Abstract

In response to an increased afterload in pulmonary arterial hypertension (PAH), the right ventricle (RV) adapts by remodeling and increasing contractility. The idea of coupling refers to maintaining a relatively constant relationship between ventricular contractility and afterload. Twenty-eight stable PAH patients (mean age 49.5 ± 15.5 years) were enrolled into the study. The follow-up time of this study was 58 months, and the combined endpoint (CEP) was defined as death or clinical deterioration. We used echo TAPSE as a surrogate of RV contractility and estimated systolic pulmonary artery pressure (sPAP) reflecting RV afterload. Ventricular–arterial coupling was evaluated by the ratio between these two parameters (TAPSE/sPAP). In the PAH group, the mean pulmonary artery pressure (mPAP) was 47.29 ± 15.3 mmHg. The mean echo-estimated TAPSE/sPAP was 0.34 ± 0.19 mm/mmHg and was comparable in value and prognostic usefulness to the parameter derived from magnetic resonance and catheterization (ROC analysis). Patients who had CEP (n = 21) had a significantly higher mPAP (53.11 ± 17.11 mmHg vs. 34.86 ± 8.49 mmHg, p = 0.03) and lower TAPSE/sPAP (0.30 ± 0.21 vs. 0.43 ± 0.23, p = 0.04). Patients with a TAPSE/sPAP lower than 0.25 mm/mmHg had worse prognosis, with log-rank test p = 0.001. the echocardiographic estimation of TAPSE/sPAP offers an easy, reliable, non-invasive prognostic parameter for the comprehensive assessment of hemodynamic adaptation in PAH patients.

Highlights

  • Pulmonary arterial hypertension (PAH) is a rare disease that causes increased pulmonary vascular resistance (PVR) and elevated pulmonary arterial pressures (PAPs)

  • right ventricular (RV)–arterial coupling is calculated as the ratio of end-systolic elastance to arterial elastance (Ees/Ea) [2,3]

  • This paper presents an echo-focused analysis of a PAH group enrolled to the project, with a grant entitled “The role of PET/magnetic resonance imaging (MRI)

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Summary

Introduction

Pulmonary arterial hypertension (PAH) is a rare disease that causes increased pulmonary vascular resistance (PVR) and elevated pulmonary arterial pressures (PAPs). The ratio of TAPSE/sPAP, introduced earlier, has been proposed as an index of in vivo RV shortening in the longitudinal axis versus developed force in patients with chronic heart failure, and was found to be a non-invasive, indirect measurement of RV contractile function and RV–arterial coupling [6,8,9]. It seems that this approach to the estimation of RV–arterial coupling may have functional and prognostic relevance, especially at bedside

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