Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The main peripheral sources of 5-hydroxytryptamine (5-HT) are as a neurotransmitter and local hormone in the gastrointestinal tract, and stored in circulating platelets and pulmonary neuroepithelial bodies. 5-HT has been shown to have many possible physiological and pathophysiological roles on the cardiovascular and renal systems. Thus, 5-HT may contribute to valvular heart disease, coronary artery disease, pulmonary hypertension, pulmonary embolism, pre-eclampsia, peripheral vascular disease and diabetic nephropathy. Consequently, modulators of the 5-HT system have diverse clinical potential. For instance, selective 5-HT subtype 3 receptor (5-HT(3)) antagonists may have potential in the treatment of the pain associated with myocardial infarction. MCI-9042 (sarpogrelate) or other 5-HT(2A) antagonists may have clinical potential for the treatment of vasospastic angina, ischaemic heart disease, reperfusion injury and hindlimb ischaemia. Several modulators of 5-HT (5-HT transporter inhibitors, 5-HT(1B) and (2B) antagonists) may have potential alone or in combination in the treatment of pulmonary hypertension. In hypertension, agonists at the 5-HT(7) and antagonists at the 5-HT(2B) may reduce blood pressure, and in diabetes, sarpogrelate may protect against nephropathy.
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PMID:The role of 5-HT on the cardiovascular and renal systems and the clinical potential of 5-HT modulation. 1272 Apr 92

Although renal failure has classically been associated with a bleeding tendency, thrombotic events are common among patients with end-stage renal disease (ESRD). A variety of thrombosis-favoring hematologic alterations have been demonstrated in these patients. In addition, "nontraditional" risk factors for thrombosis, such as hyperhomocysteinemia, endothelial dysfunction, inflammation, and malnutrition, are present in a significant proportion of chronic dialysis patients. Hemodialysis (HD) vascular access thrombosis, ischemic heart disease, and renal allograft thrombosis are well-recognized complications in these patients. Deep venous thrombosis and pulmonary embolism are viewed as rare in chronic dialysis patients, but recent studies suggest that this perception should be reconsidered. Several ESRD treatment factors such as recombinant erythropoietin (EPO) administration, dialyzer bioincompatibility, and calcineurin inhibitor administration may have prothrombotic effects. In this article we review the pathogenesis and clinical manifestations of thrombosis in ESRD and evaluate the evidence that chronic renal failure or its management predisposes to thrombotic events.
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PMID:Thrombosis in end-stage renal disease. 1471 19

As part of the National Surgical Adjuvant Breast and Bowel Project, a controlled clinical trial known as the Breast Cancer Prevention Trial (BCPT) was conducted to assess the effectiveness of tamoxifen as a preventive agent for breast cancer. In addition to the incidence of breast cancer, data were collected on several other, possibly adverse, outcomes, such as invasive endometrial cancer, ischemic heart disease, transient ischemic attack, deep vein thrombosis and/or pulmonary embolism. In this article, we present results from an illustrative analysis of the BCPT data, based on a new modeling technique, to assess the effectiveness of the drug tamoxifen as a preventive agent for breast cancer. We extended the flexible model of Gray (1994, Spline-based test in survival analysis, Biometrics 50, 640-652) to allow inference on multiple time-to-event outcomes in the style of the marginal modeling setup of Wei, Lin, and Weissfeld (1989, Regression analysis of multivariate incomplete failure time data by modeling marginal distributions, Journal of the American Statistical Association 84, 1065-1073). This proposed model makes inference possible for multiple time-to-event data while allowing for greater flexibility in modeling the effects of prognostic factors with nonlinear exposure-response relationships. Results from simulation studies on the small-sample properties of the asymptotic tests will also be presented.
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PMID:Inference in spline-based models for multiple time-to-event data, with applications to a breast cancer prevention trial. 1496 64

The Japanese Society of Anesthesiologists (JSA) conducts an annual survey of life-threatening events in operating rooms (OR) in JSA Certified Training Hospitals (JSACTH) by sending and collecting confidential questionnaires. Etiologies of the incidents were divided into four categories: those totally attributable to anesthetic management (AM), those resulting from preoperative complications (PC), those resulting from intraoperative pathological events (IP) and those related to surgical procedures (SP). IP resulted from coronary ischemia not suspected preoperatively, arrhythmias, pulmonary embolism, and other conditions. Outcomes were judged on the 7th post-operative day. In the year 2002, questionnaires were sent to 844 JSACTHs, and a total of 1,461,020 cases of anesthesia were documented from 773 JSACTHs. Of these, 1,277,045 cases of anesthesia from 712 JSACTHs were available for analysis. Seven hundred thirty nine cardiac arrests (5.79 per 10,000 anesthetics) and 806 deaths (6.31 per 10,000 anesthetics) due to life-threatening events in the OR were reported. The incidence of cardiac arrest and mortality totally attributable to AM was 0.38 and 0.11 per 10,000 anesthetics. These values tended to decrease after 1994, except the mortality totally attributable to AM, which were almost at constant level during recent years. The summary of the study between 1999 and 2002 was as follows. Among 3,855,384 anesthetics, 2,443 cardiac arrests (6.34 per 10,000 anesthetics) and 2,638 deaths (6.85 per 10,000 anesthetics) due to life-threatening events in the OR were reported. PC, SP, IP and AM were responsible for 64.7, 23.9, 9.4, and 1.5% of deaths, respectively. The major cause of PC related deaths was preoperative hemorrhagic shock, followed by cardiovascular diseases such as myocardial ischemia and congestive heart failure. Excessive surgical bleeding comprised 70.2% of SP-related deaths. The major causes of IP-related death were myocardial ischemia, pulmonary embolism, and severe arrhythmias. The incidence of cardiac arrest and death totally attributable to AM was 0.47 and 0.10/10,000 anesthetics, respectively. Among patients with ASA-PS 1(E) and 2(E), AM-related deaths occurred at a rate of 0.04/10,000 anesthetics. Half of AM-induced deaths were caused by airway or ventilatory problems. Other causes of AM-related death were medication accidents and infusion/transfusion accidents. Considerable effort is required to reduce intraoperative life-threatening events caused by human error, hemorrhage, and cardiovascular diseases.
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PMID:[Annual mortality and morbidity in operating rooms during 2002 and summary of morbidity and mortality between 1999 and 2002 in Japan: a brief review]. 1507 89

Anthracyclines, found to be efficacious in the treatment of a broad spectrum of pediatric malignancies, are cardiotoxic and may lead to heart failure even a long time after successful treatment of cancer. It is thought that subtle abnormalities can progress to the more permanent myocardial disease, resulting in cardiomyopathy which may progress to congestive heart failure. There are some precipitating factors leading to the sudden onset of cardiac symptoms such as increase in afterload or preload. We describe a young patient with congestive heart failure treated with doxorubicin (cumulative mean dose 420 mg/m2) in infancy because of pelvic sarcoma in whom the appearance of symptoms was related to pulmonary embolism. Four years before hospital admission, the patient presented echocardiographic abnormalities such as left ventricular fractional shortening and thickness reduction and he was treated with ACE-inhibitors. The myocardial ischemia, which is present in pulmonary embolism, probably worsened the left ventricular systolic function and caused congestive heart failure.
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PMID:[Biventricular heart failure in patient treated with anthracycline in childhood: myocardial dysfunction is not always the cause]. 1518 68

Patients with pulmonary embolism and right ventricle dysfunction (determined with clinical, hemodynamic or echocardiographic methods) are a subgroup at high risk for complications. One of the pathogenic factors of right ventricular dysfunction in pulmonary embolism is myocardial ischemia, usually secondary to hemodynamic overload, and sometimes worsened by underlying coronary artery disease. We described a patient with pulmonary embolism and dyskinesia of the right ventricular free wall, related to chronic atherosclerotic occlusion of the right coronary artery proximal to the acute marginal branches that irrigate the free wall.
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PMID:[Right ventricular dysfunction and ischemia in pulmonary embolism]. 1528 68

Anthracyclines, found to be efficacious in the treatment of a broad spectrum of pediatric malignancies, are cardiotoxic and may lead to heart failure even a long time after successful treatment of cancer. It is thought that subtle abnormalities can progress to the more permanent myocardial disease, resulting in cardiomyopathy which may progress to congestive heart failure. There are some precipitating factors leading to the sudden onset of cardiac symptoms such as increase in afterload or preload. We describe a young patient with congestive heart failure treated with doxorubicin (cumulative mean dose 420 mg/m2) in infancy because of pelvic sarcoma in whom the appearance of symptoms was related to pulmonary embolism. Four years before hospital admission, the patient presented echocardiographic abnormalities such as left ventricular fractional shortening and thickness reduction and he was treated with ACE-inhibitors. The myocardial ischemia, which is present in pulmonary embolism, probably worsened the left ventricular systolic function and caused congestive heart failure.
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PMID:[Heart failure in a subject treated with anthracyclines in childhood: myocardial dysfunction is not always the only reason of it]. 1534 97

The adverse and beneficial effects of postmenopausal hormone replacement therapy include: ischemic heart disease, stroke, pulmonary embolism, breast cancer, an increased rate of onset of asthma as well as reductions in the incidence of diabetes in women with known coronary artery disease and osteoporotic fractures. These varied effects can be explained by the down regulation of 11beta-hydroxysteroid dehydrogenase by estradiol, which results in a reduction of tissue specific cortisol production. The reduction in local cortisol production which diminishes the endogenous anti-inflammatory effects, also allows for the progression of both vascular and pulmonary inflammation. The decrease in cortisol activation reduces insulin resistance and anti-proliferative effects thereby reducing the potential for diabetes but allowing for the emergence of malignancy. Furthermore, the decreased local tissue availability of cortisol reduces the tendency for the development of osteoporosis. New techniques and drugs are being developed to evaluate the modulation of 11beta-HSD1 activity. Further study should result in new ways to control both inflammation and metabolism.
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PMID:Estradiol induced inhibition of 11beta-hydroxysteroid dehydrogenase 1: an explanation for the postmenopausal hormone replacement therapy effects. 1595 Mar 94

There are significant associations between moderate increases in serum homocysteine and three cardiovascular diseases: ischemic heart disease, deep vein thrombosis and pulmonary embolism, and stroke. An association between the presence of abdominal aortic aneurysm and elevated homocysteine plasma levels has been indicated. Although chronic systemic hypertension is the most common factor predisposing the aorta to dissection, homocysteinemia has never been known as the risk for aortic dissection except for that with Marfan syndrome. Homocysteinemia is suggested to be the risk for aortic dissection in Marfan syndrome and spontaneous cervical artery dissection. Reduced fibrillin-1 deposition into the extracellular matrix is found not only in Marfan syndrome but also in isolated ascending aortic aneurysm and dissection. The reduced matrix deposition produces a mild form of weakness of elastic tissue, which predisposes to ascending aortic aneurysm and dissection in patients who do not have the Marfan syndrome. The defect in fibrillin-1 leads to: (1) formation of elastin that is abnormally aggregated and more easily degraded by matrix metalloproteinases than is normal elastin; (2) upregulation of the synthesis of matrix metalloproteinases; (3) progressive destruction of connective tissue by these enzymes; (4) development of thoracic aortic aneurysms. Homocysteine causes premature breakdown in the arterial elastic fibers by activation of the elastolytic activities. Irreversible homocysteinylation of long-lived proteins should lead to cumulative damage and progressive clinical manifestations, and fibrillin-1 is seen as the paradigm of extracellular connective tissue proteins that are specially susceptible to homocysteine (and presumably homocysteine thiolactone) attack. The authors hereupon propose a novel hypothesis that homocysteine plays an important role in development of aortic dissection and that homocysteinemia is one of the risk factors for aortic dissection.
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PMID:Homocysteinemia is a risk factor for aortic dissection. 1578 May 1

Major orthopedic surgery is known to be associated with potentially serious arterial and venous vascular complications, although uncertainty exists about current event rates. Using electronic databases and investigator contact, we identified randomized and cohort studies reporting overall mortality and fatal vascular events. Where possible, studies reporting high autopsy rates (>60%) were examined. Pooled incidences were calculated from eligible studies. For Autopsy studies: Pooled overall mortality and fatal pulmonary embolism for patients undergoing elective hip and knee replacement without prophylaxis could not be calculated, while with prophylaxis they were 0.44% (95% confidence interval 0.02 to 0.87%) and 0.43% (0.01 to 0.85%). For patients undergoing hip fracture surgery, the corresponding rates without prophylaxis were 15.9% (14.5 to 17.3%) and 1.9% (1.4 to 2.4%). With prophylaxis, mortality and fatal pulmonary embolismrates were 8.5% (7.3 to 9.7%) and 1.0% (0.6 to 1.5%). Among Cohort studies: Pooled overall mortality and fatal pulmonary embolism for patients undergoing elective hip and knee replacement without prophylaxis were 0.93% (0.57 to 1.29%) and 0.36% (0.14 to 0.59%). For patients receiving prophylaxis (7 to 14 days), mortality and fatal pulmonary embolism were 0.57% (0.51 to 0.62%) and 0.18% (0.14 to 0.21%). Patients undergoing hip fracture surgery receiving prophylaxis hadmortality and fatal pulmonary embolismrates of 3.2% (2.8 to 3.6%) and 0.30% (0 to 0.61%). Vascular events contributed towards approximately 50% of all deaths with similar proportions due to ischemic heart disease, cardiac failure and pulmonary embolism. In conclusion, although prophylaxis results in a reduction in overall mortality and fatal pulmonary embolism, vascular events continue to be a common cause of mortality.
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PMID:Fatal vascular outcomes following major orthopedic surgery. 1588


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