A significant increase in the collagen content and a significant reduction in the elastin content of VV were demonstrated. The net increase in the collagen/elastin ratio is indicative of an imbalance in the connective tissue matrix. The biochemical profile of PV was similar to VV and significantly different from NV. These preliminary data support the presence of connective tissue abnormalities before valvular insufficiency. In addition, the absence of an increase in the proteolytic activity excludes enzymatic matrix degradation as an essential component in the formation of venous varicosities.

The results suggest that the latency in AAA formation in this model corresponds with a complex sequence of biochemical and cellular events. The model provides an "early window" into these interesting early phases leading to aneurysm formation.

These findings suggest that the factors (loss of consciousness, creatinine level, hemoglobin level) that are predictive of death may be a reflection of shock in this patient population. Further studies should be directed to optimizing preoperative resuscitation. Patients who have a ruptured abdominal aortic aneurysm should not be denied therapy on the basis of any specific set of preoperative factors.

Laparoscopically assisted AAA repair is technically challenging but feasible. Potential advantages may be early removal of nasogastric suction, shorter intensive care unit and hospital stays, and prompt return to full functional status. The hemodynamic data obtained from the pulmonary artery catheter and transesophageal echocardiogram during pneumoperitoneum suggest that transesophageal echocardiography may be sufficient for evaluation of volume status along with the added benefit of detection of regional wall motion abnormalities and aortic insufficiency. Further refinement in technique and instrumentation will make total laparoscopic AAA repair a reality.

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