Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0948265 (metabolic syndrome)
 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Between January 1993 and December 2001, we employed percutaneous cardiopulmonary support (PCPS) in 35 patients. PCPS was used for postcardiotomy in 25 of these patients who could not be weaned from cardiopulmonary bypass (CPB) because of severe cardiogenic shock. In the other 10 patients, PCPS was used for a non-surgical disease. Twenty-nine patients (82.9%) were weaned from PCPS, and 28 (80.0%) survived. The other 7 patients (20.0%) died due to postoperative complications. The causes of death were multiple organ failure (MOF) due to wound bleeding, low cardiac output syndrome (LOS), myonephropathic metabolic syndrome (MNMS) with severe lower limbs ischemia, cerebrovascular accident (CVA), and sepsis. The first cause for the complications was postoperative sustained severe heart failure. To improve the survival rate, it was necessary to prevent bleeding and begin PCPS at an earlier stage.
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PMID:Clinical effects of percutaneous cardiopulmonary support in severe heart failure: early results and analysis of complications. 1273 87

All cells must maintain a high ratio of cellular ATP:ADP to survive. Because of the adenylate kinase reaction (2ADP <--> ATP + AMP), AMP rises whenever the ATP:ADP ratio falls, and a high cellular ratio of AMP:ATP is a signal that the energy status of the cell is compromised. The AMP-activated protein kinase (AMPK) is the downstream component of a protein kinase cascade that is switched on by a rise in the AMP:ATP ratio, via a complex mechanism that results in an exquisitely sensitive system. AMPK is switched on by cellular stresses that either interfere with ATP production (e.g. hypoxia, glucose deprivation, or ischemia) or by stresses that increase ATP consumption (e.g. muscle contraction). It is also activated by hormones that act via Gq-coupled receptors, and by leptin and adiponectin, via mechanisms that remain unclear. Once activated, the system switches on catabolic pathways that generate ATP, while switching off ATP-consuming processes that are not essential for short-term cell survival, such as the synthesis of lipids, carbohydrates, and proteins. The AMPK cascade is the probable target for the antidiabetic drug metformin, and current indications are that it is responsible for many of the beneficial effects of exercise in the treatment and prevention of type 2 diabetes and the metabolic syndrome.
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PMID:Minireview: the AMP-activated protein kinase cascade: the key sensor of cellular energy status. 1296 15

The development of atherosclerotic cardiovascular disease is a common comorbidity in patients with the metabolic syndrome, a concurrence of cardiovascular risk factors in one individual. While multiple growth factors and adipokines are identified in atherosclerotic lesions, as well as neurotrophins implicated in both cardiac ischemia and lipid and glucose metabolism, the potential role of neurotrophins in human coronary atherosclerosis and in the metabolic syndrome still remains to be elucidated. Here we describe and discuss our results that represent a novel attempt to study the cardiovascular and metabolic biology of nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF) and mast cells (MC). The local amount of NGF, the immunolocalization of p75 neurotrophin receptor (p75NTR) and the number of MC were correlatively examined in coronary vascular wall and in the surrounding subepicardial adipose tissue, obtained from autopsy cases in humans with advanced coronary atherosclerosis. We also analyzed the plasma levels of NGF, BDNF and leptin and the number of MC in biopsies from abdominal subcutaneous adipose tissue in patients with a severe form of the metabolic syndrome. The results demonstrate that NGF levels are decreased in atherosclerotic coronary vascular tissue but increased in the subepicardial adipose tissue, whereas both tissues express a greater number of MC and a stronger p75NTR immunoreactivity, compared to controls. Metabolic syndrome patients display a significant hyponeurotrophinemia and an increased number of adipose MC; the later correlates with elevated plasma leptin levels. In effect, we provide the first evidence for (i) an altered presence of NGF, p75NTR and MC in both coronary vascular and subepicardial adipose tissue in human coronary atherosclerosis, and (ii) a significant decrease in plasma NGF and BDNF levels and an elevated amount of plasma leptin and adipose MC in metabolic syndrome patients. Together our findings suggest that neuroimmune mediators such as NGF, BDNF, leptin and MC may be involved in the development of cardiovascular disease and related disorders.
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PMID:Neurotrophin presence in human coronary atherosclerosis and metabolic syndrome: a role for NGF and BDNF in cardiovascular disease? 1469 70

Adrenomedullin was originally discovered as a vasodilative peptide, but recent studies have revealed its pleiotropic effects. Among these studies, the antioxidative properties of adrenomedullin were observed in adrenomedullin knockout mice. Through its antioxidative effect, adrenomedullin can protect organs from damage induced by high blood pressure, ischemia and aging. This indicates that antioxidants that can inhibit reactive oxygen species production but do not have a scavenging effect could be a new effective therapeutic target for organ protection in hypertension as well as metabolic syndrome, in which higher oxidative stress plays a pivotal role.
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PMID:Adrenomedullin as a potent antioxidative and antiatherosclerotic substance. 1591 20

Adrenomedullin was originally discovered as a vasodilative peptide, but recent studies have revealed its pleiotropic effects. Among these studies, the antioxidative properties of adrenomedullin were observed in adrenomedullin knockout mice. Through its antioxidative effect, adrenomedullin can protect organs from damage induced by high blood pressure, ischemia and aging. This indicates that antioxidants that can inhibit reactive oxygen species production but do not have a scavenging effect could be a new effective therapeutic target for organ protection in hypertension as well as metabolic syndrome, in which higher oxidative stress plays a pivotal role.
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PMID:Adrenomedullin as a potent antioxidative and antiatherosclerotic substance. 1594 48

The number of an elderly patient who has hypertension with diabetes mellitus has been increasing year by year since the life style of people has become Americanized in our country. Metabolic syndrome is characterized by hypertension, dyslipidemia, central adiposity and insulin resistance. It is recently recognized as the high risk for the macrovascular disease such as cerebral infarction and acute myocardial infarction. In diabetic patients, to prevent the life-threatening event or slow complications intensive blood pressure control is as efficacious as good glycemic control. The optimal blood pressure level to reduce hypertension-related morbidity and mortality in diabetic elderly has been proposed 130/80 mmHg in JSH 2004. The blood pressure level in the elderly should be lowered very slowly with careful monitoring of systemic ischemia. Early use of antihypertensive drug combinations is gaining favor. As the first step therapy would be recommended angiotensin receptor blocker, angiotensin-converting enzyme inhibitor and sustained release calcium channel blocker. Especially in the elderly, good control of life-style related diseases would be achieved through a team effort comprising the clinician, psychologist, nurse, pharmacologist, dietitian, other professionals and the patient's family. Comprehensive geriatric assessment can facilitate the maintenance of drug compliance for well control of blood pressure level.
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PMID:[Management of hypertension with diabetes mellitus in the elderly]. 1594 90

Adult vascular progenitor cells (for example endothelial progenitor cells, EPC) have been studied for their contribution to vascular repair and angiogenesis. These cells can differentiate from bone marrow cells as well as circulating cells carrying hematopoetic stem cell markers. In vivo, they take part in vasculogenesis in different animal models of limb ischemia, myocardial infarction and wound healing. In metabolic disease, the outgrowth and function of EPC in vitro is defective and numbers of EPC correlate with classical risk factors of cardiovascular disease suggesting a role of EPC in the development of vascular complications. Pilot studies for the treatment of myocardial infarction and limb ischemia with autologous bone marrow showed a distinct therapeutic benefit that is presumably mediated by vasculogenesis in damaged tissues. However, little is known about the nature of EPC and their capability to differentiate into functional cells for tissue regeneration. In this article, we review and discuss the hitherto identified physiological function of EPC, the mechanisms leading to dysfunction of these cells and potential therapeutic applications in patients with metabolic syndrome or diabetes mellitus and vascular complications.
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PMID:Adult vascular progenitor cells and tissue regeneration in metabolic syndrome. 1596 88

Nonalcoholic fatty liver disease (NAFLD) is consistently associated with features of the metabolic syndrome, a condition carrying a high risk of cardiovascular events. We measured the vasodilatory response of the brachial artery in response to ischemia (a test of endothelial function) (FMV) as well as cardiovascular risk profile in 52 NAFLD cases and 28 age- and sex-matched controls. The 10-year risk of coronary events was calculated according to the Framingham equation and the scores derived from the PROCAM study and NCEP-ATPIII proposals. FMV was 6.33% +/- 5.93% in NAFLD versus 12.22% +/- 5.05% in controls (P < .0001), and higher in pure fatty liver (9.93%) compared with nonalcoholic steatohepatitis (4.94%) (P = .010). No differences were observed in flow-independent vasodilation (response to sublingual nitroglycerin). Percent FMV was negatively associated with insulin resistance (homeostasis model assessment) in the whole population (r = -0.243; P = .030). In logistic regression analysis, NAFLD was associated with a percent FMV in the lower tertile (OR, 6.7; 95% CI, 1.26-36.1), after adjustment for age, sex, body mass index, and insulin resistance. Among NAFLD patients, low FMV was associated with nonalcoholic steatohepatitis (adjusted OR, 6.8; 95% CI, 1.2-40.2). The 10-year probability of cardiovascular events was moderately increased in NAFLD, and particularly in nonalcoholic steatohepatitis. In conclusion, our study provides evidence of endothelial dysfunction and increased risk of cardiovascular events in NAFLD. The risk of advanced liver disease is well recognized in NAFLD patients, but the large majority of cases might experience cardiovascular disease in the long term, indirectly limiting the burden of liver failure.
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PMID:Endothelial dysfunction and cardiovascular risk profile in nonalcoholic fatty liver disease. 1617 89

A novel cardiac syndrome of left ventricular apical ballooning (Takotsubo cardiomyopathy-ampulla cardiomyopathy) involves reversible left ventricular apical ballooning (during systole) of acute onset with chest pain, electrocardiographic changes, and minimal elevation of cardiac enzymes resembling acute myocardial infarction, but without evidence of myocardial ischemia or injury. Patients have no angiographic evidence of coronary artery stenosis and there is almost always a complete recovery of left ventricular function in days to weeks. The precise etiologic basic of this syndrome is not clear but most likely it is a non-ischemic, metabolic syndrome caused by stress-induced activation of the cardiac adrenoceptors in absence of ischemia and reperfusion. Reported here is a case of stress-induced transient left ventricular apical ballooning syndrome in a young woman.
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PMID:Transient left ventricular apical ballooning: a novel heart syndrome. 1598 10

Peripheral vascular disease (PVD) is very prevalent in the United States and is part of a global vascular problem. PVD patients have a heightened inflammatory state and are at high risk of death from acute cardiovascular problems rather than from progression of PVD. Modifiable risk factors for PVD include smoking, hypertension, diabetes, hyperlipidemia, elevated high sensitivity C-reactive protein, obesity, and the metabolic syndrome. Symptomatic treatment of claudication includes smoking cessation, exercise, cilostazol, statins, and revascularization with percutaneous or surgical therapy. Antithrombotic therapy with aspirin or clopidogrel is important to reduce cardiovascular events but does not affect symptoms of claudication. Patients with rest limb ischemia or ulceration should be revascularized to minimize the chance of limb loss. Percutaneous revascularization is not without significant complications, however, and future research needs to focus on inflammation, thrombosis, and restenosis in the PVD patient. Finally, new devices that tackle difficult lesions, drug-eluting stents, and pharmacologic agents that reduce global atherosclerosis are on the horizon and are likely to become critical components in the management of the PVD patient.
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PMID:Evidence-based management of peripheral vascular disease. 1610 78


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