Potential role of autoantibodies belonging to the immunoglobulin G-3 subclass in cardiac dysfunction among patients with dilated cardiomyopathy.
BACKGROUND
Immunoadsorption capable of removing circulating autoantibodies represents an additional therapeutic approach in dilated cardiomyopathy (DCM). The role played by autoantibodies belonging to the immunoglobulin (Ig) subclass G-3 in cardiac dysfunction remains to be elucidated.


RESULTS
Patients with DCM (left ventricular ejection fraction <30%) participated in this case-control study. Nine patients underwent immunoadsorption with protein A (low affinity to IgG-3), and 9 patients were treated with anti-IgG, which removes all IgG subclasses. Immunoadsorption was performed in 4 courses at 1-month intervals until month 3. In the 2 groups, immunoadsorption induced comparable reduction of total IgG (>80%). IgG-3 was effectively eliminated only by anti-IgG adsorption (eg, during the first immunoadsorption course; protein A, -37+/-4%; anti-IgG, -89+/-3%; P<0.001 versus protein A). The beta1-receptor autoantibody was effectively reduced only by anti-IgG (P<0.01 versus protein A). Hemodynamics did not change in the protein A group. In the anti-IgG group during the first immunoadsorption course, cardiac index increased from 2.3+/-0.1 to 3.0+/-0.1 L x min(-1) x m(-2) (P<0.01 versus protein A). After 3 months, before the last immunoadsorption course, cardiac index was 2.2+/-0.1 L x min(-1) x m(-2) in the protein A group and 3.0+/-0.2 L x min(-1) x m(-2) in the anti-IgG group (P<0.01 versus protein A). Left ventricular ejection fraction increased only in the anti-IgG group (P<0.05 versus protein A).


CONCLUSIONS
Autoantibodies belonging to IgG-3 may play an important role in cardiac dysfunction of DCM. The removal of antibodies of the IgG-3 subclass may represent an essential mechanism of immunoadsorption in DCM.
Staudt
Alexander
A
Klinik für Innere Medizin B, Ernst-Moritz-Arndt-Universität, Greifswald, Germany.
Böhm
Marko
M
Knebel
Fabian
F
Grosse
Yvonne
Y
Bischoff
Claudia
C
Hummel
Astrid
A
Dahm
Johannes B
JB
Borges
Adrian
A
Jochmann
Nicoline
N
Wernecke
Klaus D
KD
Wallukat
Gerd
G
Baumann
Gert
G
Felix
Stephan B
SB
D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000818:Animals; D001323:Autoantibodies / Q000097:blood* / Q000302:isolation & purification / Q000494:pharmacology; D020013:Calcium Signaling / Q000187:drug effects; D002311:Cardiomyopathy, Dilated / Q000150:complications / Q000503:physiopathology* / Q000628:therapy; D016022:Case-Control Studies; D002478:Cells, Cultured; D004232:Diuretics / Q000627:therapeutic use; D004452:Echocardiography; D005260:Female; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood* / Q000276:immunology*; D007075:Immunoglobulin M / Q000097:blood / Q000276:immunology; D007163:Immunosorbent Techniques; D008297:Male; D008875:Middle Aged; D009200:Myocardial Contraction / Q000187:drug effects; D009566:Nitrates / Q000627:therapeutic use; D011485:Protein Binding / Q000276:immunology; D051381:Rats; D018342:Receptors, Adrenergic, beta-1 / Q000276:immunology; D013318:Stroke Volume / Q000187:drug effects; D016896:Treatment Outcome; D018487:Ventricular Dysfunction, Left / Q000150:complications / Q000503:physiopathology* / Q000628:therapy
D000319:Adrenergic beta-Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D001323:Autoantibodies; D004232:Diuretics; D007074:Immunoglobulin G; D007075:Immunoglobulin M; D009566:Nitrates; D018342:Receptors, Adrenergic, beta-1