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Volume 103, Issue 6, Pages 872-876 (15 March 2009)


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Noninvasive Estimation of Pulmonary Vascular Resistance by Doppler Echocardiography in Patients With Pulmonary Arterial Hypertension

Hidemichi Kouzu, MDa, Satoshi Nakatani, MD, PhDaCorresponding Author Informationemail address, Shingo Kyotani, MD, PhDa, Hideaki Kanzaki, MDa, Norifumi Nakanishi, MD, PhDa, Masafumi Kitakaze, MD, PhDa

Received 6 September 2008; received in revised form 15 November 2008; accepted 15 November 2008. published online 27 January 2009.

Pulmonary vascular resistance (PVR) is an important hemodynamic variable in the management of patients with pulmonary hypertension. To establish a method of estimating PVR in patients with pulmonary arterial hypertension (PAH), Doppler echocardiography was performed within 24 hours of right heart catheterization in 43 patients with PAH (idiopathic PAH, n = 20; chronic thromboembolic pulmonary hypertension, n = 9; congenital heart disease, n = 9; and others). Correlations between invasive PVR and Doppler variables of pulmonary artery flow and tricuspid regurgitation were examined. Mean invasive PVR was 1,294 ± 680 dyne s cm−5. Linear regression analysis revealed significant correlations with invasive PVR for the time–velocity integral (TVI; r = −0.63, p = 0.009) of right ventricular outflow and peak tricuspid regurgitant pressure gradient (TRPG; r = 0.77, p <0.001). The TRPG/TVI ratio, which approximated the ratio of pulmonary artery pressure to pulmonary blood flow, showed an improved correlation coefficient of 0.82 (PVR = 187 + TRPG/TVI × 118, p <0.001). After excluding 5 patients with an intracardiac shunt, 26 of the remaining 38 patients (68%) met the hemodynamic criteria in international guidelines for the selection of lung transplantation candidates and were defined as the poor-prognosis group. A TRPG/TVI >7.6 showed 85% sensitivity and 92% specificity for identifying patients in the poor-prognosis group. In conclusion, TRPG/TVI provides a reliable estimation of PVR over a wide range in patients with PAH with various underlying causes.

a Division of Cardiology, Department of Internal Medicine, National Cardiovascular Center, Osaka, Japan

Corresponding Author InformationCorresponding author: Tel/fax: 81-6-6879-2561

PII: S0002-9149(08)02111-5

doi:10.1016/j.amjcard.2008.11.039


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