Validation of compliance zone at cerebral arterial bifurcation using phantom and computational fluid dynamics simulation.

OBJECTIVE: A zone compliant to pulsatile flow (compliance zone) showing evagination and flattening at the apex of the cerebral arterial bifurcation was documented in our previous report using electrocardiogram-gated computed tomographic and magnetic resonance angiography. We aimed to validate the existence of compliance zones and examine their relationship to local thin-elastic walls. METHODS: We examined different bifurcating vascular models: a phantom with a thin elastic region at the apex and computational fluid dynamics models with either an elastic or rigid region at the apex of a bifurcation. RESULTS: In the phantom, the elastic region at the apex of the bifurcation showed evagination and flattening in time with the pulsatile circulating fluids. The size of the evaginations increased when the outlet side was tilted down below the level of the flow-generating pump. Pulsatile evagination could be simulated in the computational fluid dynamics model with an elastic region at the bifurcation apex, and the pressure gradient was highest in the evaginating apex in peak systolic phase. CONCLUSIONS: We were able to demonstrate a compliance zone, which responds to pressure gradients, experimentally, in the form of a thin elastic region at an arterial bifurcation.

Echocardiogram-gated computed tomographic and magnetic resonance angiographies for the detection of pulsatile expansion at the intracranial arterial bifurcation.

OBJECTIVE: To identify the pulsatile small vascular lesion by echocardiogram (ECG)-gated computed tomographic (CT) and magnetic resonance (MR) angiographies. METHODS: Seven patients who exhibited small evagination at the cerebral artery bifurcations on 3-dimensional (3D) time-of-flight MR angiogram were enrolled. They were examined by conventional/ECG-gated CT angiogram (n = 6) and ECG-gated MR angiogram (n = 5). Echocardiogram-gated MR angiogram was performed with 3D time of flight, triggered after each time window. From ECG-gated CT and MR angiograms, consecutive 10-phase images within a single cardiac cycle were obtained. RESULTS: The pulsatile change of evagination was demonstrated on both ECG-gated CT angiogram (5 of 6 patients) and ECG-gated MR angiogram (all 5 patients). Flattening of the evagination during the diastolic phase was observed in 4 of 6 ECG-gated CT angiograms and 3 of 5 ECG-gated MR angiograms. Of note was a patient with a tiny evagination (<2 × 1 mm); pulsatile change was demonstrated only by ECG-gated MR angiogram. CONCLUSION: The pulsatile expansion of evagination at the cerebral artery bifurcation can be demonstrated on ECG-gated CT/MR angiograms.

Clinical and experimental investigation of pseudoaneurysm in the anterior communicating artery area on 3-dimensional time-of-flight cerebral magnetic resonance angiography.

OBJECTIVE: To investigate the hemodynamic mechanism of pseudoaneurysm in the anterior communicating artery (AcoA) area in magnetic resonance (MR) angiography. METHODS: For the clinical study, a total of 62 patients who undertook digital subtraction angiography (DSA) because of the rupture of an aneurysm originating from a location other than the AcoA area were examined with MR angiography. The relation between signal defect at the AcoA in MR angiography and anatomic variation of the anterior cerebral artery (ACA) was evaluated. For the experimental study, MR angiography and DSA were performed on elastic silicon vascular phantoms with 2 different bifurcation angles (70 degrees and 140 degrees). Hemodynamic factors producing signal defects were evaluated, and the results were compared by computational fluid dynamics (CFD). RESULTS: In a clinical study, 21 of 62 patients had a hypogenetic A1 segment on either side of the ACA. Their MR angiography showed signal defects in the axilla area of the bifurcated AcoA complex in 14 patients, 7 of which could make the residual normal vessel seem to be an aneurysm. All the cases with an intact AcoA complex showed no signal defect. In an experimental study, MR angiography of vascular phantoms with broad-angle bifurcation (140 degrees) showed signal defects at the axilla areas of bifurcation, and these were shown as turbulent flow in DSA and CFD. Phantoms with narrow-angle bifurcation (70 degrees) did not show a significant signal defect, however. CONCLUSIONS: A hypoplastic A1 segment accompanying a broad bifurcation angle of the contralateral A1 segment may cause a pseudoaneurysm in MR angiography because of signal defect in the AcoA area.