Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 12-year-old girl with atrial septal defect combined with pulmonary hypertension and 90% stenosis of the left main coronary artery caused by dilated pulmonary artery was scheduled for atrial septal closure and coronary artery bypass graft under general anesthesia. During the echocardiographic examination to evaluate the anatomical relationship between the pulmonary artery and left main coronary trunk, bradycardia and a depression of ST-segment on electrocardiogram appeared suddenly when the operator compressed the pulmonary artery with a probe of echocardiography from the operative field. The circulatory collapse and ischemic change on electrocardiogram might have been caused by a further reduction of blood flow to the left main coronary trunk narrowed originally by dilated pulmonary artery. Although various etiologies, such as atherosclerosis, syphilis, and congenital abnormalities are widely known to cause stenosis of the left main coronary trunk, external compression by dilated pulmonary artery has not been widely known. Malignant arrhythmias from coronary artery compression with subsequent ischemia could contribute to an incidence of sudden death. Coronary angiography and magnetic resonance imaging are useful for the preoperative evaluation. Careful management is needed to protect such a patient from ischemic event in the perioperative period.
 ...
PMID:[Left main coronary trunk compression by dilated main pulmonary artery in a patient with atrial septal defect]. 1124 76

Exercise-induced collapse and sudden death are unusual in childhood. For this reason, a study was undertaken of a series of 12 cases of sudden death in childhood occurring during physical exertion associated with sporting activities. The age range was 7 to 16 years (mean 12.3 years, M:F ratio 5:1). Deaths resulted from trauma associated with the sporting activity, from an idiosyncratic response to exertion, or from exacerbation of a known underlying disease. Trauma was directly fatal (n = 4: vascular trauma in 1, head injury in 2, drowning in 1), exacerbated an underlying medical condition (n = 1: hypertrophic obstructive cardiomyopathy), or followed collapse from underlying organic disease (n = 1: drowning in epilepsy). Deaths after exertion occurred when there was an unexpected response to underlying occult disease (n = 4: aortic stenosis in 1, cerebral arteriovenous malformation in 1, hypertrophic obstructive cardiomyopathy in 1, coronary atherosclerosis in 1) or to preexisting known disease (n = 2: surgically corrected transposition of the great vessels in 1, asthma in 1). The fatal episodes often resulted from a complex interplay of a variety of factors, including physical exertion, possible trauma, and underlying organic disease. Testing of other family members may be indicated in cases where a rare, possibly familial, disease is found. Evaluation of cases required descriptions of activities before death, information from the medical history of the deceased, and detailed findings from the autopsy.
 ...
PMID:Childhood sporting deaths. 1246 14

Obstructive sleep apnea (OSA) occurs commonly in the U.S. population and is seen in both obese as well as non-obese individuals. OSA is a disease characterized by periodic upper airway collapse during sleep, which then results in either apnea, hypopnea, or both. The disorder leads to a variety of medical complications. Neuropsychiatric complications include daytime somnolence, cognitive dysfunction, and depression. Increased incidence of motor vehicle accidents has been documented in these patients and probably reflects disordered reflex mechanisms or excessive somnolence. More importantly, vascular disorders such as hypertension, stroke, congestive cardiac failure, arrhythmias, and atherosclerosis occur frequently in these patients. The lungs may be affected by pulmonary hypertension and worsening of asthma. Recent data from several laboratories demonstrate that obstructive sleep apnea is characterized by an inflammatory response. Cytokines are elaborated during the hypoxemic episodes leading to inflammatory responses as marked clinically by elevated C-reactive protein (CRP). As elevated CRP levels are considered markers of the acute phase response and characterize progression of vascular injury in coronary artery disease, it is likely that obstructive sleep apnea could lead to worsening of vasculopathy. Moreover, as inflammatory mechanisms regulate bronchial asthma, it is also likely that cytokines and superoxide radicals generated during hypoxemic episodes could exacerbate reactive airway disease. Patients with Cough, Obstructive sleep apnea, Rhinosinusitis, and Esophageal reflux clustered together can be categorized by the acronym, "CORE", syndrome. The purpose of this manuscript is to review the inflammatory responses that occur in patients with obstructive sleep apnea and relate them to the occurrence of cardiopulmonary disease.
 ...
PMID:Obstructive sleep apnea, inflammation, and cardiopulmonary disease. 1535 23

'Functional Food' is not a new concept but it became more important recently due to the collapse of most social health system because 'Functional Foods' allow low cost prevention of numerous diseases. 'Functional Foods' are different from 'Neutraceuticals' which remain drug based with poor taste whereas 'Functional Foods' remain good food which could be consumed for years, but in addition have a disease prophylactic function. They are becoming particularly important for the prevention of food allergy in 'at risk' population, obesity, osteoporosis, cardiovascular diseases and particularly high blood pressure and atherosclerosis, but also for cancer prevention. The newest trend is that governments and health authorities allow food manufacturers to make health prevention related claims on mass media.
 ...
PMID:Impact of 'functional food'. 1570 90

Smoking is a significant risk factor for development of atherosclerosis. However, the pathophysiology of smoking-mediated vessel wall damage is not understood. With tools ranging from analytical chemistry to cell biology, we show that cigarette smoke contains metals that catalyze the direct oxidation of cellular proteins by smoke oxidants. Oxidation of cellular proteins causes a loss of microtubule function, culminating in microtubule depolymerization and proteasome-dependent degradation of alpha-tubulin. As a consequence of the microtubule collapse, cytoskeletal structures as well as intermediate filaments break down, leading finally to a contraction of vascular endothelial cells. We observed a smoke extract-induced, calpain-dependent degradation of the intracellular form of platelet-endothelial cell adhesion molecule 1/CD31, as well as a release of P-selectin/CD62P, IL-6, and IL-8 from endothelial cells into the supernatant. Increased levels of soluble CD62P and IL-6 are well known to be associated with smoking in humans. Increased permeability of the vascular endothelium is a crucial event in atherogenesis. This work highlights the compounds and mechanisms by which cigarette smoke induces leakiness of the vascular endothelium.
 ...
PMID:Cigarette smoke metal-catalyzed protein oxidation leads to vascular endothelial cell contraction by depolymerization of microtubules. 1598 33

Sleep-disordered breathing is very common and is associated with an increased risk of cardiovascular disease, cardiac arrhythmia and stroke. There are two types of sleep apnea: obstructive and central. The objective of this review is to provide a broad perspective of the pathophysiological and clinical aspects of the two types of apnea and to discuss their cardiovascular adverse effects. The diagnosis of sleep apnea syndrome is based on polysomnography, and severity is measured with an apnea-hypopnea index that counts the total number of apneas per hour of sleep. Recent large epidemiologic studies have shown that sleep apnea affects about 16% of men and 5% of women between 30 and 65 years of age. Obstructive sleep apnea is characterized by abnormal collapse of the pharyngeal airway during sleep, snoring, vigorous inspiratory efforts causing frequent arousal, and excessive daytime drowsiness. Central sleep apnea with Cheyne-Stokes respiration is a form of periodic breathing with frequent periods of hyperventilation, and carries a poor prognosis in patients with heart failure. Obstructive apnea can also have substantial health consequences. Although the exact mechanism linking sleep apnea with cardiovascular disease is unknown, there is evidence that obstructive apnea is associated with a group of proinflammatory and prothrombic factors that are also important in the development of atherosclerosis. Nocturnal and daytime sympathetic activity is elevated after sleep apnea. Autonomic abnormalities include an increased resting heart rate, decreased cardiac rhythm activity, and increased blood pressure variability. Obstructive apnea is associated with endothelial dysfunction, increased C-reactive protein and cytokine expression, elevated fibrinogen levels and decreased fibrinolytic activity. Enhanced platelet activity and aggregation, leukocyte adhesion and accumulation of endothelial cells are common in both obstructive apnea and atherosclerosis. Surges in sympathetic activity, blood pressure, ventricular wall tension and afterload adversely affect ventricular function. Many studies have shown that patients with obstructive apnea have an increased incidence of daytime hypertension, and this syndrome is recognized as an independent risk factor for hypertension. Obstructive apnea is associated with myocardial ischemia (silent or symptomatic), acute coronary events, stroke and transient ischemic attacks, cardiac arrhythmia, pulmonary hypertension and heart failure. Central sleep apnea is frequent in severe heart failure. Most heart failure patients with pulmonary congestion chronically hyperventilate because of stimulation of vagal irritant receptors and central and peripheral chemosensitivity. When PaCO2 falls below the threshold required to stimulate breathing, the central drive to respiratory muscles and air inflow ceases and central apnea ensues. Apnea, hypoxia, CO2 retention and arousals provoke elevated sympathetic activity, increased afterload and elevated left ventricular transmural pressure, and promote the progression of heart failure. Tentative relationships have been identified between central apnea and markers of inflammation, oxidative stress and endothelial dysfunction. Recent mid-terms trials showed that nocturnal use of positive airway pressure in patients with the two types of apnea alleviates symptoms, reduces sympathetic activity, improves ventricular function and quality of life, and reduces daytime drowsiness. More studies are needed to understand the mechanisms underlying the relationship between sleep apnea and cardiovascular disease, but clinicians should be aware of this link and should attempt to identify patients with these syndromes.
 ...
PMID:[Sleep apnea syndromes and cardiovascular disease]. 1614 10

The subspecialty of interventional cardiology has made significant progress in the management of coronary artery disease over the past three decades with the development of percutaneous coronary transluminal angioplasty, atherectomy, and bare-metal and drug-eluting stents (DES). Bare-metal stents (BMS) maintain vessel lumen diameter by acting as a scaffold and prevent collapse incurred by angioplasty. However, these devices cause neointimal hyperplasia leading to in-stent restenosis and requiring reintervention in more than 20% of patients by 6 mo. DES (sirolimus and paclitaxel) prevent restenosis by inhibiting neointimal hyperplasia. However, DESs also delay endothelialization, causing the stents to remain thrombogenic for an extended, yet unknown, period of time. Late stent thrombosis is associated with a 45% mortality rate. Premature discontinuation of antiplatelet therapy, particularly clopidogrel, is the strongest predictor of stent thrombosis. Sixty percent of patients receive stents for off-label (unapproved) indications, which also increases the frequency of stent thrombosis. Clopidogrel and aspirin are the cornerstone of therapy in the prevention of stent thrombosis in both BMS and DES. Recommendations pertaining to the optimal duration of dual-antiplatelet therapy have been debated. Both the Food and Drug Administration and the American Heart Association/American College of Cardiologists, in association with other major societies, have made recommendations to extend the duration of dual-antiplatelet therapy in patients with DES to 1 yr. The 6-wk duration of dual-antiplatelet therapy in patients with BMS remains unchanged. All patients with coronary stents must remain on life-long aspirin monotherapy. Since the introduction of percutaneous transluminal coronary angioplasty for the treatment of coronary atherosclerosis, the practice of percutaneous coronary intervention has undergone a dramatic transformation from simple balloon dilation catheters to sophisticated mechanical endoprostheses. These advancements have impacted the practice of perioperative medicine. In this series of two articles, in Part I we will review the evolution of percutaneous coronary intervention and discuss the issues associated with percutaneous transluminal coronary angioplasty and coronary stenting; in Part II we will discuss perioperative issues and management strategies of coronary stents during noncardiac surgery.
 ...
PMID:Coronary artery stents: Part I. Evolution of percutaneous coronary intervention. 1863 8

The obstructive sleep apnea syndrome (OSAS) is characterized by collapse of the upper airway during sleep, recurring apneas, intermittent hypoxemia and daytime somnolence. OSAS is often associated with obesity, and its prevalence is expected to rise due to the obesity epidemics worldwide. OSAS is associated with increased cardiovascular risk which appears to be normalized by treatment with nasal continuous positive airway pressure (nCPAP) during sleep, suggesting an independent role of OSAS in accelerating atherosclerosis. Insulin resistance (IR) and the metabolic syndrome (MetS) are often found in OSAS patients, but the relative role played by OSAS and obesity is still unclear. Both OSAS and MetS may exert negative synergistic effects on the cardiovascular system through multiple mechanisms (hypoxemia, sleep disruption, activation of the sympathetic nervous system, inflammatory activation). Besides nCPAP treatment, pharmacologic interventions to treat obesity and the MetS could improve cardiovascular prevention in OSAS.
 ...
PMID:Metabolic effects of the obstructive sleep apnea syndrome and cardiovascular risk. 1872 87

Obstructive sleep apnea syndrome (OSAS) is an often underestimated sleep disorder that has been associated with cardiovascular disease. OSAS is characterized by cycles of apnea and/or hypopnea during sleep caused by the collapse of the upper airways. Intermittent hypoxia deriving from the cycles of apnea/arousals (to retrieve the ventilation) plays a pivotal role in the pathogenesis of the disease. Obesity is the most frequent predisposing condition of OSAS. Recent evidence suggests that OSAS could be considered as a pro-atherosclerotic disease, independently of visceral fat amount. Oxidative stress, cardiovascular inflammation, endothelial dysfunction, and metabolic abnormalities in OSAS could accelerate atherogenesis. The present review is focused on the possible pathophysiological mediators which could favor atherosclerosis in OSAS.
 ...
PMID:Inflammation accelerates atherosclerotic processes in obstructive sleep apnea syndrome (OSAS). 2019 12

Sleep is an essential part of our daily living, and sleep disturbances may intervene with the biological and physiological processes in human body leading to the development of metabolic dysfunction. Short sleep duration and poor sleep quality have adverse effects on metabolism and hormonal processes, contributing to increased cardiovascular risk. Obstructive sleep apnoea is a chronic condition characterized by repetitive upper airway collapse during sleep, causing intermittent hypoxaemia, recurrent arousals and sleep fragmentation. Sleep disturbances can increase sympathetic activity, provoke systemic inflammation and oxidative stress, and impair vascular endothelial function. Obstructive sleep apnoea is increasingly recognized to be an independent cardiovascular risk factor. There is intense research interest in the association between obstructive sleep apnoea and the metabolic syndrome - the constellation of inter-related metabolic derangements including central obesity, hypertension, insulin resistance and dyslipidaemia, which appears to directly promote the development of atherosclerosis. The underlying pathophysiologic pathways or mechanistic links between obstructive sleep apnoea and metabolic syndrome have not been well delineated. This article reviews the current knowledge of the relationship between sleep disturbances, sleep-disordered breathing and the metabolic syndrome in adults.
 ...
PMID:Sleep & the metabolic syndrome. 2030 46


<< Previous 1 2 3 4 5 Next >>