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)

A 34-year old woman, with a 3 yr history of severe seropositive rheumatoid arthritis (RA) with lupus anticoagulant and anticardiolipin antibodies, developed a massive anterior myocardial infarction and ischemia of the lower extremities, with disseminated intravascular coagulation resulting from extensive tissue damage. Seven days after admission, she died of severe heart failure complicated by ventricular fibrillation. To our knowledge, this is the first documented case of fatal acute antiphospholipid syndrome in RA.
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PMID:Catastrophic antiphospholipid syndrome with fatal acute course in rheumatoid arthritis. 747 89

The antiphospholipid syndrome (APS) is usually defined by the association of a clinical manifestation (venous or arterial thrombosis or miscarriage) with the presence of antiphospholipid antibodies (lupus anticoagulant and/or anticardiolipin antibodies). It frequently occurs in the course of systemic lupus erythematosus but is also encountered as a "primary" disease. APS is responsible for diverse respiratory manifestations. Pulmonary embolism is common. The site of the causal venous thrombosis is frequently unusual. Pulmonary hypertension may be a consequence of repeated embolism or may belong to the primary idiopathic variety. Pulmonary manifestations may also result from left-sided heart failure due to mitral or aortic valve abnormalities, myocardial infarction or a specific myocardiopathy. APS is probably involved in the occurrence of some cases of adult respiratory distress syndrome. Long term secondary prevention of recurrent thrombosis is a central point in the management of APS.
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PMID:[Antiphospholipid syndrome and the pneumologist]. 772 79

Thirty one patients with antiphospholipid antibodies who developed multi-organ failure ("Catastrophic Antiphospholipid Syndrome") are reviewed. Thirteen suffered from a 'Primary' antiphospholipid syndrome, 13 from defined SLE, 4 from 'lupus-like' disease and one from rheumatoid arthritis. In more than one third precipitating factors were evident (e.g. infections, major/minor surgical procedures, oral contraceptives). Death occurred in 60% of patients from a variety of causes (myocardial failure, ARDS, CNS causes or, often a combination). Disseminated Intravascular Coagulation was present in 8 of 31 patients. Plasmapheresis appeared to be useful in several who had not responded to conventional therapy (e.g. IV heparin, steroids, immunosuppression).
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PMID:The catastrophic antiphospholipid syndrome 1996: acute multi-organ failure associated with antiphospholipid antibodies: a review of 31 patients. 890 72

Chronic pulmonary thromboembolism is known to be associated with poor prognosis with conservative medical treatment. Pulmonary thromboendarterectomy for chronic pulmonary thromboembolic disease is a potentially lifesaving procedure that prevents right-sided cardiac failure as a result of secondary pulmonary hypertension caused by pulmonary thromboembolism. We report a rare case of systemic lupus erythematosus with antiphospholipid syndrome in a patient who presented with pulmonary hypertension secondary to chronic proximal multiple pulmonary thromboembolism. To our knowledge, this is the first case report of chronic pulmonary thromboembolism complicated by systemic lupus erythematosus with antiphospholipid syndrome. Thromboendarterectomy was performed with satisfactory results.
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PMID:Successful thromboendarterectomy for chronic pulmonary embolism in a patient with systemic lupus erythematosus and antiphospholipid syndrome. 939 66

We present the case of a 39-year-old woman with aortic regurgitation that may have been induced by primary antiphospholipid syndrome. The patient had suffered recurrent miscarriages, thrombocytopenia, and deep-vein thrombosis for the previous 16 years, and had been diagnosed as having primary antiphospholipid syndrome 9 years previously because of a high titer of anticardiolipin antibody. She had been receiving medication for moderate hypertension for 7 years. The patient was admitted to Tenri Hospital because of heart failure, which was thought to be caused by moderate aortic regurgitation, moderate hypertension, and mild chronic renal failure. Echocardiography revealed thickened aortic and mitral valves. Primary antiphospholipid syndrome might have induced valve regurgitation as a result of valvular thickening.
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PMID:Aortic regurgitation in a patient with primary antiphospholipid syndrome--a case report. 958 54

A 51-year-old woman with overt congestive heart failure with pleural and pericardial effusion was treated with furosemide and nifedipine, leading to improvement in her condition and a decrease in effusions. An echocardiography demonstrated mitral and aortic regurgitation with mitral valve prolapse, which caused the congestive heart failure. Since leukocytopenia and lymphocytopenia with arthralgia could be observed, serological investigations were performed. She was diagnosed as having systemic lupus erythematosus (SLE) with antiphospholipid syndrome, and started on a treatment of prednisolone and aspirin. Based on the treatment, the pleural and pericardial effusion went into complete remission, indicating that the serositis related to SLE had overlapped the heart failure. Since there was no evidence of any other diseases that could be responsible for the valvular lesions, we concluded that they were due to antiphospholipid syndrome. The administration of prednisolone had no significant effect on valvular morphology or function as demonstrated by echocardiography. When patients with valvular disease are seen, a valvulopathy related to antiphospholipid syndrome should be considered as part of the differential diagnosis.
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PMID:Overt congestive heart failure with mitral and aortic regurgitation due to antiphospholipid syndrome in a patient with systemic lupus erythematosus. 1085 59

Many acquired risk factors may be identified to avoid the scholarly nature of these interminable lists, they may be reclassified with respect to their originality or their mechanism of action and those of current interest, whose data is still often hypothetical but recent, can be underlined. The following order may be proposed: risk factors which cannot be changed: age (which remains the principal factor) and gender (women being at higher risk than men); true acquired risk factors such as cancer, dysimmune conditions (more specifically, the antiphospholipid syndrome) and hormone replacement therapy (oestroprogestative contraception which has been updated by the debate about "third generation pills" and the risk related to progesterone-like substances themselves; hormone replacement therapy of the menopause which still has no clinical trials to assess "our" forms with natural hormones administered transdermally or transmucosally). Smoking has also been accused of being a risk factor for venous thrombosis in the latest clinical trials. Metabolic factors increase the risk of thrombosis: this is established for obesity, still suspected for hyperhomocystonaemia, the abnormalities being the result of complex gene-environment interactions. Other dysmetabolic conditions (diabetes, hypercholesterolaemia, hypertriglyceridaemia), responsible for arterial complications, are not clearly related to increased venous thromboembolic risk although a preventive effect of statins (yet another I) has just been reported. Similarly to these metabolic factors, the origin of which, genetic or environmental, is difficult to establish, interest has recently been shown in quantitative and functional changes in blood clotting factors. This has been established for arterial disease for fibrinogen but, in addition to this factor which slightly increases the risk of venous thrombosis, increases of factor VIII independent of inflammatory conditions, of blood group and Von Willebrand factor, which all influence the level of factor VIII, an increase by 150% of the normal increases the risk of venous thromboembolic disease by 3 or 4 times. As for factor VIII, increases in factor IX, factor XI, and resistance to activated C protein (independently of the Leiden mutation on the gene for factor V), are also associated in increased venous thromboembolic risk. Without knowing into which category to classify them, previous personal and family history of thromboembolic disease, in the absence of the already mentioned hereditary risk factors, must be noted. Finally, amongst the acquired risk factors, the authors also list conditions of blood stasis and vascular lesions with or without hypercoagulability (surgery, prolonged hospital stays, cardiac failure, paralysis, pregnancy...). Of these acquired conditions which increase the risk of thrombotic complications, particular attention has been given over the last few years to forced immobilisation in uncomfortable positions as in certain forms of transport. Although clinical reports have discordant results, it would seem that the risk is increased and the benefits of supportive elastic stockings have been confirmed. If the acquired risk is identified and quantified for a patient, it allows evaluation of global risk and the installation of appropriate therapeutic measures.
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PMID:[Venous thromboembolic pathology. New acquired risk factors or new data on acquired risk factors]. 1179 76

Large increases in mortality related to premature atherosclerosis with coronary artery disease and stroke have been reported in patients with systemic lupus erythematosus (SLE), antiphospholipid syndrome (APLS), or rheumatoid arthritis (RA). Studies found relative risks of 5 for myocardial infarction, 6 to 10 for stroke in SLE patients, and 3.6 for cardiovascular deaths in RA patients. The main risk factors for atherosclerosis included not only the classic factors identified in epidemiological studies such as the Framingham study (advanced age, high cholesterol levels, hypertension, diabetes mellitus, and obesity), but also prolonged glucocorticoid therapy, long duration of SLE, postmenopausal status, and heart failure. SLE per se is an independent risk factor. The current pathogenic hypothesis for atherosclerosis involves an inflammatory response (erythrocyte sedimentation rate, C-reactive protein, and fibrin), autoantibodies, immune complexes (containing antibodies to phospholipids, to oxidized LDLs, and to endothelial cells), cytokine-producing activated T cells, and bacterial or viral infections responsible for an immune response against heat shock proteins (endogenous HSP60 and its equivalent, bacterial HSP65). Early risk factor intervention and effective control of inflammation should be incorporated into the management of connective tissue disease with the goal of protecting patients against atherosclerosis.
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PMID:Atherosclerosis and connective tissue diseases. 1295 20

We report a case of antiphospholipid syndrome (APS) which presented with clinical and laboratory signs of an autoimmune hemolytic anemia (AHA), in the absence of manifestations typically related to APS. The diagnosis of APS was made only after the occurrence of a sudden severe heart failure due to an intraventricular thrombus requiring a surgical approach. An accurate thrombophilic screening is warranted also in patients with apparently idiopathic AHA.
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PMID:Intracardiac thrombus in a patient with autoimmune hemolytic anemia leading to a diagnosis of antiphospholipid syndrome. 1197 38

We report on an 11-year-old Omani boy who presented with acute heart failure due to dilated cardiomyopathy. Examination revealed the presence of left ventricular thrombi on echocardiography and a marked elevation of anticardiolipin antibodies. Subsequently the boy exhibited features of antiphospholipid syndrome including multiple thrombotic episodes involving the brain, and renal and iliac veins. We could not document any underlying cause of the antiphospholipid syndrome. His cardiac status subsequently deteriorated and he expired from multiorgan failure. Resistant heart failure from dilated cardiomyopathy secondary to primary antiphospholipid syndrome is uncommon and has not been reported in children.
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PMID:Antiphospholipid syndrome presenting as dilated cardiomyopathy in an 11-year-old boy. 1294 43


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