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The Effect of Right Ventricular Hypertrophy on Left Ventricular Ejection Fraction in Pulmonary Emphysema

Anton Vonk Noordegraaf; Johan T. Marcus; Bea Roseboom; Pieter E. Postmus; Theo J. Faes; Peter M. de Vries
Author and Funding Information

Affiliations: From the Department of Pulmonary Medicine, Institute for Cardiovascular Research (ICAR-VU), University Hospital Vrije Universiteit, Amsterdam, The Netherlands,  From the Departments of Medical Physics and Informatics, Institute for Cardiovascular Research (ICAR-VU), University Hospital Vrije Universiteit, Amsterdam, The Netherlands

Affiliations: From the Department of Pulmonary Medicine, Institute for Cardiovascular Research (ICAR-VU), University Hospital Vrije Universiteit, Amsterdam, The Netherlands,  From the Departments of Medical Physics and Informatics, Institute for Cardiovascular Research (ICAR-VU), University Hospital Vrije Universiteit, Amsterdam, The Netherlands


1997 by the American College of Chest Physicians


Chest. 1997;112(3):640-645. doi:10.1378/chest.112.3.640
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Abstract

Study objective: The development of right ventricular (RV) hypertrophy in emphysema is accompanied by involvement of the left ventricle (LV) and its systolic function. Our objective was to study the relation between RV hypertrophy and LV ejection fraction in emphysema by means of MRI.

Patients: Ten emphysematous patients (FEV1, 0.99±0.32 L; FEV1/vital capacity (VC), 0.32±0.11 [mean±SD]) and 10 age-matched control subjects were included. Exclusion criteria were any history of systemic hypertension, ischemic or valvular heart disease, or episodes of right- and/or left-sided cardiac failure.

Measurements and results: Rapid scout imaging was used to measure RV and LV wall mass, wall thickness, and end-diastolic volume. Stroke volume was derived from the main pulmonary artery flow. RV wall volume, RV wall thickness, and the ratio of RV to LV wall thickness were significantly larger in the patient group than in the control group (p<0.01). Furthermore, patients had significantly lower values of LV ejection fraction (p<0.01) than the control subjects. A flattening or leftward displacement of the ventricular septum during systole was observed. In addition, our study showed an increase of LV ejection fraction proportional with the RV wall thickness (r=0.78, p<0.01) in severely emphysematous patients.

Conclusion: These data are in support of the hypothesis that flattening of the interventricular septum explains the relatively normal LV ejection fraction in emphysematous patients with severe RV hypertrophy.


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