Download Right ventricular function in systemic hypertension

Journal of Human Hypertension (1998) 12, 149–155
 1998 Stockton Press. All rights reserved 0950-9240/98 $12.00
ORIGINAL ARTICLE
Right ventricular function in systemic
hypertension
´ ´
´
W Myslinski, J Mosiewicz, E Ryczak, W Barud, A Biłan, R Palusinski and J Hanzlik
First Department of Internal Medicine, Lublin University, Medical School, Staszica 16, 20-081, Lublin,
Poland
The aim of the study was the assessment of right ventricular (RV) structure and diastolic function in hypertensive subjects. The study group consisted of 44
patients with untreated, mild to moderate essential systemic hypertension. All the patients were in sinus
rhythm, no symptoms of congestive heart failure,
ischaemic or valvular heart disease and lung disorders
were found. Twenty-six healthy subjects were the control group. M-mode echocardiographic measurements
of the right ventricular wall (RVW) diastolic thickness,
right ventricular outflow tract diameter (RVOTD), left
ventricular (LV) structure and LV systolic function were
performed. Pulsed Doppler echocardiography was used
to measure peak early (TE) and peak atrial (TA) right
ventricular diastolic filling velocities as well as velocitytime integrals (VTI-TE and VTI-TA). TE:TA and VTITE:VTI-TA ratios were calculated. Similar parameters of
the left ventricular diastolic filling were recorded at the
level of mitral annulus. Mean pulmonary artery pressure
(MPAP) was measured non-invasively by the estimation
of pulmonary artery systolic flows. We demonstrated in
hypertensive patients significantly thicker RVW (3.94 vs
2.8 mm, P ⬍ 0.001) and increased LV mass. In the hypertensive, increased TA and VTI-TA and diminished TE:TA
and VTI-TE:VTI-TA ratios were recorded, indicating the
abnormalities of RV diastolic function. RV diastolic filling parameters correlated positively with corresponding
parameters of LV filling. The results of our study demonstrate that impairment of LV diastolic function, the common finding in systemic hypertension, is associated
with diastolic disturbances of the right ventricle. RVW
thickening and hypertrophy of interventricular septum
seem to be major factors influencing RV diastolic function.
Keywords: systemic hypertension; echocardiography; right ventricle; diastolic function
Introduction
Left ventricular (LV) performance in systemic hypertension is well described in numerous publications.1–5 Chronic pressure overload leads to LV
concentric hypertrophy, a major adaptive mechanism that helps to maintain normal LV systolic
function. Systemic hypertension, if not treated,
leads to heart failure and is associated with an
increased risk of coronary artery disease and stroke.
At present, the elevations in diastolic or systolic
pressure are the indications for antihypertensive
treatment.6 Unfortunately, epidemiological data
indicate that only one hypertensive patient out of
five is receiving satisfactory treatment while about
80% of hypertensive patients are not treated at all
or an antihypertensive therapy is inefficient.
It is obvious that most studies of cardiac dysfunction in essential hypertension focused on LV pathology. Congestive heart failure, the common complication of systemic hypertension, may be the
consequence of decreased LV ejection fraction.
However, Soufer et al7 and Dougherty et al8 reported
that about 40% of patients with congestive heart
´ ´
Correspondence: Dr Wojciech Myslinski, First Department of
Internal Medicine, Lublin University Medical School, Staszica
16, 20-081 Lublin, Poland
Received 14 April 1997; revised 19 July 1997; accepted 5
August 1997
failure had normal systolic function. Several radionuclide and echocardiographic studies showed the
importance of diastolic function to cardiac performance. Altered profiles of LV diastolic filling with
diminished early filling and increased late or atrial
filling are common echocardiographic findings in
hypertensive patients. LV hypertrophy and ischaemia are among the major causes of ventricular diastolic abnormalities and may be responsible for
development of heart failure even if systolic function remains normal.4,9
Most publications regarding the right ventricle
focused on right ventricular (RV) function in lung
diseases. RV hypertrophy due to alveolar hypoxia is
a common complication of chronic obstructive pulmonary disease (COPD) and obstructive sleep
apnoea syndrome (OSA).10,11 RV diastolic dysfunction was found in COPD and ischaemic heart disease.12–14 RV performance in systemic hypertension
is not well evidenced yet. Invasive studies showed
the pathology of pulmonary circulation in hypertensive patients.15–18 Only a few publications concern
echocardiographic assessment of the right ventricle
and its diastolic function in systemic hypertension,
which is all the more surprising as physical examination often demonstrates the features of RV pathology and dysfunction in hypertensive patients.19–23
The purpose of this study was the echocardiographic assessment of RV structure and diastolic
function in patients with untreated, essential
Right ventricular function in hypertension
´ ´
W Myslinski et al
150
systemic hypertension. By simultaneous echocardiographic estimation of LV performance and pulmonary circulation we tried to establish the possible
mechanisms of RV dysfunction in hypertensive
patients.
Materials and methods
The original group examined consisted of 59
patients with mild to moderate essential systemic
hypertension. Patients did not yet receive antihypertensive therapy. Blood pressure (BP) was measured
at 9.00 am on the day of examination and the
patients did not take any medication that could
influence heart and lung performance. The patients
were free of symptoms of congestive heart failure,
ischaemic heart disease, lung disorders or endocrinopathies. All patients were in sinus rhythm and
had no arrhythmias or conduction abnormalities in
standard electrocardiographic examinations.
Initially, lung function was estimated using body
plethysmography technique (Bodyscreen, Jaeger,
Germany). Total airway resistance (Raw), intrathoracic gas volume (ITGV), residual volume, total lung
capacity (TLC), forced vital capacity (FVC), forced
expiratory volume in 1 s (FEV1), Tiffeneau index
(FEV1%FVC), peak expiratory flow (PEF) and flows
at 50, 25% of FVC were measured. All values
including Raw and FEV1%FVC were expressed as a
per cent of predicated normal value calculated individually for each patient. The values of Raw below
0.3 kPa/l/s were accepted as normal. Six patients
with bronchial obturation were excluded from
further stages of the examination.
Echocardiographic examinations were performed
using Hitachi EUB-450 (Hitachi Medical Corporation, Tokyo, Japan) ultrasonograph with 3,5 MHz
transducer. Patients were in left decubitus position.
M-mode presentation in the parasternal view was
used to measure right ventricular wall (RVW) enddiastolic diameter, RV outflow tract diastolic diameter (RVOTD), interventricular septum diastolic
diameter (IVSD), posterior wall diastolic diameter
(PWD), LV end-diastolic diameter (LVEDD) and left
atrium diameter (LAD). LV mass was calculated
using the Devereux formula.24 M-mode measurements were used to calculate LV ejection fraction by
the Teichholz formula. Then, from the apical fourchamber view or alternatively from the parasternal
short axis view diastolic flows through the tricuspid
valve were recorded by pulsed Doppler echocardiography. Doppler sample volume was positioned at
the level of the tricuspid annulus. Recordings from
two consecutive cardiac cycles were averaged and
used for calculations. RV diastolic filling time
(RVFT), peak early (TE) and peak atrial (TA) diastolic filling velocities as well as velocity-time integrals of early (VTI-TE) and atrial (VTI-TA) filling
waves were measured. Additionally, deceleration
time of early filling wave was measured. TE:TA
(TE:A) and VTI-TE:VTI-TA (VTI-TE:A) ratios were
calculated. Similar recordings of transmitral flows at
the level of the mitral annulus were obtained from
the apical view—LV diastolic filling time (LVFT),
peak early (ME) and atrial (M) diastolic filling velo-
cities, early mitral wave deceleration time (DME)
and velocity-time integrals (VTI-ME, VTI-MA).
ME:MA (ME:A) and VTI-ME:VTI-MA (VTI-ME:A)
ratios were calculated. All recordings were obtained
during quiet breathing at the end of expiration. From
the parasternal short axis view pulmonary artery
systolic flows were recorded in the main pulmonary
artery. Peak pulmonary systolic velocity and pulmonary acceleration time (PAT) defined as a time
from onset to peak systolic velocity were measured.
Doppler recordings with maximal systolic velocity
were used for calculations. Based on pulmonary
artery acceleration time corrected for heart rate
(PATcorr = PAT divided by square root of R-R interval in ECG) mean pulmonary artery pressure
(MPAP) was calculated using the Kitabatake formula:25
log10 MPAP = −0.0068 PATcorr + 2.1
Six patients were excluded from statistical analysis because Doppler examination revealed the presence of valvular heart disease. Electrocardiographic
exercise test was performed by BRUCE protocol in
order to detect patients with stress-induced chest
pain. Three patients did not complete the exercise
test and were also excluded from the study group.
Finally, the study group consisted of 44 hypertensive patients, 21 women and 23 men, aged 26 to 55
(mean 43.57 ± 8.17).
Twenty-six normotensive patients, 12 women and
14 men, aged 21 to 55 (mean 41.27 ± 8.29) were the
control group. The protocol of qualification, examination and exclusion criteria were the same as in the
study group.
Statistical analysis
The statistica 4.5 for Windows was used. Values are
expressed as means ± standard deviations. Statistical methods used were linear regression models,
Pearson’s r coefficients and non-paired Student’s ttests. The coefficients of repeatability of TE and TA
(calculated according to Bland and Altman26) were
0.09 m/s and 0.07 m/s, respectively.
Results
Age, height, weight, body mass index and heart rate
were similar in both groups. Mean systolic and diastolic blood pressures were significantly higher in
the hypertensive group. Nineteen hypertensive
(43%) and 12 normotensive (46%) patients were
smokers. General characteristics of the hypertensive
and normotensive groups are listed in Table 1.
Body plethysmography
In hypertensive patients significantly higher values
of Raw were found (P ⬍ 0.001). ITGV and FEV1 were
diminished in the hypertensive (P ⬍ 0.001 and
P ⬍ 0.05, respectively). Other parameters did not
differentiate both groups, however, hypertensive
subjects showed slightly impaired lung function
compared to normotensive ones. The results of body
plethysmography are shown in Figures 1 and 2.
Right ventricular function in hypertension
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W Myslinski et al
Table 1 General characteristic of the examined population
Age (yrs)
Height (cm)
Weight (kg)
BMI (kg/m2)
DBP (mm Hg)
SBP (mm Hg)
Hypertensives
(mean ± s.d.)
Normotensives
(mean ± s.d.)
Significance
43.6 ± 8.2
168.5 ± 8.5
78.8 ± 12.6
27.7 ± 3.5
91 ± 11.8
157.3 ± 17.2
41.3 ± 8.3
167.4 ± 10.3
74 ± 13.4
26.3 ± 2.7
75.5 ± 7.1
116 ± 14
NS
NS
NS
NS
P ⬍ 0.001
P ⬍ 0.001
BMI: body mass index; DBP: diastolic blood pressure; SBP:
systolic blood pressure; NS: non-significance.
Figure 1 Pulmonary function parameters in hypertensive and
normotensive patients. Raw: total airway resistance; ITGV:
intrathoracic gas volume; FEV1: forced expiratory volume in 1 s.
(쏔 hypertensives; 쐽 normotensives).
M-mode echocardiographic examination
RVW diameter was 3.94 mm in hypertensive and
2.8 mm in normotensive subjects (P ⬍ 0.001), while
RVOTD showed no differences between both
groups. Hypertensive patients demonstrated significantly higher dimensions of IVSD (P ⬍ 0.001),
PWD (P ⬍ 0.001), LAD (P ⬍ 0.01) and increased
values of LVM (P ⬍ 0.01). Ejection fraction as well
as LVEDD were similar in hypertensive and normotensive patients (Figure 3).
Doppler-echocardiography
RV diastolic filling time was 0.44 ± 0.11 s in hypertensive and 0.47 ± 0.11 s in normotensive patients
(NS), deceleration time was 0.19 ± 0.05 s and
0.17 ± 0.05 s (NS), respectively. Also peak early
velocity (TE) did not differentiate between hypertensive and normotensive subjects (0.46 ± 0.11 m/s vs
0.5 ± 0.09 m/s, NS). Peak atrial velocity (TA) was
significantly higher in hypertensive patients
(0.39 ± 0.08 m/s vs 0.33 ± 0.07 m/s, P ⬍ 0.01). TE:A
ratio was significantly lower in patients with hypertension (1.22 ± 0.29 vs 1.53 ± 0.26, P ⬍ 0.001). Velocity-time integrals significantly varied in both examined groups. VTI-TE was 5.53 ± 2.14 cm in
hypertensive and 6.59 ± 1.26 cm in normotensive
subjects (P ⬍ 0.05). VTI-TA was 3.09 ± 0.93 cm and
2.48 ± 0.72 cm, respectively (P ⬍ 0.01). VTI-TE:A
ratio showed significant differences between study
and control groups (P ⬍ 0.001). Results of the
Doppler study are shown in Figure 4.
Peak pulmonary artery systolic flow velocities
were similar in both groups. Pulmonary artery acceleration time corrected for heart rate (PATcorr) was
significantly shortened in hypertensive compared to
normotensive
patients
(0.128 ± 0.019 s
vs
0.144 ± 0.024 s, P ⬍ 0.001). Non-invasively estimated MPAP showed higher values in patients with
hypertension (17.72 ± 5.18 mm Hg vs 14.09 ± 4.76
mm Hg, P ⬍ 0.05).
Doppler recordings of transmitral diastolic flows
in hypertensive patients demonstrated increased
values of peak atrial velocity MA (P ⬍ 0.01), lower
ME:A (P ⬍ 0.001) and VTI-ME:A (P ⬍ 0.05) ratios
and no differences regarding LVFT and ME.
Statistically significant correlations were found
between right and corresponding LV diastolic filling
parameters (Figures 5 and 6).
Figure 2 Pulmonary function parameters in hypertensive and normotensive patients (continued). RV: residual volume; TLC: total lung
capacity; FVC: forced vital capacity; FEV1%FVC: Tiffeneau index; PEF: peak expiratory flow; FEF50: forced expiratory flow at 50% of
FVC; FEF25: forced expiratory flow at 25% of FVC.
151
Right ventricular function in hypertension
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152
Figure 3 M-mode echocardiographic measurements. RVW: right ventricular wall diameter; IVSD: interventricular septum diameter;
PWD: left ventricular posterior wall diameter; RVOTD: right ventricular outflow tract diameter; LVEDD: left ventricular end-diastolic
diameter; LAD: left atrium diameter; EF: ejection fraction.
Figure 4 Doppler echocardiographic measurements of RV diastolic filling. TE: peak early velocity; TA: peak atrial velocity; TE:A: peak
early/atrial velocity ratio; VTI-TE: velocity-time integral of early filling wave; VTI-TA: velocity time integral of atrial filling wave. VTITE:A: velocity-times integrals ratio.
Discussion
The right ventricle, a thin-wall cavity, is a central
element of the low-pressure system. In our study,
hypertensive patients demonstrated an increased
RVW diastolic diameter, although, in none of them
RVW exceeded 7 mm—the upper limit of RVW diastolic thickness. Gottdiener et al27 found in healthy
subjects that the averge RVW thickness was 4 ± 1 mm
(range 3–5 mm) measured from the parasternal window.27 Measurements obtained from the subcostal
windows are usually greater than those obtained from
the parasternal view, which may depend on ultrasound beam obliqueness and papillary muscles
inclusion. We used only the parasternal view and the
high quality recordings for measurements.
The interventricular septum, common for both
ventricles, as well as posterior wall were significantly thicker in patients with hypertension.
RVOTD and LVEDD did not differ with both groups.
LV hypertrophy and tendency to RVW thickening
suggest the influence of systemic hypertension on
both ventricles. Nunez et al20 demonstrated RVW
hypertrophy in hypertensive subjects. Additionally
they showed, that in patients with LV hypertrophy
the RVW was significantly thicker compared to the
patients without LV hypertrophy.20
LV myocardial hypertrophy and increased interstitial levels of myocardial collagen are among major
causes of ventricular dysfunction in systemic hypertension. Several studies demonstrated LV diastolic
function abnormalities in patients with LT hypertrophy due to systemic hypertension, hypertrophic cardiomyopathy and aortic stenosis.1,4 LV diastolic dysfunction was also found to be aggravated in normoand hypertensive obese patients with eccentric LV
hypertrophy compared to lean subjects.3,28,29,30
Doppler examination is a useful method of estimating left and right ventricular fillings. Predominant
early diastolic filling wave and atrial filling wave,
separated by minimal flow during diastasis are usually observed in healthy subjects with sinus
rhythm.31 Recorded values of tricuspid inflow are
lower than corresponding parameters of transmitral
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Figure 5 Relationship between right and corresponding left ventricular filling parameters (early to atrial waves velocity-time
integrals ratios).
Figure 6 Relationship between right and corresponding left ventricular filling parameters (early to atrial waves velocity ratios).
diastolic flow.32 In our Doppler study we demonstrated significant differences between hypertensive
and normotensive patients regarding parameters of
RV diastolic filling. Increased TA and VTI-TA and
diminished TE:A and VTI-TE:A ratios reflect
impaired RV relaxation. These abnormalities correlated with LV diastolic function. It should be
emphasized that strong differences regarded only
indirect parameters of ventricular filling—TE:A and
VTI-TE:A. No correlations between RV filling parameters and RVW thickness or LV mass were found.
Chakko et al21 demonstrated correlations between
right and corresponding LV diastolic filling parameters in hypertensive subjects. Habib et al22
reported significant, albeit weak correlation between
RVW thickness and RV peak late inflow velocity in
hypertensive patients. They observed significant
correlations between left and right ventricular dia-
Right ventricular function in hypertension
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W Myslinski et al
154
stolic filling parameters in normo- and hypertensive patients.22
These results suggest that RVW thickening may be
of importance to RV diastolic function, although it
is not a single factor of ventricular filling abnormalities. Diastole is not only a passive process. The
active transport of calcium from sarcoplasm to sarcoplasmic reticulum is an energy-dependent process.33 The utilization of energy exceeds 15% of total
energy consumption during each cardiac cycle.33,34
Impaired tissue perfusion in hypertrophied myocardium is a substantial mechanism of delayed myocardial relaxation.
The possible mechanisms of RV hypertrophy in
systemic hypertension are not clear. In our study we
found increased values of MPAP in hypertensive
patients, but in both groups MPAP did not exceed
normal range. The elevation of MPAP may be the
consequence of increased pulmonary artery wedge
pressure (PAWP). Olivari et al15 reported in hypertensive subjects increased values of pulmonary
artery pressures, pulmonary arterioral resistance
(PAR) and PAWP. Fiorentini et al16 demonstrated
that PAR correlated positively with systemic vascular resistance and suggested that systemic and pulmonary vasculature were exposed to the same type
of dysregulation in systemic hypertension. In contrast, Fagard et al17 showed no influence of systemic
hypertension on pulmonary vasculature. Ferlinz19
demonstrated significantly lower RV ejection fraction in hypertensive patients, indicating the impairment of RV emptying.
RV hypertrophy and dysfunction is well recognized in patients with COPD and OSA.10,11,12,35 We
found in hypertensive patients significantly
increased Raw and diminished ITGV and FEV1, however, all measurements remained within normal
ranges. Therefore, it is less possible that increased
MPAP could be a result of the alveolar hypoxia and
Euler–Liljenstrand reflex.
RV diastolic filling parameters correlated with
corresponding LV filling parameters. This may suggest that interventricular septum, common for both
ventricles, may play an important part in RV diastolic dysfunction. Goldstein et al36 in their study
demonstrated interactions between ventricular function and interventricular septum performance during acute heart ischaemia. They showed that septal
ischaemia exacerbated both LV and RV diastolic
filling abnormalities. During acute right heart
ischaemia RV performance was augmented through
mechanical displacement of the interventricular
septum toward the right ventricle. Nakamura et al37
found increased RV ejection fraction during exercise
in patients with myocardial infarction and with no
evidence for interventricular septum involvement.
Years ago, interventricular septum hypertrophy due
to systemic hypertension was described as a
Bernheim syndrome.19 It is possible that inappropriate displacement of hypertrophied interventricular
septum may lead to impairment of RV diastolic suction.
As mentioned above, strong correlations between
right and left ventricular filling parameters may suggest that both ventricles are influenced by the same
factors. The influence of some systemic substances
like aldosterone, catecholamines, angiotensin, insulin or other growth factors on LV hypertrophy is
widely described and their effect is probably not
limited only to the left ventricle.38–41
The results of our study demonstrate the involvement of the right ventricle in systemic hypertension
and the relationship between right and left ventricular function. Thus, the assessment of RV performance may be an additional, sensitive indicator of the
course of hypertensive disease and also of the effectiveness of antihypertensive therapy.
Study limitations
The echocardiographic visualization of the right
ventricle is more difficult than the left one. Thus,
we assessed RV flows through the tricuspid valve
using the four chamber apical or alternatively, the
parasternal short axis view, what may have resulted
in the different position of the volume sample.
Recorded values of flows depend on the position of
the volume sample, however, we believe these differences were insignificant.42 The inspiration
enhances RV and decreases LV filling velocities.43
All Doppler measurements were obtained at the end
of expiration. Finally, the influence of lung diseases
on RV performance should be carefully considered.
The proportions of cigarette smokers were similar in
both groups. Body plethysmography tests were performed to exclude severe lung dysfunction.
Conclusions
In hypertensive patients, impaired diastolic filling is
observed both in the left and the right ventricle. RV
free wall thickening and interventricular septum
hypertrophy seem to be major factors influencing
RV performance.
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