Abstract

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. 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. 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 (>or= 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. Increased sIL-2R levels in CMP patients are an independent predictor of a more aggressive clinical course.

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