Reduced Suppressor CellActivity inCongestive Cardiomyopathy andinMyocarditis

SUMMARY We studied suppressorcell function in10patients whohadcongestive cardiomyopathy, 13 patients whohadmyocarditis and98healthy controls. Myocardial biopsy, coronaryarteriography andleft ventricular angiography wereused todefine anddifferentiate congestive cardiomyopathy andmyocarditis. The suppressorcomponent oftheimmune responsewasassessed byexamining theinvitro responses ofperipheral blood lymphoid (PBL)cells under standard conditions. Briefly, PBLcells wereincubated withconcanavalin A tostimulate suppressoractivity. Induced activity was measured bytheability ofPBLcells toinhibit 'Hthymidine uptake ofnonstimulated autologous cells whensubsequently presented withallogenic ormitogenic stimuli. CARDIOMYOPATHIESaredefined asheart musclediseases ofunknown cause. Thewidely usedclassification isbased onclinical andpathologic anatomic criteria anddistinguishes dilated, hypertrophic andrestricted forms.'-3 Thisclassification does notdescribe allaspects ofadiffering nosology. Theso-called congestive cardiomyopathy (CCM)canbedescribed by special morphologic, biochemical andimmunologic events, which haveonly amoderate specificity. Thus, theseparation between primary andsecondary diseases isoften notprecise inclinical conditions. Recently, 76%ofpatients intheacute phase ofviral carditis werefoundtohavemyocardial antibodies byindirect immunofluorescence methods. Nuclearboundantiglobulin IgMwasfound inallofthese patients.' Indilated cardiomyopathies, ahighpercentageofboundimmunoglobulins could bedetected in myocardial biopsy tissue. Immunoglobulin IgGwas mostoften demonstrated insarcolemmal structures of patients withlowejection fractions (<35%); inpatients withhigher ejection fractions, thepercentage of binding wasconsiderably lower.5 Instudies with8Hthymidine incorporation into theDNA ofstimulated lymphocytes inthepresence ofconcanavalin A-treated peripheral blood mononuclear cells, Fowles etal.6 found depressed suppressor cell function inpatients withCCM. B-lymphocytes synthesize humoralantibodies, which arefound intheserum. Helper andsuppressor T-cells modify this activity quantitatively. Asaconsequence ofadiminished suppressor T-cell function, the physiologic control oftheantibody synthesis could be disturbed. Subsequently, specifically acting pathologicagents could cause anexcessive production ofcardiotoxic antibodies, whichmaybindtomyocardial structures.