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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A retrospective study of 112 cases of lupus erythematosus, 103 acute disseminated lupus erythematosus (ADLE) and 9 chronic discoid lupus (CDL), was conducted to determine the incidence of disorders of conduction (DC), and to study their prognosis and discuss their pathogenicity. The mean age of the group was 38 +/- 16 years, and the mean follow-up period after discovery of the DC was 53 months. Cardiac lesions were present in 49.5 p. cent of the 103 patients with ADLE : pericarditis in 27 p. cent, murmur from lupus endocarditis or cardiomyopathy in 23 p. cent, heart failure in 4.8 p. cent, and hypertension in 17 p. cent. Disorders of conduction were present in 18 (17.5 p. cent) of the 112 patients studied. These included 5 partial right bundle-branch blocks (no complete right bundle-branch block), 2 complete and 3 partial left bundle-branch blocks, 5 complete, 2 first degree, and 1 second degree atrioventricular blocks (AVB). The atrioventricular blocks were usually located in the truncal or fascicular regions, but in 2 cases they were nodal in origin. The 5 complete AVB were associated with ADLE in two cases and CDL in the three other cases. The AVB in the ADLE cases appeared 9 to 20 years after the onset of the lupus, these two patients developing pericardiomyocarditis unaccompanied by disorders of conduction. The three complete AVB occurring during CDL were detected 9 to 18 months after the diagnosis. A fatal outcome was noted in 13 (12.5 p. cent) of the ADLE patients and one of the 9 cases of CDL. Ten-year survival curves showed no difference in prognosis for the groups with or without disorders of conduction, but mortality increased in patients with DC after 10 years. As disorders of conduction were more frequently observed in patients with lupus than in a control population, they can be attributed to either a lupus myocarditis or prolonged administration of synthetic antimalarial agents. Disorders of conduction, and particularly complete AVB are, in fact, observed in patients without pericardiomyocardial lesions, and when they exist usually develop a long time after the onset of the cardiac lesion. All patients had been treated with antimalarials, however, and the onset of the DC was associated with a chloroquine myopathy in some of them. Three of the five complete AVB were observed during the course of CDL in patients without cardiac lesions, this being a supplementary argument for implicating synthetic antimalarials.
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PMID:[Disorders of conduction in lupus erythematosus : frequency and incidence in a group of 112 patients (author's transl)]. 730 72

The authors had 213 patients under observation with systemic lupus erythematosus. Changes in the heart were revealed in 171 patients, all had affection of the myocardium: myocarditis was found in 66 and myocardial dystrophy in 122. Appraisal of leucocyte migration inhibition with the myocardial antigen (in 23 patients) and detection of antibodies against the myocardium by immunofluorescence (in 33) suggest that disorders in cellular immunity play an important part in the development of lupus myocardial affection. Involvement of the heart in patients with systemic lupus erythematosus was partly associated with renal hypertension, which was conducive, first and foremost, to the development of myocardial hypertrophy and could be attended with increased cardiac ejection and peripheral resistance. A decrease in the cardiac output with a gradual growth in the activity of systemic lupus erythematosus was noted. Steroid myocardial affection was found in 1/4 of patients, which sometimes occurred with cardiac insufficiency and signs of inflammation. Besides mitral valve sclerosis (7%), mitral stenosis was revealed in 3 patients and aortic insufficiency in one. Echocardiography helped to make an early diagnosis of hypertrophy of the heart and pericardial effusion in patients with systemic lupus erythematosus.
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PMID:[Cardiovascular aspects of systemic lupus erythematosus pathology]. 739 79

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

There are two aspects to considerations of the value of peritoneal dialysis (PD) in the treatment of renal insufficiency with associated pathology. The first involves the effects of the treatment on the symptoms or evolution of the pathology. Examples include the improvement of dyspnea due to cardiac insufficiency (CI) and of cirrhotic ascites (CA). However, there is also an undefined risk of reactivation lupus. The second facet is the increased risk of peritoneal infection, particularly for patients who are HIV + or who are immunosuppressed due to lupus or myeloma. In certain types of case (lupus with intractable vascular thrombosis, intolerance of ultrafiltration in cases of CI, AC or generalised amyloidosis) PD has particular advantages. Nevertheless, there has been no appropriate prospective study to demonstrate or otherwise the advantages in terms of survival. The use of PD remains therefore a matter of choice for individual patients and experienced health care team.
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PMID:[Peritoneal dialysis in cases of associated pathology]. 770 Apr 12

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

A case of systemic lupus erythematosus (SLE) associated with fever, heart failure, and left ventricular (LV) aneurysm is reported. A diagnosis of SLE was suspected owing to the presence of active lymphocytic myocarditis and fibrinous endocarditis at LV endomyocardial biopsy and was confirmed by identification of 4 of the 11 criteria proposed by the American Rheumatism Association for the definition of SLE. A 2-month period of steroid therapy was followed by a remarkable recovery of LV function and progression of endomyocarditis to a healed phase at control LV biopsy. The LV aneurysm disappeared, likely because thrombosis occurred as a result of the hypercoagulable state accompanying the presence of anticardiolipin antibodies. This is the first reported case of LV aneurysm induced by SLE and is a rare clinicohistologic documentation of the effectiveness of steroid treatment on lupus endomyocarditis.
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PMID:Acute myocarditis and left ventricular aneurysm as presentations of systemic lupus erythematosus. 854 1

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

Complete congenital heart block (CCHB) is the most severe manifestation of neonatal lupus syndrome, associated with a mortality rate of up to 31%. It is caused by irreversible damage to the cardiac conduction system due to the transplacental passage of maternal antibodies to the fetus. Anti-Ro (SSA) and anti-La (SSB) antibodies are usually detected in sera of mothers of children with prenatally diagnosed CCHB and in cardiac tissues of affected newborns. Their pathogeneic role in the development of CCHB has been established in several studies. When CCHB is detected during pregnancy, careful monitoring and delivery are needed before heart failure is developed. Treatment strategies are debatable and may include prophylactic therapy for high-risk pregnant women and a combination of intrauterine plasmapheresis with plasma exchange or with corticosteroids. Pacemaker insertion is required in most infants during the first three months of life. Assays for anti-Ro (SSA) and anti-La (SSB) antibodies should be performed on sera of pregnant women with SLE and newborns with CCHB.
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PMID:Anti-Ro (SSA) and anti-La (SSB) antibodies and complete congenital heart block. 925 27

Clinical presentation, laboratory findings, renal biopsy findings and subsequent clinical course were studied retrospectively in 90 children with acute renal failure to intrinsic renal damage. The mean age at presentation was 8.1 years. Diagnosis and number of patients were as follows: Hemolytic uremic syndrome (HUS) in 32 patients, tubulo-interstitial nephritis in 19, idiopathic nephrotic syndrome in 10, IgA nephropathy on 9, membranoproliferative glomerulonephritis in 8, lupus in 5, poststreptococcal glomerulonephritis in 4, cortical necrosis in 1, Henoch Schoenlein purpura nephritis in 1 and anti-neutrophil cytoplasmic antibody associated glomerulonephritis in 1. Thirty-nine patients needed dialysis, but 36 of these were able to stop dialysis, 3 patients with HUS without gastrointestinal symptoms needed chronic dialysis. The mean follow-up period was 7.3 years from onset, and the the latest follow-up 82 patients had normal renal function, 3 showed chronic renal failure, 2 had regular dialysis, 2 had successful renal transplantation, an 1 had died due to heart failure. A poor outcome was associated with diffuse crescents and the presence of severe vascular changes. The early biopsy findings were very useful for the management of children with acute renal failure.
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PMID:[A clinicopathological study of 90 children with acute renal failure]. 928 14

A 46-year-old man was admitted to our clinic because of acute heart failure. Six years before admission he was pointed out cardiomegary and hematuria. One year later, he was diagnosed as having jugular foramen syndrome. On admission, he had a fever and dyspnea. Pansystolic blowing murmur was audible at the apex. The chest ratio on his chest X-ray was 52.5%. An electrocardiogram showed left ventricular hypertrophy. An echocardiogram showed marked dilatation and severe dysfunction of left ventricle. Radionuclide scanning with technetium 99 m pyrophosphate identified inflammatory change in the apex. Myocardial biopsy showed fibrotic degeneration and IgG deposits in myocardium. Blood examination showed anemia, lymphopenia. positive anti-nuclear antibody (1000 times, shaggy pattern), positive anti ds-DNA antibody and hypocomplementemia. Furthermore, proteinuria was pointed out. Renal biopsy showed focal segmental glomerulonephritis with active necrotizing lesion (type III nephritis). Lupus myocarditis and nephritis was diagnosed. After prednisolone (80 mg/day) was administered. left ventricular function and hypocomplementemia improved. The ACE inhibitor was also used for proteinuria. In spite of a little amount of blood transfusion, he showed hepatic hemosiderosis. We suspect that the cause of hemosiderosis was related chronic inflammation of active lupus. It was treated with Erythropoietin.
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PMID:[A case of lupus myocarditis and nephritis with transient foramen jugular syndrome]. 939 74


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