doi: 10.1161/CIRCULATIONAHA.107.704460
(Circulation. 2007;116:e336-e337.)
© 2007 American Heart Association, Inc.
Images in Cardiovascular Medicine |
Sclerotic Aortic Valve
Flow-Sensitive 4-Dimensional Magnetic Resonance Imaging Reveals 3 Distinct Flow-Pattern Changes
From the Departments of Diagnostic Radiology, Medical Physics (M.M., M.L., J.H., A.F.), Neurology and Clinical Neurophysiology (A.H.), and Cardiology and Angiology (D.F.), University Hospital, Albert-Ludwigs-University, Freiburg, Germany.
Correspondence to Dr M. Markl, University Hospital Freiburg, Department of Diagnostic Radiology. Medical Physics, Hugstetter Straße 55, 79106 Freiburg, Germany. E-mail michael.markl{at}uniklinik-freiburg.de
We present findings in a 67-year-old male patient who was examined during diagnostic workup because of arrhythmia and pulmonary vein ablation. During transthoracic and transesophageal echocardiography, a nonstenotic, sclerosed aortic valve with slightly reduced area (1.7 cm2) and mild aortic regurgitation were observed. Standard contrast-enhanced magnetic resonance angiography was performed for arterial and venous status.
To evaluate the effect of altered valve function on blood flow in the entire aorta, flow-sensitive 4-dimensional magnetic resonance imaging was performed. Data were acquired with cardiac and navigator gating to permit ECG synchronized measurement of 3-directional blood flow in the entire thoracic aorta during free breathing (Magnetom Trio, Siemens, Erlangen, Germany; flip angle =15°, velocity sensitivity =150 cm/s, spatial resolution 3.2x2.1x3.0 mm3, time to echo =3.5 ms, repetition time=5.6 ms, temporal resolution =48.8 ms). Data analysis was performed with a commercially available software package (EnSight, CEI, Apex, NC). Visual evaluation of the resulting 3-dimensional (3D) anatomic and blood flow images was based on the calculation of time-resolved 3D particle traces, which depicted the spatial and temporal evolution of blood flow as traces along the paths of virtual particles released within measured blood flow velocities.1
Compared with the evolution of normal systolic and early diastolic blood flow in a healthy volunteer (Figure 1), 3D blood flow visualization for the patient (Figure 2) demonstrated 3 distinct flow-pattern changes: locally constrained and accelerated early systolic outflow, reversed and considerably enhanced helical outflow patterns, and an early onset of markedly increased helical retrograde flow (online Data Supplement, Movie I).
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In contrast to normal flow characteristics, early systolic outflow in the patient with the sclerosed and regurgitant valve followed a distinct and isolated flow channel along the outer curvature of the ascending aorta, with substantially accelerated flow velocities (red traces). The flow channel reached its maximum extent during peak systole, as indicated by the open white arrows in Figure 2C.
In addition, the formation of considerable systolic left-handed helical outflow throughout the entire ascending aorta can clearly be appreciated in Figure 2B through 2F. For clarity, a helical flow path was illustrated by the curved arrow in Figure 2D. Note that helix formation in the patient is markedly increased and even rotationally reversed compared with the typically observed mild right-handed outflow helix in volunteers, as illustrated by the magnified particle traces in Figure 1D.
Moreover, during late systole and early diastole, the early formation of an inner retrograde flow pattern was observed. The progression of a central helical flow channel originating from the distal aorta (Figure 2D) into the proximal ascending aorta is indicated by the solid white arrows in Figure 2D through 2K.
These flow characteristics in the patient demonstrate that drastic hemodynamic changes can be associated with relatively minor changes in valve geometry and function. Such alterations may lead to changes in strength and variation of shear forces along the aortic wall that may offer an explanation for vascular remodeling and aneurysm formation, which is often observed as a secondary morphological alteration in patients with aortic valve disease.2–4
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Disclosure |
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Dr Markl is supported by research grant MA 2383/3-1 from Deutsche Forschungsgemeinschaft. The other authors report no conflicts.
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Footnotes |
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The online-only Data Supplement, consisting of a movie, is available with this article at http://circ.ahajournals.org/cgi/content/full/CIRCULATIONAHA.107.704460/DC1.
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References |
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1. Markl M, Harloff A, Bley TA, Zaitsev M, Jung B, Weigang E, Langer M, Hennig J, Frydrychowicz A Time-resolved 3D MR velocity mapping at 3T: improved navigator-gated assessment of vascular anatomy and blood flow. J Magn Reson Imaging. 2007; 25: 824–831.[CrossRef][Medline] [Order article via Infotrieve]
2. Glagov S, Weisenberg E, Zarins CK, Stankunavicius R, Kolettis GJ. Compensatory enlargement of human atherosclerotic coronary arteries. N Engl J Med. 1987; 316: 1371–1375.[Abstract]
3. Langille BL, O’Donnell F. Reductions in arterial diameter produced by chronic decreases in blood flow are endothelium-dependent. Science. 1986; 231: 405–407.
4. Cheng C, Tempel D, van Haperen R, van der Baan A, Grosveld F, Daemen MJ, Krams R, de Crom R. Atherosclerotic lesion size and vulnerability are determined by patterns of fluid shear stress. Circulation. 2006; 113: 2744–2753.
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