PURPOSE: To investigate pressure and maximum rate of rise of systolic pressure (peak dP/dt) in completely excluded aneurysms and endoleaks to determine the hemodynamic impact of endoleaks. METHODS: In mongrel dogs (n = 36) experimental aneurysms were created by insertion of a patch (portion of rectus abdominis muscle sheath) into the infrarenal aorta. In group I (n = 18), all aortic branches of the aneurysm were ligated and all aneurysms were completely excluded by stent grafts. Group II (n = 18) consisted of aneurysms with patent aortic side branches that represented sources of endoleaks. One week (n = 12), six weeks (n = 12), and six months (n = 12) after stent grafting, hemodynamic measurements were obtained in thrombosed aneurysms and proved endoleaks. Systemic blood pressure and intraaneurysmal pressure were simultaneously measured and the respective peak dP/dt were computed. RESULTS: At the six-month follow-up, the systolic-pressure ratio (intraaneurysmatic pressure: systemic pressure) was significantly increased in endoleaks compared to non-perfused areas (0.879 +/- 0.042 versus 0.438 +/- 0.176, p < 0.01, group II) or completely excluded aneurysms (0.385 +/- 0.221, group I). Peak dP/dt ratio (intraaneurysmal peak dP/dt: systemic peak dP/dt) was 0.922 +/- 0.154 in endoleaks, compared to 0.084 +/- 0.080 in non-perfused areas (group II, p < 0.01), and was 0.146 +/- 0.121 in completely excluded aneurysms (group I). The diastolic-pressure ratio was also increased in endoleaks compared to non-perfused areas (0.929 +/- 0.088 versus 0.655 +/- 0.231, p < 0.01, group II) or completely excluded aneurysms (0.641 +/- 0.278, group I). In excluded aneurysms, pressure exposure declined as the length of the follow-up period increased. CONCLUSION: Type II endoleaks transmit pulsatile pressure of near systemic level and indicate insufficient treatment result. In contrast, complete endovascular exclusion of aneurysms results in significantly reduced pressure exposure.
PURPOSE: To investigate pressure and maximum rate of rise of systolic pressure (peak dP/dt) in completely excluded aneurysms and endoleaks to determine the hemodynamic impact of endoleaks. METHODS: In mongrel dogs (n = 36) experimental aneurysms were created by insertion of a patch (portion of rectus abdominis muscle sheath) into the infrarenal aorta. In group I (n = 18), all aortic branches of the aneurysm were ligated and all aneurysms were completely excluded by stent grafts. Group II (n = 18) consisted of aneurysms with patent aortic side branches that represented sources of endoleaks. One week (n = 12), six weeks (n = 12), and six months (n = 12) after stent grafting, hemodynamic measurements were obtained in thrombosed aneurysms and proved endoleaks. Systemic blood pressure and intraaneurysmal pressure were simultaneously measured and the respective peak dP/dt were computed. RESULTS: At the six-month follow-up, the systolic-pressure ratio (intraaneurysmatic pressure: systemic pressure) was significantly increased in endoleaks compared to non-perfused areas (0.879 +/- 0.042 versus 0.438 +/- 0.176, p < 0.01, group II) or completely excluded aneurysms (0.385 +/- 0.221, group I). Peak dP/dt ratio (intraaneurysmal peak dP/dt: systemic peak dP/dt) was 0.922 +/- 0.154 in endoleaks, compared to 0.084 +/- 0.080 in non-perfused areas (group II, p < 0.01), and was 0.146 +/- 0.121 in completely excluded aneurysms (group I). The diastolic-pressure ratio was also increased in endoleaks compared to non-perfused areas (0.929 +/- 0.088 versus 0.655 +/- 0.231, p < 0.01, group II) or completely excluded aneurysms (0.641 +/- 0.278, group I). In excluded aneurysms, pressure exposure declined as the length of the follow-up period increased. CONCLUSION: Type II endoleaks transmit pulsatile pressure of near systemic level and indicate insufficient treatment result. In contrast, complete endovascular exclusion of aneurysms results in significantly reduced pressure exposure.