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

Endothelial dysfunction (ED) is actively involved in the mechanism of occurrence, development and progression of all the degrees of atherosclerosis. The established impact of ED on the progress and outcome of cardiovascular diseases, together with convincing indications of a possible successful therapeutic modification, necessitate the changeover of ED assessment from experimental to a routine practice. As there is no appropriate method for a clinical practice, scientists anticipate significant research efforts in the further development. Among numerous methods already available, von Willebrand Factor (vWF) stands out significantly. In accordance with the accepted leading diagnostic role of vWF baseline levels in the group of peripheral endothelial markers, and earlier scientific observations on the absence of its expected reactivation during physical exercise, we hypothesised this promising theory. We believe that a constant stronger release of vWF in endothelial cell injury leads to the exhaustion of its stores in Weibel-Palade bodies with the consequent absence of the expected rise of concentration during the exercise. Therefore, we hypothesised that ED could be exhaustible vWF endothelopathy and the exercise induced release of vWF a new, simple, safe and reliable test for the detection of ED and monitoring of the expected therapeutic effect. In order to have a final clinical usability of the proposed diagnostic model, it is necessary to test its reliability in different pathological and risk states, and establish susceptibility in therapeutic procedures. The correlation with invasive functional angiographic tests and the flow mediated dilatation test of peripheral arteries also needs to be validated. We expect the proposed test of vWF inducibility to find its place in clinical practice, i.e. in prevention, prediction and therapy of cardiovascular diseases.
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PMID:Exercise induced von Willebrand Factor release -- new model for routine endothelial testing. 1750 74

This study aimed to determine whether vital exhaustion (VE) was associated with BMI cross-sectionally and after 3 and 6 years of follow-up. Extant data from the Atherosclerosis Risk in Communities (ARIC) study were used to examine the relationship between VE and BMI among 13,727 white and African-American adults cross-sectionally (baseline) and longitudinally (3 and 6 years later). We used adjusted and nonadjusted general linear regression models. Associations with excess weight gain (>or=5.0%) were also examined using logistic regression. Results showed that BMI was significantly higher among both white and African-American men and women in the highest VE quartile compared to those with no VE. Similarly, high VE at baseline was associated with higher BMI 3 and 6 years later, although VE was not able to predict future BMI after adjusting for baseline BMI. Baseline VE predicted future excess weight gain in white men and women, but not in African Americans. These results suggest that reducing VE levels may play an important role in reducing the prevalence of obesity. High VE was associated with higher current BMI (all races) and excess weight gain (whites only). Although high VE predicted future weight gain without baseline BMI adjustment, the magnitude of change in BMI over time was similar among those with low and high VE; suggesting that any relationship between VE and BMI was already established at baseline. Assessment of VE and BMI over time would help to elucidate uncertainties between the temporal nature of the relationship between them.
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PMID:Obesity and vital exhaustion: analysis of the Atherosclerosis Risk in the Communities study. 1845 77

The present study examined the interaction between vital exhaustion and cardiac reactivity and recovery on preclinical atherosclerosis assessed by carotid intima-media thickness (IMT) in young men and women. We measured heart rate (HR), respiratory sinus arrhythmia (RSA), and pre-ejection period (PEP) in response to mental arithmetic and speech tasks. Vital exhaustion and carotid IMT were also measured. Significant associations were observed for men aged 28-37 years, but not for men aged 22-25 years, nor for women in these age groups. It was shown that, among highly exhausted men in the older age group, lower HR reactivity was related to greater IMT. Our results also imply that, among non-exhausted men in this age group, slow HR and RSA recovery after acute stress predicted higher IMT. These results suggest that long-term stress as assessed by vital exhaustion is a risk only if it has resulted in ineffective cardiac stress reactivity. Autonomic imbalance resulting from chronic stress may be the common mechanism linking vital exhaustion and cardiac responsiveness to an increased risk of atherosclerosis.
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PMID:Interactive effect of long-term mental stress and cardiac stress reactivity on carotid intima-media thickness: the Cardiovascular Risk in Young Finns study. 1895 Dec 43

This study aims to explore the interactive effect of vital exhaustion (VE) and endothelial dysfunction on preclinical atherosclerosis, assessed by carotid intima-media thickness (IMT). Furthermore, interaction between VE and carotid elasticity is examined. Participants were 1,596 young healthy adults from the Cardiovascular Risk in Young Finns study. Endothelial dysfunction was measured by brachial flow-mediated dilatation (FMD), and carotid elasticity by carotid artery compliance (CAC). Significant interactions between FMD and VE, and between CAC and VE, for IMT were found in participants with the very lowest FMD and CAC. Thus, VE may be harmful if the endothelium is not working properly.
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PMID:Chronic stress and the development of early atherosclerosis: moderating effect of endothelial dysfunction and impaired arterial elasticity. 2004 36

Vital exhaustion, defined as excessive fatigue, feelings of demoralization, and increased irritability, has been identified as a risk factor for incident and recurrent cardiac events, but there are no population-based prospective studies of this association in US samples. We examined the predictive value of vital exhaustion for incident myocardial infarction or fatal coronary heart disease in middle-aged men and women in 4 US communities. Participants were 12,895 black or white men and women enrolled in the Atherosclerosis Risk In Communities (ARIC) study cohort and followed for the occurrence of cardiac morbidity and mortality from 1990 through 2002 (maximum follow-up 13.0 years). Vital exhaustion was assessed using the 21-item Maastricht Questionnaire and scores were partitioned into approximate quartiles for statistical analyses. High vital exhaustion (fourth quartile) predicted adverse cardiac events in age-, gender-, and race-center-adjusted analyses (1.69, 95% confidence interval 1.40 to 2.05) and in analyses further adjusted for educational level, body mass index, plasma low-density lipoprotein and high-density lipoprotein cholesterol levels, systolic and diastolic blood pressure levels, diabetes mellitus, cigarette smoking status, and pack-years of cigarette smoking (1.46, 95% confidence interval 1.20 to 1.79). Risk for adverse cardiac events increased monotonically from the first through the fourth quartile of vital exhaustion. Probabilities of adverse cardiac events over time were significantly higher in people with high vital exhaustion compared to those with low exhaustion (p = 0.002). In conclusion, vital exhaustion predicts long-term risk for adverse cardiac events in men and women, independent of established biomedical risk factors.
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PMID:Vital exhaustion as a risk factor for adverse cardiac events (from the Atherosclerosis Risk In Communities [ARIC] study). 2053 11

Exposure to military combat has been associated with myriad adverse health effects. Mechanisms are not well understood, but may include negative emotional states. The authors investigated the relationship between combat and trait anger and vital exhaustion among 5,347 middle-aged male participants in the Atherosclerosis Risk in Communities Study. Combat was significantly associated with trait anger, although results were limited to men of the Korean and Vietnam War eras. Among men of the Korean War era, combat- and noncombat veterans, compared to their nonveteran counterparts, reported more trait anger. Compared to their noncombat and nonveteran counterparts, Vietnam War era combat veterans reported more trait anger. Noncombat veterans from the World War II and Vietnam War eras reported lower vital exhaustion compared to nonveterans. Anger proneness may be a mechanism through which combat stress is associated with adverse health outcomes.
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PMID:Association between exposure to combat-related stress and psychological health in aging men: the Atherosclerosis Risk in Communities (ARIC) Study. 2056 69

In order to maintain cellular homeostasis against endogenous and exogenous aggressions, different cellular mechanisms of defence, maintenance and repair are continuously activated throughout life. Hormesis, a concept based on the fact that mild stresses protect cells against subsequent stresses, amplifies the efficacy of the cellular mechanisms of defence and repair. Ageing, senescence and ultimately death, result from the exhaustion of these mechanisms maintaining cellular functions. One of the major sources of vascular endothelial damage is oxidative stress. The age-dependent shift in the redox environment towards pro-oxidation contributes to a progressive compensatory remodelling of the endothelium, an accumulation of damages, and its dysfunction, the premises for atherosclerosis. We propose that in agreement with the concept of hormesis, a moderate exposure during endothelial maturation to mild physiological oxidative stressors determines -vascular longevity.
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PMID:[Age-dependent oxidative stress: toward an irreversible failure in endothelial maintenance]. 2092 80

Atherosclerosis and its associated complications remain the primary cause of death in humans. Aging is the main contributor to atherosclerosis, compared with any other risk factor, yet the specific manner in which age increases risk (the 'aging-risk' mechanism) remains elusive. A novel concept for atherosclerosis risk implicates a lack of endothelial progenitor cell (EPC)-dependent arterial repair in the development of the disease that is secondary to exhaustion of repair-competent EPCs. Molecular evidence derived from genetic techniques indicates atherosclerotic lesions may begin to form as arterial repair fails, rather than merely following arterial injury. Thus, chronic arterial injury may overwhelm the ability of EPCs to maintain arterial homeostasis, particularly when EPCs capable of arterial repair become exhausted. Recent studies have reported genes identified using non-biased approaches (ie, genetic linkage studies and genome-wide association studies) that are associated with susceptibility for atherosclerosis and related thromboembolic disorders; these genes may be implicated in the control of arterial wall inflammation and EPC-mediated tissue repair. Most of the genes identified by using non-biased genomic techniques are associated with inflammation, immune response and stem cells. This review focuses on new genetic data in the field of atherosclerosis and arterial homeostasis.
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PMID:Inflammation, stem cells and atherosclerosis genetics. 2115 63

Atherosclerosis is classed as a disease of aging, such that increasing age is an independent risk factor for the development of atherosclerosis. Atherosclerosis is also associated with premature biological aging, as atherosclerotic plaques show evidence of cellular senescence characterized by reduced cell proliferation, irreversible growth arrest and apoptosis, elevated DNA damage, epigenetic modifications, and telomere shortening and dysfunction. Not only is cellular senescence associated with atherosclerosis, there is growing evidence that cellular senescence promotes atherosclerosis. This review examines the pathology of normal vascular aging, the evidence for cellular senescence in atherosclerosis, the mechanisms underlying cellular senescence including reactive oxygen species, replication exhaustion and DNA damage, the functional consequences of vascular cell senescence, and the possibility that preventing accelerated cellular senescence is a therapeutic target in atherosclerosis.
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PMID:Aging and atherosclerosis: mechanisms, functional consequences, and potential therapeutics for cellular senescence. 2277 27

This article explores the concept of allostatic load and its utility as an integrative framework for thinking about the impact of chronic stress on children and adolescents. Allostatic load refers to the failure or exhaustion of normal physiologic processes that occurs in response to severe, frequent, or chronic stressors. This persistent physiologic dysregulation may lead to secondary health problems such as immunosuppression, obesity, atherosclerosis, and hypertension. Allostatic load can be measured and followed as a composite index of a group of physiologic parameters which fall outside of a normal range. Although research regarding allostatic load in children is limited, this article explores relevant studies and identifies ways in which the concept of allostatic load can be used to broaden approaches to assessment, case formulation, and treatment in children. The concept of allostatic load may be of particular interest to psychodynamic psychiatrists in recognizing the ways in which chronic stress and adverse childhood experiences lead not only to negative psychological sequelae but also to long-term health consequences including the possibility of premature death. It underscores the importance of monitoring patients' physical as well as psychological health and thinking about the complex interrelations between the two.
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PMID:The cost of chronic stress in childhood: understanding and applying the concept of allostatic load. 2300 5


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