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

One important cardioprotective function of HDL is to remove cholesterol from lipid-laden macrophages in the artery wall. HDL also exerts anti-inflammatory effects that might inhibit atherogenesis. However, HDL has been proposed to be dysfunctional in humans with established coronary artery disease (CAD), though the underlying mechanisms are unclear. Therefore, we used mass spectrometry to investigate the roles of HDL proteins in inflammation and cardiovascular disease. Shotgun proteomic analysis identified multiple complement regulatory proteins, protease inhibitors, and acute-phase response proteins in HDL, strongly implicating the lipoprotein in inflammation and the innate immune system. Moreover, mass spectrometry and biochemical analyses demonstrated that HDL3 from subjects with clinically significant CAD was selectively enriched in apolipoprotein E, suggesting that it carries a distinctive protein cargo in humans with atherosclerosis. HDL from CAD subjects also contained markedly elevated levels of chlorotyrosine and nitrotyrosine, two characteristic products of myeloperoxidase, indicating that oxidative damage might generate dysfunctional HDL. Aggressive lipid therapy with a statin and niacin remodeled the HDL proteome to resemble that of apparently healthy subjects. Collectively, our observations indicate that quantifying the HDL proteome by mass spectrometry should help identify novel anti-inflammatory and cardioprotective actions of HDL and provide insights into lipid therapy.
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PMID:The HDL proteome: a marker--and perhaps mediator--of coronary artery disease. 1906 Feb 51

Left main (LM) coronary artery aneurysm is rare and usually found incidentally during coronary angiography. Except for rare Kawasaki disease, iatrogenic and mycotic aneurysms, atherosclerosis is the primary cause of coronary aneurysm. In most clinical scenarios, coronary artery disease is accompanied with LM coronary aneurysm. Although coronary artery aneurysm does not confer added risk in patients with coexisting obstructive coronary artery disease, LM coronary aneurysm itself remains a significant clinical concern. Thrombosis and distal embolization are the most likely reasons to cause morbidities. Aggressive surgical treatment should be considered. Here, we report a 65-year-old man presenting with effort angina. LM coronary aneurysm was noted in coronary angiogram and images including computed tomography, transesophageal echocardiography and operative photography were presented.
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PMID:Surgical treatment of left main coronary artery aneurysm: a case report. 1907 21

The presence of kidney disease, manifested by low glomerular filtration rates (GFR) and/or large amounts of protein in the urine, is independently associated with increased rates of cardiovascular disease (CVD). The severity of kidney disease is associated with graded increases in risk for CVD and death. Chronic kidney disease (CKD) should be recognized and treatment initiated early to maximize the chances for slowing nephropathy progression and reducing proteinuria. We recommend screening for CKD in all patients with CVD, including computing an estimated GFR and evaluating for proteinuria using a spot urine albumin:creatinine ratio. Aggressive management of traditional cardiovascular risk factors should be employed in this high-risk population, specifically rigorous hypertension control (including the use of angiotensin-converting enzyme inhibitors (ACEI)/angiotensin receptor blocking agents (ARB)), management of hyperglycemia, hyperlipidemia and smoking cessation. Further studies are needed to identify the unique renal failure-related (non-traditional) risk factors that contribute to accelerated atherosclerosis in this population and performance of randomized trials to assess the effects of cardiovascular interventions in individuals with CKD.
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PMID:Cardiovascular disease in chronic kidney disease. 1912 39

Typically involving the renal artery ostium or proximal segment of the renal artery, atherosclerosis is the major cause of renal artery stenosis. While commonly without direct clinical consequences, the presence of renal artery atherosclerosis is associated with atherosclerotic disease in other vascular beds and in some subjects may give rise to systemic hypertension, progressive renal dysfunction and/or heart failure. Aggressive blood pressure control, atherosclerotic risk factor modification and use of anti-platelet therapy are indicated once diagnosed. The role for concomitant renal artery revascularization remains unclear and the decision should be individualized depending on patient preferences, co-morbidities, institutional expertise, and carefully weighed risks and benefits. Ongoing trials including CORAL and ASTRAL will hopefully provide critical evidence for or against this additive invasive strategy.
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PMID:Update on the management of atherosclerotic renal artery disease. 1920 21

Our previous work in cynomolgus monkeys demonstrated significant relationships between (i) social reorganization stress and visceral fat deposition, and (ii) central fat deposition and coronary artery atherosclerosis (CAA). Nevertheless, direct relationships between CAA and visceral fat have not been demonstrated in people or animals, nor have relationships among stress, visceral obesity, and CAA been observed within a single study. Here, we examine the hypothesis that visceral obesity provides a link between social stress and CAA. Subjects were 41 socially housed females that consumed an atherogenic diet for 32 months. Social behavior and ovarian function were continuously recorded; dexamethasone suppression tests, telemetered overnight heart rate, BMI, visceral (VAT) and subcutaneous abdominal (SAT) adipose tissue were measured before necropsy. Females with high VAT:SAT were relatively subordinate, socially isolated, received more aggression and less grooming, desensitized to circulating glucocorticoids, had impaired ovarian function, higher heart rates late in the day, and more CAA than low VAT:SAT females. High-BMI females had higher heart rates than low-BMI females. Poor ovarian function in high VAT:SAT females is a novel observation suggesting the need for studies of fat distribution and ovarian function in women. The results of this study are the first to demonstrate a relationship between CAA and visceral obesity, and suggest that social stress may exacerbate CAA in part by increasing the ratio of visceral:subcutaneous fat mass in selected individuals susceptible to diet-induced CAA. Further studies are needed to understand the complex and multifactorial temporal relationship among relative visceral obesity, physiological stress responses, and CAA.
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PMID:Social stress, visceral obesity, and coronary artery atherosclerosis in female primates. 1932 45

We report here the case of a 53-year-old man who suddenly fell to the ground after being involved in a physical aggression by two younger men. Forensic autopsy revealed no significant injury except for slight, pale abrasions on the face. There were extensive signs of hypertensive and severe coronary artery atherosclerosis, corresponding to the data available from clinical history. The cause of death was established as acute myocardial ischemia due to hypertensive and atherosclerotic cardiovascular disease, probably related to the physical and/or emotional stress due to the aggression. We discuss medico-legal aspects of the death.
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PMID:Homicide by heart attack? 1934 74

Cerebrovascular and cardiovascular diseases are a major cause of morbidity and mortality. Soluble P-selectin (sP-selectin) is a biomarker for platelet/endothelial activation and is considered a risk factor for vascular disease. sP-selectin enhances procoagulant activity by inducing leukocyte-derived microparticle production and promotes activation of leukocyte integrins. However, it is not known whether it directly contributes to vascular complications. We investigated the effect of increased levels of sP-selectin on blood-brain barrier (BBB) function, stroke outcome, and atherosclerosis by comparing wild-type mice with P-sel(DeltaCT/DeltaCT) mice in which the endogenous P-selectin gene was replaced with a mutant that produces abnormally high plasma levels of sP-selectin. P-sel(DeltaCT/DeltaCT) mice presented several abnormalities, including (1) higher BBB permeability, with 25% of the animals showing differential permeability between the right and left hemispheres; (2) altered social behavior with increased aggression; (3) larger infarcts in the middle cerebral artery occlusion ischemic stroke model; and (4) increased susceptibility to atherosclerotic, macrophage-rich lesion development in both male and female mice on the apoE(-/-) genetic background. Thus, elevated sP-selectin is not only a biomarker for vascular disease, but also may contribute directly to atherosclerosis and cerebrovascular complications.
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PMID:Elevated levels of soluble P-selectin in mice alter blood-brain barrier function, exacerbate stroke, and promote atherosclerosis. 1934 21

Despite improving strategies for control of risk factors, progression of atherosclerosis may lead to recurrent cardiac events related to a lesion other than that treated with initial percutaneous coronary intervention (PCI) after ST-elevation myocardial infarction (STEMI). Of 1,007 consecutive patients undergoing primary or rescue PCI for STEMI, 897 who were discharged alive were followed for up to 3 years. Those who underwent nontarget lesion revascularization (non-TLR) were compared with those who did not. Those who underwent a second procedure were followed for an additional 1 year. Altogether, 94 patients (10.5%) required a non-TLR. The median time from the first to the second PCI was 396 days (interquartile range 131 to 533). Subsequent PCI was required for non-STEMI in 46.1% and STEMI in 9.7% of cases. Independent predictors of need for non-TLR were diabetes mellitus, history of coronary bypass surgery, or peripheral vascular disease. By 1 year after the second PCI, 9 patients (9.6%) died, 4 (4.3%) had sustained MI, and 4 (4.3%) had TLR. One of these major adverse events had occurred in 17 (18%). In conclusion, after STEMI, nearly 10% of patients will develop an event that requires subsequent PCI to an unrelated lesion. Patients with diabetes mellitus, history of coronary bypass surgery, or peripheral vascular disease are at increased risk for this event. Aggressive preventive and medical management should be applied to this population for prevention of these subsequent events.
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PMID:Incidence, predictors, and outcome of new, subsequent lesions treated with percutaneous coronary intervention in patients presenting with myocardial infarction. 1940 57

To understand and promote vascular health, we must reduce the aggression to the vessel wall and enhance the physiologic mechanisms leading to restoration of vessel wall function. Three main defense mechanisms are responsible for maintaining cardiovascular homeostasis: the regenerative production of endothelial progenitor cells, vessel wall angiogenesis, and macrophage-mediated reverse cholesterol transport. Endothelial progenitor cells can restore vessel wall function and reduce atherosclerosis. In patients with risk factors, high levels of circulating progenitor cells increase event-free survival from cardiovascular events. Mobilization of progenitor cells includes physical and pharmacological approaches, of which exercise and statin therapy have great potential. Angiogenesis is a pivotal defense mechanism to counteract hypoxia and is needed for plaque regression. However, neovessels are susceptible for intraplaque hemorrhage, particularly in diabetes mellitus. In these patients, the haptoglobin 2-2 genotype is the more affected, and may benefit from an antioxidant approach. Finally, the reverse cholesterol transport system is the main mechanism for plaque regression. In addition to high-density lipoprotein cholesterol, apolipoprotein A-I therapies and the promotion of cholesterol efflux from macrophages by the ABCA1 and ABCG1 transporter systems hold great promise and may be available for therapeutic application in the near future.
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PMID:Promoting mechanisms of vascular health: circulating progenitor cells, angiogenesis, and reverse cholesterol transport. 1953 40

Chlamydia trachomatis (CT) infection is one of the most common causes of reproductive tract diseases and infertility. CT-Hsp60 is synthesized during infection and is released in the bloodstream. As a consequence, immune cells will produce anti-CT-Hsp60 antibodies. Hsp60, a ubiquitous and evolutionarily conserved chaperonin, is normally sequestered inside the cell, particularly into mitochondria. However, upon cell stress, as well as during carcinogenesis, the chaperonin becomes exposed on the cell surface (sf-Hsp60) and/or is secreted from cells into the extracellular space and circulation. Reports in the literature on circulating Hsp and anti-Hsp antibodies are in many cases short on details about Hsp60 concentrations, and about the specificity spectra of the antibodies, their titers, and their true, direct, pathogenetic effects. Thus, more studies are still needed to obtain a definitive picture on these matters. Nevertheless, the information already available indicates that the concurrence of persistent CT infection and appearance of sf-Hsp60 can promote an autoimmune aggression towards stressed cells and the development of diseases such as autoimmune arthritis, multiple sclerosis, atherosclerosis, vasculitis, diabetes, and thyroiditis, among others. At the same time, immunocomplexes composed of anti-CT-Hsp60 antibodies and circulating Hsp60 (both CT and human) may form deposits in several anatomical locations, e.g., at the glomerular basal membrane. The opposite side of the coin is that pre-tumor and tumor cells with sf-Hsp60 can be destroyed with participation of the anti-Hsp60 antibody, thus stopping cancer progression before it is even noticed by the patient or physician.
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PMID:Chlamydia trachomatis infection and anti-Hsp60 immunity: the two sides of the coin. 1971 22


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