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© The European Society of Cardiology 2007. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Magnetic resonance and nuclear imaging of the right ventricle in pulmonary arterial hypertension

Anton Vonk-Noordegraaf1,*, Jan-Willem Lankhaar1,3, Marco J.W. Götte2, J. Tim Marcus3, Pieter E. Postmus1 and Nico Westerhof1,4

1 Department of Pulmonary Diseases, Institute for Cardiovascular Research, VU University Medical Center, De Boelelaan 1117, 1081 HV Amsterdam, The Netherlands
2 Department of Cardiology, Institute for Cardiovascular Research, VU University Medical Center, Amsterdam, The Netherlands
3 Department of Physics and Medical Technology, Institute for Cardiovascular Research, VU University Medical Center, Amsterdam, The Netherlands
4 Department of Physiology, Institute for Cardiovascular Research, VU University Medical Center, Amsterdam, The Netherlands

* Corresponding author. Tel: +31 20 44 47 82; fax: +31 20 44 43 28. E-mail address: a.vonk{at}vumc.nl


   Abstract
Top
 Abstract
Introduction
 Quantification of right...
 Right ventricular flow...
 Right ventricular function and...
 Right ventricular wall and...
 Concluding remarks
 References
 
Many clinicians have recognized the unique possibilities of magnetic resonance imaging (MRI) for the study of right ventricular (RV) anatomy. Especially for the assessment of the RV in pulmonary hypertension, MRI has been proven to be of clinical importance. It is, however, less well known that if MRI measures of volume and flow are combined with pressure measurements, accurate description of RV function in relation to its afterload is possible. Furthermore, nuclear imaging techniques offer the opportunity to study the altered RV metabolism and to elucidate the possible contribution of ischaemia to RV failure in pulmonary hypertension. Since RV failure in pulmonary hypertension is the result of the complex interaction between geometry, structure, function, perfusion, and metabolism, MRI and nuclear imaging are promising techniques to study these mechanisms and to evaluate the effects of therapy aimed at improving RV function in pulmonary hypertension.

Key Words: Ventricular structure • Ventricular function • Perfusion • PET • SPECT • Delayed-contrast enhancement


   Introduction
Top
 Abstract
 Introduction
Quantification of right...
 Right ventricular flow...
 Right ventricular function and...
 Right ventricular wall and...
 Concluding remarks
 References
 
Pulmonary arterial hypertension (PAH) is a disease characterized by increased pulmonary vascular resistance (PVR), resulting in right ventricular (RV) pressure overload, and RV hypertrophy to compensate for the increased wall stress. Other adaptations compromising RV function include RV and atrial dilatation, tricuspid regurgitation, and in severe cases, prominent leftward displacement of the interventricular septum (septal bowing) during early diastole.1

Accurate assessment of RV structure and function in patients with PAH is essential for two reasons. First, direct visualization of the site of the disease in PAH patients, the arteriolar wall, is currently not possible in patients. Therapeutic effects can thus only be monitored indirectly by studying RV function and (non-invasive) estimates of pulmonary artery resistance. Second, the primary cause of death in PAH patients is RV failure. However, the mechanisms of RV failure are currently poorly understood and can only be unravelled if the complex interaction between altered structure and function of the RV and the pivotal role of myocardial perfusion and metabolism on these parameters can be elucidated.

Magnetic resonance imaging (MRI) and nuclear imaging techniques offer the possibility to study the effects of treatment on the RV in detail. In addition, both techniques will allow the determination of the role of the different factors contributing to RV failure, and subsequently to develop new therapeutic strategies.

This article provides an overview of the latest developments in MRI and nuclear imaging techniques that are aimed at getting an integral picture of RV structure, function, and metabolism in PAH.


   Quantification of right ventricular geometry and mass
Top
 Abstract
 Introduction
 Quantification of right...
Right ventricular flow...
 Right ventricular function and...
 Right ventricular wall and...
 Concluding remarks
 References
 
In the early years of MRI, it was already recognized that this technique allows us to measure the RV volume accurately.2–4 Initially, the accuracy of global RV volume and function measurements was verified using water-filled latex balloons and ventricular casts of excised bovine hearts.4 Using a stack of ECG-triggered transverse images encompassing the RV and central pulmonary arteries, it was demonstrated that the severity of RV hypertrophy was in proportion to the elevated pulmonary artery pressure. Nowadays, short-axis images are often used in daily clinical practice for the quantification of RV volume. The principle of MRI measurement of RV volume and mass is demonstrated in Figure 1, which also shows the consecutive steps to be taken in the planning of the stack of short-axis cines in order to measure RV mass and volume.


Figure 1
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  		Figure 1 Consecutive steps in the planning of the stack of short-axis cines. (A) Coronal view, (B) transversal view, (C) vertical long-axis view, and (D) short-axis view. The white lines indicate the projection lines used for planning the next step in localizing. The line on the coronal view defines the transversal view, and similarly the next views are obtained. Signs of PAH are enlarged right atrium [(A) and (B)] and pulmonary artery (A), leftward ventricular septal bowing [(A), (B), and (D)], and increased pericardial fluid [(B) and (D)].

 
In recent years, temporal and spatial resolutions have further improved, allowing more accurate quantification of global function of both the left ventricle and RV, and the complex interaction between both ventricles in pulmonary hypertension.5 Only in the late 1990s, reference values for RV were published.6,7

Owing to these technical improvements, assessment of RV mass and volume in chronic obstructive pulmonary disease (COPD) patients, difficult to study with echocardiography, became feasible.8 The accuracy of MRI in this patient group was demonstrated by Calverley et al.,9 showing that RV mass measured by MRI-acquired pre-mortem in COPD patients corresponds with findings obtained during post-mortem studies.

The value of a single MR derived parameter measured at a single time point is limited.10 For example, increased RV mass reflects increased RV afterload on the one hand –undesirable in itself– and normal adaptation to this afterload on the other. Furthermore, although RV mass is related to pulmonary arterial pressure,11,12 this sole parameter does not reveal whether the RV is adapted to the increased afterload or not. Also, a dilated RV may reflect normal adaptation to volume overload (e.g. in portopulmonary arterial hypertension) or it may reflect RV failure.

In contrast, assessing the changes of these structural parameters over time provides a tool to monitor therapy. An increase in RV end-diastolic volume and/or reduction in stroke volume measured by MRI, has been shown to strongly predict a poor prognosis.9a Several studies have demonstrated the ability of MRI to assess the effects of PAH therapy on the RV.13–15 In these studies, increased RV stroke volume and decreased mass were associated with improvement in symptoms and 6-minutes walking distance.

The SERAPH study,16 a randomized study on the different effects of bosentan and sildenafil, demonstrated that MRI-derived parameters have the potential to be used as primary end-points for the comparison of treatments. The study demonstrated that sildenafil, in contrast to bosentan, reduces the RV mass. This finding is interesting because it underlines that MR provides additional insights above the functional parameters currently used to evaluate the efficacy of medication. Furthermore, it is interesting because it confirms the finding that most of the PAH medication currently used not only acts on the pulmonary vasculature, but also has an intrinsic effect on the cardiac myocytes. Detailed studies of RV function in patients under treatment are necessary to elucidate these effects.


   Right ventricular flow quantification
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 Abstract
 Introduction
 Quantification of right...
 Right ventricular flow...
Right ventricular function and...
 Right ventricular wall and...
 Concluding remarks
 References
 
Velocity-encoded cine MRI (Figure 2) provides an accurate and reproducible tool for the quantification of pulmonary artery flow and lung perfusion.17–21 In 1992, Kondo et al.22 described the application of this technique in PAH patients for the first time. It was found that, in comparison to controls, flow acceleration time and distensibility of the pulmonary artery were decreased in patients with primary PAH. Similar observations were made in studies that used Doppler echocardiography for measuring velocity flow.23


Figure 2
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  		Figure 2 Magnetic resonance phase-contrast flow quantification in the main pulmonary artery. (A) Planning on the RV outflow tract cine. (B) Magnitude image. (C) Velocity-encoded image. Signs of PAH are hypertrophic RV (A) and enlarged pulmonary artery (all images).

 
The major advantage of MRI volumetric flow measurements is that a precise quantification of the effective forward stroke volume of both the right and left ventricle is possible. Whereas thermodilution and the Fick method may be inaccurate in the presence of an intra-cardiac shunt, which is often the case in patients with PAH because of a patent foramen ovale or underlying congenital heart disease, MRI provides an excellent tool to quantify right and left stroke volume and to calculate the shunt fraction. This approach was validated and further improved by Beerbaum et al.19,20 showing that right-to-left and left-to-right intra-cardiac shunts in children with congenital heart disease can be measured accurately in <60 s. This technique offers a new way to monitor treatment efficacy in children and adults with PAH secondary to congenital heart disease, since a decrease in right-to-left or an increase in left-to-right shunt reflects improved pulmonary haemodynamics.

By combining MRI-measured flow with pulmonary artery pressure, accurate estimations of PVR can be made. In a group of 24 patients with either suspected PAH or congenital heart disease, it was shown that this approach is feasible and valid.24 A limitation of this method remains that still a right-heart catheterization is required and that for simultaneous measurements an interventional (X-)MRI suite together with a special catheterization set must be used. For these reasons, it is unlikely that this type of measurement will be performed routinely in the near future.

A more attractive idea is the estimation of pulmonary pressure and vascular resistance from the volume–flow curve. Several attempts have been made to accomplish this.23,25,26 However, a validation study performed at our institute showed that all of these approaches fail to estimate pulmonary arterial pressure with sufficient accuracy.12


   Right ventricular function and afterload
Top
 Abstract
 Introduction
 Quantification of right...
 Right ventricular flow...
 Right ventricular function and...
Right ventricular wall and...
 Concluding remarks
 References
 
The most common description of RV systolic function is the ejection fraction based on volumetric assessment. Diastolic function of the RV can be estimated by end-diastolic volume and can be approximated by isovolumic relaxation time.27 Both parameters can be derived from MRI or SPECT (single photon emission computed tomography) equilibrium radionuclide angiography of the RV.27 Since the influence of afterload on these functional parameters is considerable, they have to be interpreted with care. An accurate description of RV afterload is therefore required.

Magnetic resonance imaging is a promising method to arrive at a better description of RV function and afterload if used together with pressure measurements. The most complete description of ventricular afterload is arterial input impedance, which can be obtained from spectral analysis of pressure and flow.29–31 The impedance spectrum represents both the resistance (i.e. impedance, modulus, the amplitude ratio) and phase delay of the sinusoidal components of blood pressure and flow. The impedance at zero frequency represents PVR. Impedance thus gives a comprehensive description of steady and pulsatile afterload. Although physiologists have been familiar with the impedance concept for a long time, and its clinical relevance has been acknowledged,29,30,32–34 clinical application has been hampered by the requirement of measurement of instantaneous pulmonary pressure and flow at the same time.

Alternatively, ventricular afterload can be quantified using lumped models,35,36 i.e. models in which all spatial information is accumulated in a limited number of parameters. Recently, we have shown that it is possible to detect differences between three patient groups with a three-element windkessel model using the MR flow signal as an input signal.37 As was in our study, MRI may be a crucial tool in the translation of the physiological concepts into clinical practice, because it allows accurate quantification of instantaneous blood flow in the pulmonary artery, non-invasively.38 Especially, with the advent of MRI scanners in the catheterization laboratory,39–41 pressure and flow can be measured simultaneously, which will enable advanced haemodynamic characterization of individual patients in clinical practice. Since these scanners are not yet available on a wide scale, some assumptions should be made about the stationarity of the haemodynamic state of the patient if flow and pressure measurement are performed in a more conventional setting.37

In a similar way, insight can be obtained in RV function by combining RV volume measures and pressure. Although not applied in patients with pulmonary hypertension yet, measurements in animals with increased afterload have shown the feasibility of this concept.42 Since it has recently been shown that patients exercising in an MR scanner is a feasible technique, these concepts might also be applicable during exercise.43


   Right ventricular wall and coronary perfusion
Top
 Abstract
 Introduction
 Quantification of right...
 Right ventricular flow...
 Right ventricular function and...
 Right ventricular wall and...
Concluding remarks
 References
 
Little attention has been paid to RV ischaemia in relation to RV function in PAH. From animal studies it is known that RV coronary perfusion, and especially the systolic part, is impeded in pulmonary hypertension.44 In addition, nuclear techniques have shown that the RV metabolic need is proportionally increased with RV afterload measures45 and can be reduced during treatment.46 Although RV myocardial infarction in patients with PAH is rare, ongoing ischaemia (stunning) might be present in patients with PAH. Using stress myocardial scintigraphy, Gomez et al.47 showed that nine of the 23 PAH patients examined had images consistent with RV ischaemia. In addition, they found a significant correlation between RV ischaemia obtained through myocardial perfusion scintigraphy and haemodynamic measures of RV failure, underlining the possible contributing role of ischaemia to RV failure.

A second factor that may contribute to impaired RV function is the deposition of collagen in the RV myocardium. A recent study by Blyth et al.48 showed the potential of MRI to identify such regions in the RV myocardial wall of patients with pulmonary hypertension. Interestingly, delayed-contrast enhancement (DCE) was confined to the RV insertion points in seven patients and extended to the interventricular septum in the remaining 16 patients (Figure 3). In these 16 patients, the septal-contrast enhancement was associated with interventricular septal bowing. This finding suggests a mechanical factor such as increased wall stress, which may contribute to the occurrence of fibrosis. The extent of contrast enhancement correlated positively with mean pulmonary artery pressure and PVR, and correlated inversely with RV ejection fraction.


Figure 3
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  		Figure 3 Delayed-contrast enhancement in a scleroderma patient with pulmonary hypertension. This figure shows extensive delayed-contrast enhancement at the insertion points.

 
Although considerable forces acting on the RV insertion points may explain the DCE at these points, the DCE in the septum is less clear. Since it is known from the left ventricle that DCE may occur in ischaemic regions, it is conceivable that ischaemia might also explain the septal DCE in pulmonary hypertension. Indeed, Nelson et al.49 showed in an animal model of pulmonary hypertension that increased mechanic compression of the septum might impede septal blood flow and provoke ischaemia. This also illustrates that combined imaging modalities may provide new insight in RV failure in pulmonary hypertension.


   Concluding remarks
Top
 Abstract
 Introduction
 Quantification of right...
 Right ventricular flow...
 Right ventricular function and...
 Right ventricular wall and...
 Concluding remarks
References
 
Although much attention has been paid to the development of effective treatments directed to reverse pulmonary vascular remodelling, less attention has been paid to the RV. Given the central role that RV failure plays in PAH and the fact that most of PAH patients die because of RV failure, a search for a better treatment of RV failure is warranted. Both MRI and nuclear techniques are promising candidates to help in this quest. MRI not only offers the possibility to measure accurately RV structure and function and its relation with changes in the pulmonary vasculature, but also provides information on morphological changes of the RV wall and coronary blood flow. In addition, although the clinical role of MRI has not been defined yet, the clinical advantage of MRI for monitoring PAH patients has been recognized by many clinicians. Combining volumetric and flow measurements with pressure measurements will lead to an improved description of RV function and its afterload. Although nuclear techniques have not been frequently used for studying RV failure, lessons learned from the left ventricle—especially with respect to perfusion and metabolism—suggest that this modality may play an important role in the near future.

Conflict of interest: none declared.


   References
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 Abstract
 Introduction
 Quantification of right...
 Right ventricular flow...
 Right ventricular function and...
 Right ventricular wall and...
 Concluding remarks
 References
 

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