Hemodynamic mechanism of pulsatile tinnitus caused by venous diverticulum treated with coil embolization.

BACKGROUND AND

OBJECTIVE

Coil embolization has become a new treatment method for pulsatile tinnitus (PT) caused by sigmoid sinus diverticulum (SSD). Although this therapy has achieved good results in clinical reports, the hemodynamic mechanism of coils in the treatment of PT in SSD remained unclear.

METHODS

Finite element method (FEM) and computational fluid dynamics (CFD) were combined to explore the hemodynamic mechanism of coil embolization in SSD treatment. Three personalized geometric models of sigmoid sinus were established according to the CTA data of patients. Coil model were established by FEM, and the hemodynamic differences of SSD before and after coiling were compared by transient CFD method.

RESULTS

Velocity streamlines disappeared in the SSD after coiling. At the peak time (t1 = 0.22 s), the SSD-average velocity decreased in every patient. The average value of the decreased in three patients was 0.154 ± 0.028 m/s (mean ± SD). Wall average pressure (Pavg) also showed a decline in every patient. Average of decrements of three patients was 17.69 ± 4.91 Pa (mean ± SD). Average WSS (WSSavg) was also reduced in every patient. The average value of WSS drop was 9.74 ± 3.02 Pa (mean ± SD). After coiling, the proportion of low-velocity region in the sigmoid sinus cortical plate dehiscence (SSCPD) area increased. Average of increments was 22.1 ± 5.36% (mean ± SD).

CONCLUSIONS

A reduction in SSD-average velocity, wall pressure, and WSS were the short-term hemodynamic mechanism of coil embolization for PT. Coil embolization increased the proportion of low-velocity region in the SSCPD area, thereby creating a hemodynamic environment that easily produced thrombus and protects blood vessels from the impact of blood flow. This phenomenon was the long-term effect of coil embolization.