Fatal cardiac failure due to myocardial microthrombi in systemic lupus erythematosus

Brown, J; Doherty, C C; Allen, Derek C.; Morton, Paul D.

doi:10.1136/bmj.296.6635.1505

Cited by 65 publications

(24 citation statements)

References 2 publications

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“…A link between the presence of antiphospholipid antibodies and microvascular lesions resulting in myocardial ischaemia has thus been suspected in patients with lupus.' 27 filling, in the same manner as reported in patients with coronary heart disease. '2 We fournd an abnormal filling pattern in patients affected by primary antiphospholipid syndrome without any previous history of myocardial infarction or coronary artery disease.…”

Section: Discussionmentioning

confidence: 60%

M mode and Doppler echocardiographic assessment of left ventricular diastolic function in primary antiphospholipid syndrome.

Coudray

Zuttere

Blëtry

et al. 1995

Heart

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Background-High titres of serum antiphospholipid antibodies are a possible pathogenic factor for cardiac lesions in patients with systemic lupus erythematosus.Objective-To test the hypothesis of a causal link between high titres of antiphospholipid antibodies in the serum and myocardial involvement in patients without systemic lupus erythematosus. Patients and design-18 patients with primary antiphospholipid syndrome (recurrent fetal loss, arterial and/or venous thrombosis, high titres of antiphospholipid antibodies, and no criteria for systemic lupus erythematosus) were prospectively studied by cross sectional, M mode, and pulsed Doppler echocardiography, and compared with 18 healthy controls. The pulsed Doppler indices of left ventricular diastolic function included isovolumic relaxation time and four mitral outflow indices: peak velocity of early flow, peak velocity of late flow, early to late peak flow velocity ratio, and rate of deceleration of early flow. Four computerised M mode indices were also measured: peak rate of left ventricular enlargement in diastole, peak rate of posterior wall thinning, peak velocity of lengthening of the posterior wall, and velocity of circumferential chamber lengthening.

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Section: Discussionmentioning

confidence: 60%

M mode and Doppler echocardiographic assessment of left ventricular diastolic function in primary antiphospholipid syndrome.

Coudray

Zuttere

Blëtry

et al. 1995

Heart

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“…Widespread acute intramyocardial arteriolar thrombosis, without evidence of vasculitis, is responsible for extensive muscle necrosis in patients with aPL. 7 Although the biopsy specimen of our patient did not show intramyocardial arteriolar thrombosis, it may be possible that the process is not acute but recurrent, and affects small groups of vessels, resulting in a clinical picture and a course similar to a chronic cardiomyopathy. Myocardial involvement is also known in patients with SLE without APS.…”

Section: Discussionmentioning

confidence: 60%

Autologous hematopoietic stem cell transplantation for refractory antiphospholipid syndrome causing myocardial necrosis

Hashimoto

Iwasaki

Sekiguchi

et al. 2004

Bone Marrow Transplant

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Summary:Autologous hematopoietic stem cell transplantation (HSCT) is currently being evaluated as a treatment for autoimmune diseases, including systemic lupus erythematosus (SLE), that are associated with a very severe prognosis. We describe a 27-year-old woman with SLE with a 10-year history of refractory antiphospholipid syndrome (APS). She developed progressive myocardial necrosis despite treatment with corticosteroids, cyclophosphamide (CYC), cyclosporine, and immunopheresis. After conditioning with CYC, fludarabine, and antithymocyte globulin, autologous HSCT using CD34 þ selection was performed. After transplantation, the clinical symptoms caused by APS remitted, and the serum anticardiolipin antibody level decreased. Remission has persisted for 21 months after transplantation. Although a longer follow-up is required for the assessment of efficacy, autologous HSCT may cure patients with refractory APS.

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“…38 The patient succumbed from circulatory failure. It is possible that our patient 2 suffered from a similar process, producing an echocardiographic impression of 'myocarditis' or 'pseudocardiomyopathy'.…”

Section: Discussionmentioning

confidence: 99%

Diagnostic and therapeutic problems in two patients with antiphospholipid antibodies, heart valve lesions, and transient ischaemic attacks.

Asherson

Gibson

Evans

et al. 1988

Annals of the Rheumatic Diseases

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SUMMARY Two young women (aged 32 and 25 years) with systemic lupus erythematosus and heart valve lesions in association with antiphospholipid antibodies are presented. In addition to the presence of the 'lupus anticoagulant' and false positive Venereal Disease Research Laboratory (VDRL) tests, both patients had high levels of IgG anticardiolipin antibodies. The first patient additionally had contraceptive induced chorea, chorea gravidarum, seven miscarriages, livedo reticularis, pulmonary embolism, and thrombocytopenia and developed culture negative endocarditis as well as hypertension. The second patient, who had presented with hypertension, developed aortic and mitral regurgitation, suspected myocarditis, manifested transient ischaemic attacks, and responded well to anticoagulation and steroid treatment.

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Fatal cardiac failure due to myocardial microthrombi in systemic lupus erythematosus

Abstract: antisocial, and had intellectual difficulties. A psychotherapist she saw regularly diagnosed a narcissistic personality disorder. After four years of self bleeding she stopped for one year, and her haemoglobin concentration became 120-130 g/l.

Cited by 65 publications

References 2 publications

M mode and Doppler echocardiographic assessment of left ventricular diastolic function in primary antiphospholipid syndrome.

M mode and Doppler echocardiographic assessment of left ventricular diastolic function in primary antiphospholipid syndrome.

Autologous hematopoietic stem cell transplantation for refractory antiphospholipid syndrome causing myocardial necrosis

Diagnostic and therapeutic problems in two patients with antiphospholipid antibodies, heart valve lesions, and transient ischaemic attacks.

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