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DOI: 10.1148/radiol.2431060067
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(Radiology 2007;243:63-69.)
© RSNA, 2007

Cardiac Imaging

Pulmonary Hypertension: Accuracy of Detection with Left Ventricular Septal-to–Free Wall Curvature Ratio Measured at Cardiac MR1

Santo Dellegrottaglie, MD, Javier Sanz, MD, Michael Poon, MD, Juan F. Viles-Gonzalez, MD, Roxana Sulica, MD, Martin Goyenechea, MD, Frank Macaluso, RT, Valentin Fuster, MD, PhD and Sanjay Rajagopalan, MD

1 From the Zena and Michael A. Wiener Cardiovascular Institute and the Marie-Josée and Henry R. Kravis Center for Cardiovascular Health, Mount Sinai Medical Center, New York, NY (S.D., J.S., M.P., J.F.V., R.S., M.G., F.M., V.F., S.R.); and Division of Cardiovascular Medicine, CT/MR Imaging Program, Ohio State University, 473 W 12th Ave, Columbia, OH 43210 (S.R.). Received January 13, 2006; revision requested March 10; revision received April 11; accepted May 17; final version accepted August 4. Supported in part by the Mount Sinai School of Medicine Consortium for Cardiovascular Imaging Technology, New York, NY. S.D. supported by a research grant from the Italian Society of Cardiology. J.S. supported by a research grant from the Spanish Society of Cardiology. Address correspondence to S.R. (e-mail: Sanjay.Rajagopalan{at}osumc.edu).


   ABSTRACT
TOP
 ABSTRACT
MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 ADVANCE IN KNOWLEDGE
 References
 
Purpose: To retrospectively evaluate the accuracy and reproducibility of the cardiac magnetic resonance (MR) imaging–derived left ventricular septal-to–free wall curvature ratio for prediction of the right ventricular systolic pressure (RVSP) in patients clinically known to have or suspected of having pulmonary hypertension (PH), with same-day right-side heart catheterization (RHC) as the reference standard.

Materials and Methods: Institutional review board approval was received for this HIPAA-compliant study. Sixty-one patients clinically known or suspected of having PH underwent cardiac MR and RHC on the same day. Interventricular septal curvature (CIVS) and left ventricular free wall curvature (CFW) measured at end systole were used to derive the curvature ratio (CIVS/CFW). Effective distending transmural pressure (dPFW) and transseptal pressure gradient (dPIVS) were assumed to be equivalent, respectively, to the systolic blood pressure (SBP) and the difference between SBP and RVSP. Curvature ratio and SBP were used to noninvasively estimate RVSP. Linear regression analysis was performed to assess the difference between curvature ratio and rate of pressure rise (dP) ratio (dPIVS/dPFW). The accuracy of the dichotomized curvature ratio in PH detection was analyzed by using receiver operating characteristic (ROC) curves.

Results: PH, defined as RVSP higher than 40 mm Hg, was confirmed with RHC in 46 patients. A direct linear correlation between dP ratio and curvature ratio was observed (r = 0.85, P < .001). Bland-Altman analysis revealed moderate agreement between cardiac MR– and RHC-derived RVSPs (mean difference, –1.1 mm Hg ± 15.9 [standard deviation]). ROC analysis of the accuracy of the curvature ratio for detection of increased RVSP revealed 87% sensitivity and 100% specificity (area under ROC curve, 0.95; P < .001). Intraobserver (r = 0.97) and interobserver (r = 0.95) curvature ratio measurements were closely correlated.

Conclusion: In patients clinically known to have or suspected of having PH, cardiac MR–derived curvature ratio, as compared with RHC measurement, was an accurate and reproducible index for estimation of RVSP.

© RSNA, 2007

Noninvasive estimation of the right ventricular systolic pressure (RVSP) performed by measuring the tricuspid regurgitation peak velocity at Doppler echocardiography enables accurate prediction of the pulmonary artery systolic pressure derived by using invasive methods (1,2). This method has been applied for many years to noninvasively determine the presence and magnitude of pulmonary hypertension (PH). However, the clinical feasibility of this technique may be substantially affected by several conditions, such as absence of a detectable jet of tricuspid regurgitation, limited acoustic window, and advanced lung disease (3,4).

Cardiac magnetic resonance (MR) imaging is considered the reference-standard modality for evaluation of biventricular size, geometry, and function, as it reportedly enables imaging of cardiac structures with superb delineation of the endocardial border (5,6). This strength of cardiac MR can be applied potentially to derive quantitative hemodynamic information by means of evaluation of left ventricular (LV) geometric deformation secondary to PH.

In previous studies involving the use of echocardiography or cardiac MR, the distortion of the LV cavity observed in patients with PH has been quantified by measuring the interventricular septal (IVS) curvature (CIVS) or the curvature ratio (ie, CIVS/CFW, where CFW is the LV free wall curvature) (7–11). During the cardiac cycle, the position of the IVS is primarily determined by the difference in pressure between the LV and the right ventricle—that is, the transseptal pressure gradient (11,12). Similarly, the configuration of the LV free wall is determined by the difference between the LV pressure and the surrounding pressure—that is, the effective distending transmural pressure (13). Patients with PH may have a substantially reduced transseptal pressure gradient, which may lead to the frequently observed flattening (or bowing) of the IVS (12,14). According to the Laplace law (15), wall stress is proportional to the rate of pressure rise (dP) divided by the product of wall thickness times curvature, and this relationship may be independently applied to derive wall stress information across the IVS and the free wall. In the absence of asymmetric hypertrophy, the wall stress in the IVS and in the free wall may be assumed to be similar; thus, any change in the dP ratio (ie, transseptal pressure gradient divided by effective distending transmural pressure) should affect the curvature ratio proportionally (16). By assuming a minimal influence of external (pericardial) pressure across the LV in systole, one can then apply a simplified method to measure the dP ratio.

Reisner et al (17) previously proposed using the curvature ratio as a noninvasive index for predicting the RVSP. However, the diagnostic accuracy of this method in identifying patients with abnormal RVSP values, as compared with that of invasive measurement at right-side heart catheterization (RHC), has not been validated. Thus, the aim of the present study was to retrospectively evaluate the accuracy and reproducibility of the cardiac MR imaging–derived left ventricular septal-to–free wall curvature ratio in the prediction of RVSP in patients clinically known to have or suspected of having PH, with same-day RHC as the reference standard.


   MATERIALS AND METHODS
TOP
 ABSTRACT
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 ADVANCE IN KNOWLEDGE
 References
 
Patients
This retrospective study was approved by the institutional review board of Mount Sinai Medical Center and Health Insurance Portability and Accountability Act compliant; the requirement for informed consent was waived. Between January 2003 and July 2004, a total of 77 patients who were referred for evaluation of clinically known or suspected PH were examined with cardiac MR and RHC on the same day. In all patients, the cardiac MR and invasive measurements were obtained within 2 hours of each other. Six patients were excluded because of breathing artifacts that substantially affected cardiac MR image quality. Other reasons for exclusion were regional LV wall motion abnormalities (n = 5), asymmetric LV hypertrophy (n = 4), and history of cardiopulmonary surgery (n = 1). Thus, the study sample consisted of 61 patients aged 24–88 years (mean, 53 years ± 15 [standard deviation]) and included a larger proportion of women (n = 53 [88%]) (Fig 1). All included patients had a normal sinus rhythm and had no contraindications to cardiac MR imaging.


Figure 1
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  		Figure 1: Flow diagram illustrates the process leading to selection of the final study group from the initial population of patients known to have or suspected of having PH. All enrolled patients underwent cardiac MR imaging (CMR) followed on the same day by RHC, the reference standard for measurement of pulmonary and intracardiac pressures.

 
Cardiac MR Protocol
Cardiac MR imaging was performed by using a 1.5-T unit (Magnetom Sonata; Siemens Medical Systems, Erlangen, Germany) with a multielement phased-array surface coil. The examinations began with the acquisition of survey chest images in the three orthogonal planes (transverse, coronal, and sagittal) to localize the heart and obtain breath-hold localizer images in the two-chamber short-axis view and finally in the four-chamber view in succession. By using the four-chamber view, a series of parallel short-axis image planes (encompassing the entire LV from the base to the apex) were defined, and images were acquired during short breath holds by using a retrospective electrocardiographically gated steady-state free precession sequence. Cine images were acquired by using 3.2/1.6 (repetition time msec/echo time msec), a high flip angle (60°–90°), an 8-mm section thickness, a matrix of 256 x 166 (typical), a minimal field of view (typical), a spatial resolution of 1.7 x 1.4 mm (typical), an acquired temporal resolution of 33–45 msec, 11–15 segments, 20–25 reconstructed cardiac phases (reconstructed by using view sharing when required), and a bandwidth of 900–1000 Hz/pixel. Cardiac MR examination was successfully completed in all patients.

RHC Procedure
At completion of the cardiac MR examination, each patient was transferred to the cardiac catheterization laboratory. All RHC procedures were performed by an experienced team familiar with patients who have PH (M.P., R.S., 7 and 4 years experience, respectively, performing RHC in patients with PH) and unaware of the patients' cardiac MR results. In all patients, RHC was performed with fluoroscopic guidance through the right internal jugular vein by using a four-lumen thermodilution catheter and a multiparameter monitor. The following pressures were measured: RVSP, pulmonary artery systolic pressure, pulmonary artery mean pressure (MP), and pulmonary capillary wedge pressure (WP). Cardiac output (CO) was estimated from the mean of three thermodilution curves (created after rapid injection of 10 mL of cool saline), and the cardiac index was computed by dividing the mean cardiac output by the patient's body surface area. Pulmonary vascular resistance (PVR, in Wood units) was subsequently calculated by using the formula PVR = (MP – WP)/CO. At the time of RHC, the systemic systolic blood pressure (SBP) was also measured noninvasively. All patients completed the RHC procedure without incurring complications. For the purpose of this study, the diagnosis of PH was defined as an RVSP higher than 40 mm Hg.

Image Analysis
Cine cardiac MR images were downloaded to an off-line workstation (Leonardo; Siemens Medical Solutions) for analysis. In each patient, the depicted LV was divided into three equal portions (basal, middle, and apical) by using two lines orthogonal to the LV long axis. Measurements of LV cavity deformation were performed on the cine-loop images (in the short-axis series) corresponding to the middle level of the basal segments of the LV. By using this image series, measurements of LV geometry were performed on the image corresponding to the smallest LV area, which was considered to be representative of the end-systolic frame.

Several parameters were used to derive the RVSP noninvasively (Table 1). The radius of the CIVS and the radius of the CFW were measured by using the method originally described by Brinker et al (18) (Fig 2). A circle (ie, "circumcircle") passes through each of the three vertices of a triangle. Thus, when three points are defined, the radius of the subtended arc segment can be geometrically determined: Two chords, each spanning separate parts of the same arc segment, can be drawn, and the lines orthogonal to these chords define the center, or circumcenter, of a circle described by the arc segment (19). This method was applied to the selected image to calculate the end-systolic radii of the CIVS and CFW (Fig 2). The end-systolic CIVS (1 divided by radius of CIVS) and CFW (1 divided by radius of CFW) were subsequently derived. The curvature ratio was calculated as CIVS/CFW. In previous studies, the curvature ratio has been approximately 1 in healthy subjects (in whom CIVS and CFW are similar) and significantly decreased in patients with PH (in whom CIVS is reduced compared with CFW) (17,20).


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  		Table 1. Methods Used to Derive Geometric and Hemodynamic Parameters

 

Figure 2
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  		Figure 2: Curvature calculation. Two points—junction 1 (J1) and junction 2 (J2)—are initially positioned at the junctions between the IVS and the free wall. Two additional points are then marked in the middle portion of IVS (M1) and the free wall (M2). By considering J1, J2, and M1, the radius of the CIVS (RIVS) is derived by applying the three-point circle method (see Materials and Methods). J1, J2, and M2 are used similarly to derive the radius of the CFW (RFW).

 
All curvature ratio measurements were performed by a reader (S.D., 1 year of cardiac MR experience) blinded to the patient identities. To assess the inter- and intraobserver reproducibility of the curvature ratio measurements, more than 3 months after the first reading, 15 (25%) imaging studies randomly selected from the total sample were separately reexamined by the first reader (S.D.) and a second independent blinded observer (J.F.V., 1 year of cardiac MR experience). The readers performed the measurements in the patients after completing training in the specific analysis required for the study, under the supervision of J.S. (3 years cardiac MR experience) and with use of a separate series of cardiac MR images with normal and abnormal findings.

Statistical Analyses
SPSS, version 12.0 (SPSS, Chicago, Ill), and MedCalc, version 8.0.0.1 (MedCalc Software, Mariakerke, Belgium), software programs were used for statistical computations. Linear regression analysis of the relationship between curvature ratio and dP ratio was performed, and Pearson correlation coefficients were obtained. A regression equation in which the dP ratio was modeled by using the curvature ratio was derived. By using this equation, the RVSP was computed in each patient (by including the actual curvature ratio and SBP values), and a plot of these values compared with RHC-derived RVSPs was generated by using Bland-Altman analysis. By using receiver operating characteristic curves, a dichotomized curvature ratio was analyzed for accuracy in the detection of PH. A logistic model was generated, and a cutoff curvature ratio value with balanced sensitivity and specificity was derived to predict elevated RVSP (>40 mm Hg).

Confidence intervals for sensitivity and specificity were calculated by using the exact binomial method. Intra- and interobserver agreement was assessed by using linear regression and Bland-Altman analyses. Power analysis of the sample size (61 patients) was conducted by using SAS, version 9.1 (SAS Institute, Cary, NC), statistical software.


   RESULTS
TOP
 ABSTRACT
 MATERIALS AND METHODS
 RESULTS
DISCUSSION
 ADVANCE IN KNOWLEDGE
 References
 
RHC measurement confirmed the diagnosis of PH in 46 (75%) of the 61 patients (Table 2) (21). The hemodynamic measurements obtained at RHC in the study patients are given in Table 3.


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  		Table 2. Final Diagnoses in Study Population

 

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  		Table 3. Hemodynamic Measurements Obtained at RHC in 61 Patients

 
Correlation between Curvature Ratio and dP Ratio
Linear regression analysis of the relationship between curvature ratio (RC) and dP ratio (RdP) revealed good correlation (r = 0.85; 95% confidence interval: 0.78, 0.92; P < .001) in the total patient group (Fig 3). The equation derived from the linear regression was RC = (1.03 · RdP) + 0.01. Thus, by taking into account that the dP ratio can be simplified as (SBP – RVSP)/SBP, an estimation of the RVSP might be obtained by using the formula RVSP = SBP · [1 – (RC/1.03)].


Figure 3
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  		Figure 3: Scatterplot shows direct correlation between curvature ratio (C-Ratio) and dP ratio. bullet = patients with PH, {blacktriangleup} = patients without PH. SEE = standard error of estimate.

 
There was a progressive increase in LV cavity deformation in the patients with elevated RVSP, as revealed by the curvature ratio reduction on the cardiac MR images (Fig 4). With Bland-Altman analysis, the measurements derived from the above equation for RVSP showed satisfactory limits of agreement with the RVSP values obtained invasively at RHC (Fig 5); the mean difference in values was –1.1 mm Hg ± 15.9 (standard deviation).


Figure 4
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  		Figure 4: End-systolic short-axis cine cardiac MR images (3.2/1.6, 60° flip angle) show that compared with the curvature ratio (C-Ratio) value in a person with a normal RVSP (A), proportional reductions in curvature ratio are associated with abnormal increases in RVSP (B and C).

 

Figure 5
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  		Figure 5: Bland-Altman plot shows satisfactory levels of agreement between cardiac MR (CMR) and RHC measurements of RVSP. SD = standard deviation.

 
The area under the receiver operating characteristic curve for curvature ratio in the detection of PH was 0.95 (Fig 6). A cutoff curvature ratio of 0.67 yielded the best balanced sensitivity (87% [40 of 46 patients]; 95% confidence interval: 74%, 95%) and specificity (100% [15 of 15 patients]; 95% CI: 78%, 100%) for detection of an RVSP higher than 40 mm Hg.


Figure 6
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  		Figure 6: Receiver operating characteristic curve shows the curvature ratio (C-ratio) to have good diagnostic accuracy in the prediction of PH (RVSP > 40 mm Hg). AUC = area under receiver operating characteristic curve.

 
Reproducibility of Curvature Ratio Measurements
Intraobserver (r = 0.97, standard error of estimate = 0.08, P < .001) and interobserver (r = 0.95, standard error of estimate = 0.09, P < .001) measurements of curvature ratio were closely correlated. At Bland-Altman analysis, the mean difference in curvature ratio measurements between the two readers was –0.09 ± 0.08. The mean intraobserver difference in curvature ratio measurements was within –0.04 ± 0.07.


   DISCUSSION
TOP
 ABSTRACT
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
ADVANCE IN KNOWLEDGE
 References
 
In this study, we measured curvature ratio at cardiac MR imaging as a direct index of LV cavity deformation in a group of patients known to have or suspected of having PH. By using RHC findings obtained on the same day that MR imaging was performed as the reference standard, we demonstrated that cardiac MR–derived curvature ratio measurements are accurate and reproducible in the prediction of RVSP. Our data show a clear direct correlation between curvature ratio and dP ratio (r = 0.85), and a formula for the noninvasive calculation of RVSP was derived: RVSP = SBP · [1 – (RC/1.03)]. This calculation represents a simple method of measuring RVSP noninvasively from the known SBP and curvature ratio.

In our study, the curvature ratio enabled prediction of the presence of PH with high sensitivity and specificity (87% and 100%, respectively), but the concordance of curvature ratio measurements with invasive measures was not excellent. However, we should consider that the study group included individuals with PH of different etiologies (consistent with real-world conditions) and that the cardiac MR and invasive assessments were performed on the same day but not simultaneously. (Changes in hemodynamic conditions during the 2-hour interval cannot be excluded.) In addition, numerous other uncontrollable variables (eg, conditions inherent to cardiac MR image acquisition at end expiration, and administration of sedatives in some claustrophobic patients before cardiac MR) probably play a role in reducing the concordance between the pressure values obtained with the two modalities.

As a direct consequence of the complex ventricular interdependence, IVS flattening is frequently observed in patients with right ventricular pressure overload (7,20,22). Earlier studies were performed to determine the relationships between transmural gradients and LV cavity shape. In the "unloaded" human heart, the IVS has a flat configuration and its normal concave shape is due to a left-to-right positive transseptal pressure gradient (11). In patients with PH, the right ventricular pressure overload causes a decrease in the transseptal pressure gradient, which is associated with IVS flattening (or bowing) (12,14).

The observed linear relationship between dP ratio and curvature ratio was not surprising and may be readily explained on the basis of the Laplace law (15). During systole, the shape of the LV is influenced to some extent by wall contraction but to a large extent is a reflection of transmural gradients. By using a simplified model for LV geometry and postulating the homogeneity of wall stress, one can discern that there is a direct relationship between dP ratio and curvature ratio.

In conjunction with the eccentricity index (obtained by determining the ratio between the two orthogonal short-axis diameters of the LV), the CIVS and the curvature ratio have been the most frequently used parameters to quantify the deformation of the LV cavity profile (23–26). Roeleveld et al (10) recently observed a significant correlation between maximal CIVS and pulmonary artery systolic pressure measurements obtained invasively and within the same week in 39 adults who were suspected of having PH and underwent cardiac MR imaging. Moreover, a clear correlation between systolic CIVS and transseptal pressure gradient has been reported in studies of echocardiography performed in children with congenital heart disease (14,20).

By using echocardiography, Reisner et al (17) demonstrated that the RVSP could be noninvasively derived by using the curvature ratio as a measure of the degree of LV cavity deformation. In their study, the RVSP was derived noninvasively at Doppler echocardiography and a strong correlation between echocardiographically derived curvature ratio and dP ratio was reported. Our study findings obtained at cardiac MR imaging are a direct extension of findings from Reisner et al (17) and validate (with RHC) a method of deriving RVSP from curvature ratio measurements.

We acknowledge several limitations of this study. First and foremost, assumptions were made in the calculation of LV wall stress forces in the free wall and IVS. In the absence of asymmetric LV hypertrophy, the degree of forces may be similar, but they may not be equivalent. The effective distending transmural pressure was estimated with the assumption that the pressure surrounding the right ventricle in systole is negligible. This may not be the case in all patients, and increased values of the surrounding pressure have been documented in patients with right-sided heart failure (27). LV systolic pressure was estimated from the SBP, and this simplification may not be applicable to patients with concurrent aortic valve disease. In addition, relevant valvular diseases cause LV systolic and/or diastolic overload, which may result in changes in the LV geometry.

The cardiac MR image frame with the smallest LV area was used to measure end-systolic values of LV cavity deformation (7,28), but this frame may not correspond to actual end systole in all patients. To ensure a clinically applicable approach, alternative ways of identifying end systole (the time frame corresponding to the aortic valve closure or the maximal CFW value), although potentially more accurate, were excluded because they were not considered to be feasible (aortic valve closure cannot be identified on the short-axis images used for analysis) or were excessively time consuming (with calculation of CFW in each image frame) (9,17). These assumptions and the associated simplifications of the formulas may have contributed to some of the discordance observed between the cardiac MR– and RHC-derived RVSP measurements.

An additional limitation was related to the inherent selection bias due to the exclusion of patients with regional LV wall motion abnormalities, asymmetric LV hypertrophy, and/or a history of cardiopulmonary surgery in an effort to eliminate potential confounding variables that may have affected the relationship between transmural pressure gradient and LV cavity configuration. As a consequence, our conclusions cannot be extended to patients with these characteristics.

Finally, in this study, PH was defined by using a cutoff RVSP higher than 40 mm Hg. There is some debate in the literature as to what cutoff RVSP value defines PH. As with other continuous variables, with RVSP there may not be a strict cutoff value: A number of healthy patients have pressures of between 30 and 40 mm Hg. Prior studies conducted with large numbers of patients have revealed that up to 28% of subjects with normal echocardiographic findings have estimated RVSPs higher than 30 mm Hg (29,30).

In conclusion, our study results demonstrate that in patients clinically known to have or suspected of having PH, the curvature ratio measured at cardiac MR imaging, as compared with the RHC measurement, is an accurate and reproducible index for estimation of the RVSP. Further studies, including head-to-head comparisons between cardiac MR imaging and Doppler echocardiography, are needed to identify the advantages and disadvantages of these two techniques in the estimation of pulmonary pressures.


   ADVANCE IN KNOWLEDGE
TOP
 ABSTRACT
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 ADVANCE IN KNOWLEDGE
References
 


   ACKNOWLEDGMENTS
 
We gratefully acknowledge Mbabazi Kariisa, MA, of the Cardiovascular Institute, Mount Sinai Medical Center, for her excellent statistical assistance.


   FOOTNOTES
 

Abbreviations: CFW = LV free wall curvature • CIVS = IVS curvature • dP = rate of pressure rise • IVS = interventricular septum • LV = left ventricle • PH = pulmonary hypertension • RHC = right-side heart catheterization • RVSP = right ventricular systolic pressure • SBP = systolic blood pressure

Authors stated no financial relationship to disclose.

Author contributions: Guarantor of integrity of entire study, S.D.; study concepts/study design or data acquisition or data analysis/interpretation, all authors; manuscript drafting or manuscript revision for important intellectual content, all authors; manuscript final version approval, all authors; literature research, S.D., J.S., J.F.V., M.G.; clinical studies, S.D., J.S., M.P., R.S., F.M.; statistical analysis, S.D., J.F.V., S.R.; and manuscript editing, S.D., J.S., M.G., V.F., S.R.


   References
TOP
 ABSTRACT
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 ADVANCE IN KNOWLEDGE
 References
 

  1. Yock PG, Popp RL. Noninvasive estimation of right ventricular systolic pressure by Doppler ultrasound in patients with tricuspid regurgitation. Circulation 1984;70:657–662.[Abstract/Free Full Text]
  2. Currie PJ, Seward JB, Chan KL, et al. Continuous wave Doppler determination of right ventricular pressure: a simultaneous Doppler-catheterization study in 127 patients. J Am Coll Cardiol 1985;6:750–756.[Abstract]
  3. Berger M, Haimowitz A, Van Tosh A, Berdoff RL, Goldberg E. Quantitative assessment of pulmonary hypertension in patients with tricuspid regurgitation using continuous wave Doppler ultrasound. J Am Coll Cardiol 1985;6:359–365.[Abstract]
  4. Arcasoy SM, Christie JD, Ferrari VA, et al. Echocardiographic assessment of pulmonary hypertension in patients with advanced lung disease. Am J Respir Crit Care Med 2003;167:735–740.[Abstract/Free Full Text]
  5. Constantine G, Shan K, Flamm SD, Sivananthan MU. Role of MRI in clinical cardiology. Lancet 2004;363:2162–2171.[CrossRef][Medline]
  6. Pennell DJ, Sechtem UP, Higgins CB, et al. Clinical indications for cardiovascular magnetic resonance (CMR): consensus panel report. Eur Heart J 2004;25:1940–1965.[Free Full Text]
  7. Dong SJ, Crawley AP, MacGregor JH, et al. Regional left ventricular systolic function in relation to the cavity geometry in patients with chronic right ventricular pressure overload: a three-dimensional tagged magnetic resonance imaging study. Circulation 1995;91:2359–2370.[Abstract/Free Full Text]
  8. Marcus JT, Vonk Noordegraaf A, Roeleveld RJ, et al. Impaired left ventricular filling due to right ventricular pressure overload in primary pulmonary hypertension: noninvasive monitoring using MRI. Chest 2001;119:1761–1765.[CrossRef][Medline]
  9. Giorgi B, Mollet NR, Dymarkowski S, Rademakers FE, Bogaert J. Clinically suspected constrictive pericarditis: MR imaging assessment of ventricular septal motion and configuration in patients and healthy subjects. Radiology 2003;228:417–424.[Abstract/Free Full Text]
  10. Roeleveld RJ, Marcus JT, Faes TJ, et al. Interventricular septal configuration at MR imaging and pulmonary arterial pressure in pulmonary hypertension. Radiology 2005;234:710–717.[Abstract/Free Full Text]
  11. Lima JA, Guzman PA, Yin FC, et al. Septal geometry in the unloaded living human heart. Circulation 1986;74:463–468.[Abstract/Free Full Text]
  12. Jessup M, Sutton MS, Weber KT, Janicki JS. The effect of chronic pulmonary hypertension on left ventricular size, function, and interventricular septal motion. Am Heart J 1987;113:1114–1122.[CrossRef][Medline]
  13. Belenkie I, Smith ER, Tyberg JV. Ventricular interaction: from bench to bedside. Ann Med 2001;33:236–241.[Medline]
  14. King ME, Braun H, Goldblatt A, Liberthson R, Weyman AE. Interventricular septal configuration as a predictor of right ventricular systolic hypertension in children: a cross-sectional echocardiographic study. Circulation 1983;68:68–75.[Abstract/Free Full Text]
  15. Yin FC. Ventricular wall stress. Circ Res 1981;49:829–842.[Free Full Text]
  16. Nakatani S, White RD, Powell KA, Lever HM, Thomas JD. Dynamic magnetic resonance imaging assessment of the effect of ventricular wall curvature on regional function in hypertrophic cardiomyopathy. Am J Cardiol 1996;77:618–622.[CrossRef][Medline]
  17. Reisner SA, Azzam Z, Halmann M, et al. Septal/free wall curvature ratio: a noninvasive index of pulmonary arterial pressure. J Am Soc Echocardiogr 1994;7:27–35.[Medline]
  18. Brinker JA, Weiss JL, Lappe DL, et al. Leftward septal displacement during right ventricular loading in man. Circulation 1980;61:626–633.[Free Full Text]
  19. Pedoe D. Circles: a mathematical view. Washington, DC: Mathematical Association of America, 1995; 22–27.
  20. Agata Y, Hiraishi S, Misawa H, Takanashi S, Yashiro K. Two-dimensional echocardiographic determinants of interventricular septal configurations in right or left ventricular overload. Am Heart J 1985;110:819–825.[CrossRef][Medline]
  21. Simonneau G, Galie N, Rubin LJ, et al. Clinical classification of pulmonary hypertension. J Am Coll Cardiol 2004;43(12 suppl S):5S–12S.[Abstract/Free Full Text]
  22. Louie EK, Lin SS, Reynertson SI, Brundage BH, Levitsky S, Rich S. Pressure and volume loading of the right ventricle have opposite effects on left ventricular ejection fraction. Circulation 1995;92:819–824.[Abstract/Free Full Text]
  23. Schreiber TL, Feigenbaum H, Weyman AE. Effect of atrial septal defect repair on left ventricular geometry and degree of mitral valve prolapse. Circulation 1980;61:888–896.[Abstract/Free Full Text]
  24. Ryan T, Petrovic O, Dillon JC, Feigenbaum H, Conley MJ, Armstrong WF. An echocardiographic index for separation of right ventricular volume and pressure overload. J Am Coll Cardiol 1985;5:918–927.[Abstract]
  25. Feneley M, Gavaghan T. Paradoxical and pseudoparadoxical interventricular septal motion in patients with right ventricular volume overload. Circulation 1986;74:230–238.[Abstract/Free Full Text]
  26. Hinderliter AL, Willis PW 4th, Barst RJ, et al. Effects of long-term infusion of prostacyclin (epoprostenol) on echocardiographic measures of right ventricular structure and function in primary pulmonary hypertension: Primary Pulmonary Hypertension Study Group. Circulation 1997;95:1479–1486.[Abstract/Free Full Text]
  27. Baker AE, Dani R, Smith ER, Tyberg JV, Belenkie I. Quantitative assessment of independent contributions of pericardium and septum to direct ventricular interaction. Am J Physiol 1998;275(2 pt 2):H476–H483.[Medline]
  28. Walker RE, Moran AM, Gauvreau K, Colan SD. Evidence of adverse ventricular interdependence in patients with atrial septal defects. Am J Cardiol 2004;93:1374–1377, A6.[CrossRef][Medline]
  29. Moraes DL, Colucci WS, Givertz MM. Secondary pulmonary hypertension in chronic heart failure: the role of the endothelium in pathophysiology and management. Circulation 2000;102:1718–1723.[Abstract/Free Full Text]
  30. McQuillan BM, Picard MH, Leavitt M, Weyman AE. Clinical correlates and reference intervals for pulmonary artery systolic pressure among echocardiographically normal subjects. Circulation 2001;104:2797–2802.[Abstract/Free Full Text]




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