The Effect of Acute Pulmonary Hypertension on Tricuspid Annular
Height, Strain, and Curvature in Sheep
Department of Aerospace Engineering & Engineering Mechanics, Department of Biomedical Engineering, University of Texas
at Austin, 210 E 24th Street, Austin, TX 78703, USA;
Department of Cardiac Surgery, Medical University of Silesia, School
of Medicine in Katowice, Ziolowa 47, 40-635 Katowice, Poland; and
Meijer Heart and Vascular Institute at Spectrum Health,
100 Michigan St NE, 49503 Grand Rapids, MI, USA
(Received 12 February 2018; accepted 24 May 2018)
Associate Editor Wei Sun and Ajit P. Yoganathan oversaw the review of this article.
Abstract—The tricuspid annulus shows signiﬁcant alterations
in patients with functional tricuspid regurgitation–tricuspid
valve dysfunction that is secondary to other diseases such as
pulmonary hypertension. Early changes in annular shape and
dynamics may provide an understanding of disease mechanisms
and could predict disease progression. To gain a mechanistic
insight into these early changes we perform a spatially-resolved
analysis of the effect of acute pulmonary hypertension on the
tricuspid annulus in sheep. To this end, we suture sonomicrom-
etry crystals to the annulus of nine sheep and record their
locations in the beating heart, before and after inducing acute
pulmonary hypertension. Using least-squares cubic splines, we
derive mathematical representations of the annulus to describe
pulmonary hypertension-induced annular shape changes via
strain, relative curvature, and relative annular height between
the control group and the acute pulmonary hypertension group.
Moreover, we determine hypertension-induced alterations to
annular dynamics as within-group strains, relative curvature,
and relative height throughout the cardiac cycle for each group.
We conﬁrm that the annulus in acute pulmonary hypertension
dilates signiﬁcantly, becomes more circular, and ﬂattens. Our
regional analysis reveals that annular dilation, circularization,
and ﬂattening are driven by highly localized changes in annular
strains, curvature, and height. Additionally, we ﬁnd that acute
pulmonary hypertension alters annular dynamics, albeit min-
imally. This regionally-resolved analysis of acute hypertension-
induced changes of annular shape and dynamics provides
insight into early disease mechanisms, and may inspire future
generations of annuloplasty devices and techniques that address
spatial annular heterogeneities.
Keywords—Functional tricuspid regurgitation, Least-squares
cubic splines, Shape, Dynamics, Sonomicrometry.
The tricuspid annulus has a complex three-dimen-
sional shape with peaks and valleys, and an approxi-
mately elliptical two-dimensional projection.
shape is likely of teleological origin and may aid in
minimizing leaﬂet stresses, similarly to the mitral
Furthermore, this three-dimensional con-
ﬁguration changes sphincterically throughout the car-
diac cycle ensuring successful valve closure.
Consequently, insults to annular shape and its
dynamics contribute to valvular dysfunction and
regurgitation of blood from the right ventricle into the
To date, approximately 1.6 mil-
lion Americans suffer from tricuspid valve dysfunction
or tricuspid regurgitation.
In most cases, tricuspid valve dysfunction is sec-
ondary or functional in nature, meaning that leakage is
not due to a primary valve lesion. Rather, leakage re-
sults from other conditions that cause annular dilation
and ventricular remodeling, subsequently preventing
proper leaﬂet coaptation.
For example, functional
tricuspid regurgitation can be secondary to pulmonary
Patients with pulmonary hypertension
present with chronically elevated right ventricular
blood pressure leading to signiﬁcant ventricular
remodeling, concomitant papillary muscle displace-
ment, and restricted leaﬂet motion. These, combined
with annular dilation, result in valvular dysfunction.
We are interested in the acute effects of pulmonary
hypertension because they may provide insight into the
early development of functional tricuspid regurgitation
and possibly serve as predictors for disease progres-
Address correspondence to Manuel K. Rausch, Department of
Aerospace Engineering & Engineering Mechanics, Department of
Biomedical Engineering, University of Texas at Austin, 210 E 24th
Street, Austin, TX 78703, USA. Electronic mail: manuel.rausch@
Cardiovascular Engineering and Technology (
2018 Biomedical Engineering Society