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. Author manuscript; available in PMC: 2015 Dec 1.
Published in final edited form as: Curr Heart Fail Rep. 2014 Dec;11(4):500–508. doi: 10.1007/s11897-014-0217-5

Table 1.

Summary of Studies of AAbs in DCM

Epitope
of AAb		 Physiological effect
on
pathology		 Reproduction of
disease
by
passive
transfer		 Induction
of
disease
by
immunization of
epitope		 Association with
phenotype
or
outcomes
in human		 Improvement of
pathology
after
removal		 Comments
Myosin +[12] ±[10,11]* +[8] +[13,15] ? *Transfer of AAbs causes myocarditis only in certain strains of mice [10,11]
β1AR +++[4,20–27,29]
−[32,33]*		 +[5] +[4] ++[28,83]†
[30]‡		 ±[57]
+[31,55]		 *AAbs from some patients are functionally inactive [32,33].
†Associated with ventricular arrhythmia, sudden death [83] and cardiovascular death[28].
‡Associated with more favorable response to β-blocker[30]
M2R ++[35,37–39] *(See comments) +[6,7] +[38,41]† ? *Reproduced by adoptive transfer into Rag2 knockout mice of splenocytes from M2R knockout mice immunized with M2R protein.
†Association with Af comorbid with DCM and recurrent after ablation[38,41]
Troponin I +[9] +[9] +[42] −?[46]
+[44]*		 −?[58] *Associated with higher LVEF and more favorable outcomes in DCM[44]
Na-K-ATPase +[84] ? +[85] +[84]* ? *Associated with ventricular arrhythmia and sudden death [84]
“Cardio-depressant AAb” +[59,60,61] ? ? ? +[60,62] Epitope unknown

AAb, autoantibody; DCM, dilated cardiomyopathy; β1AR, β1-adrenergic receptor; M2R, muscarinic M2 acetylcholine receptor; Af, atrial fibrillation; LVEF, left ventricular ejection fraction.