Shuang Leng1, Ru-San Tan1,2, Ping Chai3,4, Wen Ruan1, Ting Ting Low3,4, Lynette Teo4,5, Tee Joo Yeo3,4, Xiaodan Zhao1, John C. Allen2, Jonathan Yap1, Soo Teik Lim1,2, James W. Yip3,4, Ju Le Tan1,2, and Liang Zhong1,2
1National Heart Centre Singapore, Singapore, Singapore, 2Duke-NUS Medical School, Singapore, Singapore, 3National University Heart Centre, Singapore, Singapore, 4Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore, 5National University Hospital, Singapore, Singapore
Synopsis
Pulmonary artery (PA) stiffness in pulmonary
arterial hypertension (PAH) is strongly associated with clinical progression of
the disease. This study aimed to introduce a novel parameter—PA global
longitudinal strain (GLS)—for PA stiffness assessment using a semi-automated
feature-tracking approach with standard cine cardiovascular magnetic resonance
(CMR). Reduced PA GLS was significantly associated with increased pulmonary
artery pressure and pulmonary vascular resistance in PAH. In addition, PA GLS
was significantly impaired in PAH patients with hemodynamically decompensated
right ventricular (RV) function compared to those with compensated RV function.
Background and Purpose
Pulmonary arterial hypertension (PAH) is a
chronic and severe cardiopulmonary disorder that is characterized by a stiff
pulmonary artery (PA) resulting in progressive elevation of pulmonary artery
pressure (PAP) and pulmonary vascular resistance (PVR). PA stiffness is usually
quantified as the ratio of change in luminal diameter of PA and change in
pressure. However, the need for invasive pressure measurements limits its use
for detection of early PA remodeling or for serial measurements. Pulse wave
velocity (PWV) has been described as a noninvasive measure of arterial
stiffness.1 However, it has not been adopted for clinical use
because of difficulty in reliably measuring PWV and its dependence on
hemodynamic conditions.2 In this study, we propose a novel parameter—PA
global longitudinal strain (GLS)—to quantify PA stiffness in PAH based on a
semi-automated strain measurement approach using standard cine cardiovascular
magnetic resonance (CMR) images.Methods
Thirty-five PAH patients (48±12 years, 27
female) and 35 age- and sex-matched normal controls (47±14 years, 27 female) were
enrolled (Table 1). PAH was diagnosed based on invasive hemodynamic
measurements3: mean PAP ≥25 mmHg, pulmonary capillary wedge pressure (PCWP) ≤15
mmHg, and PVR >3 Woods units. PAH patients were stratified into 2 groups by invasively
measured mean right atrial pressures (RAP)4,5: PAH with
hemodynamically compensated (PAH-C) and decompensated right ventricular (RV)
function (PAH-D) with mean RAP <10
mmHg and ≥10 mmHg, respectively. All subjects underwent CMR scans on a 3T
system (Ingenia, Philips Healthcare) or 1.5T system (MAGNETOM Aera, Siemens
Healthineers). Standard end-expiratory breath-held cine images (steady-state
free precession pulse sequence, retrospective electrocardiographic gating, typical
temporal resolution 30 frames per cardiac cycle) were acquired in the PA
bifurcation, RV outflow tract (RVOT), coronal RVOT, and RV 3-chamber views (Figure
1A) in addition to routine imaging planes. On these CMR views, the PA
longitudinal strain parameters were measured using an in-house semi-automated
algorithm6-9 that tracked the PA bifurcation and pulmonary valve in three-dimensional (3D) space: (1) landmarks
on the PA bifurcation (red star) and pulmonary valve annulus (blue squares,
yellow diamonds, red dots) were automatically tracked over the cardiac cycle (Figure
1A), (2) Two-dimensional (2D) spatial coordinates of the above points were mapped onto a 3D
coordinate system, (3) the distance ($$$L$$$) between the PA bifurcation and pulmonary valve
projected along the longitudinal direction was calculated, (4) instantaneous PA
longitudinal strain at time point ($$$t$$$) relative to initial time point (time 0) at end-diastole
was calculated using the formula for Lagrangian strain $$$\frac{(L(t)-L(0))\times100}{L(0)}$$$, and (5) PA GLS was defined as the peak absolute
strain value (Figure 1B).Results
PA GLS assessment was successful in all
subjects. Compared with controls, PAH patients had significantly lower PA GLS (10.0±3.5 vs. 19.4±4.8%,
P<0.0001) (Table 1). There was a positive
correlation between PA GLS and RV ejection fraction (EF) in the entire cohort (n=70, r=0.30, P=0.011). Among PAH patients, PA GLS was inversely
correlated with mean RAP (r=-0.54, P=0.001), PVR (r=-0.43,
P=0.018), mean PAP (r=-0.39, P=0.022), and PCWP (r=-0.52,
P=0.005). PAH-D patients had significantly lower PA GLS than PAH-C (8.2±2.8 vs. 11.3±3.4%,
P=0.007) (Table 1). On receiver operating
characteristic (ROC) analysis, PA GLS (Area under the ROC Curve=0.77, Sensitivity=67%, Specificity=85%,
Cut-off=8.6%) was superior to RVEF (AUC=0.64) for discriminating PAH-D from
PAH-C.Conclusion
We have demonstrated the feasibility of
measuring PA GLS, a novel cine CMR feature-tracking parameter for quantitation
of PA stiffness. Impaired PA GLS was more prevalent among PAH patients compared
with controls, was associated with elevated PAP and PVR, and discriminated well
for RV decompensation in PAH. PA GLS may represent a useful non-invasive
imaging index for characterization of PA stiffness as well as therapeutic
monitoring in PAH.Acknowledgements
No acknowledgement found.References
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