{"id":{"repo_id":"aachen","oai_identifier":"oai:publications.rwth-aachen.de:61792"},"canonical_url":"https://search.dev.ndltd.org/etd/aachen/oai:publications.rwth-aachen.de:61792","repository":{"repo_id":"aachen","name":"RWTH Aachen University","base_url":"https://publications.rwth-aachen.de/oai2d"},"display":{"title":"Versuch der Etablierung eines experimentellen Modells zum chronischen Hibernating Myocardium am Schweineherzen","abstract":"BACKGROUND: Congenital origin of the left coronary artery from the pulmonary artery (ALCAPA-syndrome) can result in chronic left ventricular dysfunction due to hypoxic hypoperfusion of the myocardium supplied by the left anterior descending coronary artery (LAD). Portions of this dysfunctional tissue might recover after revascularization and thus, might represent hibernating myocardium. In the present experimental study we tried to establish an artificial ALCAPA syndrome in anaesthetized pigs as a model for chronic hibernating myocardium. METHODS AN RESULTS: A segment of the carotid artery was interposed between the pulmonary artery and the LAD as a bypass graft. Coronary blood flow in the LAD was reduced by sequential inflations of a cuff occluder. Simultaniously, incremental increases of antegrade blood flow through the artificial bypass graft resulted in reduction of regional wallmotion, as assessed by reduced segment shortening measured by ultrasonic crystals. Histologic analysis of the hypoperfused, hypoxic myocardial territory showed severe cellular degeneration, myolysis, and alteration of the chromatin structure comparable to ischemic cell death after one hour of LAD occlusion. CONCLUSION: Hypoxic hypoperfusion of the myocardium via an artificial bypass graft from the pulmonary artery results in ischemic cell necrosis of the depending myocardium. These findings are in contrast to the concept of myocardial hibernation in the congenital ALCAPA-syndrome. The presented artificial ALCAPA-syndrome failed to induce myocardial adaptive processes and did not induce a stable condition of preserved cellular integrity but resulted in ischemic cell death.","abstract_html":"BACKGROUND: Congenital origin of the left coronary artery from the pulmonary artery (ALCAPA-syndrome) can result in chronic left ventricular dysfunction due to hypoxic hypoperfusion of the myocardium supplied by the left anterior descending coronary artery (LAD). Portions of this dysfunctional tissue might recover after revascularization and thus, might represent hibernating myocardium. In the present experimental study we tried to establish an artificial ALCAPA syndrome in anaesthetized pigs as a model for chronic hibernating myocardium. METHODS AN RESULTS: A segment of the carotid artery was interposed between the pulmonary artery and the LAD as a bypass graft. Coronary blood flow in the LAD was reduced by sequential inflations of a cuff occluder. Simultaniously, incremental increases of antegrade blood flow through the artificial bypass graft resulted in reduction of regional wallmotion, as assessed by reduced segment shortening measured by ultrasonic crystals. Histologic analysis of the hypoperfused, hypoxic myocardial territory showed severe cellular degeneration, myolysis, and alteration of the chromatin structure comparable to ischemic cell death after one hour of LAD occlusion. CONCLUSION: Hypoxic hypoperfusion of the myocardium via an artificial bypass graft from the pulmonary artery results in ischemic cell necrosis of the depending myocardium. These findings are in contrast to the concept of myocardial hibernation in the congenital ALCAPA-syndrome. The presented artificial ALCAPA-syndrome failed to induce myocardial adaptive processes and did not induce a stable condition of preserved cellular integrity but resulted in ischemic cell death.","abstract_has_math":false,"creators":["Schütz, Thorsten"],"institution":"Publikationsserver der RWTH Aachen University","degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":["Schwarz, Ernst Rüdiger"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2004,"date_issued":"2004","date_published":"2004","updated_at":"2026-07-30T19:43:19Z","subjects":["info:eu-repo/classification/ddc/610","Medizin"],"languages":["ger"],"rights":["info:eu-repo/semantics/openAccess"],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["https://publications.rwth-aachen.de/search?p=id:%22RWTH-CONV-123416%22"],"render_values":[{"text":"https://publications.rwth-aachen.de/search?p=id:%22RWTH-CONV-123416%22","href":"https://publications.rwth-aachen.de/search?p=id:%22RWTH-CONV-123416%22","code":true}]}]},"links":{"outbound_url":"https://publications.rwth-aachen.de/record/61792","outbound_label":"Repository record","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Schwarz, Ernst Rüdiger"]},{"key":"dc:creator","label":"Author","values":["Schütz, Thorsten"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:coverage","label":"Dc Coverage","values":["DE"]},{"key":"dc:date","label":"Dc Date","values":["2004"]},{"key":"dc:publisher","label":"Institution","values":["Publikationsserver der RWTH Aachen University"]},{"key":"dc:relation","label":"Dc Relation","values":["info:eu-repo/semantics/altIdentifier/urn/urn:nbn:de:hbz:82-opus-8743"]},{"key":"dc:type","label":"Dc Type","values":["info:eu-repo/semantics/doctoralThesis","info:eu-repo/semantics/publishedVersion"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["info:eu-repo/classification/ddc/610","Medizin"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["ger"]},{"key":"dc:rights","label":"Dc Rights","values":["info:eu-repo/semantics/openAccess"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://publications.rwth-aachen.de/record/61792","https://publications.rwth-aachen.de/search?p=id:%22RWTH-CONV-123416%22"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["BACKGROUND: Congenital origin of the left coronary artery from the pulmonary artery (ALCAPA-syndrome) can result in chronic left ventricular dysfunction due to hypoxic hypoperfusion of the myocardium supplied by the left anterior descending coronary artery (LAD). Portions of this dysfunctional tissue might recover after revascularization and thus, might represent hibernating myocardium. In the present experimental study we tried to establish an artificial ALCAPA syndrome in anaesthetized pigs as a model for chronic hibernating myocardium. METHODS AN RESULTS: A segment of the carotid artery was interposed between the pulmonary artery and the LAD as a bypass graft. Coronary blood flow in the LAD was reduced by sequential inflations of a cuff occluder. Simultaniously, incremental increases of antegrade blood flow through the artificial bypass graft resulted in reduction of regional wallmotion, as assessed by reduced segment shortening measured by ultrasonic crystals. Histologic analysis of the hypoperfused, hypoxic myocardial territory showed severe cellular degeneration, myolysis, and alteration of the chromatin structure comparable to ischemic cell death after one hour of LAD occlusion. CONCLUSION: Hypoxic hypoperfusion of the myocardium via an artificial bypass graft from the pulmonary artery results in ischemic cell necrosis of the depending myocardium. These findings are in contrast to the concept of myocardial hibernation in the congenital ALCAPA-syndrome. The presented artificial ALCAPA-syndrome failed to induce myocardial adaptive processes and did not induce a stable condition of preserved cellular integrity but resulted in ischemic cell death."]},{"key":"dc:source","label":"Dc Source","values":["Aachen : Publikationsserver der RWTH Aachen University 115 S. : Ill., graph. Darst. (2004). = Aachen, Techn. Hochsch., Diss., 2004"]},{"key":"dc:title","label":"Title","values":["Versuch der Etablierung eines experimentellen Modells zum chronischen Hibernating Myocardium am Schweineherzen"]}]}],"canonical_facts":{"dc:contributor":["Schwarz, Ernst Rüdiger"],"dc:coverage":["DE"],"dc:creator":["Schütz, Thorsten"],"dc:date":["2004"],"dc:description":["BACKGROUND: Congenital origin of the left coronary artery from the pulmonary artery (ALCAPA-syndrome) can result in chronic left ventricular dysfunction due to hypoxic hypoperfusion of the myocardium supplied by the left anterior descending coronary artery (LAD). Portions of this dysfunctional tissue might recover after revascularization and thus, might represent hibernating myocardium. In the present experimental study we tried to establish an artificial ALCAPA syndrome in anaesthetized pigs as a model for chronic hibernating myocardium. METHODS AN RESULTS: A segment of the carotid artery was interposed between the pulmonary artery and the LAD as a bypass graft. Coronary blood flow in the LAD was reduced by sequential inflations of a cuff occluder. Simultaniously, incremental increases of antegrade blood flow through the artificial bypass graft resulted in reduction of regional wallmotion, as assessed by reduced segment shortening measured by ultrasonic crystals. Histologic analysis of the hypoperfused, hypoxic myocardial territory showed severe cellular degeneration, myolysis, and alteration of the chromatin structure comparable to ischemic cell death after one hour of LAD occlusion. CONCLUSION: Hypoxic hypoperfusion of the myocardium via an artificial bypass graft from the pulmonary artery results in ischemic cell necrosis of the depending myocardium. These findings are in contrast to the concept of myocardial hibernation in the congenital ALCAPA-syndrome. The presented artificial ALCAPA-syndrome failed to induce myocardial adaptive processes and did not induce a stable condition of preserved cellular integrity but resulted in ischemic cell death."],"dc:identifier":["https://publications.rwth-aachen.de/record/61792","https://publications.rwth-aachen.de/search?p=id:%22RWTH-CONV-123416%22"],"dc:language":["ger"],"dc:publisher":["Publikationsserver der RWTH Aachen University"],"dc:relation":["info:eu-repo/semantics/altIdentifier/urn/urn:nbn:de:hbz:82-opus-8743"],"dc:rights":["info:eu-repo/semantics/openAccess"],"dc:source":["Aachen : Publikationsserver der RWTH Aachen University 115 S. : Ill., graph. Darst. (2004). = Aachen, Techn. Hochsch., Diss., 2004"],"dc:subject":["info:eu-repo/classification/ddc/610","Medizin"],"dc:title":["Versuch der Etablierung eines experimentellen Modells zum chronischen Hibernating Myocardium am Schweineherzen"],"dc:type":["info:eu-repo/semantics/doctoralThesis","info:eu-repo/semantics/publishedVersion"]},"updated_at":"2026-07-30T19:43:19Z"}