1347517 - Intimal Flap Motion is Associated with Altered True Lumen Pulse Wave Velocity in Type B Aortic Dissection

Background: Type B aortic dissection (TBAD) is characterized by the formation of a true (TL) and a false lumen in the descending aorta, separated by an intimal flap. TBAD is associated with a high rate of complications primarily due to progressive aortic growth. Traditional risk metrics for predicting growth are limited and do not include measurement of aortic flow, considered to be a key driver of outcomes. Recent studies have shown that 4D flow MRI hemodynamic parameters have the potential to improve risk stratification¹. In particular, early evidence points to pulse wave velocity (PWV), a biomarker of arterial stiffness, as a strong predictor of growth^2,3. High PWV could, in fact, indicate a stiff dissection that is less prone to dilation. However, the mechanisms underlying PWV variations in TBAD are not fully understood and need further investigation. The aim of this study was to analyze the effect of intimal flap motion - an unexplored potential mechanism for changes in stiffness - on PWV in the TL.

Methods: As part of an ongoing prospective study, patients with TBAD underwent a cardiothoracic MRI, which included a 4D flow MRI of the aorta (spatial resolution=2.5mm³, temporal resolution=50msec, venc=160cm/s, scan time=11.1±2.6min), followed by multiple 2D CINE SSFP scans to assess intimal flap motion. 2D CINE SSFP consisted of 3 axial oblique acquisitions orthogonal to the aorta and at the level of the proximal, mid, and distal descending aorta. After 4D flow data pre-processing and TL manual 3D segmentation, PWV in the TL was calculated using multiple analysis planes for flow waveforms extraction, and cross-correlation for flow-time differences determination⁴ (fig.1). To quantify intimal flap motion, the contours of the TL were manually traced on all time frames of CINE SSFP scans and the relative area changes (RAC) were calculated. The maximum RAC (RAC_max) was extracted from each axial acquisition (fig.2). The average RAC_max was then calculated as a global measure of dissection flap motion and correlated to TL PWV. A correlation analysis between RAC_max and time since diagnosis was also performed.

Results: Seven patients were included (age: 58.7±5.3y; 5M). All patient’s RAC profiles over one cardiac cycle are represented in fig.3A. Pearson’s test showed a significant association between increased TL PWV with reduced RAC_max (r = -0.78, p=0.04, fig.3B). However, there was no significant correlation between RAC_max and time since diagnosis (r = -0.34, p=0.45, fig.3C).

Conclusion: Given the strong correlation between RAC_max and TL PWV, we conclude that intimal flap motion is an important mechanism of PWV in TBAD. High flap motion could, in fact, reduce aortic stiffness resulting in slower TL PWV and thus a higher risk of aortic growth. It is notable, however, that TL PWV was considerably lower than the measurements usually observed in non-dissected aortas. In addition, we found that flap motion was independent of time since diagnosis, suggesting a nonuniform motion course between patients.