ABSTRACT
OBJECTIVES: With traditional instruments, endoscopic coronary artery bypass grafting has not been possible. This study was designed to determine the clinical feasibility of using a robotically assisted microsurgical system to create endoscopic coronary anastomoses. METHODS AND RESULTS: Ten patients underwent endoscopic coronary artery bypass grafting of the left internal thoracic artery to the left anterior descending artery. Subxiphoid endoscopic ports (2 for instruments, 1 for a camera) were placed, and a robotic system was used to perform the left internal thoracic artery-left anterior descending artery bypass graft. Conventional techniques were used to perform the other grafts. Blood flow through the left internal thoracic artery graft was measured in the operating room and was adequate in 8 of 10 patients. The 2 inadequate grafts were revised successfully by hand. Six weeks after the operation, selective coronary angiography demonstrated a graft patency of 100% (8/8). There were no technical failures of the robotic system. The only postoperative complication was mediastinal hemorrhage in 1 patient. CONCLUSIONS: This pilot study demonstrates the feasibility of robotically assisted endoscopic coronary artery bypass grafting.
Subject(s)
Anastomosis, Surgical/methods , Coronary Artery Bypass/methods , Endoscopy/methods , Robotics/methods , Anastomosis, Surgical/instrumentation , Coronary Artery Bypass/instrumentation , Coronary Disease/surgery , Feasibility Studies , Female , Humans , Male , Middle Aged , Pilot Projects , Robotics/instrumentation , Thoracic Arteries/transplantation , Treatment Outcome , United States , Vascular PatencyABSTRACT
Males of the MyK-103 line of transgenic mice are fertile and sire litters of normal size, but they never transmit the transgene, whereas females transmit the transgene with normal frequency. The chromosome originally bearing the transgene can be transmitted through the male germ line, but only after the transgene is deleted or rearranged by intrachromosomal recombination. The transgene encodes a functional herpes simplex virus (HSV) thymidine kinase gene that causes sperm infertility when expressed in postmeiotic germ cells. Immunocytochemistry revealed clones of germ cells that fail to express HSV thymidine kinase. We postulate that these cells arose by transgene deletion in embryonic germ cells and postnatal spermatogonial stem cells and that they are responsible for the normal fertility of MyK-103 males. The frequency of recombination events at the integration locus suggests that it contains a hotspot for mitotic recombination.
