International Journal of Cardiology 206 (2016) 5153
Contents lists available at ScienceDirect
International Journal of Cardiology
journal homepage: www.elsevier.com/locate/ijcard
Correspondence
Right ventricular dysfunction in systemic hypertension: A call to action
Kamilu M. Karaye a,, Aim Bonny b
a
Department of Medicine, Bayero University, Kano, Nigeria
b
Cardiovascular Research Centre, University of Douala, Douala, Cameroon
a r t i c l e i n f o
Article history:
Received 13 December 2015
Accepted 2 January 2016
Available online 6 January 2016
Keywords:
Right ventricular dysfunction
Remodeling
Systemic hypertension
The earliest description of the importance of right ventricular (RV)
function was by Sir William Harvey in 1616, who opined that it was
made for the sake of transmitting blood through the lungs and not
for nourishing them [1,2]. Perhaps as a consequence, the RV continued
to be grossly undervalued for many years and considered to function
mainly as a conduit, while its contractile performance was considered
hemodynamically unimportant. Since the early 1950s however, the rel-
evance of the chamber in the maintenance of normal cardiac physiology
was recognized in several cardiovascular disorders [3]. Unfortunately,
studies on RV dysfunction among hypertensive patients are still few
with several limitations, and information on outcome is lacking [4,5].
This article aimed to review some key studies on RV dysfunction in
hypertension, in order to make a case for starting a large multicentre
longitudinal study to assess RV dysfunction in hypertension, the
possibility of its reverse remodeling and potential outcomes.
The RV weighs about one-sixth of the left ventricle (LV) mass and
performs about one-quarter of its stroke work to propel blood into the
pulmonary circulation, whose resistance is about one-tenth of the sys-
temic values due to its large cross-sectional area [6]. As compared
with the LV, the RV can adapt to accept large volumes of blood with
negligible changes in pressure. However, chronic pulmonary pressure
overload stimulates an adaptive response consisting of compensatory
RV hypertrophy (RVH) [3]. Long-term increases in pulmonary vascular
resistance seems to originate from both functional components due to
an unbalanced production of endothelium-derived vasoactive media-
Grant support: none.
Corresponding author at: Department of Medicine, Bayero University, 3 New Hospital
Road, PO Box 4445, Kano, Nigeria.
E-mail addresses: kkaraye@yahoo.co.uk (K.M. Karaye), aimebonny@yahoo.fr
(A. Bonny).
http://dx.doi.org/10.1016/j.ijcard.2016.01.049
0167-5273/ 2016 Elsevier Ireland Ltd. All rights reserved.
tors (e.g. nitric oxide, prostacyclin, endothelin-1) and structural remod-
eling of pulmonary arterioles caused by proliferating endothelial cells,
vascular smooth muscle cells and broblasts [3]. RV and LV are function-
ally and structurally interdependent; force is transmitted from one to
the other ventricle through the myocardium independently from neu-
ral, humoral and haemodynamic inuences, so that about 2040% of
the beat-to-beat RV systolic pressure and volume outow is conditioned
by LV contraction [7].
Although the RV is a chamber that is difcult to image due to its
crescent-like shape wrapping around the LV, cardiac magnetic reso-
nance imaging (MRI) overcomes that problem through the acquisition
of parallel and contiguous tomographic images with high temporal res-
olution thus optimising the contrast between blood and myocardium as
well as epicardium and surrounding fat [8]. In a cardiac MRI study com-
prising of 25 patients with uncomplicated, mild to moderate essential
hypertension, compared with 24 healthy age and gender matched con-
trols, Todiere et al. reported that RV mass index (RVMI), ventricular wall
thickness and remodeling index were greater in hypertensive subjects
and associated with reduced peak lling rate; a pattern consistent
with concentric RV remodeling [8]. However, RVMI was signicantly
higher only in hypertensive men and not women as compared with
controls, and RV ejection fraction (RVEF) and volumes were not
signicantly different between the 2 groups [8]. Although none of the
subjects had RVH, 48% of them had LV hypertrophy [8]. These ndings
suggest that in mildmoderate hypertension, the processes of hypertro-
phy are different between the 2 ventricles as well between the sexes,
but more studies are needed to corroborate these ndings.
In spite of its advantages, MRI is not widely available or affordable in
developing countries. However, echocardiography is cheap and widely
available, and various echocardiographic indices have been used to
further characterise hypertensive patients [4,5,911]. In an echocardio-
graphic cross-sectional study among hypertensive subjects with abnor-
mal LV geometric patterns and diastolic or systolic LV dysfunctions, we
found RV systolic dysfunction (RVSD), dened as tricuspid annular
plane systolic excursion (TAPSE) b 15 mm, in 29.6% of them [9]. Subjects
with RVSD were older, had higher prevalence of peripheral oedema,
moderatesevere dyspnoea, higher heart rate and prevalence of atrial
arrhythmias and lower LV ejection fraction (LVEF) than those with
preserved RV systolic function [9]. In another study, we reported the
prevalence, determinants and correlates of RVSD and RV diastolic
dysfunction (RVDD) in hypertensive subjects with various LV geometric
patterns [10]. RVSD was dened as TAPSE b 16 mm or S b 10 cm/s, and
RV diastolic dysfunction (RVDD) as a ratio b 1.0 of the peak velocities of
the early (Em) to late (Am) diastolic waves in the tissue Doppler
52 Correspondence

Fig. 1. Assessment of RV function using TAPSE. Assessment of RV function using tricuspid annular plane systolic excursion (TAPSE). RV long axis amplitude of motion (i.e. TAPSE) is
measured from end-systolic to end-diastolic points during held end-expiration.

imaging (TDI) of the RV lateral tricuspid annulus [10] [Figs. 1 and 2].
RVDD was found in 61.7% of the subjects while 31.0% had RVSD.
Subjects with eccentric hypertrophy (EH) had the highest prevalence
of RVSD, while RVDD was common across all the groups. LVEF and
age were the only independent determinants of RVSD and RVDD,
respectively [10]. Pedrinelli et al. described the relationship between in-
creasing systemic blood pressure (BP) and RV function, among never-
treated, non-obese patients with BP values varying from the optimal
to the mild hypertensive range [11]. They found that RV diastolic and
systolic function deteriorates in response to slightly increased systemic

Fig. 2. Assessment of RV systolic function using Tissue Doppler Imaging echocardiography. Legend: Fig. 2: S, e and a are the tissue Doppler imaging-derived tricuspid lateral annular
systolic, and early and late diastolic velocities.
 Correspondence
blood pressure [11]. The process paralleled homologous changes at the
LV side and was driven by interventricular septum remodeling, perhaps
as a reection of its role in RV function and biventricular interdepen-
dence [11]. Tumuklu et al. additionally showed that patients with
hypertension and normal LV systolic function could exhibit a subtle
disturbance in RV systolic contractility. This was demonstrated by the
use of strain imaging of RV free wall but not other echocardiography de-
rived techniques [5]. Therefore, echocardiography is useful in assessing
RVSD and RVDD in hypertensive subjects in spite of its limitations in
assessing RV geometry.
The relationship between mortality and other outcomes in relation
to RV geometry or dysfunction in hypertensive subjects does not seem
to have been previously reported, in spite of its high prevalence globally
and associated morbidity and mortality. However, in the Multi-Ethnic
Study of Atherosclerosis (MESA), investigators examined the associa-
tion of abnormal RV structure and function with the risk of heart failure
(HF) or cardiovascular (CV) death in a population-based multiethnic
sample free of clinical CV disease at baseline [12]. They performed cardi-
ac MRI on 4144 participants and followed them up for incident HF and
CV death over a time of 5.8 years. The mean age of subjects was
61.4 10.1 years, 47.6% were males and 42.8% had hypertension. The
presence of RVH (dened as increased RV mass) was associated with
a more than twice the risk of HF or CV death after adjustment for several
confounding factors including hypertension (HR = 2.52, p b 0.001) and
a doubling (or more) of risk with LV mass at the mean value or lower
(p = 0.05) [16]. In this study, the relationships between RV volumes,
RVSD and the outcomes were not statistically signicant [12].
As mentioned above, there is striking paucity of multicentre
longitudinal studies among hypertensive subjects to study RV dysfunc-
tion and its associated morbidities and mortality, as well as the possible
impact of treatments on RV reverse remodeling and cardiovascular or
all-cause mortality. Such studies will further characterise RV disease in
hypertensive patients, and give more insight into how to prevent and
treat it.
53
Conict of interest
None to declare.
References
[1] W. Harvey, Exercitatio Anatomica de Motu Cordis et Sanguinis in Animalibus, 1628.
[2] J. Goldstein, The right ventricle: what's right and what's wrong, Coron. Artery Dis. 16
(2005) 13.
[3] F. Haddad, R. Doyle, D.J. Murphy, S.A. Hunt, Right ventricular function in cardiovas-
cular disease, part II: pathophysiology, clinical importance, and management of
right ventricular failure, Circulation 117 (2008) 17171731.
[4] W. Myslinski, J. Mosiecwicz, E. Ryczak, W. Barud, A. Bian, R. Palusinski, et al., Right
ventricular function in systemic hypertension, J. Hum. Hypertens. 12 (1998)
149155.
[5] M.M. Tumuklu, U. Erkorkmaz, A. Ocal, The impact of hypertension and
hypertension-related left ventricle hypertrophy on right ventricle function,
Echocardiography 24 (2007) 374384.
[6] F. Haddad, S.A. Hunt, D.N. Rosenthal, D.J. Murphy, Right ventricular function in car-
diovascular disease, part I: anatomy, physiology, aging, and functional assessment of
the right ventricle, Circulation 117 (2008) 14361448.
[7] W.P. Santamore, L.J. Dell'Italia, Ventricular interdependence: signicant left ventric-
ular contributions to right ventricular systolic function, Prog. Cardiovasc. Dis. 40
(1998) 289308.
[8] G. Todiere, D. Neglia, S. Ghione, E. Fommei, P. Capozza, G. Guarini, et al., Right
ventricular remodelling in systemic hypertension: a cardiac MRI study, Heart 97
(15) (2011) 12571261.
[9] K.M. Karaye, A.G. Habib, S. Mohammed, M. Rabiu, M.N. Shehu, Assessment of right
ventricular systolic function using tricuspid annular-plane systolic excursion in
Nigerians with systemic hypertension, Cardiovasc. J. Afr. 21 (4) (2010) 186190.
[10] K.M. Karaye, H. Sai'du, M.N. Shehu, Right ventricular dysfunction in a hypertensive
population stratied by patterns of left ventricular geometry, Cardiovasc. J. Afr. 23
(9) (2012) 478482.
[11] R. Pedrinelli, M.L. Canale, C. Giannini, E. Talini, G. Penno, G. Dell'Omo, et al., Right
ventricular dysfunction in early systemic hypertension: a tissue Doppler imaging
study in patients with high-normal and mildly increased arterial blood pressure, J.
Hypertens. 28 (3) (2010) 615621.
[12] S.M. Kawut, R.G. Barr, J.A. Lima, A. Praestgaard, W.C. Johnson, H. Chahal, et al., Right
ventricular structure is associated with the risk of heart failure and cardiovascular
death. The Multi-Ethnic Study of Atherosclerosis (MESA)-Right Ventricle Study,
Circulation 126 (14) (2012) 16811688.