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Research Article Free access | 10.1172/JCI105803

Left ventricular function in patients with chronic obstructive pulmonary disease

John F. Williams Jr., Richard H. Childress, Daniel L. Boyd, Lawrence M. Higgs, and Roy H. Behnke

Medical Service, Veterans Administration Hospital and the Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana 46202

Find articles by Williams, J. in: PubMed | Google Scholar

Medical Service, Veterans Administration Hospital and the Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana 46202

Find articles by Childress, R. in: PubMed | Google Scholar

Medical Service, Veterans Administration Hospital and the Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana 46202

Find articles by Boyd, D. in: PubMed | Google Scholar

Medical Service, Veterans Administration Hospital and the Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana 46202

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Medical Service, Veterans Administration Hospital and the Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana 46202

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Published May 1, 1968 - More info

Published in Volume 47, Issue 5 on May 1, 1968
J Clin Invest. 1968;47(5):1143–1153. https://doi.org/10.1172/JCI105803.
© 1968 The American Society for Clinical Investigation
Published May 1, 1968 - Version history
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Abstract

Left ventricular function was assessed in six patients with essentially normal cardiopulmonary function, in five patients with primary myocardial disease, and in 16 patients with chronic obstructive pulmonary disease by determining the response of the ventricle to an increased resistance to ejection. Studies were performed at the time of cardiac catheterization and increased resistance to left ventricular ejection was produced by the intravenous infusion of methoxamine.

In the control patients, methoxamine produced an increase in stroke volume index (SVI), in stroke work index (SWI), and stroke power index (SPI), whereas left ventricular end-diastolic pressure (LVEDP) increased only moderately. In contrast SVI, SWI, and SPI fell, whereas LVEDP increased inordinately in the patients with myocardiopathy. The patients with chronic obstructive pulmonary disease responded to the infusion with an increase in SVI, SWI, SPI, and LVEDP comparable to the control patients. Furthermore, in this latter group of patients, a quantitatively similar response was observed in those with essentially normal resting hemodynamics, in those with resting pulmonary hypertension, and in those whose disease had progressed to the stage of right ventricular failure.

This study provides no evidence that chronic obstructive pulmonary disease results in chronic impairment of left ventricular function, but on the contrary, has demonstrated that the left ventricle responds normally to an increased pressure load in these patients.

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