PURPOSE: To ascertain the nature of the pressure wave transmitted through aneurysm thrombus and the changes produced after endovascular repair and the development of type I and II endoleaks. METHODS: A 25 mm Talent endovascular graft was deployed in a latex model of an abdominal aortic aneurysm, which was incorporated in a pulsatile flow unit. The graft was surrounded by thrombus analogue to simulate conditions in vivo. Pressure waveforms in the sac were captured over 5s at 1000 Hz in these settings: (i) no endoleaks (baseline), after introduction of (ii) type I (iii) type II and (iv) combined type I and II endoleaks. The arterial blood pressure settings used were 140/100 and 130/90 mmHg, denoted the high and low settings, respectively. ANOVA in Minitab 13 was applied for statistical analysis. RESULTS: Pulsatile waveforms were transmitted through the thrombus. Intrasac pressure after stent-grafting reduced to 110/107, 99/96 mmHg (p<0.001) (high, low settings, respectively). Introduction of a type I endoleak caused this to rise to 120/112, 115/107 mmHg (p<0.001, vs. baseline); after producing a type II endoleak these were 101/98, 91/88 mmHg (p<0.001, vs. baseline). A combined type I and II endoleak produced intrasac pressures identical to that of a type I endoleak. CONCLUSIONS: Intrasac pressure waveforms following EVAR are easily defined following a type I endoleak. Waveforms obtained following type II endoleak simulation resemble the baseline waveform in an attenuated form. Intrasac pressures are, therefore, a reliable marker for type I, but not a type II endoleak. In the case of a combined endoleak, the type I endoleak waveform effectively masks that of the type II. Intrasac thrombus faithfully transmits intrasac pressures.
PURPOSE: To ascertain the nature of the pressure wave transmitted through aneurysm thrombus and the changes produced after endovascular repair and the development of type I and II endoleaks. METHODS: A 25 mm Talent endovascular graft was deployed in a latex model of an abdominal aortic aneurysm, which was incorporated in a pulsatile flow unit. The graft was surrounded by thrombus analogue to simulate conditions in vivo. Pressure waveforms in the sac were captured over 5s at 1000 Hz in these settings: (i) no endoleaks (baseline), after introduction of (ii) type I (iii) type II and (iv) combined type I and II endoleaks. The arterial blood pressure settings used were 140/100 and 130/90 mmHg, denoted the high and low settings, respectively. ANOVA in Minitab 13 was applied for statistical analysis. RESULTS: Pulsatile waveforms were transmitted through the thrombus. Intrasac pressure after stent-grafting reduced to 110/107, 99/96 mmHg (p<0.001) (high, low settings, respectively). Introduction of a type I endoleak caused this to rise to 120/112, 115/107 mmHg (p<0.001, vs. baseline); after producing a type II endoleak these were 101/98, 91/88 mmHg (p<0.001, vs. baseline). A combined type I and II endoleak produced intrasac pressures identical to that of a type I endoleak. CONCLUSIONS: Intrasac pressure waveforms following EVAR are easily defined following a type I endoleak. Waveforms obtained following type II endoleak simulation resemble the baseline waveform in an attenuated form. Intrasac pressures are, therefore, a reliable marker for type I, but not a type II endoleak. In the case of a combined endoleak, the type I endoleak waveform effectively masks that of the type II. Intrasac thrombus faithfully transmits intrasac pressures.