the assessment of heart disease risk. Time for a paradigm shift? 1840 66

Aging is a process of irreversible decline in physiological function over the time. Several postulated mechanisms for aging include cumulative DNA damage, mitochondrial dysfunction, telomere loss, altered gene expression, and oxidative damages. Those factors affecting the aging process were implicated in hypertension, diabetes, lipid metabolic disorder, heart failure, smoking and psychological stress and so on. Subjects with those disorders are manifested the increased insulin resistance and oxidative stress which are more likely to accelerate aging, atherosclerosis and premature death. Both are also associated with accelerated telomere attrition in leucocytes and chronicle the cumulative burden of oxidative stress and inflammation over a life course. Here, recent evidences including our data about the relationship between telomere attrition and age-related disorders are introduced. Finally, we identify improving life-style as well as pharmacological interventions as potent anti-aging effects to be important for keeping of healthy long life.
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PMID:[Role of the environmental factors on aging]. 1959 Dec 81

This study focuses on the role of sex steroids on the libido, sexual life, emotional and physiological heart of men of all ages. Sex steroids play a significant role throughout a man's life, with a gradual decline in old age. The foetal testis secretes testosterone and dehydroepiandrosterone at about nine weeks gestation. At puberty, testosterone increases dramatically in boys. Changes in weight and height of boys across this period are associated with increasing testosterone concentration and sex hormone binding globulin (SHBG). Romantic thoughts, fantasy, and sexual pleasure-seeking behaviour in adolescents are associated with exposure to high androgens secretion. Thus, the libido and sexual life of a man is initiated and maintained by testosterone and SHBG. Lower testosterone levels are associated with erectile dysfunction among other risk factors: diabetes, hypertension, heart disease, psychological stress and obesity. Men with proven coronary atherosclerosis have lower levels of testosterone and SHBG, which have negative correlation with very low-density lipoprotein, triglycerides, body mass index and body fat mass. These are some of the risk factors for cardiovascular diseases. Thus, in men, endogenous sex steroids impart beneficial effects on the heart. How exactly endogenous sex steroids act on the heart is not clear. Further study is needed to understand the interaction between endogenous sex steroids, higher centers in the brain and the heart of a man.
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PMID:Hormonal profiles behind the heart of a man. 1965 70

Acute psychophysiological stress testing, involving measurement of cardiovascular and biological responses to laboratory-induced mental stress, is an important tool to investigate mechanisms that might account for the association between psychosocial stress and cardiovascular diseases (CVD). Accumulating evidence has demonstrated associations of disturbed psychophysiological responses with sub-clinical measures of atherosclerosis, hypertension, and metabolic risk. The complex pattern of stress responding is influenced by individual differences, such as coping style, race and ethnicity, genetics, background stress, and lifestyle habits, which should be taken into account when interpreting results. For example, an unique interplay between cardiac and vascular responses in black Africans and African Americans is thought to contribute towards a heightened risk of hypertension in this group. Whether or not psychophysiological risk markers provide prognostic information over and above that of established risk markers is not clear. In summary, controlled trials that examine if the modification of psychophysiological responses through lifestyle and psychosocial interventions can reduce the risk of CVD outcomes are needed to establish causality. Further work is also required that examines the associations of ambulatory responses to real life stress in relation to risk of CVD.
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PMID:Psychophysiological risk markers of cardiovascular disease. 1990 73


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