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Query: UMLS:C0409974 (lupus)
 22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Apoplexy of the heart can be responsible for sudden and for recurring instability of cardiac rhythm and conduction, and for the clinical counterparts of syncope and sudden death. Every pathophysiological mechanism which produces cerebral apoplexy has its counterpart in apoplexy of the heart. Among the mechanisms documented are thrombosis, embolism and rupture of those special vessels supplying the sinus node, atrioventicular (A-V) node and His bundle. Apoplexy of the heart can occur either with or without significant or recognizable ventricular myocardial infarction. Acute vascular accidents within the critical centers of cardiac impulse formation and conduction deserve more frequent consideration in the explanation of unusual cases of "epilepsy", of seizure disorders of the elderly, of neurologic manifestations (which may be secondary as well as primary) of systemic diseases such as lupus erythematosus or thrombotic thrombocytopenic purpura, and indeed of every case of otherwise unexplanined syncope or sudded death at any age.
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PMID:De subitaneis mortibus. XXVIII. Apoplexy of the heart. 61 31

Right and left heart pressures, left ventricular volumes, indices of contractility, myocardial wall stiffness, and coronary blood flow were determined in five young women with systemic lupus erythematosus (SLE) during diagnostic right and left heart catheterization. Examinations revealed (1) increases of right and left ventricular enddiastolic pressures; (2) decreases of cardiac output, stroke volume, ejection fraction, contractility indices, diastolic left ventricular volume inflow; (3) decreases of pharmacologically induced coronary vasodilation in SLE. The results demonstrate impaired pump function, reduced contractility, increased myocardial wall stiffness, and decreased coronary vascular reserve in SLE. It is concluded that lupus cardiomyopathy associated with an impairment of left ventricular function may be apparent in young women with SLE who have no clinical signs of cardiac dysfunction.
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PMID:Lupus cardiomyopathy: cardiac mechanics, hemodynamics, and coronary blood flow in uncomplicated systemic lupus erythematosus. 99 77

Haemodynamic functions, myocardial contractility, and coronary blood flow were measured in five young women with systemic lupus erythematosus. There had been no signs of cardiac involvement. Left and right heart catherterisation excluded abnormal pressure gradients and valvar regurgitation. But left ventricular end-diastolic pressures were considerably raised while cardiac output, stroke volume, ejection fraction, and left ventricular compliance were decreased. Isovolumic indices of myocardial contractility were altered, corresponding to a decreased contractile state of the myocardium. Coronary blood flow was moderately increased at rest, but pharmacologically induced coronary vascular reserve was markedly reduced. It is concluded that in young women with this disease there may be, in the absence of clinical signs of cardiac involvement, haemodynamic abnormalities which must be ascribed to the consequences of a lupus cardiomyopathy.
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PMID:[Cardiomyopathy in uncomplicated systemic lupus erythematosus (author's transl)]. 116 89

We retrospectively evaluated the clinical outcome of 45 female and 11 male patients with biopsy-proven lupus nephritis, followed at our hospital between February 1974 and February 1990. In the majority signs of nephritis were present at the time systemic lupus erythematosus was diagnosed (range: -42-156 months) and the median time from onset of nephritis to biopsy was 2 months. The median follow-up from the time of the biopsy was 53.5 months (range: 2-192), the median age at biopsy 25 years and the median serum creatinine level 1.2 mg/dl. Initial renal biopsies had the following histopathological classes according to the World Health Organization criteria (n): I (2); II (10); III (10); IV (28); V (5); VI (1). Over the study period active episodes were treated with high-dose oral prednisone alone or combined with intravenous nitrogen mustard and oral chlorambucil (1974-75), azathioprine (1978-86), cyclophosphamide (1986-90) and/or plasma-exchange (1976-84). These strategies were based on literature data or multicenter studies in which we participated. Eight patients developed end-stage renal disease (ESRD) (median: 47 months post-biopsy; range: 20-120). In these, initial biopsies showed class IV in seven, and class V in one. Confounded risk factors for ESRD were class IV biopsy, male gender and serum creatinine level above 1.4 mg/dl. The calculated proportion without ESRD 5 years post-biopsy was 87% (95% confidence limits: 98-76%), and at 10 years 70% (95% confidence limits: 90-49%). Five patients (11.2%) died; causes of death were cerebrovascular accident (n = 2), cerebral lupus (n = 2) and S. aureus sepsis (n = 1).(ABSTRACT TRUNCATED AT 250 WORDS)
Lupus 1992 Feb
PMID:The long-term clinical outcome of 56 patients with biopsy-proven lupus nephritis followed at a single center. 130 70

Antibodies directed against phospholipids are highly associated with episodes of venous and arterial thrombosis, which are often recurrent. There seems to be a skewed frequency of cerebral thrombosis when the arterial circulation is affected. Clinical clues that should lead to evaluation for aPL include stroke in a young adult, recurrent thrombosis or miscarriage, and thrombocytopenia. Associated laboratory abnormalities include a biologically false-positive test for syphilis, abnormal antinuclear antibody titers, and a high erythrocyte sedimentation rate. If the activated partial thromboplastin time is prolonged on routine screening and does not correct with mixing studies, a lupus anticoagulant should be suspected. However, more sensitive and specific tests are usually necessary to detect aPL. Many in vitro and more recently in vivo systems strongly suggest that aPL may be directly implicated in the pathogenesis of thrombosis. Optimal management of patients with aPL-associated thrombosis is unknown. The use of aggressive therapeutic management schemes with such agents as warfarin or corticosteroids is sometimes required.
Heart Dis Stroke
PMID:Antiphospholipid antibodies and ischemic stroke. 134 35

Racial differences in stroke are known to exist with persons in the black race having a higher morbidity, mortality and incidence of stroke compared to whites. We evaluated coagulation factors in black and white stroke patients and compared the results between races. D-dimer was elevated more frequently in blacks than whites to a statistically significant degree. There were non-significant trends for blacks to have a positive lupus anticoagulant, low protein C and protein S, higher platelet factor 4, and hyporesponsive platelets to 10 microM epinephrine. The significance of these findings in understanding racial differences in stroke is discussed.
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PMID:Racial differences in coagulation studies in stroke. 135 61

A case of antiphospholipid syndrome (APPS) is presented. A 33-year-old female presented with a right hemispheric stroke secondary to thrombosis of the middle cerebral artery. Shortly thereafter, she developed thrombosis of the right brachial artery. Despite thrombolytic therapy, progressive occlusion of this artery occurred as demonstrated by a follow-up angiogram. The patient had a history of multiple recurrent spontaneous abortions. Lupus anticoagulant, anticardiolipin antibodies, and VDRL were positive on two different occasions. The angiographic findings of multiple and progressive arterial thrombosis in young women should alert the angiographer to the possibility of APPS.
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PMID:Angiographic findings in a patient with primary antiphospholipid syndrome: case report. 139 62

Lupus anticoagulant antibodies and anticardiolipin antibodies are acquired circulating immunoglobulins that interact with phospholipids. These factors may exert anticoagulant properties in vitro and so interfere with coagulation tests that use phospholipids. These antibodies are not, however, associated with a hemorrhagic diathesis. Indeed, despite their name and their in vitro anticoagulant properties, they have been associated right from the earliest reports with systemic and cerebral thromboembolic episodes. We report the clinical and instrumental findings in a patient with ischemic stroke and anticoagulant antibodies in the serum.
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PMID:The primary antiphospholipid syndrome: case report. 142 95

Central nervous system (CNS) dysfunction in patients with systemic lupus erythematosus (SLE) is highly variable, although it is often described under a single heading of "neuropsychiatric" or "CNS" SLE. To clarify these CNS abnormalities, we studied 91 lupus patients, 63 of whom had CNS symptoms or signs, over 599 patient years. By placing patients in relatively homogeneous clinical groups (stroke, seizure, suicide attempt, hallucination, confusion, decreased alertness) we detected significant (but variable among groups) correlations with other manifestations of SLE, suggesting separate mechanisms for each CNS disorder. These correlations were lost if all "CNS-SLE" was considered as a single group. Patients with decreased alertness often had undetected systemic infections and had a high death rate from infection, rather than from CNS-SLE. The understanding of the pathogenesis and potential treatment of CNS disorders in lupus will depend on classifying the patients into homogeneous groups.
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PMID:Central nervous system disease in patients with systemic lupus erythematosus. 151 50

We examined the relationship between free protein S deficiency and cerebrovascular disease by reviewing the records of all patients with the diagnoses of cerebral thrombosis, cerebral embolism, and cerebral vascular occlusion who were referred for coagulation studies over a 12-month period. We assayed for free protein S antigen, protein C antigen, and antithrombin III and tested for lupus-like anticoagulant and anticardiolipin antibody. Twenty-two of 267 patients (8.2%) admitted with thrombotic strokes were referred for coagulation studies. Free protein S antigen was significantly lower in women than in men (62 +/- 25% versus 88 +/- 24%, p = 0.03; n = 11 in each group). Six women had free protein S antigen levels below the range recorded for a contemporary group of 24 age-matched normal women (17 to 59% versus 70 to 102%, p less than 0.001); four of these women had cerebral arterial thrombosis and two had venous dural sinus thrombosis. The six women were aged 29 to 55 at the time of their first strokes; two had family members with protein S deficiency, and one of these had died of a stroke at age 52. Other abnormalities in this population included a positive test for lupus-like anticoagulant or anticardiolipin in five patients, a modest decrease in protein S in two men, and one patient with an isolated deficiency of antithrombin III. We conclude that protein S deficiency may be an important risk factor for stroke in middle-aged women but this requires confirmation by prospective studies in unselected patients.
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PMID:Protein S deficiency in middle-aged women with stroke. 153 5


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