Publicaciones científicas

Autologous human serum for cell culture avoids the implantation of cardioverter-defibrillators in cellular cardiomyoplasty

01-jun-2004 | Revista: International Journal of Cardiology

Chachques JC, Herreros J, Trainini J, Juffe A, Rendal E, Prosper F, Genovese J.

Current clinical experience with cellular cardiomyoplasty (using serum bovine-cultivated myoblasts) has demonstrated significant malignant ventricular arrhythmias and sudden deaths in patients. In some ongoing clinical trials the implantation of cardioverter-defibrillator is mandatory.

We have hypothesized that contact of human cells with fetal bovine serum results after 3-week fixation of animal proteins on the cell surface, representing an antigenic substrate for immunological and inflammatory adverse events.

Autologous myoblasts were transplanted into infarcted LV in 20 patients (90% males, mean age 62+/-8 years). Cells were cultivated in a complete human medium during 3 weeks, using the patients' own serum obtained from a blood sample or from plasmapheresis. Injections were performed during CABG (2.1 grafts/pt). All patients had an uneventful recovery.

At a mean follow-up of 14 +/- 5 months without mortality, no malignant cardiac arrhythmias are reported. LV ejection fraction improved from 28 +/- 3% to 52 +/- 4.7% (p = 0.03), and regional wall motion score index (WMSI) from 3.1 to 1.4 (p = 0.04) in the cell-treated segments. Myocardial viability tests showed areas of regeneration. Patients moved from mean NYHA class 2.5 to class 1.2.

A total autologous cell culture procedure was used in cellular cardiomyoplasty reducing the risk of arrhythmia. Human-autologous-serum cell expansion avoids the risk of prion, viral or zoonoses contamination. Since patients treated with noncultivated bone marrow cells are free of arrhythmia, the bovine-culture medium seems to be responsible for this complication. Cellular cardiomyoplasty may be efficient to avoid progression of ventricular remodeling and subsequent heart failure in ischemic heart disease.

CITA DEL ARTÍCULO  Int J Cardiol. 2004 Jun;95 Suppl 1:S29-33