Artigo Revisado por pares

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

2009; Elsevier BV; Volume: 103; Issue: 6 Linguagem: Inglês

10.1016/j.amjcard.2008.11.039

ISSN

1879-1913

Autores

Hidemichi Kouzu, Satoshi Nakatani, Shingo Kyotani, Hideaki Kanzaki, Norifumi Nakanishi, Masafumi Kitakaze,

Tópico(s)

Cardiovascular Issues in Pregnancy

Resumo

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 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. 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 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.

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