Background Activation of T lymphocytes is thought to mediate myocardial dysfunction in dilated cardiomyopathy (CMP), probably through cytotoxic cytokines, but its value as a prognostic factor has not been evaluated.

Methods For 2 years we prospectively followed 76 patients (65 males, 11 females, age 49 ± 7 years) with CMP and New York Heart Association(NYHA) Class II–III heart failure; left ventricular (LV) function was assessed echocardiographically. Thirty‐three patients (28 males, five females, age 52 ± 6 years) with ischaemic heart disease (IHD) and similar NYHA and LV function characteristics were used as controls. Serum sIL‐2R levels, peripheral blood lymphocyte proliferation (basal, + concanavalin A) and HLA‐DQB1 genotyping was carried out in all patients.

Results The CMP patients had increased sIL‐2R levels (1259 ± 130 pg mL⁻¹) compared with the IHD patients (703 ± 80 pg mL⁻¹, P < 0·01, only 3 > 800 pg mL⁻¹). In the CMP patients, there was a significant (r = +0·45, P= 0·04) correlation between sIL‐2R and the LV end‐diastolic diameter but not with the LV ejection fraction or NYHA Class. During the 24‐month follow up, 17 of the CMP patients had an adverse clinical course (death, need for cardiac transplantation, or worsening heart failure). Of these, 14 (75%) had elevated (≥ 800 pg mL⁻¹) sIL‐2R levels (Group I) compared with only five (6%) with a stable clinical course (Group II). Neither [3H] thymidine incorporation into the peripheral blood lymphocytes nor the excess of HLA‐DQB1‐30 histidine homozygotes in the Group I patients (38% vs. 17%, P < 0·05) could predict the clinical outcome.

Conclusion Increased sIL‐2R levels in CMP patients are an independent predictor of a more aggressive clinical course.