Home Quantitative Assessment of Asymmetric Aortic Dilation with Valve-related Aortic Disease
Post
Cancel

Quantitative Assessment of Asymmetric Aortic Dilation with Valve-related Aortic Disease

Posted Dec 31, 2012 Updated Apr 10, 2023
By Michael T. Lu MD , Samir R. Thadani MD MEng , Michael D. Hope MD
11 min read

Rationale and Objectives

Previous work suggests that ascending aortic (AsAo) dilation can be asymmetric and is potentially related to valve-related blood flow abnormalities. The aim of this study was to investigate the relationship between the aortic valve and AsAo dilation using a quantitative, three-dimensional assessment of aortic shapes.

Materials and Methods

Computed tomographic and magnetic resonance images of the thorax were retrospectively reviewed. Four groups with aortic dilation were studied: those with tricuspid aortic valves (TAVs) with and without stenosis and those with bicuspid aortic valves (BAVs) with and without stenosis. Controls had either TAVs or BAVs but no aortic stenosis or dilation. In additional to standard orthogonal diameters, a unique measurement of AsAo asymmetry was used: the ratio of the greater to lesser curvatures measured using three-dimensional reformats in a “candy-cane” orientation.

Results

A total of 105 patients were identified. Ratios of greater to lesser curvature in patients with aortic dilation and nonstenotic TAVs were not significantly different from those in controls (1.69 vs 1.55, P > .20), but the asymmetry reflected by this ratio was markedly increased in patients with aortic dilation and stenotic TAVs (1.94, P < .001). Patients with aortic dilation and BAVs had significantly elevated ratios regardless of the status of the aortic valve (1.96 for nonstenotic and 2.05 for stenotic vs 1.53 for controls, P < .001).

Conclusions

Asymmetric AsAo dilation with relative bulging of the greater curvature is linked to aortic stenosis, but it is also seen with nonstenotic BAVs. This suggests that the hemodynamic forces that contribute to aortic dilation are not fully revealed by conventional assessment of the aortic valve.

Previous work suggests that ascending aortic (AsAo) dilation can be asymmetric and is potentially related to valve-related blood flow abnormalities. Most studies have focused on bicuspid aortic valve (BAVs), a congenital lesion seen in 1% to 2% of the general population . Dilation of the ascending aorta is a frequent complication of BAV. Because aortic dilation is often asymptomatic, it may progress unchecked to aneurysm, dissection, or rupture . Studies have suggested that using the size of the ascending aorta alone is inadequate to predict the risk for dissection, necessitating the development of better risk assessment tools .

The etiology of AsAo dilation in patients with BAVs is controversial. There is convincing evidence that it is related to intrinsic fragility of the aortic wall . Patients with BAVs have dilation out of proportion to valvular dysfunction , dilation of the main pulmonary artery in the absence of pulmonary valvular abnormality , and first-degree relatives with aortic dilation but normal aortic valves . Yet the reported asymmetric shape of the ascending aorta with BAV would be unusual if intrinsic aortic wall fragility were the sole etiology for dilation. With Marfan syndrome, the quintessential connective tissue disorder, aortic dilation is typically symmetric and most prominent at the sinuses of Valsalva. However, with BAV, unique patterns of AsAo dilation have been associated with specific aortic leaflet fusion patterns , and asymmetric bulging of the greater curvature has been reported . A potential explanation for this asymmetry is abnormal blood flow.

Get Radiology Tree app to read full this article<

Get Radiology Tree app to read full this article<

Methods

Patient Selection

Get Radiology Tree app to read full this article<

Get Radiology Tree app to read full this article<

Get Radiology Tree app to read full this article<

Get Radiology Tree app to read full this article<

Imaging Protocols

Get Radiology Tree app to read full this article<

Reconstruction and Measurement Techniques

Get Radiology Tree app to read full this article<

Get Radiology Tree app to read full this article<

Figure 1, Measurement of the greater and lesser ascending aortic curvatures. (a) The superior margin of the main pulmonary artery (MPA) is labeled on a two-dimensional oblique multiplanar reconstruction with an asterisk . (b) An orthogonal line is drawn from the superior margin of the MPA across the ascending aorta on the three-dimensional volume rendering in “candy-cane” orientation. (c) The outer and inner curvatures are measured from the aortic valve plane to this line.

Figure 2, Ascending aortic morphology for four representative patients. Three-dimensional computed tomographic angiographic volume renderings of the ascending aorta are provided in “candy-cane” view for each subgroup, with asterisks denoting the superior margin of the main pulmonary artery: (a) a control patient with a tricuspid aortic valve (TAV) and a ratio of greater to lesser curvature of 1.5; (b) a patient with aortic dilation and a nonstenotic TAV and a ratio of greater to lesser curvature of 1.7; (c) a control patient with a bicuspid aortic valve (BAV) and a ratio of greater to lesser curvature of 1.6; and (d) a patient with aortic dilation and a stenotic BAV and a ratio of greater to lesser curvature of 2. Bulging of the greater curvature is most pronounced in the patient with aortic dilation and a stenotic BAV (d) . AS, aortic stenosis.

Get Radiology Tree app to read full this article<

Statistical Analysis

Get Radiology Tree app to read full this article<

Results

Patient Characteristics

Get Radiology Tree app to read full this article<

Table 1

Patient Characteristics

Variable Control TAV Control BAV Dilated TAV, No AS Dilated TAV, AS Dilated BAV, No AS Dilated BAV, AS ( n = 25) ( n = 24) ( n = 25) ( n = 9) ( n = 15) ( n = 7) Age (y) 53.68 ± 17.425 34.4 ± 15.8 70.4 ± 9.46 67.6 ± 10.1 40.2 ± 15.0 42.4 ± 17.0 Men 11 (44%) 13 (54%) 17 (68%) 9 (100%) 14 (93%) 4 (57%) CTA 24 7 24 8 4 3 MRA 1 17 1 1 11 4 Aortic leaflet fusion Right to left – 17 – – 9 3 Unknown – 7 – – 6 4 Aortic stenosis None 25 15 25 0 15 0 Mild 0 6 0 0 0 3 Moderate/severe 0 3 0 9 0 4

AS, aortic stenosis; BAV, bicuspid aortic valve; CTA, computed tomographic angiography; MRA, magnetic resonance angiography; TAV, tricuspid aortic valve.

Data are expressed as mean ± standard deviation or as number (percentage).

Get Radiology Tree app to read full this article<

Orthogonal Aortic Diameters

Get Radiology Tree app to read full this article<

Figure 3, Graph of ascending aortic diameters measured at the aortic valve, sinuses of Valsalva, sinotubular junction, mid ascending aorta at the main pulmonary artery, and pre-arch for each of the patient subgroups. All patients with aortic dilation had significantly larger orthogonal diameters than controls, with one exception: no significant difference between diameters at the level of the aortic valve was found for the stenotic bicuspid aortic valve (BAV) group. AS, aortic stenosis; TAV, tricuspid aortic valve.

Get Radiology Tree app to read full this article<

Aortic Curvature Measurements

Get Radiology Tree app to read full this article<

Table 2

Ascending Aortic Curvature Measurements

Curvature Measurement Control TAV Control BAV Dilated TAV, No AS Dilated TAV, AS Dilated BAV, No AS Dilated BAV, AS Greater curvature (cm) 6.83 ± 1.06 6.73 ± 1.53 9.66 ± 1.02 10.2 ± 2.01 10.6 ± 1.48 10.4 ± 1.75 Lesser curvature (cm) 4.44 ± 0.737 4.39 ± 0.837 5.74 ± 0.692 5.22 ± 0.541 5.48 ± 0.988 5.03 ± 0.498 Greater/lesser ratio 1.55 ± 0.185 1.53 ± 0.210 1.69 ± 0.139 1.94 ± 0.270 1.96 ± 0.201 2.05 ± 0.155

AS, aortic stenosis; BAV, bicuspid aortic valve; TAV, tricuspid aortic valve.

Data are expressed as mean ± standard deviation.

Get Radiology Tree app to read full this article<

Get Radiology Tree app to read full this article<

Figure 4, Box-and-whisker plot of the ratio of greater to lesser curvatures for patients with aortic dilation. Patients with stenotic tricuspid aortic valves (TAVs) and both stenotic and nonstenotic bicuspid aortic valves (BAVs) had significantly greater ratios compared to those with nonstenotic TAVs ( P < .05). The horizontal gray line corresponds to the mean ratio of the nondilated controls, which was not significantly different from the nonstenotic TAV group ( P > .20) but was significantly smaller than the other three groups with aortic dilation ( P < .001). AS, aortic stenosis.

Get Radiology Tree app to read full this article<

Discussion

Get Radiology Tree app to read full this article<

Get Radiology Tree app to read full this article<

Get Radiology Tree app to read full this article<

Get Radiology Tree app to read full this article<

Get Radiology Tree app to read full this article<

Get Radiology Tree app to read full this article<

Conclusions

Get Radiology Tree app to read full this article<

References

  • 1. Ward C.: Clinical significance of the bicuspid aortic valve. Heart 2000; 83: pp. 81-85.

  • 2. Tzemos N., Therrien J., Yip J., et. al.: Outcomes in adults with bicuspid aortic valves. JAMA 2008; 300: pp. 1317-1325.

  • 3. Siddiqi H., Isselbacher E., Suzuki T., et. al.: Is size a good predictor of dissection risk in patients with Marfan syndrome or bicuspid aortic valves? Insights from the International Registry of Acute Aortic Dissection (IRAD). J Am Coll Cardiol 2012; 59: pp. E1883.

  • 4. Elefteriades J.A.: Thoracic aortic aneurysm: reading the enemy’s playbook. Curr Probl Cardiol 2008; 33: pp. 203-277.

  • 5. Keane M.G., Wiegers S.E., Plappert T., et. al.: Bicuspid aortic valves are associated with aortic dilatation out of proportion to coexistent valvular lesions. Circulation 2000; 102: pp. III35-III39.

  • 6. Hahn R.T., Roman M.J., Mogtader A.H., et. al.: Association of aortic dilation with regurgitant, stenotic and functionally normal bicuspid aortic valves. J Am Coll Cardiol 1992; 19: pp. 283-288.

  • 7. Bonderman D., Gharehbaghi-Schnell E., Wollenek G., et. al.: Mechanisms underlying aortic dilatation in congenital aortic valve malformation. Circulation 1999; 99: pp. 2138-2143.

  • 8. Fedak P.W., Verma S., David T.E., et. al.: Clinical and pathophysiological implications of a bicuspid aortic valve. Circulation 2002; 106: pp. 900-904.

  • 9. Niwa K., Perloff J.K., Bhuta S.M., et. al.: Structural abnormalities of great arterial walls in congenital heart disease: light and electron microscopic analyses. Circulation 2001; 103: pp. 393-400.

  • 10. Cecconi M., Manfrin M., Moraca A., et. al.: Aortic dimensions in patients with bicuspid aortic valve without significant valve dysfunction. Am J Cardiol 2005; 95: pp. 292-294.

  • 11. Kutty S., Kaul S., Danford C.J., et. al.: Main pulmonary artery dilation in association with congenital bicuspid aortic valve in the absence of pulmonary valve abnormality. Heart 2010; 96: pp. 1756-1761.

  • 12. Biner S., Rafique A.M., Ray I., et. al.: Aortopathy is prevalent in relatives of bicuspid aortic valve patients. J Am Coll Cardiol 2009; 53: pp. 2288-2295.

  • 13. Jackson V., Petrini J., Caidahl K., et. al.: Bicuspid aortic valve leaflet morphology in relation to aortic root morphology: a study of 300 patients undergoing open-heart surgery. Eur J Cardiothorac Surgery 2011; 40: pp. e118-e124.

  • 14. Fernandes S.M., Sanders S.P., Khairy P., et. al.: Morphology of bicuspid aortic valve in children and adolescents. J Am Coll Cardiol 2004; 44: pp. 1648-1651.

  • 15. Schaefer B.M., Lewin M.B., Stout K.K., et. al.: Usefulness of bicuspid aortic valve phenotype to predict elastic properties of the ascending aorta. Am J Cardiol 2007; 99: pp. 686-690.

  • 16. Bauer M., Gliech V., Siniawski H., et. al.: Configuration of the ascending aorta in patients with bicuspid and tricuspid aortic valve disease undergoing aortic valve replacement with or without reduction aortoplasty. J Heart Valve Dis 2006; 15: pp. 594-600.

  • 17. Cotrufo M., Della Corte A.: The association of bicuspid aortic valve disease with asymmetric dilatation of the tubular ascending aorta: identification of a definite syndrome. J Cardiovasc Med (Hagerstown) 2009; 10: pp. 291-297.

  • 18. Viscardi F., Vergara C., Antiga L., et. al.: Comparative finite element model analysis of ascending aortic flow in bicuspid and tricuspid aortic valve. Artif Organs 2010; 34: pp. 1114-1120.

  • 19. Wigstrom L., Sjoqvist L., Wranne B.: Temporally resolved 3D phase-contrast imaging. Magn Reson Med 1996; 36: pp. 800-803.

  • 20. Hope M.D., Hope T.A., Meadows A.K., et. al.: Bicuspid aortic valve: four-dimensional MR evaluation of ascending aortic systolic flow patterns. Radiology 2010; 255: pp. 53-61.

  • 21. Markl M., Draney M.T., Hope M.D., et. al.: Time-resolved 3-dimensional velocity mapping in the thoracic aorta: visualization of 3-directional blood flow patterns in healthy volunteers and patients. J Comput Assist Tomogr 2004; 28: pp. 459-468.

  • 22. den Reijer P.M., Sallee D., van der Velden P., et. al.: Hemodynamic predictors of aortic dilatation in bicuspid aortic valve by velocity-encoded cardiovascular magnetic resonance. J Cardiovasc Magn Reson 2010; 12: pp. 4.

  • 23. Hope M.D., Hope T.A., Crook S.E., et. al.: 4D flow CMR in assessment of valve-related ascending aortic disease. JACC Cardiovasc Imaging 2011; 4: pp. 781-787.

  • 24. Hope M.D., Wrenn J., Sigovan M., et. al.: Imaging biomarkers of aortic disease: increased growth rates with eccentric systolic flow. J Am Coll Cardiol 2012; 60: pp. 356-357.

  • 25. Webb R.W., Higgins C.B.: Thoracic Imaging.2005.Lippincott Williams & WilkinsPhiladelphia, PA

  • 26. Roman M.J., Devereux R.B., Kramer-Fox R., et. al.: Two-dimensional echocardiographic aortic root dimensions in normal children and adults. Am J Cardiol 1989; 64: pp. 507-512.

  • 27. Baumgartner H., Hung J., Bermejo J., et. al.: Echocardiographic assessment of valve stenosis: EAE/ASE recommendations for clinical practice. J Am Soc Echocardiogr 2009; 22: pp. 1-23.

  • 28. Hiratzka LF, Bakris GL, Beckman JA, et al. 2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM guidelines for the diagnosis and management of patients with thoracic aortic disease. A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, American Association for Thoracic Surgery, American College of Radiology, American Stroke Association, Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, Society of Interventional Radiology, Society of Thoracic Surgeons, and Society for Vascular Medicine. J Am Coll Cardiol;55:e27–e129.

  • 29. Bauer M., Siniawski H., Pasic M., et. al.: Different hemodynamic stress of the ascending aorta wall in patients with bicuspid and tricuspid aortic valve. J Card Surg 2006; 21: pp. 218-220.

  • 30. Della Corte A., Quarto C., Bancone C., et. al.: Spatiotemporal patterns of smooth muscle cell changes in ascending aortic dilatation with bicuspid and tricuspid aortic valve stenosis: focus on cell-matrix signaling. J Thorac Cardiovasc Surg 2008; 135: pp. 8-18.

  • 31. Fry D.L.: Certain histological and chemical responses of the vascular interface to acutely induced mechanical stress in the aorta of the dog. Circ Res 1969; 24: pp. 93-108.

  • 32. Slager C.J., Wentzel J.J., Gijsen F.J., et. al.: The role of shear stress in the destabilization of vulnerable plaques and related therapeutic implications. Nat Clin Pract Cardiovasc Med 2005; 2: pp. 456-464.

  • 33. Nistri S., Sorbo M.D., Marin M., et. al.: Aortic root dilatation in young men with normally functioning bicuspid aortic valves. Heart 1999; 82: pp. 19-22.

  • 34. Thanassoulis G., Yip J.W., Filion K., et. al.: Retrospective study to identify predictors of the presence and rapid progression of aortic dilatation in patients with bicuspid aortic valves. Nat Clin Pract Cardiovasc Med 2008; 5: pp. 821-828.

Academic Radiology, Volume 20, Issue 1
Journals General Radiology
This post is licensed under CC BY 4.0 by the author.
Recently Updated
Contents