Chest
Volume 120, Issue 3, September 2001, Pages 809-815
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Clinical Investigations
Pulmonary Vasculature
Intravascular Ultrasound Assessment of Pulmonary Vascular Disease in Patients With Pulmonary Hypertension

https://doi.org/10.1378/chest.120.3.809Get rights and content

Abstract

Background

Measurements of pulmonary pressure and resistance are still considered to be the “gold standard” in the evaluation of pulmonary hypertension (PH), despite their limitations in predicting irreversible disease. Hemodynamic assessment also only provides a global evaluation of the pulmonary vascular bed, whereas PH is an inhomogeneous disease of the vessel wall.

Methods and results

We assessed the value of intravascular ultrasound (IVUS) in 30 patients with suspected PH and correlated the structural changes in distal pulmonary arteries found on IVUS with conventional hemodynamic data. Plasma endothelin (ET)-1 levels and pulmonary ET-1 extraction also were measured as markers of the severity of PH. The anatomic abnormalities revealed by IVUS were more severe in the lower lobes than in the upper lobes, as evidenced by the greater percentage of wall thickness (WT), the smaller lumen diameter/WT and lumen area/total vessel area (p < 0.05 for each). IVUS anatomic indexes correlated directly with hemodynamic data (eg, with pulmonary arterial systolic pressure; r = 0.56; p < 0.001) and ET-1 levels but inversely with pulmonary ET-1 extraction.

Conclusion

Patients with PH have greater pulmonary arterial WT that is more severe in the lower lobes than in the upper lobes. The severity of structural abnormalities found on IVUS is directly correlated with hemodynamic findings and ET-1 levels. IVUS may provide useful additional information in the assessment of patients with PH.

Section snippets

Study Population

The study population consisted of 30 patients (10 men and 20 women) ranging in age from 33 to 73 years (mean, 54 years) who had suspected primary or secondary PH and were undergoing cardiac catheterization. The causes for PH were the following: severe left ventricular dysfunction (8 patients); mitral valve stenosis (16 patients); mitroaortic valvular disease (3 patients); Eisenmenger syndrome (1 patient); CREST (ie, calcinosis, Raynaud’s phenomenon, esophageal dysmotility, sclerodactyly, and

Hemodynamic Data

The baseline values for PASP and mean PA pressure ranged from 21 to 136 mm Hg (mean [± SD], 49 ± 22) and from 13 to 85 mm Hg (33 ± 14), respectively. Pulmonary vascular resistance (PVR) and indexed PVR were 3.4 ± 3.3 Wood units (WU) (range, 0.4 to 16.3 WU) and 5.5 ± 4.7 WU × m2 (range, 0.8 to 22.4 WU × m2), respectively.

IVUS Measurements

We were able to perform the IVUS examination in all patients without complication (Fig 1). An average of two lobes were assessed per patient. The upper and lower lobes both were

Assessment of the Pulmonary Circulation Using IVUS and Correlations With Hemodynamic Abnormalities

The use of IVUS imaging allowed for the in vivo identification of regional differences in pulmonary vascular abnormalities found in patients with PH. Greater vascular wall hypertrophy already had been demonstrated in the lower lobes by histopathology,2 a finding attributed to the higher hydrostatic pressure chronically present in these segments with the patient in the upright posture. In contrast, there was no difference in IVUS indexes between the right and left lungs, demonstrating the

Conclusion

IVUS brings additional useful information to the evaluation of patients with PH. IVUS confirms in vivo the in vitro observation of greater vascular hypertrophy in the more dependent regions of the lung. IVUS-derived indexes correlate with classic hemodynamic indexes of PH and with two biochemical markers of PH, plasma ET-1 levels and reduced ET-1 clearance. Additional studies are necessary to determine whether the structural information derived from IVUS may help in the evaluation of the

Acknowledgment

The authors thank Joanne Vincent and Nathalie Ruel for their technical assistance, and Suzanne Taillefer for her help in the preparation of the manuscript.

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    Supported by the Fonds de la Recherche en Santé du Québec, the Medical Research Council of Canada, the Quebec Heart and Stroke Foundation, the CAFIR of the University of Montreal, and the Fonds de Recherche de l’Institut de Cardiologie de Montréal.

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