This Article Full Text Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Dörffel, W. V. Articles by Reinke, P. Search for Related Content PubMed PubMed Citation Articles by Dörffel, W. V. Articles by Reinke, P. Pubmed/NCBI databases 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