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Original Research: PULMONARY VASCULAR DISEASE |

Longitudinal Shortening Accounts for the Majority of Right Ventricular Contraction and Improves After Pulmonary Vasodilator Therapy in Normal Subjects and Patients With Pulmonary Arterial HypertensionLongitudinal Shortening and the Right Ventricle

Suzanne B. Brown, MD; Amresh Raina, MD; David Katz, MD; Molly Szerlip, MD; Susan E. Wiegers, MD; Paul R. Forfia, MD, FCCP
Author and Funding Information

From the Division of Cardiology (Drs Brown, Raina, Wiegers, and Forfia), Hospital of the University of Pennsylvania, Philadelphia, PA; Division of Cardiology (Dr Katz), University of Colorado, Aurora, CO; and the Division of Cardiology (Dr Szerlip), University of Arizona, Tucson, AZ.

Correspondence to: Paul R. Forfia, MD, FCCP, Hospital of the University of Pennsylvania, Penn Heart and Vascular Center, Perelman Center-2nd Floor, E Pavilion, 3400 Civic Center Blvd, Philadelphia, PA 19104; e-mail: paul.forfia@uphs.upenn.edu


Funding/Support: The authors have reported to CHEST that no funding was received for this study.

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(1):27-33. doi:10.1378/chest.10-1136
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Background:  The right ventricle has a unique contraction pattern, with a greater portion of the shortening occurring in the longitudinal plane. However, the relative contributions of longitudinal and transverse shortening to overall right ventricular (RV) function have not been quantified. We sought to quantify the proportions of longitudinal and transverse shortening to RV function in normal subjects and in patients with pulmonary arterial hypertension (PAH) at baseline and following PAH-specific therapy.

Methods:  The normal cohort comprised 90 subjects with normal clinical echocardiograms, whereas the PAH cohort included 36 patients, of whom 25 had echocardiograms before and after initiation of PAH-specific therapy. Assessment of RV function included tricuspid annular plane systolic excursion, RV fractional area change (RVFAC), and relative change in RV area in longitudinal and transverse planes.

Results:  Longitudinal fractional area change (LFAC) accounted for the majority of total RVFAC (77% ± 14%) in normal subjects. Among patients with PAH, longitudinal shortening still represented the majority of RVFAC, even though it was less than in normal subjects (63% ± 18%, P < .0001). Following PAH therapy, overall RV function improved (RVFAC, 30% ± 13% to 36% ± 9%; P = .026), solely because of an increase in longitudinal area change. As a result, the proportion of longitudinal shortening increased (LFAC, 58% ± 18% to 69% ± 17%; P = .002), whereas transverse shortening fell (transverse fractional area change, 42% ± 18% vs 31% ± 17%; P = .002).

Conclusions:  Longitudinal shortening accounts for the majority of RV contraction in normal subjects and patients with PAH, although less so in PAH. Improved RV function following pulmonary vasodilator therapy occurs solely from improvements in longitudinal contraction, suggesting that longitudinal shortening may represent the afterload-responsive element of RV functional recovery.

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