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Paul R. Forfia, MD, FCCP
Author and Funding Information

From the Cardiovascular Division, Pulmonary Hypertension Program, University of Pennsylvania School of Medicine.

Correspondence to: Paul R. Forfia, MD, FCCP, Cardiovascular Division, Pulmonary Hypertension Program, University of Pennsylvania School of Medicine, 3400 Civic Center Blvd, Perelman Center, 2 E Philadelphia, PA 19104; e-mail: paul.forfia@uphs.upenn.edu


Financial/nonfinancial disclosures: The author has reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).


© 2011 American College of Chest Physicians


Chest. 2011;140(2):557-558. doi:10.1378/chest.11-0292
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To the Editor:

First, I would like to thank Dr Kind and colleagues for their comments and questions regarding our recent article in CHEST.1 I have great respect for their work. Our study set out to determine the proportion of total right ventricular (RV) contraction accounted for by transverse (RV free wall to septum) and longitudinal (RV base to apex) shortening in normal subjects and patients with incident pulmonary arterial hypertension (PAH), and in patients with PAH following pulmonary hypertension (PH)-specific therapy.

We chose RV fractional area change (RVFAC) as the metric of global RV function for two reasons: (1) RVFAC is a well-established method of determining global RV function by two-dimensional (2-D) echocardiography in patients with normal hearts and PH and (2) RVFAC is, in essence, what the clinician is visualizing on 2-D echocardiography in practice. Using this approach, we were able to objectify the relative proportion of both components of RV contraction and also to learn how much the “eye” must account for longitudinal contraction when trying to appreciate global RV function by 2-D echocardiography. As such, we hoped that our study would have scientific as well as practical value.

The findings of Kind et al2 are somewhat at odds with ours. However, it is challenging to directly compare the results of these studies, given that their imaging modality was cardiac MRI and they used a volume-based (RV ejection fraction) measure of RV function as their reference metric of RV function. Previous work has shown that longitudinal RV function closely relates to cardiac stroke volume in PAH at baseline and in response to epoprostenol infusion.3,4 Is it possible that the better relationship between RV transverse shortening and RV ejection fraction in their study was driven by a close relationship between transverse RV shortening and RV end-diastolic volume? It would be interesting to see how well both transverse and longitudinal shortening correlated with cardiac stroke volume in their data set.

I agree that the large surface-volume ratio of the RV free wall leads to higher volume ejected per lesser absolute free-wall excursion. However, it is also true that normal global RV systolic function typically requires preservation of both transverse and longitudinal shortening. It is plausible that, because of inherent limitations in RV free-wall imaging by 2-D echocardiography, it is less able to resolve the differences in transverse wall motion over a small absolute distance. In contrast, measures of longitudinal RV function are not typically subject to these limitations.5 Thus, by 2-D echocardiography, it may be that well-visualized longitudinal shortening parameters are preferable to less well-visualized measures of transverse RV free-wall motion.

Although we reported a larger absolute transverse area change in subjects with PAH vs normal subjects, this occurred in the context of an RV end-diastolic area that was nearly 70% larger. We also found that the contribution of transverse contraction was higher in subjects with PAH (pretherapy) vs subjects with normal hearts, which, at least qualitatively, parallels the findings of Kind et al.2 In response to PH-specific therapy, however, we observed a relatively selective improvement in longitudinal function and a change in the RV contractile pattern to one more similar to that of normal hearts. These results suggest that the RV contractile pattern is dynamic and that serial assessment of longitudinal RV function is rational.

Overall, I agree that both transverse and longitudinal shortening of the right ventricle are important contributors to RV function, and, in fact, they may work in concert. Rushmer6 hypothesized that base-to-apex shortening of the right ventricle serves to lengthen circumferentially oriented RV muscle fibers, thus aiding in transverse shortening. My suspicion is that the relative contribution of longitudinal and transverse shortening to overall RV function varies with RV loading conditions and the degree of hypertrophy vs dilatation, as well as the perspective provided by different methods of RV imaging.

Brown SB, Raina A, Katz D, Szerlip M, Wiegers SE, Forfia PR. Longitudinal shortening accounts for the majority of right ventricular contraction and improves after pulmonary vasodilator therapy in normal subjects and patients with pulmonary arterial hypertension. Chest. 2011;1401:27-33. [CrossRef] [PubMed]
 
Kind T, Mauritz GJ, Marcus JT, van de Veerdonk M, Westerhof N, Vonk-Noordegraaf A. Right ventricular ejection fraction is better reflected by transverse rather than longitudinal wall motion in pulmonary hypertension. J Cardiovasc Magn Reson. 2010;12:35. [CrossRef] [PubMed]
 
Forfia PR, Fisher MR, Mathai SC, et al. Tricuspid annular displacement predicts survival in pulmonary hypertension. Am J Respir Crit Care Med. 2006;1749:1034-1041. [CrossRef] [PubMed]
 
Urheim S, Cauduro S, Frantz R, et al. Relation of tissue displacement and strain to invasively determined right ventricular stroke volume. Am J Cardiol. 2005;968:1173-1178. [CrossRef] [PubMed]
 
Lamia B, Teboul JL, Monnet X, Richard C, Chemla D. Relationship between the tricuspid annular plane systolic excursion and right and left ventricular function in critically ill patients. Intensive Care Med. 2007;3312:2143-2149. [CrossRef] [PubMed]
 
Rushmer RF. Cardiovascular Dynamics. 1976;4th ed Philadelphia, PA WB Saunders Company
 

Figures

Tables

References

Brown SB, Raina A, Katz D, Szerlip M, Wiegers SE, Forfia PR. Longitudinal shortening accounts for the majority of right ventricular contraction and improves after pulmonary vasodilator therapy in normal subjects and patients with pulmonary arterial hypertension. Chest. 2011;1401:27-33. [CrossRef] [PubMed]
 
Kind T, Mauritz GJ, Marcus JT, van de Veerdonk M, Westerhof N, Vonk-Noordegraaf A. Right ventricular ejection fraction is better reflected by transverse rather than longitudinal wall motion in pulmonary hypertension. J Cardiovasc Magn Reson. 2010;12:35. [CrossRef] [PubMed]
 
Forfia PR, Fisher MR, Mathai SC, et al. Tricuspid annular displacement predicts survival in pulmonary hypertension. Am J Respir Crit Care Med. 2006;1749:1034-1041. [CrossRef] [PubMed]
 
Urheim S, Cauduro S, Frantz R, et al. Relation of tissue displacement and strain to invasively determined right ventricular stroke volume. Am J Cardiol. 2005;968:1173-1178. [CrossRef] [PubMed]
 
Lamia B, Teboul JL, Monnet X, Richard C, Chemla D. Relationship between the tricuspid annular plane systolic excursion and right and left ventricular function in critically ill patients. Intensive Care Med. 2007;3312:2143-2149. [CrossRef] [PubMed]
 
Rushmer RF. Cardiovascular Dynamics. 1976;4th ed Philadelphia, PA WB Saunders Company
 
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