Thorac Cardiovasc Surg 2012; 60 - P74
DOI: 10.1055/s-0031-1297865

The impact of the Ca-binding protein S100A1 in muscular cardiac assist

NW Guldner 1, D Thalmann 1, A Remppis 2, P Klapproth 3, M Großherr 4, R Noel 5, HH Sievers 1
  • 1Universitätsklinikum Schleswig-Holstein, Campus Lübeck, Klinik für Herzchirurgie, Lübeck, Germany
  • 2Herzzentrum Bad Bevensen, Bad Bevensen, Germany
  • 3Klinik für Herz- und thorakale Gefäßchirurgie, Universitätsklinikum Schleswig-Holstein, Campus Lübeck, Lübeck, Germany
  • 4Klinik für Anästhesie, Universitätsklinikum Schleswig-Holstein, Campus Lübeck, Lübeck, Germany
  • 5Allgemeine Tierhaltung der Universität zu Lübeck, Lübeck, Germany

Objectives: Muscle powered cardiac assist using latissimus dorsi muscle (LDM) with 100% type I fibers as a cardiomyoplasty was stopped clinically due a severe power loss, decreased muscle mass and muscle damage. The Ca-binding protein S100A1 is an important component of the electromechanical coupling and increases the contraction power in skeletal and cardiac muscle. Single fiber experiments with type I fibers recently demonstrated a limited efficacy of S100A1 during contraction. Thus this study investigates the effect of S100A1 within skeletal muscle ventricles (SMVs) of 100% type I fibers of group A (100% MHCI) in comparison with SMVs of 50% fatigue-resistant type IIa fibres (group B).

Methods: Left LDM of male Bore Goats were wrapped around an intra-thoracic elastic training device as a skeletal muscle ventricle (SMV). Electrical stimulation patterns for the transformation into100% type I-fibres were chosen in group A (n=6) and those resulting in 50% fatigue-resistant type IIa fibres in group B (n=6). Myosin heavy chain-, S100A1- and morpho- metric muscle analysis were performed after a time period over 4–9 months of pumping.

Results: In group A with 100% MHCI there was found no correlation between stroke volume and S100 A1 concentration. In total the stroke volume was low (14ml). In group B however with a 50% type IIa fibre muscle the correlation between stroke volume and S100 A1 was high (R2=0.933) and linear and the stroke volumes more than threefold higher than in A (46ml). Stroke volumes differed significantly(P<0.01). Muscles of group A demonstrated muscle damage and those of B were well preserved.

Conclusion: These data relating on S100A1 concentration and stroke volumes and muscle damage indicate, muscle powered cardiac assist with100% type I fibers was a big misunderstood with extremely reduced muscle power and severe muscle damage. Myo-stimulators with controlled stimulation regimes, enabling 50% type IIa fiber muscle, for clinical use, which are available commercially(Microstim GmbH, Germany) let us expect an effective muscular myocardial support in future.