Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Obstructive sleep apnea (OSA) is a common medical condition that occurs in approximately 5% to 15% of the population. The pathophysiology of OSA is characterized by repetitive occlusions of the posterior pharynx during sleep that obstruct the airway, followed by oxyhemoglobin desaturation, persistent inspiratory efforts against the occluded airway, and termination by arousal from sleep. Obstructive sleep apnea is associated with daytime sleepiness and fatigue, likely due to fragmented sleep from recurrent arousals. Substantial evidence shows that patients with OSA have an increased incidence of hypertension compared with individuals without OSA and that OSA is a risk factor for the development of hypertension. Recent studies show that OSA may be implicated in stroke and transient ischemic attacks. Obstructive sleep apnea appears to be associated with coronary heart disease, heart failure, and cardiac arrhythmias. Pulmonary hypertension may be associated with OSA, especially in patients with preexisting pulmonary disease. Although the exact cause that links OSA with cardiovascular disease is unknown, there is evidence that OSA is associated with a group of proinflammatory and prothrombotic factors that have been identified to be important in the development of atherosclerosis. Obstructive sleep apnea is associated with increased daytime and nocturnal sympathetic activity. Autonomic abnormalities seen in patients with OSA include increased resting heart rate, decreased R-R interval variability, and increased blood pressure variability. Both atherosclerosis and OSA are associated with endothelial dysfunction, increased C-reactive protein, interleukin 6, fibrinogen, and plasminogen activator inhibitor, and reduced fibrinolytic activity. Obstructive sleep apnea has been associated with enhanced platelet activity and aggregation. Leukocyte adhesion and accumulation on endothelial cells are common in both OSA and atherosclerosis. Clinicians should be aware that OSA may be a risk factor for the development of cardiovascular disease.
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PMID:Obstructive sleep apnea and cardiovascular disease. 1530 32

Albuminuria is a predictor of cardiovascular morbidity and mortality in patients with diabetes. In this study, the relationship of albuminuria with left ventricular function by using myocardial performance (Tei) index together with conventional function parameters was aimed to be examined. We studied 123 patients with diabetes but without obvious coronary artery disease and heart failure. The patients were divided into 3 groups: 50 with no albuminuria; 49 with microalbuminuria; and 24 with macroalbuminuria. The Tei index in the patients with diabetes was increased (0.59 +/- 0.12). A significant stepwise increase in the Tei index was seen from no albuminuria to macroalbuminuria (0.51 +/- 0.1, 0.61 +/- 0.1, and 0.7 +/- 0.08, respectively). Tei index was positively correlated with isovolumic relaxation time, isovolumic contraction time, the duration of diabetes, left ventricular mass index, the levels of fibrinogen, creatinine, total cholesterol, and low-density lipoprotein cholesterol. The association of amount of secreted albumin into urine with echocardiographic parameters (Tei index, ejection fraction, peak early and late transmitral filling velocity ratio, peak early transmitral filling velocity decelaration time, isovolumic relaxation time, left ventricle mass index) was evaluated by using regression analysis. It was observed that amount of albumin was significantly associated with only Tei index ( P = .001, B = 0.3). It was found that there was a strong relation between Tei index and albuminuria and also its degree. Therefore, it was concluded that Tei index may be a sensitive marker for diagnosis of ventricular dysfunction in patients with diabetes and prognosis of diabetes.
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PMID:Association of Doppler-derived myocardial performance index with albuminuria in patients with diabetes. 1550 95

Clinical studies in patients with acromegaly have shown that growth hormone (GH) exerts both short- and long-term effects on the structure and function of the heart. Moreover, chronic growth hormone deficiency (GHD) has been associated with impaired cardiac performance, low heart rate and impaired left ventricular systolic function. Exercise capacity in patients with GHD is significantly reduced and in some severely affected individuals, dilated cardiomyopathy and heart failure has been reported. GHD has also been associated with a number of risk factors for cardiovascular disease. Altered lipoprotein metabolism and elevated fibrinogen and plasminogen activator inhibitor-1 activity are associated with GHD, and the risk of hypertension is increased in GH-deficient men. Subcutaneous and intra-abdominal fat mass have also been found to be abnormally high in these patients. These effects may contribute to an increased risk of death from cardiovascular disease. GH is therefore an important factor in the development and function of the cardiovascular system. In this paper, the effects of GH on the physiological mechanisms of the cardiovascular system are discussed, including the effect of GHD on cardiovascular disease risk. We will also discuss the effects of long-term GH replacement therapy in this patient population.
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PMID:Cardiovascular disease and risk factors: the role of growth hormone. 1559 64

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.
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PMID:[Sleep apnea syndromes and cardiovascular disease]. 1614 10

Modern approaches to prevention of venous thromboembolic complications in patients with chronic heart failure are analyzed in this review which contains results of large studies of low molecular weight heparins. In MEDENOX trial the use of enoxaparin in medical patients was associated with 63% reduction of risk of thrombosis. The authors own experience showed that 2 weeks of therapy with enoxaparin in patients with chronic stage IIB-III heart failure caused significant lowering of soluble fibrin-monomer complexes, fibrinogen, and index of turbo-dynamic potential. These changes evidenced for decreased intravascular blood coagulation. Thus enoxaparin can be effectively used for prevention of thrombosis and thromboembolism in patients with chronic heart failure. Novel antithrombotic agents fondaparinux, idraparinux, ximelagatran, recombinant thrombomodulin are perspective medications for prevention of venous thromboses and embolism in medical patients.
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PMID:[Novel possibilities of antithrombotic therapy in patients with chronic heart failure]. 1635 54

Obstructive sleep apnea (OSA) is a common medical condition that occurs in a considerable percentage of the population. Substantial evidence shows that patients with OSA have an increased incidence of hypertension compared with individuals without OSA, and that OSA is a risk factor for the development of hypertension. It is established that OSA may be implicated in stroke and transient ischemic attacks. OSA is associated with coronary heart disease, heart failure, and cardiac arrhythmias. Pulmonary hypertension may be associated with OSA, especially in patients with pre-existing pulmonary disease. Although the exact cause that links OSA with cardiovascular disease is unknown, there is evidence that OSA is associated with a group of proinflammatory and prothrombotic factors that have been identified as important in the development of atherosclerosis. OSA is associated with increased daytime and nocturnal sympathetic activity. Autonomic abnormalities seen in patients with OSA include increased resting heart rate, decreased R-R interval variability, and increased blood pressure variability. Both atherosclerosis and OSA are associated with endothelial dysfunction, increased C-reactive protein, interleukin 6, fibrinogen, plasminogen activator inhibitor, and reduced fibrinolytic activity. OSA has been associated with enhanced platelet activity and aggregation. Leukocyte adhesion and accumulation on endothelial cells are common in both OSA and atherosclerosis. Clinicians should be aware that OSA may be a risk factor for the development of cardiovascular disease.
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PMID:Inflammatory aspects of sleep apnea and their cardiovascular consequences. 1646 39

Circulating apoptotic proteins are increased in patients with heart failure. We evaluated whether circulating soluble (s) apoptosis-related proteins and inflammation markers are increased in long-term disease free breast cancer survivors and associated with cardiotoxicity, and if subgroups could be identified based on the applied treatments. Circulating tumour necrosis factor (TNF) alpha, sTNF-receptor (sTNF-R) 1 and 2, sFas, sFas ligand, sTNF-related apoptosis inducing ligand (sTRAIL) and serum HER2 were measured with immunoassay. High-sensitivity C-reactive protein (HS-CRP), fibrinogen, plasma B-type and N-terminal atrial natriuretic peptide (NT-ANP and BNP) were also determined. Thirty-four patients with median 6.0 years follow-up and 12 healthy age-matched women were enrolled. Chemotherapy, consisting of five cycles fluorouracil, epirubicin (90 mg/m(2)), cyclophosphamide (FEC) (n=14) or four cycles FEC followed by myeloablation with high-dose carboplatin, cyclophosphamide, thiotepa (n=20), preceded irradiation and tamoxifen. Circulating apoptosis markers were higher in patients than in controls. No associations with cardiac dysfunction were observed. sFas ligand and sTRAIL were higher in the high-dose than in the standard-dose group. In conclusion, we observed increased circulating apoptotic protein levels in long-term disease-free breast cancer survivors, treated with adjuvant chemoradiotherapy, particularly after myeloablative chemotherapy. The potential relation with late cardiotoxicity of antineoplastic therapy deserves further study.
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PMID:Circulating apoptotic proteins are increased in long-term disease-free breast cancer survivors. 1654 63

Plasma fibrinogen, C-reactive protein (CRP), and interleukin-6 (IL-6) levels in patients with acute myocardial infarction (AMI) receiving thrombolysis have been related to prognosis. The aim of this study was to investigate the time course of plasma fibrinogen, CRP, and IL-6 levels during the in-hospital phase in patients with AMI receiving thrombolysis, and their relationship to in-hospital and prognosis after 12-months follow-up. In 40 patients presenting with AMI within 6 hours of symptom onset and treated with thrombolysis, plasma fibrinogen, CRP, and IL-6 levels were measured on admission and after 6, 12, 24, 48, and 72 hours; 7 days; and 6 months. Patients with other diseases that can alter fibrinogen, CRP, or IL-6 levels were excluded. Patients had a clinical follow-up at 6 and 12 months, and the following cardiac events were recorded: cardiac death, recurrent angina, recurrent AMI, and heart failure. Plasma fibrinogen concentrations decreased significantly (p <0.01 vs admission levels) at 12 hours (425 +/-94 vs 322 +/-132 mg/dL), started to increase at 24 hours, reached peak value at 72 hours (602 +/-209 mg/dL), remained elevated at 7 days, and were back to admission levels at 6 months (375 +/-79 mg/dL). CRP levels increased significantly at 12 hours (0.73 +/-0.43 vs 0.23 +/-0.11 mg/dL, p <0.01), reached peak value at 72 hours (7.66 +/-3.28 mg/dL), decreased significantly on day 7 (2.32 +/-1.17 mg/dL), and at 6 months were within normal limits (0.49 +/-0.29 mg/dL). IL-6 levels increased significantly at 6 hours (14.03 +/-8.13 vs 6.37 +/-3.88 pg/mL, p <0.05), reached peak value at 24 hours (59.49 +/-23.57 pg/mL), started to decrease at 48 hours, and at 6 months were within normal limits (2.25 +/-1.24 pg/mL). During the in-hospital phase 33 patients had an uneventful course and 7 patients had complications (3 post-AMI angina; 4 heart failure). During the 12-month follow-up period 28 patients had an uneventful course, and 12 patients had complications (1 cardiac death, 5 recurrent angina, 2 recurrent AMI, and 4 heart failure). Regarding the in-hospital prognosis, fibrinogen, CRP, and IL-6 levels were significantly higher (p <0.05) in patients with complications from 48 to 72 hours, from 12 hours until day 7, and from 6 hours until day 7, respectively. During the 12-month follow-up period fibrinogen, CRP, and IL-6 levels were significantly higher in patients with complications (at 48, 24, and 24 hours, respectively) only in the subgroup of patients who had complications within the first 6 months following AMI. Multivariate analysis showed that CRP at 48 hours was the most important factor related to in-hospital prognosis (p = 0.02), and ejection fraction followed by CRP at 24 hours (p = 0.02) to 6-month prognosis (p = 0.018). Fibrinogen, CRP, and IL-6 levels alter in patients with AMI receiving thrombolysis, and are related both to in-hospital and to 6-month follow-up prognosis.
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PMID:In-hospital and long-term prognostic value of fibrinogen, CRP, and IL-6 levels in patients with acute myocardial infarction treated with thrombolysis. 1670 88

The observed 26 subjects with chronic heart failure (CHF) resulted from ischemic heart disease and it was found that the state of correlation interrelation between indices of lipid peroxidation of the antioxidant system and hemocoagulation is determined by the severity of decompensation. Patients with stage I CHF were seen to have a close direct interrelation between the content of primary and secondary by-products of lipid peroxidation and prothrombin time (PT). Patients with stage IIA CHF were observed with a close negative interrelation between the level of common lipids and recalcification time; vitamin A concentration and fibrinogen F. Patients with stage II CHF had direct interrelation between the level of common lipids, vitamins E, A and prothrombin index and inversely proportional to prothrombin time at the same time the catalase activity of the patients inversely correlated with fibrinogen F.
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PMID:[Interrelation between lipid peroxidation and indices of hemocoagulation in patients with chronic heart failure resulted from ischemic heart disease]. 1768 13

This study was conducted to assess the relationship among circulating markers of inflammation, endothelial dysfunction and angiogenesis in 59 chronic heart failure (CHF) patients. Increased concentrations of C-reactive protein (CRP), tumour necrosis factor-alpha (TNF-alpha), von Willebrand factor (VWF) and fibrinogen are strongly implicated in the development of CHF. Increased vascular endothelium grow factor (VEGF) and decreased thrombospondin-1 (TSP-1) concentrations suggest a role of angiogenesis in the maintenance and repair of luminal endothelium in CHF. A relationship among markers of endothelial dysfunction (VWF) and inflammation (fibrinogen, CRP) and angiogenesis (VEGF, TSP-1) was found in CHF patients.
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PMID:Inflammation, endothelial dysfunction and angiogenesis markers in chronic heart failure patients. 1772 86


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