Tumor necrosis factor-α predicts response to cardiac resynchronization therapy in patients with chronic heart failure

Circ J. 2014;78(9):2232-9. doi: 10.1253/circj.cj-14-0023. Epub 2014 Jun 20.

Abstract

Background: Pro-inflammatory cytokines contribute to the pathophysiology of heart failure (HF) and are up-regulated in affected patients. We investigated whether pro-inflammatory cytokines might predict the response to cardiac resynchronization therapy (CRT). METHODS AND RESULTS: Plasma levels of tumor necrosis factor-α (TNF-α) and interleukin-6 were assessed in 91 patients before CRT. Response to CRT was defined as a decrease ≥15% in left ventricular end-systolic volume (LVESV) at 6 months. Baseline TNF-α did correlate with LVESV reduction (P=0.001) after CRT. The subject group was divided according to tertiles of TNF-α. From the lower to the upper tertile LVESV (-31±28%, -17±17%, -9±22%) and LV end-diastolic volume (-23±25%, -14±16%, -4±18%) were progressively less reduced after CRT (P<0.001). The proportion of responders to CRT was 70%, 42% and 33%, according to the lower, intermediate and upper tertile of TNF-α distribution (P=0.01). Serious cardiac events (cardiac death, HF hospitalization or urgent heart transplantation) occurred in 63% of patients in the upper tertile vs. 32% and 17% in the intermediate and lower tertiles, respectively, during a median follow-up of 47 months (P<0.001).

Conclusions: Circulating TNF-α predicts the degree of LV reverse remodeling after CRT and may contribute to the early identification of those patients at higher risk of events after device implantation.

Publication types

  • Clinical Trial

MeSH terms

  • Aged
  • Cardiac Resynchronization Therapy
  • Chronic Disease
  • Death
  • Female
  • Follow-Up Studies
  • Heart Failure / blood*
  • Heart Failure / therapy*
  • Heart Transplantation
  • Humans
  • Interleukin-6 / blood
  • Male
  • Middle Aged
  • Prospective Studies
  • Tumor Necrosis Factor-alpha / blood*
  • Ventricular Remodeling*

Substances

  • IL6 protein, human
  • Interleukin-6
  • TNF protein, human
  • Tumor Necrosis Factor-alpha