Morphologic and Functional Remodeling of the Right Ventricle in
Pulmonary Hypertension by Real Time Three Dimensional
Echocardiography
Julia Grapsa, MD, PhD
a,
*, J. Simon R. Gibbs, MD
a,b
, David Dawson, MSc
a
, Geoffrey Watson, MD
a
,
Ravi Patni, MBBS
c
, Thanos Athanasiou, MD, PhD
c
, Prakash P. Punjabi, MBBS
c
,
Luke S.G.E. Howard, DPhil
a,b
, and Petros Nihoyannopoulos, MD
a
The aims of this study were to assess the right ventricle in different causes of pulmonary
hypertension (PH) and to assess the changes of the tricuspid apparatus during this
remodeling. The functional and morphologic changes of the right ventricle and the tricus-
pid apparatus in relation to different causes of PH remain elusive. A total of 141 consec-
utive patients were prospectively recruited, of whom 55 had pulmonary arterial hyperten-
sion (PAH), 32 had chronic thromboembolic disease (CTED), and 34 had PH secondary to
mitral regurgitation (MR). Twenty age- and gender-matched healthy volunteers were also
studied to serve as controls. Real-time 3-dimensional echocardiography was used to assess
right ventricular (RV) volumes and tricuspid valve mobility. Overall, RV diastolic volumes
were greater and RV ejection fractions lower in patients with PAH compared to those with
CTED and MR (186.4 48.8 vs 113.5 vs 109.4 ml, p <0.001, and 33.2% vs 36.8% vs 66.8%,
p <0.001, respectively). Among the 3 PH groups, tricuspid valve mobility was most
restricted in the CTED group and least restricted in the MR group. Tricuspid tenting
volume was greater in the CTED and PAH groups than in the MR group (p <0.01). Most
patients with PAH (54.6%) had at least moderate tricuspid regurgitation, while in the
CTED group, most (59.4%) had mild and only 37.5% had moderate tricuspid regurgitation
(p <0.01). Conversely, patients with MR (85%) had only mild tricuspid regurgitation.
There was no correlation between RV systolic pressures and the RV ejection fraction or
tenting volume. In conclusion, this study demonstrates that different causes of PH may
lead to diverse RV remodeling, with the most adverse remodeling being in patients with
PAH. In addition, changes of the tricuspid apparatus also differed, with the most adverse
effects seen in patients with CTED. Crown Copyright © 2012 Published by Elsevier Inc.
All rights reserved. (Am J Cardiol 2012;109:906 –913)
In this study, we hypothesized that different causes of
pulmonary hypertension (PH) may lead to diverse patterns
of right ventricular (RV) remodeling and that as a conse-
quence, the tricuspid apparatus would change in shape and
leaflet mobility. The purpose of this study was to charac-
terize the RV remodeling, including the tricuspid apparatus,
in different causes of PH using 3-dimensional echocardiog-
raphy.
Methods
Consecutive patients with PH were prospectively en-
rolled from patients referred for clinical evaluation at our
institution. The following inclusion criteria were used: (1)
chronic PH that had been diagnosed for 6 months before
the study with cardiac catheterization, (2) tricuspid regur-
gitant velocity 2.7 m/s, and (3) sinus rhythm. Patients with
cardiomyopathy, aortic valve disease, free-flow tricuspid
regurgitation, and poor RV or tricuspid valve image quality
were excluded. Patients were distributed into 3 groups ac-
cording to the cause of PH (Figure 1): 55 patients had
pulmonary arterial hypertension (PAH; precapillary PH), 32
had chronic thromboembolic disease (CTED; precapillary
PH), and 34 had secondary PH due to mitral regurgitation
(MR; postcapillary PH).
All patients underwent comprehensive right- and left-
sided cardiac catheterization
1,2
and contrast-enhanced pul-
monary angiography,
2
which was performed using a multi-
detector helical computed tomographic scanner (LightSpeed
Ultra; GE Medical Systems, Milwaukee, Wisconsin), with
collimation of 1.25 mm, and a ventilation perfusion lung
scan. Standard criteria for the diagnosis of PH were used.
1,2
Twenty healthy volunteers were used as the control group.
The protocol was approved by the local ethics committee.
A comprehensive baseline study was first performed,
including the assessment of right-sided heart pressures and
a
Department of Cardiology,
b
National PH Service, and
c
Department of
Cardiothoracic Surgery, Hammersmith Hospital, Imperial College London
NHS Trust, London, United Kingdom. Manuscript received July 16, 2011;
revised manuscript received and accepted October 28, 2011.
Dr. Grapsa was supported by a research grant from the European
Society of Cardiology, Sophia Antipolis, France. This study was supported
by the National Institute for Health Research, London, United Kingdom,
under the Biomedical Research Centre Scheme.
*Corresponding author: Tel: 44-20-8383-2333; fax: 44-20-8383-4392.
E-mail address: jgrapsa@gmail.com (J. Grapsa).
0002-9149/12/$ – see front matter Crown Copyright © 2012 Published by Elsevier Inc. All rights reserved. www.ajconline.org
doi:10.1016/j.amjcard.2011.10.054