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 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Postoperative venous thromboembolic disease (VTED) affects approximately one in four general surgery patients who do not receive preventive measures. In addition to the risk of pulmonary embolism, which is often fatal, patients with VTED may develop long-term complications such as post-thrombotic syndrome or chronic pulmonary hypertension. In addition, postoperative VTED is usually asymptomatic or produces clinical manifestations that are attributed to other processes and consequently this complication is often unnoticed by the surgeon who performed the procedure. Thus, the most effective strategy consists of effective prevention of VTED using the most appropriate prophylactic measures against the patient's thromboembolic risk. There is sufficient evidence that VTED can be prevented by pharmacological methods, especially heparin and its derivatives and with mechanical methods such as support tights or intermittent pneumatic compression of the lower extremities. To reduce the incidence of VTED as far as possible, strategies have been proposed that include a combination of drugs and mechanical methods, new antithrombotic drugs, or prolonging the duration of prophylaxis in patients at very high risk, such as those who have undergone surgery for cancer. Another important aspect is the optimal moment to initiate prophylaxis with anticoagulant drugs with the aim of achieving an adequate equilibrium between antithrombotic efficacy and the risk of hemorrhagic complications. The present article reviews the available evidence to attempt to optimize prevention of VTED in general surgery and in some special groups, such as laparoscopic surgery, short-stay surgery and obesity.
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PMID:[Prevention of venous thromboembolic disease in general surgery]. 1958 11

The term "cor pulmonale" is still popular but there is presently no consensual definition and it seems more appropriate to define the condition by the presence of pulmonary hypertension (PH) resulting from diseases affecting the structure and/or the function of the lungs: PH results in right ventricular enlargement and may lead with time to right heart failure (RHF). Chronic obstructive pulmonary disease (COPD) is the first cause of cor pulmonale, far before idiopathic pulmonary fibrosis and obesity-hypoventilation syndrome. In chronic respiratory disease (CRD) PH is "pre-capillary," due to an increase of pulmonary vascular resistance (PVR). The first cause of increased PVR is chronic long-standing alveolar hypoxia which induces pulmonary vascular remodeling. The main characteristic of PH in CRD and particularly in COPD is its mild to moderate degree, resting pulmonary artery mean pressure (PAP) in a stable state of the disease usually ranging between 20 and 35 mmHg. However, PH may worsen during exercise, sleep, and exacerbations of the disease. These acute increases in afterload can favor the development of RHF. A minority (<5%) of COPD patients exhibit severe or "disproportionate" PH (PAP >40 mmHg), the mechanism of which is not well understood. At present long-term oxygen therapy (LTOT) is the logical treatment of PH since alveolar hypoxia is considered to be the major determinant of the elevation of PAP and PVR. LTOT stabilizes or at least attenuates and sometimes reverses the progression of PH, but PAP seldom returns to normal. Vasodilators (prostacyclin, endothelin receptor antagonists, sildenafil, nitric oxide) could be considered in patients with severe PH but controlled studies in this field are presently lacking.
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PMID:Cor pulmonale. 1964 33

The prevalence of right ventricular cardiac failure (CF) and its characteristics were analysed in 326 hospitalized elderly patients with chronic obstructive pulmonary disease (COPD) (average age 70+/-11 years). At admission right ventricular CF was diagnosed in 107 (33%) patients with COPD; its prevalence did not depend to sex but increased with age, especially among men. In patients with COPD right ventricular CF was associated with atrial fibrillation, anemia and obesity as well as a history of myocardial infarction. In patients with right ventricular CF dimensions of right ventricle and left atrium were significantly larger than those in patients without CF. Right ventricular CF was often associated with dilation of right atrium and pulmonary hypertension, especially with severe pulmonary hypertension. These data suggested that age (especially among men), pulmonary hypertension, atrial fibrillation, anemia, obesity and probably a history of myocardial infarction are risk factors for right ventricular CF in hospitalized elderly patients with COPD.
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PMID:[Right ventricular cardiac failure in hospitalized patients with chronic obstructive pulmonary disease: prevalence and clinical and instrumental characteristics]. 1965 6

Obesity is becoming a worldwide problem of epidemic proportions, and its effect on the heart is increasingly being recognized. Obesity is often associated with an increased risk for heart failure. In this article, the authors review the evidence for obesity-related cardiomyopathy. The importance of metabolic disturbances in the development of cardiomyopathy in obese patients is highlighted. The authors also briefly explore whether obesity plays a role in the development of pulmonary hypertension. Better recognition and understanding of both obesity cardiomyopathy and pulmonary hypertension are needed in the obese patient population.
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PMID:Role of obesity in cardiomyopathy and pulmonary hypertension. 1970 49

Severe pulmonary hypertension is a lethal group of disorders which preferentially afflicts women. It appears that in recent years the patient profile has shifted towards older, obese, and postmenopausal women, suggesting that endocrine factors may be important. Several studies have revealed an increased prevalence of thyroid disease in these patients, but no studies have evaluated for a coexistence of endocrine factors. In particular, no studies have attempted to evaluate for concurrent thyroid disease, obesity and long-term estrogen exposure in patients. 88 patients attending the Pulmonary Hypertension Association 8th International meeting completed a questionnaire and were interviewed. Information was collected regarding reproductive history, height, weight, and previous diagnosis of thyroid disease. 46% met criteria for obesity. 41% reported a diagnosis of thyroid disease. 81% of women reported prior use of hormone therapy. 70% reported greater than 10 years of exogenous hormone use. 74% of female patients reported two or more of potentially disease modifying endocrine factors (obesity, thyroid disease or estrogen therapy). The coexistent high prevalence in our cohort of exogenous estrogen exposure, thyroid disease and obesity suggests that an interaction of multiple endocrine factors might contribute to the pathogenesis of pulmonary hypertension and may represent epigenetic modifiers in genetically-susceptible individuals.
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PMID:Estrogen exposure, obesity and thyroid disease in women with severe pulmonary hypertension. 1974 50

The correlates and consequences of pulmonary hypertension (PH) associated with obstructive sleep apnea (OSA) are poorly understood. Patients undergoing pulmonary artery catheterization within 6 months of an overnight polysomnography showing OSA were included in the present analysis. A total of 83 patients with complete data were analyzed (no PH, n = 25 [30%]; PH, 58 [70%]; of these, 18 had a pulmonary capillary wedge pressure of <15 mm Hg). No significant differences were observed between the PH and no PH groups regarding age or apnea-hypopnea index. The correlates of PH were elevated right ventricular systolic pressure (p <0.001), body mass index (p = 0.026), female gender (p = 0.01), nocturnal desaturation (82% vs 18%), and forced vital capacity <70% (p = 0.04) on univariate analysis and female gender (p = 0.03), age <49 years (p = 0.02), body mass index of > or =26 kg/m(2) (p = 0.08), and right ventricular systolic pressure of > or =30 mm Hg (p <0.001) on multivariate analysis. Patients with PH had a lower 6-minute walk distance (285.5 +/- 122 m vs 343 +/- 213 m, p = 0.4). The survival rate at 1, 4, and 8 years for patients with PH was 93%, 75%, and 43% compared to 100%, 90%, and 76% for patients without PH, respectively. Patients with severe PH (n = 27; 33%) had more nocturnal desaturation (p = 0.045), worse pulmonary hemodynamics, and greater mortality (37%) than the groups with mild or moderate PH (16%) or no PH (16%). In conclusion, our results have shown that, although generally mild to moderate, severe PH can occur in patients with OSA. Female gender, younger age, obesity, and nocturnal desaturation were associated with PH. PH can cause functional limitations and increased mortality in patients with OSA.
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PMID:Frequency and impact of pulmonary hypertension in patients with obstructive sleep apnea syndrome. 1984 May 81

Obesity places a significant load on the respiratory system, affecting lung volumes, respiratory muscle function, work of breathing, and ventilatory control. Despite this, most morbidly obese individuals maintain eucapnia. However, a subgroup of morbidly obese individuals will develop chronic daytime hypercapnia, described as the obesity hypoventilation syndrome (OHS). While obesity is obviously a crucial component of this syndrome, the relationship between excess fat accumulation and the development of awake hypercapnia is complex and extends beyond simply impairments of pulmonary mechanics and lung volumes as a consequence of obesity. Various compensatory mechanisms operate to maintain eucapnia even in the presence of extreme obesity. However, if compensation is impaired, hypoventilation will ensue. While obesity alone does not account for the development of hypoventilation, weight loss will produce significant improvements in lung function and awake gas exchange. Such improvements have the potential to substantially reduce morbidity and mortality in these individuals. Nevertheless, many individuals remain overweight despite substantial weight loss, with persistence of upper airway obstruction. Attention to this residual abnormality is important given the high incidence of cardiovascular abnormalities, including pulmonary hypertension, in individuals with OHS.
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PMID:Big breathing: the complex interaction of obesity, hypoventilation, weight loss, and respiratory function. 1987 12

Heterocyclic indazole derivatives are claimed in patent WO2008138448 as inhibitors of the serum- and glucocorticoid-inducible-kinase 1 (SGK1) and drugs for the pharmacological treatment of SGK1-related diseases, such as diabetes, obesity, metabolic syndrome, systemic and pulmonary hypertension, cardiac fibrosis, hypertrophy and insufficiency, arteriosclerosis, glomerulosclerosis, nephrosclerosis, nephritis, nephropathy, deranged electrolyte excretion, fibrosing and inflammatory disease (e.g., liver cirrhosis, lung fibrosis, rheumatism, arthrosis, Crohn s disease, chronic bronchitis, radiation fibrosis, sclerodermia, cystic fibrosis, scar formation and Alzheimer' disease), tumor growth, peptic ulcers and some disorders hitherto not conclusively shown to involve SGK1. Most of the claims are supported by the literature. SGK1 is ubiquitously expressed and its expression is stimulated by hyperglycemia, cell shrinkage, ischemia, glucocorticoids, mineralocorticoids and several inflammatory mediators including TGF-ss. SGK1 is activated by insulin and growth factors via the phosphatidylinositol-3-kinase pathway. SGK1 regulates ion channels (including ENaC, KCNE1/KCNQ1), carriers (including NCC, NHE3, SGLT1), Na(+)/K(+)-ATPase, enzymes (including glycogen-synthase-kinase-3) and transcription factors (including FOXO3a, ss-catenin, NF-kappaB). A gain-of-function SGK1 gene variant, carried by approximately 3 - 5% of Caucasians and approximately 10% of Africans, is associated with increased blood pressure, obesity and type 2 diabetes. In vitro and in vivo experiments suggested a critical role of SGK1 in renal fluid retention and hypertension, glucose-induced obesity, coagulation and increased matrix protein formation.
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PMID:Heterocyclic indazole derivatives as SGK1 inhibitors, WO2008138448. 2002 Dec 89

The term obesity cardiomyopathy has previously been used to describe a clinical syndrome in obese patients typically consisting of eccentric left ventricular hypertrophy with preserved ejection fraction and diastolic dysfunction and is often associated with right ventricular dysfunction independent of the presence of the obstructive sleep apnea syndrome. Although several publications have described the early stages of this syndrome, little is known about the end stages of the disease. The authors conducted a retrospective study of a subset of edematous obese patients with multiple common medical comorbidities who present with a clinical syndrome in the setting of physiologic stress or infection. Under severe physiologic stress these patients developed pulmonary hypertension, right-sided volume overload, decreased effective arterial blood volume, and renal failure. Often, these findings were in the setting of obstructive sleep apnea. This retrospective study focuses on an obesity-related cardiorenal syndrome but also serves to provide a foreground for acknowledging the broad spectrum of cardiovascular pathology, including pulmonary hypertension, diastolic dysfunction, and sleep apnea, seen in the obese.
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PMID:Obesity-related cardiorenal syndrome. 2004 33

A high serum uric acid is common in subjects with pulmonary hypertension. The increase in serum uric acid may be a consequence of the local tissue ischemia and/or hypoxia, and it may also result from other factors independent of ischemia or hypoxia that occur in various forms of pulmonary hypertension. While classically viewed as a secondary phenomenon, recent studies suggest that hyperuricemia may also have a role in mediating the local vasoconstriction and vascular remodeling in the pulmonary vasculature. If uric acid does have a contributory role in pulmonary hypertension, we may see an increasing prevalence of pulmonary hypertension as hyperuricemia is common in subjects with obesity and metabolic syndrome. We propose studies to investigate the role of uric acid in pulmonary hypertension and to determine if lowering serum uric acid may have clinical benefit in this condition.
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PMID:Could uric acid be a modifiable risk factor in subjects with pulmonary hypertension? 2006 95


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