Published online before print September 27, 2004, doi: 10.1161/01.CIR.0000143138.02493.DD
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(Circulation. 2004;110:2010-2016.)
© 2004 American Heart Association, Inc.
Imaging |
Magnetic Resonance Imaging Analysis of Right Ventricular Pressure-Volume Loops
In Vivo Validation and Clinical Application in Patients With Pulmonary Hypertension
From the Departments and Divisions of Congenital Heart Diseases and Pediatric Cardiology (T.K., S.Y., P.E., I.S.-N., P.L.) and Cardiology (M.G., E.F., E.N.), German Heart Institute, Berlin, Germany; Cardiology, Leiden University Medical Center, Leiden, Germany (P.S.); and Pediatric Cardiology (P.M.) and Radiology (M.S., O.W., C.B.H.), University of California, San Francisco.
Correspondence to Titus Kuehne, MD, Department of Congenital Heart Diseases and Pediatric Cardiology, German Heart Institute, Augustenburger Platz 1, Berlin 13353 Germany. E-mail titus.k{at}t-online.de
Received February 29, 2004; de novo received April 20, 2004; accepted June 17, 2004.
Background— The aims of this study were to validate MRI-derived right ventricular (RV) pressure-volume loops for assessment of RV myocardial contractility and then to apply this technique in patients with chronic RV pressure overload for assessment of myocardial contractility, ventricular pump function, and VA coupling.
Methods and Results— Flow-directed catheters were guided under MR fluoroscopy (1.5 T) into the RV for invasive pressure measurements. Simultaneously, ventricular volumes and myocardial mass were assessed from cine MRI. From sampled data, RV pressure-volume loops were constructed, and maximal ventricular elastance indexed to myocardial mass (Emax_i) was derived by use of a single-beat estimation method. This MRI method was first validated in vivo (6 swine), with conductance techniques used as reference. Bland-Altman test showed good agreement between methods (Emax_i=5.1±0.5 versus 5.8±0.7 mm Hg · mL–1 · 100 g–1, respectively; P=0.08). Subsequently, the MRI method was applied in 12 subjects: 6 control subjects and 6 patients with chronic RV pressure overload from pulmonary hypertension. In these patients, indexes of RV pump function (cardiac index), Emax_i, and VA coupling (Emax/Ea) were assessed. In patients with pulmonary hypertension, RV pump function was decreased (cardiac index, 2.2±0.5 versus 2.9±0.4 L · min–1 · m–2; P<0.01), myocardial contractility was enhanced (Emax_I, 9.2±1.1 versus 5.0±0.9 mm Hg · mL–1 · 100 g–1; P<0.01), and VA coupling was inefficient (Emax/Ea, 1.1±0.3 versus 1.9±0.4; P<0.01) compared with control subjects.
Conclusions— RV myocardial contractility can be determined from MRI-derived pressure-volume loops. Chronic RV pressure overload was associated with reduced RV pump function despite enhanced RV myocardial contractility. The proposed MRI approach is a promising tool to assess RV contractility in the clinical setting.
Key Words: heart defects, congenital • hypertension, pulmonary • magnetic resonance imaging • myocardial contraction • ventricles
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