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Circulation. 1997;95:1994-1997

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*Substance via MeSH
Medline Plus Health Information
*Autoimmune Diseases
*Cardiomyopathy

(Circulation. 1997;95:1994-1997.)
© 1997 American Heart Association, Inc.


Articles

Short-term Hemodynamic Effects of Immunoadsorption in Dilated Cardiomyopathy

Wolf V. Dörffel, MD; Stephan B. Felix, MD; Gerd Wallukat, MD; Stefan Brehme, MD; Knut Bestvater, MD; Torsten Hofmann, MD; Franz X. Kleber, MD; Gert Baumann, MD; Petra Reinke, MD

From the Departments of Internal Medicine I (W.V.D., S.B.F., S.B., F.X.K., G.B.) and V (K.B., T.H., P.R.), Charité, Humboldt University, Berlin, and the Max Delbrück Center for Molecular Medicine (G.W.), Berlin-Buch, Germany.

Correspondence to Dr Stephan Felix, Department of Internal Medicine I, Charité, Schumannstr 20-21, 10098 Berlin, Germany.

Background Previous studies have shown that the sera of many patients with dilated cardiomyopathy (DCM) are positive for several antibodies directed against cardiac antigens. Anti–ß1-adrenergic receptor antibodies occur in 70% to 90% of DCM patients. These antibodies are extractable by immunoadsorption (IA). In an investigation of the functional significance of antibodies for hemodynamics, IA was performed throughout 5 consecutive days on nine patients with severe DCM who were on stable drug therapy.

Methods and Results Immunoglobulins were eliminated in nine patients with severe DCM (mean age, 43.5 years; range, 25 to 58 years; left ventricular ejection fraction, <25%). IA was performed over 5 consecutive days with an immunoadsorber for immunoglobulin. All patients were on stable medication, including ACE inhibitors, digitalis, and diuretics. All patients received ß-blockers. During therapy, hemodynamic parameters (mean±SD) were monitored with a Swan-Ganz thermodilution catheter. IA elicited a decrease of anti–ß1-adrenergic receptor antibodies from 6.4±1.3 to 1.0±0.5 relative units. During IA, cardiac output increased from 3.7±0.8 to 5.5±1.8 L/min, P<.01. Mean arterial pressure decreased from 76.0±9.9 to 65.0±11.2 mm Hg, P<.05; mean pulmonary arterial pressure, from 27.6±7.7 to 22.0±6.5 mm Hg, P<.05; left ventricular filling pressure, from 16.8±7.4 to 12.8±4.7 mm Hg, P<.05; and systemic vascular resistance, from 1465±332 to 949±351 dyne·s·cm-5, P<.01.

Conclusions In addition to conventional medical treatment, IA may be an additional therapeutic possibility for acute hemodynamic stabilization of patients with severe DCM.


Key Words: cardiomyopathy • immunoadsorption • hemodynamics




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