Vascular Disease
Josh Engel, BSc
Medical Student
Northwestern University
Chicago, Illinois, United States
Josh Engel, BSc
Medical Student
Northwestern University
Chicago, Illinois, United States
Ozden Kilinc, MD
Clinical Research Associate
Northwestern University
Chicago, Illinois, United States
Justin Baraboo, BSc
PhD Candidate
Northwestern University
Chicago, Illinois, United States
Elizabeth Weiss, BSc
MD/PhD Candidate
Northwestern University
Chicago, Illinois, United States
Christopher Mehta, MD
Cardiac Surgeon
Northwestern University, United States
Andrew Hoel, MD
Vascular Surgeon
Northwestern University, United States
S. Chris Malaisrie, MD
Cardiac Surgeon
Northwestern University, United States
Mark Markl, PhD
Professor
Northwestern University
Bradley D. Allen, MD, MSc, FSCMR
Assistant Professor, Cardiovascular and Thoracic Imaging
Northwestern University
Chicago, Illinois, United States
Aortic diameter growth is associated with increased mortality in patients with both de novo type B aortic dissection (TBAD) and residual dissection after type A dissection repair (rTAAD). Preemptive surgical intervention in chronic TBAD has been shown to improve mortality, however, it remains unclear which subgroups of patients benefit most from early intervention. Current imaging-based risk stratification is limited to evaluation of baseline aortic diameter on conventional images and growth over time. Assessment of true and false lumen (TL, FL) hemodynamics using 4D flow MRI (4DF) may better capture the drivers of adverse outcomes in TBAD. In this study, we hypothesize that changes in 4DF quantified TL and FL kinetic energy (KE), maximum velocity (MV), forward and reverse flow (FF, RF) over serial imaging correlate with aortic growth.
Methods:
We retrospectively identified TBAD patients with baseline and follow-up 4DF at least 120 days apart. Patients with TBAD intervention before baseline or between scans were excluded. The TL and FL were manually segmented for each scan and voxel-wise total KE, MV, FF, and RF were calculated using a Matlab tool. KE was summed over the cardiac cycle and luminal volume. FF and RF were summed over the cardiac cycle then averaged over luminal volume. 4DF data sets included prospective and retrospective ECG gating. To account for the effect of partial coverage of cardiac cycle by prospective gating, analysis was only performed on the percentage of the cardiac cycle captured by all scans (67.3%). Aortic diameter was measured from MRA images acquired at the time of 4DF. Pearson correlation coefficients were calculated between growth rate and parameter changes over time.
Results:
32 patients met inclusion criteria (age: 56.9±14.1 years, Female: 13, n=19 rTAAD, n=13 de novo TBAD (8 chronic, 5 acute at baseline). Mean follow up time was 538.3±470.7 days. Baseline diameter did not correlate with growth rate. In the entire cohort, Δ TL KE (r=.39, p=.025), Δ TL MV (r=.42, p=.02), Δ TL FF (r=.45, p=.009), Δ FL KE (r=.42, p=.02), Δ FL MV (r=.42, p=.02), and Δ FL RF (r=.61, p< .001) correlated with growth rate. In rTAAD only, Δ FL RF (r=.53, p=.02) correlated with growth, while in de novo TBAD only, all six correlations remained significant.
Conclusion:
This study suggests that changes in 4DF derived hemodynamic parameters over time correlate with aortic growth rate in TBAD. High energy, high velocity flow through the TL to the FL correlates with growth. Moreover, high energy flow and RF in the FL, which continues into diastole, increased with growth. These results may be capturing FL pressurization and dynamism as drivers of expansion and are consistent with treatment approaches that reduce flow into the FL as a protective mechanism. Our study also suggests de novo TBAD and rTAAD are hemodynamically distinct and warrant separate evaluation. Baseline diameter did not correlate with growth, illustrating a need for improved risk stratification tools in TBAD.