Cadaveric evaluation of sternal reconstruction using the pectoralis muscle flap.

BACKGROUND: Deep sternal wound infection is a significant complication of open cardiac surgery associated with increased mortality and morbidity. The use of muscle flaps, such as the pectoralis major advancement flap, in deep sternal wound infection reconstruction reduces hospital stay and mortality. However, the lower end of the sternum is remote from the vascular supply and cover is therefore problematic in many cases. METHODS: This study aimed to determine the distance (cm) and surface area (cm2 ) of sternum covered when the pectoralis major muscle is sequentially dissected from the sternocostal origin and humeral insertion using 10 cadaveric specimens. RESULTS: The largest proportion of sternum was covered when both the origin and insertion were divided, allowing the flap to be islanded on its vascular pedicle. There was a statistically significant difference when the pectoralis major was divided from the origin and insertion compared to division of the origin alone (P < 0.01). The average area covered with sternocostal origin division alone was 55.43 cm2 compared to 85.36 cm2 after division of both the origin and insertion. CONCLUSION: Division of both the sternocostal origin and humeral insertion of the pectoralis major muscle represents an effective means to increase sternal coverage. This study describes the average distance and area covered by sliding pectoralis major muscle advancement flaps. These measurements could better inform plastic surgeons when evaluating reconstructive options in sternal defects.

A non-apoptotic role for caspase-9 in muscle differentiation.

Caspases, a family of cysteine proteases most often investigated for their roles in apoptosis, have also been demonstrated to have functions that are vital for the efficient execution of cell differentiation. One such role that has been described is the requirement of caspase-3 for the differentiation of skeletal myoblasts into myotubes but, as yet, the mechanism leading to caspase-3 activation in this case remains elusive. Here, we demonstrate that caspase-9, an initiator caspase in the mitochondrial death pathway, is responsible for the activation of caspase-3 in differentiating C2C12 cells. Reduction of caspase-9 levels, using an shRNA construct, prevented caspase-3 activation and inhibited myoblast fusion. Myosin-heavy-chain expression, which accompanies myoblastic differentiation, was not caspase-dependent. Overexpression of Bcl-xL, a protein that inhibits caspase-9 activation, had the same effect on muscle differentiation as knockdown of caspase-9. These data suggest that the mitochondrial pathway is required for differentiation; however, the release of cytochrome c or Smac (Diablo) could not be detected, raising the possibility of a novel mechanism of caspase-9 activation during muscle differentiation.