1349524 - Right Ventricular Diastolic Kinetic Energy is Increased in Patients With Precapillary Pulmonary Hypertension

Patients with precapillary pulmonary hypertension (PH_precap) have increased pulmonary vascular resistance (PVR) which alters the right ventricular (RV) hemodynamics (1). Despite complex treatments, the RV may rapidly deteriorate, and new means of monitoring treatment effect are needed. Intracardiac hemodynamics may be analyzed non-invasively by measuring kinetic energy (KE) using 4D flow cardiovascular magnetic resonance imaging. KE has the potential to be an early marker of cardiac dysfunction (1). Therefore, the aim of this project was to investigate if RV KE differ in patients with PH_precap compared to controls without PH_precap, and to investigate if KE is associated with PVR in patients with PH_precap.

Methods:

Twenty patients with PH_precap (pulmonary arterial hypertension, n=13, and chronic thromboembolic pulmonary hypertension, n=7) and twelve age- and sex matched healthy controls underwent CMR at 1.5T (MAGNETOM Aera, Siemens Healthcare, Erlangen, Germany). Cine images, 2D flow phase contrast images and 4D flow using a prototype sequence were acquired. Peak RV KE was computed as previously published (2), using Segment v2.2 R7052 (Medviso, Lund, Sweden)(3). Stroke volume was computed from 2D flow images of the pulmonary artery, or from 4D flow when 2D was of insufficient quality. Right heart catheterization including PVR was performed in patients. The Mann-Whitney U test was performed for group comparisons, and the Spearman correlation and simple linear regression analysis for associations.

Results:

Patients with PH_precap had increased diastolic RV KE compared to controls (presented as median [IQR]: 2.7 mJ [1.6] vs 1.3 mJ [0.86], p=0.0004, Table 1, Figure 1). Systolic RV KE was similar between patients and controls (4.0 mJ [2.8] vs 4.5 mJ [2.9], p=0.9, Table 1, Figure 1), and correlated negatively with PVR in patients (r=-0.48, p=0.03, Figure 2). Furthermore, stroke volume and PVR correlated negatively (r=-0.70, p=0.0006, Figure 2), and systolic RV KE and SV correlated positively (r=0.62, p=0.003). When systolic RV KE was indexed to stroke volume there was no correlation to PVR (p=0.7, Figure 2).

Conclusion:

Diastolic, but not systolic, RV KE was increased in patients with PH_precap, suggesting that PH_precap leads to diastolic rather than systolic dysfunction, and that the RV can still generate sufficient blood flow during systole despite the increased PVR. The loss of association between PVR and systolic RV KE when indexed to SV suggests that peak systolic KE is more related to changes in SV rather than changes in PVR per se.

Acknowledgements

We thank Ning Jin at Siemens Medical Solutions USA Inc., Cleveland, Ohio, USA for providing the 4D flow sequence as a work-in-progress package. We also thank the SCAPIS study for allowing access to data to identify 10 healthy controls.