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Published online before print October 2, 2003, 10.1148/radiol.2292020559
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Real-Time MR Imaging of Aortic Flow: Influence of Breathing on Left Ventricular Stroke Volume in Chronic Obstructive Pulmonary Disease1

Rik J. van den Hout, MD{dagger}, Hildo J. Lamb, PhD, Joost G. van den Aardweg, MD, Robert Schot, BSc, Paul Steendijk, PhD, Ernst E. van der Wall, MD, Jeroen J. Bax, MD and Albert de Roos, MD

1 From the Departments of Radiology (R.J.v.d.H., H.J.L., E.E.v.d.W., A.d.R.), Pulmonology (J.G.v.d.A., R.S.), and Cardiology (P.S., J.J.B.), Leiden University Medical Center, Albinusdreef 2, 2333 ZA Leiden, the Netherlands. From the 2001 RSNA scientific assembly. Received May 15, 2002; revision requested July 15; final revision received February 12, 2003; accepted March 28. Address correspondence to H.J.L. (e-mail: H.J.Lamb@lumc.nl).



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Figure 1. Diagram illustrates the sequence of hemodynamic events during inspiration. Interaction between intrathoracic pressure (Pthor) and right (RV) and left (LV) ventricle is shown. For clarity, atria are not depicted. In the following explanation of the sequence, -> = leads to, {downarrow} = decrease, and {uparrow} = increase. Inspiration -> intrathoracic pressure {downarrow}-> gradient with extrathoracic pressure {uparrow}-> inferior vena cava (VCI) flow {uparrow}-> right ventricular filling volume and pressure (P&V) {uparrow}-> right ventricular SV {uparrow}-> aortic pulmonary flow (A. PULM) {uparrow}-> blood pooling in lungs because of increased vascular capacity -> ventricular pulmonary flow (V. PULM) {downarrow}-> left ventricular filling volume and pressure {downarrow}-> left ventricular SV {downarrow}-> aortic flow {downarrow}. Note that increased right ventricular filling also causes shifting of the interventricular septum toward the left ventricle, compromising left ventricular filling and contraction. Note that during expiration the opposite occurs and left ventricular SV {uparrow}.

 


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Figure 2. Images in a healthy 25-year-old man. A, Modulus and phase images of real-time MR flow imaging in the ascending aorta are displayed and resulted in the corresponding flow peak, as illustrated. B, Simultaneous real-time recording of flow in the ascending aorta. C, Breathing curve (gray line) and SV curve (black line with data points). Calculated SVs for all flow peaks result in the SV curve. SV acceleration (SVacc) and SV deceleration (SVdec) are indicated with dotted black lines. These lines demonstrate the mean slope of the ascending and descending curve. a.u. = arbitrary units. D, Electrocardiographic signal.

 


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Figure 3. Graphs of typical breathing maneuvers performed by the same subject as in Figure 2. Gray line represents the breathing curve. Black line is the SV curve, with each data point representing an SV value. Dotted horizontal line represents mean SV. This value does not differ between normal and deep breathing. a.u. = arbitrary units. A, Normal breathing. Note that SV increases with expiration and decreases with inspiration. B, Deep breathing. Note the exaggerated effect of an SV increase with expiration and an SV decrease with inspiration. C, Valsalva maneuver. Note a sudden increase in SV followed by a slow decrease in SV.

 


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Figure 4. Graph shows correlation between thoracic excursion (inspiration or expiration) and SV during normal breathing in the same subject as in Figure 2. Each data point represents an SV value. Note that SV decreases from end-expiration toward end-inspiration (r2 = 0.77, P < .05). For the whole group, mean r2 = 0.78 ± 0.09. a.u. = arbitrary units.

 


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Figure 5. Graph shows SV curves of the same subject as in Figure 2 and of a 69-year-old man with COPD obtained during spontaneous breathing. Curve obtained in patient with COPD is in all aspects at a lower level, the range between minimal and maximal SV is wider (compare gray areas), and the acceleration-deceleration ratio of SV is higher as compared with values in the healthy subject. For all healthy subjects, mean SV range is 13.1 mL ± 2.7, and for the patients with COPD, the range is 19.5 mL ± 5.6 (P < .05). The acceleration-deceleration ratio is 1.0 ± 0.5 in healthy subjects and 1.8 ± 0.6 in patients with COPD. SVacc = SV acceleration, SVdec = SV deceleration.

 


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Figure 6. Graph shows comparison of all SV parameters as a result of normal breathing in both healthy subjects and patients with COPD. COPD causes a decrease of minimal, maximal, and mean SV (P < .05). Note the increase in SV range and acceleration-deceleration ratio in patients with COPD as compared with values in healthy subjects (P < .05). * = P < .05, unpaired two-tailed Student t test, comparison between healthy subjects and patients with COPD.

 





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