Jing SONG1, Yousan CHEN2, Xiangchuang KONG1, Yue CUI1, Yukun CAO1, Jia LIU1, Xiaoyue ZHOU3, Heshui SHI1, and JING SONG1
1Department of Radiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, WUHAN, China, 2Department of Radiology, Wuhan General Hospital of Chinese People’s Liberation Army, WUHAN, China, 3MR Collaboration,Siemens Healthcare Ltd,Shanghai,China, SHANGHAI, China
Synopsis
There is little understanding
about the mechanism of left ventricular strain in pulmonary hypertension (PH)
patients at present. In this study, we compared left ventricular strain between
PH patients and the healthy controls. For PH patients with preserved or mildly improved
left ventricular ejection fraction (LVEF), the ventricular strain parameters decreased
compared to the healthy controls. We found that left ventricular myocardial
strain impairment in HP patients is associated with right ventricular overload
of volume or pressure and decreased ejection capacity.
Introduction
Left
ventricular ejection fraction (LVEF) is considered to be an important clinical index
of reflecting the ventricular function. However, for many pulmonary
hypertension (PH) patients, the LVEF appears normal or, even mildly elevated.
Myocardial strain, on the other hand, is more sensitive to the early
ventricular deformation change[1]. At present, there is little
understanding about the mechanism of left ventricular (LV) strain in PH
patients. In this study, we aim to determine whether LV strain may be affected in
PH patients, especially those with preserved or mildly improved LVEF and,
whether chronic right heart failure affects regional LV function.Method
After
informed consent, a total of 30 PH patients were evaluated with right heart
catheterization (RHC) and cardiac magnetic resonance (CMR) imaging and were
compared with 19 healthy volunteers. The presence of PH was defined as a mean
pulmonary artery pressure >25 mm Hg at RHC. Patients with other LV disease
unrelated to PH or ventricular shunt were excluded. All subjects were
classified into: group A (healthy volunteers, LVEF ≥ 50%, N=19), group B
(PH patients, LVEF ≥
50%, N=18), and group C (PH patients, LVEF < 50%, N= 12). CMR studies were
performed on two 1.5 Tesla MR scanners (MAGNETOM Aera or MAGNETOM Avanto;
Siemens Healthcare, Erlanger, Germany) using a 18-channel phased-array body
coil combined with the spine coil (12 of 36 channels used). Long-axis 4-chamber
cine images and short-axis covering the whole heart cine images were obtained.
Scan parameters for MAGNETOM Aera were: FOV = 340×255 mm2,acquisition matrix = 256×205,TR = 2.93 ms, TE
= 1.16 ms,flip angle 80°,slice thickness = 6 mm;
Scan parameters for MAGNETOM Avanto were: FOV = 360×288 mm2,acquisition matrix = 168×192, TR = 47.69 ms, TE
= 1.08 ms, flip angle 65°, slice thickness = 8 mm. Cardiac
function analysis was performed on a dedicated workstation (Argus, Siemens
Medical Solutions, Erlangen, Germany) by manually outlining the endocardial
contour of the left and right ventricles. LV and RV volumes were indexed to
body surface area. Biventricular ejection fraction (EF), end-diastolic volume
index (EDVI), end-systolic volume index (ESVI) were calculated. For the
myocardial strain analyses, CMR cine images were loaded into a prototype
post-processing software (TrufiStrain, version 2.0, Siemens Healthcare,
Erlangen, Germany) to measure the global
peak systolic longitudinal (Ell) strain, circumferential (Ecc) strain, and radial (Err) strain. Besides,
LV regional Ecc and Err, including septum(AHA segments 2, 3, 8, 9, 14),lateral
wall (AHA segments 5,6,11,12,16), anterior wall (AHA segments 1,7,13) and
inferior wall(AHA segments 4,10,15)were measured on the short-axis cine images
as well (Figure 1). Differences in two group were
established using a 2-tailed unpaired Student t test, or in cases involving
multiple groups, the ANOVA test and Kruskal Wallis test were used. Correlation
between variables was assessed by Pearson or Spearman correlation coefficients.Result
The global LV Ell and Err decreased in PH patients
with preserved or mildly elevated LVEF, and all strain parameters decreased in PH
patients with decreased LVEF (Table2 and 3). The
regional LV Ecc
was significantly associated with RVEDVI, especially in the septum (r = 0.732, P<0.01). The LV Err in the lateral wall was related to the mean
pulmonary artery pressure (r =
-0.419, P<0.05); and the global LV
Err was significantly correlated with RVEF (r
= 0.722, P<0.01).Discussion
The
strain abnormality in patients with preserved or mildly elevated LVEF may be
due to the fact that LVEF only reflects volume changes in LV and cannot reflect
changes in myocardial ultrastructure associated with LV systolic function[2]. Ecc was
significantly associated with RVEDVI, especially in the septum, which suggests
that ventricular interdependence may be a potential etiology for abnormal LV
function in PH patients[3]. when the right
ventricular (RV) afterload is increased ,the ventricular septum bulges to the
left side, so that the curve radius of the LV free wall and the tension are
significantly higher than the ventricular septum, which may be the mechanism of
decreased lateral Err caused by increased RV afterload. The RVEF is mainly the
compression of the inner diameter between the free wall and the
interventricular septum, and the power comes from the left ventricle. Increased
RVEDV limits the LV filling and changes the shape and spatial structure of the
left ventricle, making the left ventricle contraction does not continue to
power the RV ejection ,which leads to further deterioration of RV function.
Early
contractile dysfunction of left ventricle was found in PH patients with
preserved or mildly elevated LVEF. LV myocardial strain impairment in PH patients
is associated with RV overload of volume or pressure and decreased ejection
capacity.Acknowledgements
No acknowledgement foundReferences
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