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)

Serious side effects of (OCs) oral contraceptives involve blood pressure, the kidneys, and urinary bladder, glucose and lipid metabolism, liver and gall bladder, blood coagulation, and the cardiovascular system. Causes for increased morbidity and mortality resulting from OCs are: venous thrombosis and pulmonary embolism, cerebrovascular ischemia and hemorrhage, as well as myocardial infarctions. Among the pathogenetic mechanisms responsible for vascular complications, a possible atherogenic effect of OCs is frequently discussed which might be mediated by adverse effects on blood pressure, glucose, and lipid metabolism, and by a direct lesion of the vascular wall. We compared past history, atherogenic risk factors, and coronary arteriograms of 9 young females with a history of acute myocardia infarctions on an OC regimen and 21 premenopausal women with advanced coronary atherosclerosis angiographically (of the same age). These observations suggest that myocardial infarctions during OC ingestion may occur in absence of coronary atherosclerosis and of atherogenic risk factors with the possible exception of cigarette smoking. The incidence of serious cardiovascular side effects from OCs is estimated from epidemiologic data, and therapeutic guidelines are derived. (authors' modified)
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PMID:[Cardiovascular side effects resulting from oral contraceptives]. 738 86

The clinical and pathologic findings are reported in seven consecutive patients with progressive and fatal pulmonary hypertension which was not explained by predisposing cardiac or pulmonary diseases. Pulmonary arterial lesions consisted of atherosclerosis of the elastic pulmonary arteries, and medial hypertrophy and concentric laminar fibrosis of the muscular pulmonary arteries in seven patients, plexiform lesions in six patients and necrotizing vasculitis in one patient. Pulmonary emboli were not identified. Five patients had manifestations of autoimmune disease, including laboratory abnormalities (positive antinuclear antibody, positive latex agglutination for rheumatoid factor, hypergammaglobulinemia or antimitochondrial antibody) in four, necrotizing vasculitis in one, Raynaud's phenomenon in two and clinical evidence of multisystem collagen vascular disease in two. Five patients had liver disease which developed prior to or concomitant with the onset of pulmonary hypertension. At autopsy, one patient had prominent periportal fibrosis and four had macronodular (postnecrotic) cirrhosis (active in three and inactive in one). Four of these five patients with liver disease and pulmonary hypertension had evidence of autoimmune phenomena. The findings in the seven patients suggest an association between autoimmune disease, plexogenic pulmonary hypertension and liver disease of the chronic active hepatitis-postnecrotic cirrhosis type.
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PMID:Severe pulmonary hypertension associated with macronodular (postnecrotic) cirrhosis and autoimmune phenomena. 742 41

The extensive homology between apolipoprotein(a) and plasminogen has led to the hypothesis that the increased risk for atherosclerosis, cardiac disease and stroke associated with elevated levels of apolipoprotein(a) may reflect modulation of fibrinolysis. We have investigated the role of apolipoprotein(a) on clot lysis in transgenic mice expressing the human apolipoprotein(a) gene. These mice develop fatty streak lesions resembling early lesions of human atherosclerosis. Pulmonary emboli were generated in mice by injection, through the right jugular vein, of a human platelet-rich plasma clot radiolabelled with technetium-99m-labelled antifibrin antibodies. Tissue plasminogen activator was introduced continuously via the right jugular vein. Clot lysis, determined by ex vivo imaging, was depressed in mice carrying the apolipoprotein(a) transgene relative to their sex-matched normal littermates. These results directly demonstrate an in vivo effect of apolipoprotein(a) on fibrinolysis, an effect that may contribute to the pathology associated with elevated levels of this protein.
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PMID:Antifibrinolytic activity of apolipoprotein(a) in vivo: human apolipoprotein(a) transgenic mice are resistant to tissue plasminogen activator-mediated thrombolysis. 758 43

Patients with morbid obesity have high rates of sudden, unexpected cardiac death. The mechanism of death in these patients is uncertain. Twenty-eight patients with morbid obesity (22 sudden cardiac deaths, 6 unnatural deaths) were compared to 11 age-matched nonobese patients with traumatic deaths. Heart weight, left ventricular cavity diameter, left and right ventricular wall thickness, ventricular septal thickness, epicardial fat thickness, and extent of coronary artery atherosclerosis were determined; myocyte size, nuclear size, and degree of interstitial fibrosis were calculated morphometrically. Mean heart weights in the patients with morbid obesity were increased but remained constant as a percentage of body weight. Of the gross parameters, only heart weight and left ventricular cavity size were independent predictors of obesity. Of microscopic parameters, only nuclear area was an independent predictor of obesity. Of 22 patients with morbid obesity, dilated cardiomyopathy was the most frequent cause of sudden cardiac death in (10 patients), followed by severe coronary atherosclerosis (6), concentric left ventricular hypertrophy without left ventricular dilatation (4), pulmonary embolism (1), and hypoplastic coronary arteries (1). The cardiomyopathy of morbid obesity is characterized by cardiomegaly, left ventricular dilatation, and myocyte hypertrophy in the absence of interstitial fibrosis. It is the most common cause of sudden cardiac death in these patients.
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PMID:Sudden death as a result of heart disease in morbid obesity. 763 12

The occurrence of cardiac manifestations and their relationship with the lupus anticoagulant (LA) in SLE was studied in 74 patients who were followed up for 22 years (median), of which 16 years were after the initial LA testing. Pericarditis was the most common cardiac event occurring in 16 (22%) patients but it did not correlate with LA. Valvular heart disease, coronary artery disease, left ventricular failure and/or cor pulmonale were observed in 16 (22%) patients. Taken together, their occurrence was associated with a history of leg ulcers (odds 3.8, P = 0.028) but not with LA or other common clinical manifestations of the antiphospholipid syndrome. Valvular heart disease in five patients was significantly associated with LA (P = 0.05). Cor pulmonale due to chronic pulmonary embolism was present in two patients with LA. Myocardial infarctions in five patients occurred late in the course of disease but in relatively young patients (mean 43 years). Fatal myocardial infarction in the absence of atherosclerosis in two LA-positive patients supports a pathogenetic role for LA in these cases. In conclusion, of the various cardiac complications in SLE, valvular heart disease and cor pulmonale appear to be connected with the antiphospholipid syndrome. Both conditions should be actively sought in patients with LA to decrease possible adverse events (arterial emboli and right ventricular failure) affecting the patients' prognosis.
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PMID:Lupus anticoagulant and cardiac manifestations in systemic lupus erythematosus. 795 2

This study of 49 patients with spontaneous venous and arterial thrombosis identified 27 with hypercoagulable states: 13 had only venous thrombosis (VT), six had episodes of VT followed by arterial thrombosis (AT) and eight had AT only. All 27 patients were less than 42 years of age; 22 had specific natural anticoagulant or fibrinolytic deficiencies: antithrombin III (nine patients), protein C (eight patients), protein S (three patients), heparin cofactor II (two patients), tissue plasminogen activator release (one patient) and mixed antithrombin III and protein S (one patient). The remaining five patients had recurrent thrombotic events associated with resistance to heparin anticoagulation, but no established laboratory diagnosis. Clotting complications included recurrent VT, pulmonary embolism, multiple failed arterial procedures and lower extremity amputation. The remaining 22 patients (mean age of 53 years, range of 46 to 63 years), 12 with VT and ten with AT, did not have laboratory evidence of hypercoagulability and none had recurrent vascular occlusions. All these patients were successfully treated by conventional therapy without any additional thrombotic events during the follow-up period. Young adults with spontaneous thrombotic events should be screened for possible hypercoagulable states. Additionally, these young patients need further evaluation and treatment of cardiovascular risk factors. Those with premature atherosclerosis have an especially poor prognosis despite surgical intervention and anticoagulant therapy.
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PMID:Hypercoagulable states as an evolving risk for spontaneous venous and arterial thrombosis. 792 7

Low molecular weight heparins are well established in the prophylaxis of deep vein thrombosis in patients with general surgery, in high risk patients undergoing elective hip surgery or emergency surgery and also in patients with an enhanced risk of thrombosis who are treated in medical wards. There are, however, many possibilities for improving prophylaxis and treatment with LMWH. The mechanisms by which low molecular weight heparins and also unfractionated heparin inhibit thrombus formation are not fully understood. The inhibition of thrombin formation and local effects at the endothelial level may be more important than antithrombin-III mediated effects on factor IIa and on factor Xa. For most low molecular weight heparins the most effective dose regimens to be used in patients at high risk have not yet been established. Low molecular weight heparins may be more effective in the treatment of deep venous thrombosis than unfractionated heparin. In the therapeutic studies published so far the major intention was to show that low molecular weight heparins can prevent the progression of deep venous thrombosis and pulmonary embolism to the same extent as unfractionated heparin. Extended treatment regimens, however, may lead to a relevant thrombus reduction. Outpatient treatment for a longer period of time with results not far from those obtained with thrombolysis seem possible especially in elderly patients. Low molecular weight heparins in their present form or modified low molecular weight heparins may be useful for long-term treatment of patients with atherosclerosis with the aim of regression of atherosclerotic lesions. New forms of application, e.g. inhalation, may render long-term treatment more feasible.
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PMID:Low molecular weight heparins--state-of-the-art and unsolved issues. 818 Mar 24

We analysed the causes of 67 deaths, over a 4 y period, in our oriental population with systemic lupus erythematosus (SLE). The median disease duration was 48 +/- 60.5 months (range 1-250 months). The mean age at diagnosis and death were 30 and 35.1 y respectively. SLE alone accounted for death in 30 patients (44.8%), infection in 27 (40.3%), pulmonary embolism in 5 (7.5%), malignancy in 4 (5.9%) and rheumatic heart disease in 1 (1.5%). The major organ involvement in those with active disease at death were SLE related thrombocytopenia (n = 23/44, 52.3%), nephritis (n = 21/44), 47.7%), cerebral lupus (n = 16/44, 36.4%), and pulmonary haemorrhage (n = 12/44, 27.3%). As in other series, SLE and infection were the principal causes of death in our population. During this 4 y period, there was no late death due to atherosclerosis.
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PMID:SLE mortality in an oriental population. 911 15

The Prevalence of Early Atherosclerosis study aims to define the prevalence of subclinical atherosclerosis in a typical population of central Italy. A concomitant study evaluates the prevalence of venous diseases. The prevalence of superficial and deep venous disease, the prevalence of venous thrombosis and pulmonary embolism, and the prevalence of the most common venous malformations were studied through use of medical history, a questionnaire, and noninvasive investigations. The costs of venous problems were also considered. Of some 2000 inhabitants, 746 (379 women; mean age 46.3 +/- 7 years; range eight to ninety-four) have been screened. No significant difference in trend increase of the relationship age/percent of subjects with venous problems was observed for superficial venous disease. The increase in the proportion of subjects with lipodermatosclerosis and venous ulcerations appeared to be correlated with age (r = 0.543). Evidence accepted for pulmonary embolisms was pulmonary angiogram or evidence on ventilation+perfusion lung scans. According to these criteria the number of documented deep vein thromboses and pulmonary embolisms was very limited with a larger number of suspected disease entities. There was no significant correlation between age and pulmonary embolism or deep venous thrombosis distribution. The number of venous and/or arteriovenous malformations was comparable along the age axis in the different age groups. Only a limited number of these malformations (in less that 1% of subjects) had caused a clinical problem. The treatments used for venous problems have been reported in a questionnaire and subdivided into occasional treatments and chronic treatments (when used for periods longer than twelve months). The percent of subjects using different treatment was also studied. Treatments were divided in: (1) over-the-counter products (or any treatment not requiring prescription); (2) specialized drug (for venous diseases); (3) compression; (4) surgery (any type of surgical treatment); (5) sclerotherapy; (6) combined treatments (ie, sclerotherapy and surgery); (7) alternative treatments (herbal products etc). Finally, the average costs per year for treatment, for investigations, and the costs due to lost working days were recorded. In conclusion some 12% of the evaluated population sample (male population 46%) had or had been affected in the past by a venous problem and 50% of them had received some type of treatment.
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PMID:Epidemiology and costs of venous diseases in central Italy. The San Valentino Venous Disease Project. 924 56

The PAP/PEA (Prevalence of Early Atherosclerosis) study aims to define the prevalence of subclinical atherosclerosis in a typical population of central Italy. A concomitant study evaluates the prevalence of venous diseases. The first group of 850 patients evaluated, indicated the prevalence of superficial ve-nous disease, the prevalence of deep venous thrombosis and pulmonary embolism and the prevalence of the most common venous malformations. Also the costs of venous problems was considered. In conclusion some 12% of the evaluated population sample (male population 46%) had or had been affected in the past by a venous problem and 50% of them had been under some form of treatment.
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PMID:[Prevalence of venous diseases. The San Valentino screening and prevalence study]. 927 70


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