Review
Right ventricular hypertrophy in systemic
hypertension: an updated review of clinical studies
Cesare Cuspidi a,b, Carla Sala c, Maria Lorenza Muiesan d, Nicola De Luca e, and Giuseppe Schillaci f,g,
on behalf of the Working Group on Heart, Hypertension of the Italian Society of Hypertension
Aim: Experimental and clinical evidence supports the view
that right ventricular hypertrophy (RVH) may parallel left
ventricular hypertrophy in systemic hypertension; a
comprehensive analysis of this issue, however, is lacking.
Thus, we analyzed the literature in order to provide an
updated information on the right ventricular structural
changes associated to systemic hypertension.
Design: A literature search using the key words ‘right
ventricle’ ‘right ventricular hypertrophy’, ‘biventricular
hypertrophy’ ‘right and left ventricular hypertrophy’.
‘hypertension’, ‘echocardiography’ was performed in order
to identify relevant articles. Full articles published in English
language in the last three decades reporting studies in
adult hypertensive individuals were considered.
Results: A total of 13 studies, including 1290 untreated
(45%) and treated hypertensive patients and 259
normotensive controls, were considered. Overall, in
hypertensive individuals right ventricular wall was thicker
than in normotensive counterparts (standardized difference
1.3 mm, P < 0.001). RVH prevalence consistently varied
among studies (17.0–80.0%) with an average of 28.6%
in the pooled population. This was also the case for LVH
prevalence rates (9.0–100%) with an average value of
30.6%.
Conclusion: Clinical studies consistently indicate that RVH
is a common cardiac phenotype in systemic hypertension.
As this finding is based on a limited number of cross-
sectional studies including small population samples,
further investigations are needed to determine the clinical
utility and prognostic value of this phenotype in clinical
practice.
Keywords: echocardiography, hypertension, right
ventricular hypertrophy
Abbreviations: BP, blood pressure; CIs, confidence
intervals; LVH, left ventricular hypertrophy; ORs, odd ratios;
RVH, right ventricular hypertrophy
INTRODUCTION
L
eft ventricular hypertrophy (LVH) is a cardinal mani-
festation of hypertensive heart disease reflecting
an adaptive response to chronic elevation of systemic
blood pressure (BP) aimed to counterbalance left ventri-
cular wall stress [1–3]. A variety of structural and functional
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alterations of the heart such as left atrial enlargement, aortic
dilatation, systolic/diastolic dysfunction, impaired coronary
reserve, arrhythmias and right ventricular hypertrophy
(RVH) may also occur in hypertensive patients as a
consequence of haemodynamic and nonhaemodynamic
factors [4–8].
Gottdiener et al. [9] in the mid-1980s were the first
to report that right ventricular wall thickness was increased
in 40 (80%) out of 49 essential hypertensive patients with
no evidence of pulmonary hypertension and that the
magnitude of right ventricular wall increment was linearly
related (r ¼ 0.76, P < 0.005) with left ventricular wall thick-
ness. The lack of correlation between right ventricular wall
thickness and pulmonary pressure observed in that study,
however, was not in keeping with the pioneering studies by
Guazzi and co-workers [10,11] who suggested that pulmon-
ary circulation in essential hypertension was exposed to the
same dysregulation as the systemic one, by showing that
hypertensive patients had significantly heightened pulmon-
ary arterial pressure and pulmonary arteriolar resistances
as compared to their normotensive counterparts. Moreover,
elevated left ventricular pressure due to diastolic dys-
function in hypertrophied hearts is an important mech-
anism leading to venous pulmonary hypertension and to
right ventricular pressure overload [12,13]. Finally, left
ventricular hypertrophic adaptation to systemic hyper-
tension is multifactorial being sustained by a number of
growth factors including aldosterone, catecholamines,
angiotensin, insulin, cytokines and inflammatory markers
[14,15]. All these circulating or locally produced substances
may be responsible of the hypertrophic response of the
right ventricular independently of haemodynamic altera-
tions of the pulmonary circulation.
Journal of Hypertension 2013, 31:858–865
a
Department of Health Science, University of Milano-Bicocca, bIstituto Auxologico
Italiano, cDepartment of Clinical Sciences and Community Health, University of Milano
and Fondazione Policlinico di Milano, Milano, dDepartment of Medical and Surgical
Sciences, University of Brescia, Brescia, eDipartimento di Medicina Clinica e Scienze
Cardiovascolari ed Immunologiche, Università Federico II, Napoli, fDipartimento di
Medicina Clinica Sperimentale, Università di Perugia, Perugia and gAzienda Ospeda-
liera ‘S.Maria della Misericordia’, Terni, Italy
Correspondence to Professor Cesare Cuspidi, Istituto Auxologico Italiano, Clinical
Research Unit, Viale della Resistenza 23, Meda 20036, Italy. Tel: +39 0362 772433;
fax: +39 0362 772416; e-mail: cesare.cuspidi@unimib.it
Received 16 October 2012 Revised 18 November 2012 Accepted 17 January 2013
J Hypertens 31:858–865 ß 2013 Wolters Kluwer Health | Lippincott Williams &
Wilkins.
DOI:10.1097/HJH.0b013e32835f17e5
Volume 31
Number 5
May 2013

To date, only few studies have examined the impact
of systemic hypertension on right ventricular structure
[16]. This may be related to several reasons, including
the anatomy of right ventricular, characterized by thin-
wall cavity and irregular geometry that may interfere with
accurate measurements of wall thickness and volume [17].
In the present article, we report the findings of a systematic
analysis of clinical studies focusing on RVH, as assessed by
echocardiography, in order to provide a comprehensive
information on the relevance of this cardiac phenotype and
related pathophysiological as well as diagnostic implica-
tions in a pooled population of 1290 hypertensive patients.
METHODS
Search strategy and study selection
Medical literature was reviewed in order to identify all
articles evaluating right ventricular structure in hyperten-
sive patients.
A computerized search was performed using PubMed,
OVID and EMBASE databases from 1 January 1985 up to 31
July 2012. The studies were identified by the following
keywords ‘right ventricle’ ‘right ventricular hypertrophy’,
‘biventricular hypertrophy’ ‘right and left ventricular
hypertrophy’, ‘hypertension’, ‘echocardiography’. Checks
of the reference lists of selected articles and pertinent
reviews complemented the electronic search. Data have
been extracted by two independent investigators (C.C. and
C.S.); additional data have been obtained by personal
contact with authors of selected articles.
Inclusion criteria were: full articles published in English
in peer-reviewed journals from January 1st 1985 up to July
31st 2012; available data on right ventricular structure as
assessed by echocardiography; studies including at least
15 adult patients with arterial hypertension defined accord-
ing to current guidelines.
Only the up-dated or largest report was considered
when multiple publications by the same research group
were found. The first literature search identified 642 articles,
66 of these were potentially eligible for the analysis, but
only 13 could be included in the final review [9,18–29].
In particular, 32 studies were excluded as no data on
right ventricular structure (i.e. right ventricular wall thick-
ness) were provided in the hypertensive cohorts examined,
10 as double or serial publications, six because includ-
ing less than 15 individuals, three as the right ventricular
anatomy was assessed by MRI and two due to the lack of a
minimum set of clinical data.
Statistical analysis
For the purpose of the present study we considered
data provided by the studies on right ventricular wall
thickness in hypertensive individuals as compared to their
normotensive counterparts, and, when available, on the
prevalence of RVH.
In order to calculate the average prevalence of RVH
in the pooled population, the number of patients fulfilling
RVH criteria provided by the authors in each study was
divided by the total number of patients (n ¼ 1290). Data are
expressed as absolute numbers, percentage, mean  SD or
Journal of Hypertension
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
Hypertensive right ventricular hypertrophy
median and inter-quartile range. Differences between
groups/studies were assessed by ANOVA. The limit of
statistical significance was set at P < 0.05.
For the dichotomous outcome RVH present/absent,
the results were expressed as odds ratios (ORs) with 95%
confidence intervals (CIs). Heterogeneity was estimated
using the I-square test; random effect models were applied
when the heterogeneity across studies was high (I2 > 75).
Statistical analysis was done with Comprehensive Meta-
Analysis Version 2 (Biostat, Englewood, New Jersey, USA).
RESULTS
Characteristics of the studies
Table 1 shows the main characteristics of analyzed studies,
including sample size, setting, ethnicity, mean age, BMI,
office blood pressure (BP), as well as prevalence rates of
men, type 2 diabetes mellitus, cardiovascular disease and
antihypertensive treatment. Overall, 1290 hypertensive
patients and 259 normotensive controls of both sexes
were included in 13 studies performed in different clinical
settings; the assessment of right ventricular structure and
RVH prevalence was not the primary aim of all studies. Out
of 13 studies, six were conducted in internal medicine
departments [9,18,22–25], four in out-patient hypertension
clinics [19,21,26,27] and three in cardiology departments
[20,28,29].
Characteristics of the patients
Mean age range was 36–58 years [21,26]; 64.0% of
participants were men (n ¼ 798). Average SBP ranged
from 139  10 mmHg [27] to 161  20 mmHg [19], DBP from
87  9 mmHg [27] to 101  10 mmHg [19] and average BMI
from 25.0  4.0 [22] to 28.6  2.4 kg/m2 [24].
The vast majority of the pooled population (>95%) was
Caucasian (data provided from 11 studies including 1198
patients); approximately 3% had type 2 diabetes (10 studies,
1169 patients); all patients were free from overt cardio-
vascular disease (11 studies, 1206 patients).
As reported by all selected studies, about 45% of patients
(n ¼ 577) were not taking antihypertensive drugs; of these,
27% (n ¼ 157) had discontinued antihypertensive treatment
during a brief placebo wash-out period (1–4 weeks) at the
time of echocardiographic examination [37]. The fraction of
patients receiving antihypertensive medications ranged
from 28 [29] to 100% [9] across the studies.
Echocardiographic findings
Right ventricular wall measurement
As shown in Table 2, right ventricular wall thickness was
measured at end-diastole in the parasternal long-axis view
(anterior wall) at the outflow tract level in all studies. In five
out of 13 studies [9,26–29], right ventricular wall thickness
was also determined in the sub-costal view at the tips
level of the tricuspid valve. Estimation of right ventricular
wall thickness was carried out by two-dimensionally
guided M-mode tracings in all but two studies [18,23].
Intra-observer and inter-observer coefficient of variation
of measurement of right ventricular wall thickness were
www.jhypertension.com 859
Cuspidi et al.

provided by only three out of 13 studies [22,26,29]. Overall,

No (75),PWO (25)
no (70),PWO (30)
no/years (%)
these studies showed satisfactory reproducibility data

AA, African–American; BP, blood pressure; C, Caucasian; CD, cardiology department; DM, type 2 diabetes mellitus; HC, hypertension center; MD, medicine department; n.a., not available; PCVD, previous cardiovascular disease; PWO,
Treatment (ranging from 8 to 10% for intra-observer and from 10 to
13% for inter-observer variability).

PWO
PWO

PWO
100

No

No

No

No
90

70
28
Right ventricular hypertrophy criteria and right
ventricular hypertrophy prevalence
PCVD no/
years (%)

Five studies, encompassing about three quarter of the

pooled patients, provided diagnostic criteria for RVH
definition [9,24,26,28,29]. All diagnostic criteria were based
n.a.
n.a.
No
No
No
No
No
No
No
No
No
No
No
on right ventricular wall thickness measured from the
parasternal window; two out of five criteria were nonsex
TABLE 1. List of echocardiographic studies published in the last three decades focusing on right ventricular structure in human hypertension

10.3
DM
(%)

specific [9,24]. One study reported normal upper limits

n.a.
n.a.

n.a.
No

No
No
No
No
No

No
No
No
indexed to body size (i.e. body surface area) [26].
Overall, 277 patients (28.6%) were found to have RVH
161  20/101  10
150  21/100  16

154  20/101  12

according to the thresholds listed in Table 2. The pre-

157  17/91  12
156  14/96  9

155  10/99  6

149  10/99  7
145  13/97  7
139  14/88  9
139  10/87  9
155  16/94  9
153  19/95  9
Clinic BP

valence of RVH consistently varied among the studies

(mmHg)
n.a.

ranging from 17 [28] to 80% [9]. This was also the case
for LVH prevalence, ranging from 9 [27] to 100% [9,24].

Comparison between hypertensive patients and

normotensive controls
25.0  4.0
27.7  3.5
28.6  2.4
27.6  3.0
26.3  3.7
25.7  2.1
27.0  5.1
25.5  5.4
(kg/m2)

Ten out of 13 studies [9–25,26] included normotensive

BMI

n.a.
n.a.
n.a.
n.a.
n.a.

controls in their series and all but one study [27] showed
a significant increase in right ventricular wall thickness in
hypertensive patients as compared to their normotensive
counterparts. Fig. 1 reports the results of the meta-analysis
Men
(%)
100
63
62
56
87
76

70
70
62
78
56
66
n.a.

from nine studies providing data on average right ventri-

cular wall thickness and SD. The standardized difference
in means was positive in favour of hypertensive patients
(years)

52  10
47  10
43  12

58  12
50  11
51  12
50  10
60  9

31  6
49  9
44  8
50  3
52  6
Age

(1.31 mm, CI 0.86–1.77, P < 0.001). As shown in Table 2,

average right ventricular thickness ranged from 3.9 [23] to
7.0 mm [9] in patients with systemic hypertension and from
2.8 [23] to 5.0 mm [20] in controls, respectively.
Ethnicity (%)

C (83) AA (17)

Correlation between right ventricular and left

ventricular thickness
n.a.

n.a.

The relationship of right ventricular to left ventricular wall

C

C
C
C
C
C
C
C
C
C

thickness was assessed by five studies [9] including a total of

712 normotensive and hypertensive individuals. A positive
Sample
size (n)
49
35
58
43
15
41
44
20
30
330
60
376
189

correlation between right ventricular anterior wall and

left ventricular posterior wall thickness was present, the
correlation coefficient (r) ranging from 0.47 [26] to 0.76 [9]
with an average value (r ¼ 0.62) being highly significant
Setting

(P < 0.001) (Fig. 2). Similar, but less stringent correlations

MD
MD

MD
MD
MD
MD

were found between right ventricular anterior wall and

HC
CD
HC

HC
HC
CD
CD

interventricular wall thickness (data not shown).

publication

DISCUSSION
Year of

The present analysis of 13 studies published in the last three

1985
1987
1989
1992
1993
1995
1998
2001
2002
2009
2010
2011
2012

decades provides an updated information on right ventri-

cular structural changes and RVH prevalence, as assessed
by echocardiography, in a pooled hypertensive population
Habib and Zoghbi [20]

of 1290 patients from different hypertensive settings and

Gottdiener et al. [9]

Myslinski et al. [23]

Pedrinelli et al. [27]

Galderisi et al. [24]
Cittadini et al. [22]

Ivanovic et al. [28]

Cuspidi et al. [19]

Cuspidi et al. [26]

characterized by various grades of BP elevation and hyper-

Nunez et al. [18]

Lonati et al. [21]

Cicala et al. [25]

Tadic et al. [29]

(Reference)

placebo wash-out.

tensive heart disease. The main findings of our review are :

echocardiographic RVH is frequently detected in treated
Author

and untreated hypertensive patients, its frequency ranging

from 17 to 80% in the different reports depending on the
criteria employed and the clinical characteristics of the

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 Journal of Hypertension
TABLE 2. Echocardiographic findings concerning right ventricular wall thickness (RVWT) and hypertrophy (RVH) in clinical studies on systemic hypertension published in the last
three decades
RVWTd (mm)
Author hypertensive RVWTd (mm) Echocardiographic
(Reference) patients (n) controls (n) method Site of measurement RVH criteria RVH (%)
Gottdiener et al. [9] 7.0  2.0 (n ¼ 49) 4.0  1.0 (n ¼ 20) M-mode under two-dimensional Right ventricular outflow tract RVWTd  6.0 mm 80%
control and subcostal view
Nunez et al. [18] 5.9  1.5 (n ¼ 35) 3.7  0.8 (n ¼ 15) M-mode Right ventricular outflow tract n.a. n.a.
Cuspidi et al. [19] 5.1 þ 0.9 (n ¼ 58) 3.6  0.8 (n ¼ 20) M-mode under two-dimensional right ventricular outflow tract n.a. n.a.
control
Habib and Zoghbi [20] 6.0  1.2 (n ¼ 43) 5.0  1.0 (n ¼ 42) M-mode under two-dimensional Right ventricular outflow tract n.a. n.a.
control
Lonati et al. [21] 4.6  0.6 (n ¼ 15) 3.2  0.3 (n ¼ 15) M-mode under two-dimensional Right ventricular outflow tract n.a. n.a.
control
Cittadini et al. [22] 7.0  2.0 (n ¼ 41) 4.0  2.0 (n ¼ 40) M-mode under two-dimensional Right ventricular outflow tract n.a. n.a.
control
a a
Myslinski et al. [23] 3.9 (n ¼ 44) 2.8 (n ¼ 26) M-mode Right ventricular outflow tract n.a. n.a.
Galderisi et al. [24] 4.6  0.8 (n ¼ 20) 4.0  0.6 (n ¼ 30) M-mode under two-dimensional right ventricular outflow tract RVWTd 5.0 mm 47
control
Cicala et al. [25] 4.8  1.1 (n ¼ 30) 3.8  0.9 (n ¼ 30) M-mode under two-dimensional Right ventricular outflow tract n.a. n.a.
control
Cuspidi et al. [26] 5.5  1.0 (n ¼ 330) n.a. M-mode under two-dimensional Right ventricular outflow tract RVWTd 3.1 mm/m2 (M); 33.5
control and subcostal view 3.0 mm/m2 (W)
Pedrinelli et al. [27] 3.8  0.9 (n ¼ 60) 3.7  0.7 (n ¼ 29) M-mode under two-dimensional Right ventricular outflow tract n.a. n.a.
control and subcostal view (?)
Ivanovic et al. [28] 4.4  0.8 (n ¼ 376) n.a. M-mode under two-dimensional Right ventricular outflow tract RVWTd 6.0 mm (M); 17.5
control and subcostal view 5.5 mm (W)
Tadic et al. [29] 4.5  0.9 (n ¼ 189) n.a. M-mode under two-dimensional Right ventricular outflow tract RVWTd 6.0 mm (M); 27.5
control and subcostal view 5.5 mm (W)

n.a., not available.

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861
Hypertensive right ventricular hypertrophy
Cuspidi et al.

Study name Statistics for each study Std. difference in means and 95% CI
Std. Diff. Lower Upper P- Weight
in means limit limit Value %
Gottdiener (1985) 1.69 1.09 2.28 <0.01 11.8
Nunez (1987) 1.65 0.96 2.33 <0.01 10.5
Cuspidi (1989) 1.71 1.14 2.29 <0.01 11.3
Habib (1992) 0.90 0.46 1.35 <0.01 12.2
Lonati (1993) 2.95 1.92 3.99 <0.01 8.0
Cittadini (1995) 1.50 1.01 1.99 <0.01 11.9
Galderisi (2001) 0.87 0.28 1.47 <0.01 11.2
Cicala (2001) 0.99 0.46 1.53 <0.01 11.6
Pedrinelli (2010) 0.12 –0.32 0.56 0.59 12.2
Total 1.31 0.86 1.77 <0.01 100
Random model –4.0 –2.0 0.0 2.0 4.0
Heterogeneity test I2 = 82.4 % Favours control Favours EH
FIGURE 1 Meta-analysis of studies comparing right ventricular wall thickness in essential hypertensive patients (EH) and normotensive controls (c): the analysis supports the
presence of a positive difference in favor of EH.

examined patients. Overall, RVH was observed in approxi-
mately 25% of the whole study population; right ventricular
structure was determined by a single linear measurement of
right ventricular anterior wall from the parasternal long axis
view by two-dimensionally guided M-mode tracings in the
vast majority of the studies; significant differences in right
ventricular wall thickness between hypertensive patients
and normotensive controls were found in all studies but
one; right ventricular anterior wall thickness was signifi-
cantly correlated with left ventricular posterior wall thick-
ness (average r ¼ 0.62).
The data of the present review, although based on a
small series of studies including about one thousand
patients, reinforce the concept that left ventricular structural
alterations induced by systemic hypertension are paralleled
by similar changes in right ventricular chamber. These
echocardiographic findings are in keeping with previous
reports in experimental animals about the pathophysiology
of inter-ventricular interaction. Left ventricular pressure
overload induced by proximal aorta banding in experi-
mental animals was found to be associated with increased
biochemical and haemodynamic function of the ‘non-
stressed’ ventricle as well as with development of bi-
ventricular hypertrophy [30]. Furthermore, banding of the
dog pulmonary artery, in addition to causing right ventricular
wall thickening, resulted in increased left ventricular mass
and stiffness [31]. Finally, in cats undergoing pulmonary
artery constriction Buccino et al. [32] were able to demon-
strate a marked increase in connective tissue synthesis, as
indicated by the raised concentration and total content of
hydroxyproline both in the ‘stressed’ right ventricle as in the
‘unstressed’ left ventricle.
The mechanism(s) of RVH in systemic hypertension are
still unclear due to the paucity of clinical investigations
specifically addressed to this issue. A combination of
haemodynamic, anatomical and humoral factors may have
an important role in modulating right ventricular mor-
phology and function in essential hypertension.
Guazzi and co-workers [10] were the first to report that
systemic hypertension is associated with increased pulmon-
ary arterial pressure and pulmonary arteriolar resistances
even in the presence of preserved left ventricular function

Study name Statistics for each study Correlation and 95% CI

Correlation Lower Upper P- Weight
limit limit value %

Gottdiener (1985) 0.76 0.65 0.84 <0.01 19.6

Nunez (1987) 0.66 0.47 0.79 <0.01 16.6

Cuspidi (1989) 0.72 0.57 0.82 <0.01 17.5

Cuspidi (2009) 0.47 0.38 0.55 <0.01 23.8

Tadic (2012) 0.49 0.37 0.59 <0.01 22.5

Total 0.62 0.49 0.73 <0.01 100

–1.00 –0.50 0.00 0.50 1.00
Random model
Heterogeneity test I2 = 82.5% Favours Favours
negative positive
FIGURE 2 Meta-analysis of studies evaluating the relationship between right ventricular anterior wall and left ventricular posterior wall thickness: the analysis supports the
presence of a positive correlation between the two parameters.

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and normal left ventricular mass. Furthermore, the same
investigators showed that pulmonary vascular over-
reactivity to catecholamines is present in patients with
systemic hypertension suggesting that a vasoconstriction
in the pulmonary circulation occurs in parallel with the
development of systemic high blood pressure [11,33]. These
observations, however, were not confirmed by other
reports. For instance, in a group of 71 men with essential
hypertension, Fagard et al. [34] failed to demonstrate
a significant relationship between pulmonary vascular
resistances and mean intra-arterial brachial pressure.
Left ventricular diastolic dysfunction related to LVH,
especially of the concentric type, has been demonstrated
to markedly affect right-sided cardiac morphology and
haemodynamics. Pulmonary venous hypertension caused
by elevated left-sided pressures as a consequence of a
reduced left ventricular relaxation is a powerful deter-
minant of right ventricular hypertrophy and functional
impairment. This pathophysiologic link is supported by
the concomitant increase of right ventricular wall thickness
with the progressive worsening of left ventricular diastolic
parameters as assessed by conventional and pulsed tissue
Doppler analysis [25,26]. Furthermore, a number of studies
have shown that a parallel impairment of left ventricular
and right ventricular diastolic function may occur in
systemic hypertension even before the development of
biventricular hypertrophy [27,35,36].
Although myocyte disposition in the right ventricular
wall substantially differs (i.e. predominantly oriented in the
longitudinal direction in the sub-endocardial layer) from
the three-layered left ventricular wall, mechanical transfer
of stress from the left ventricular to the right ventricular
trough common muscle bands is a plausible mechanism
leading to RVH in systemic hypertension [37,38]. It is note-
worthy that right ventricular function is strictly influenced
by left ventricular performance owing to ventricular
interaction. Interventricular septum (which includes
fibres arising from both ventricular chambers), pericardium
and common muscle fibres all play a pivotal role in
facilitating force transmission from left ventricular to
right ventricular. Notably, approximately one-third of
right ventricular pressure is generated by left ventricular
contraction.
A further possibility is that humoral/hormonal
factors mediate both right ventricular and left ventricular
hypertrophy in response to pressure overload of either
ventricle; thus, biventricular hypertrophy may be a
secondary response to the activation of sympathetic tone
and renin–angiotensin–aldosterone system in patients with
systemic hypertension. Experimental data from Laks et al.
[39] showed that pressure overload following long-term
banding of the pulmonary artery causes noradrenaline
release in both ventricles. Ventetuolo et al. [40] examining
the relationship of administration of angiotensin-converting
enzyme inhibitors and angiotensin II receptor blockers with
right ventricular structure and function, assessed by cardiac
MRI, in a large cohort of participants without clinical
cardiovascular disease recruited in the Multi-Ethnic Study
of Atherosclerosis (MESA) found that African–American
subjects treated with these drugs had lower right ventricular
mass independently of several confounders suggesting a
Journal of Hypertension
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Hypertensive right ventricular hypertrophy
possible role of the renin–angiotensin system in modulat-
ing right ventricular structure and function.
Some further aspects of our review deserve to be
commented. Imaging of the right ventricular by echo-
cardiography is challenging due to the complex geometry
of this cardiac chamber, right ventricular can be divided in
three anatomical parts: the inlet part including tricuspid
valve, the trabeculated apex and the outlet [41]. This com-
plex morphology can be hardly assimilated to a geometric
model, at difference from the conical shape of the left
ventricular; this represents a major methodological limita-
tion for a reliable assessment of right ventricular dimension
and function based on standard echocardiography. In spite
of these limitations, Foale et al. [42] showed that mean
absolute right ventricular wall thickness measured from five
echocardiographic views at 10 different right ventricular
sites in 41 normal controls varied within a narrow interval:
from 3 to 4 mm (range 2–7 mm). In that article, right
ventricular wall thickness obtained by the subcostal view
was greater than that measured from the parasternal view;
this finding has been confirmed by subsequent obser-
vations. It is unclear why right ventricular wall measured
by subcostal windows is thicker that that obtained by
different echocardiographic views (i.e. parasternal long-
and short-axis view). A difficult alignment of the M-mode
cursor and inclusion of trabeculations, chordae tendineae
as well as papillary muscles are among the technical
and biological factors that may explain the differences
in right ventricular wall thickness between subcostal
and parasternal view. Notably, the above-mentioned
factors may also explain the higher intra-observer and
inter-observer coefficient of variation of right ventricular
wall measurement from subcostal view as compared to
parasternal view documented in some reports [26].
On the basis of echocardiographic studies conducted in
normotensive healthy controls, right ventricular muscular
wall not including trabeculations may range from 2 to 5 mm
[41,43]; thus, right ventricular mass is approximately one-
quarter that of left ventricular.
Accordingly, RVH is defined by authoritative guidelines
and scientific reports on the basis of right ventricular free
wall thickness equal [17] or exceeding [41] 5 mm regardless
of sex and indexation for body size. This occurs in spite of
the fact that in healthy as well as diseased patients, cardiac
parameters are closely related to anthropometric variables
such as height and weight. Furthermore, the extension
of such diagnostic thresholds to the older fraction of the
general population should be considered with caution as
the above-mentioned upper limits of normality of right
ventricular wall thickness have been derived from young
or middle-aged individuals [17,43].
Alterations in right ventricular morphology and function
have been demonstrated to have a relevant prognostic
value in patients with pulmonary hypertension, myocardial
infarction involving the right ventricular and left ventricular
dysfunction [44,45] and more recently in a population-
based multi-ethnic sample free of clinical cardiovascular
disease at baseline [46]. This has not been documented for
patients with systemic hypertension, as no prospective
studies have investigated the impact of RVH on cardiovas-
cular morbidity and mortality. Nonetheless, it is conceivable
www.jhypertension.com 863
Cuspidi et al.
that the development of bi-ventricular hypertrophy may
have a worse prognosis than isolated LVH. In one article
included in the present review, abdominal obesity, left
ventricular systolic dysfunction, high-fasting glucose and
elevated SBP were in ranking order the most important
independent correlates of biventricular hypertrophy [26].
These data underline the fact that this cardiac phenotype is
associated with a clustering of modifiable conditions of
adverse prognostic significance.
A further point worthy of comment relates to the lack
of available data on right ventricular changes as assessed
by standard electrocardiogram in the setting of systemic
hypertension. For what concerns MRI, to the best of our
knowledge, a few studies addressed this topic. Todiere
et al. [47] evaluating 25 patients with mild-to-moderate
essential hypertension and 24 age-matched controls found
that right ventricular mass index, ventricular wall thickness
and remodelling index were greater in the former group
and were associated with reduced peak filling rate. Notably,
none of hypertensive patients fulfilled the criteria for RVH
(i.e. 48 g/m2 in men and 37 g/m2 in women).
In conclusion, our analysis clearly shows that
hypertensive heart disease is characterized by the parallel
involvement of both ventricles and that RVH is a frequent
echocardiographic finding in systemic hypertension.
RVH may relate to multiple factors including ventricular
interdependence, loading conditions, pulmonary hyper-
tension, hormonal agents and sympathetic activation.
Whether right ventricular structural alterations occur
in the early phases of hypertensive heart disease or in a
later step after pulmonary vascular changes have been
developed, remains to be clarified. More importantly,
future prospective investigations addressing the associ-
ation between RVH and outcomes are needed to define
the clinical and prognostic value of this phenotype in
patients with systemic hypertension. Indeed, detection
of alterations in right ventricular structure and function
could refine the evaluation of hypertensive cardiac target
organ damage and improve cardiovascular risk stratifica-
tion and decision making therapeutic strategies in addition
to the traditional assessment of left ventricular structure
and function.
ACKNOWLEDGEMENTS
We are grateful to Dr Marjana Tadic (MD) for providing the
data of her study, Dr Francesca Negri (MD) and Dr Marta
Rescaldani (MD) for their contribution in statistical analysis.
Conflicts of interest
There are no conflicts of interests.
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trophy as a determinant of atrial fibrillation) and therapeutic
response (whether, e.g. RAS blockers are more effective
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than other agents) have not been satisfactory addressed by
specific investigations yet.
Reviewer 2
This review provides evidence of structural changes of
the right ventricle in hypertensive patients, which appear
to be in parallel with changes in the left ventricle. The
strength is a carefully conducted systematic review and
meta-analysis. However, echocardiographic examination
of the right ventricle can be challenging and these meth-
odological issues are difficult to account for in this meta-
analysis. Also, the number of patients in the separate studies
is limited.
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