Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0014118 (endocarditis)
 15,629 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cardiovascular diseases are the leading cause of death worldwide. Endothelial dysfunction, inflammation and oxidative stress are at the forefront in the onset and development of atherosclerosis and many cardiovascular diseases. Epidemiological evidence is that low serum albumin levels are linked to incident ischemic heart disease, heart failure, atrial fibrillation, stroke and venous thromboembolism, independent of risk factors, body mass index and inflammation. Hypoalbuminemia has also emerged as an independent prognosticator in many cardiovascular diseases, such as coronary artery disease, heart failure, congenital heart disease, infective endocarditis and stroke, even after adjusting for usual causal factors and prognostic markers. Given physiological properties of serum albumin that include anti-inflammatory, antioxidant, anticoagulant and antiplatelet aggregation activity as well as colloid osmotic effect, hypoalbuminemia could act as an unrecognized modifiable risk factor. The purpose of this review is to provide an overview of the physiological properties of serum albumin, as well as prevalence, causes, prognostic value and potential contribution to the disease emergence and progression of hypoalbuminemia, and the resulting clinical implications.
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PMID:Human serum albumin in cardiovascular diseases. 2968 Jan 74

The endothelium is a monolayer of cells that covers the inner surface of blood vessels and its integrity is essential for the maintenance of vascular health. Endothelial dysfunction is a key pathological component of antiphospholipid syndrome (APS). Its systemic complications include thrombotic endocarditis, valvular dysfunction, cerebrovascular occlusions, proliferative nephritis, deep vein thrombosis, and pulmonary embolism. In women, APS is also associated with pregnancy complications (obstetric APS). The conventional treatment regimens for APS are ineffective when the clinical symptoms are severe. Therefore, a better understanding of alterations in the endothelium caused by antiphospholipid antibodies (aPL) may lead to more effective therapies in patients with elevated aPL titers and severe clinical symptoms. Currently, while in vivo analyses of endothelial dysfunction in patients with APS have been reported, most research has been performed using in vitro models with endothelial cells exposed to either patient serum/plasma, monoclonal aPL, or IgGs isolated from patients with APS. These studies have described a reduction in endothelial cell nitric oxide synthesis, the induction of inflammatory and procoagulant phenotypes, an increase in endothelial proliferation, and impairments in vascular remodeling and angiogenesis. Despite these lines of evidence, further research is required to better understand the pathophysiology of endothelial dysfunction in patients with APS. In this review, we have compared the current understanding about the mechanisms of endothelial dysfunction induced by patient-derived aPL under the two main clinical manifestations of APS: thrombosis and gestational complications, either alone or in combination. We also discuss gaps in our current knowledge regarding aPL-induced endothelial dysfunction.
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PMID:Mechanisms of Endothelial Dysfunction in Antiphospholipid Syndrome: Association With Clinical Manifestations. 3062 4