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Original Research: CARDIOVASCULAR DISEASE |

Ventilatory Inefficiency Reflects Right Ventricular Dysfunction in Systolic Heart Failure

Amanda B. Methvin, MD; Anjali T. Owens, MD; Anthony G. Emmi, RCS; Michael Allen, RN; Susan E. Wiegers, MD; Daniel L. Dries, MD; Kenneth B. Margulies, MD; Paul R. Forfia, MD, FCCP
Author and Funding Information

From the Cardiovascular Division, Heart Failure/Transplant and Pulmonary Hypertension Programs (Drs Methvin, Owens, Dries, Margulies, and Forfia, and Mr Allen) and the Echocardiography Laboratory (Mr Emmi and Dr Wiegers), University of Pennsylvania School of Medicine, Philadelphia, PA.

Correspondence to: Paul R. Forfia, MD, FCCP, Cardiovascular Division, Heart Failure/Transplant, and Pulmonary Hypertension Programs, Perelman Center for Advanced Medicine, Heart and Vascular Center, 2 E Pavilion, Philadelphia, PA 19104; e-mail: paul.forfia@uphs.upenn.edu


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;139(3):617-625. doi:10.1378/chest.10-0318
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Background:  An increased minute ventilation (V˙ e)/carbon dioxide production (Vco2) relationship, an expression of ventilatory inefficiency (VI), is associated with increased morbidity and mortality in patients with left ventricular systolic dysfunction (LVSD). A direct link between VI and a specific cardiac abnormality has not been established.

Methods:  We analyzed cardiopulmonary exercise test (CPET) data from patients (N = 83) with severe LVSD (ischemic and nonischemic; left ventricular ejection fraction [LVEF] 19% ± 7%) and at least moderate exercise intolerance. Subjects were stratified into two groups based on the (V˙ e/Vco2 ratio at anaerobic threshold (V˙ e/Vco2@AT) (group 1 V˙ e/Vco2@AT ≤ 34; group 2 V˙ e/Vco2@AT > 34). Clinical, CPET, echocardiographic, and hemodynamic data were compared between groups.

Results:  Group 2 subjects had lower exercise capacity (peak (V˙ o2, 45.7% ± 11.8% vs 50.4 ± 8.9% predicted; P < .05), with a significantly lower oxygen pulse (71.6% ± 24.5% vs 85.4 ± 18.5% predicted) and maximum systolic BP (122 ± 19 mm Hg vs 138 ± 22 mm Hg; P < .001 for both), suggesting a more blunted stroke volume to exercise vs group 1. There were no differences in left ventricular (LV) size, LVEF, or mitral regurgitation between the two groups. In sharp contrast, group 2 had larger right ventricular (RV) dimensions (4.5 ± 1.1 cm vs 3.9 ± 0.8 cm) and more severe RV systolic dysfunction (RV fractional area change 26% ± 11% vs 33% ± 12%; tricuspid annular plane systolic excursion [TAPSE] 1.6 ± 0.5 cm vs 2.0 ± 0.5 cm; all P < .001) vs group 1. Multivariable analysis revealed that only TAPSE and Doppler-estimated pulmonary artery systolic pressure were independently associated with V˙ e/Vco2@AT and the (V˙ e/Vco2slope. The V˙ e/Vco2@AT, V˙ e/Vco2 slope, and TAPSE had nearly identical predictive value for death or transplant.

Conclusions:  The present study suggests that VI is a functional, noninvasive marker of more advanced right-sided heart dysfunction in patients with severe LVSD.

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