Short-term hemodynamic effects of immunoadsorption in dilated cardiomyopathy

WV Dörffel, SB Felix, G Wallukat, S Brehme… - Circulation, 1997 - Am Heart Assoc
WV Dörffel, SB Felix, G Wallukat, S Brehme, K Bestvater, T Hofmann, FX Kleber…
Circulation, 1997Am Heart Assoc
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–β1-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 …
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–β1-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 β-blockers. During therapy, hemodynamic parameters (mean±SD) were monitored with a Swan-Ganz thermodilution catheter. IA elicited a decrease of anti–β1-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.
Am Heart Assoc