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Effect of Right Ventricular Function and

Pulmonary Pressures on Heart Failure
Srilakshmi M. Adhyapak, DNB
The relationship of right ventricular function and
pulmonary systolic pressure in patients with con-
gestive heart failure was evaluated to risk-stratify
them. The study included 147 consecutive
patients with symptomatic heart failure who
underwent clinical and laboratory examination
and echocardiography including Doppler tissue
echocardiography. They were followed for a
mean of 11.26.4 months. During follow-up, 16
patients died and 45 patients had nonfatal
cardiac events. There were 60 readmissions for
heart failure. Pulmonary artery systolic pressure
and right ventricular systolic function were
inversely related (r
=0.66, P<.001). On Cox
multivariate survival analysis, early worsening
of pulmonary arterial pressures was an indepen-
dent prognostic predictor (hazard ratio, 0.44;
condence interval, 0.280.91, P=.024). The
patients with pulmonary hypertension and right
ventricular systolic dysfunction had the worst
prognosis. The assessments of right ventricular
function help to risk-stratify patients with heart
failure. The early worsening of pulmonary
hypertension is a powerful predictor of worse
prognosis. Prev Cardiol. 2010;13:7277.

2009 Wiley Periodicals, Inc.

n patients with primary (idiopathic) dilated car-
diomyopathy (DCM) or ischemic heart disease
(IHD), left ventricular (LV) dysfunction is the ori-
ginal physiologic disorder leading to the clinical
syndrome of chronic heart failure. A reduced LV
ejection fraction is a powerful predictor of death
in a general population of patients with heart fail-
ure; however, its prognostic value loses strength
when applied to patients with advanced heart
Recent studies
have demonstrated that
reduced right ventricular (RV) ejection fraction is
an independent prognostic factor in moderate to
severe heart failure. Combined RV systolic and dia-
stolic dysfunction are strong predictors of poor
prognosis in symptomatic heart failure.
hypertension frequently complicates heart failure
and is considered an indicator of worse prognosis
irrespective of RV function.
We sought to examine the relationship of RV
systolic function and pulmonary artery systolic pres-
sure in symptomatic patients with heart failure, by
2-dimensional echocardiography and Doppler tissue
echocardiography, in order to risk-stratify them.
The study population comprised 147 consecutive
patients with symptomatic heart failure. The study
period was December 2004 to June 2007. Institu-
tional ethics committee approval was obtained, and
informed consent was obtained from all study
patients. All patients were in sinus rhythm and in
moderate to severe heart failure as dened by the Fra-
minghamcriteria, with an etiology of DCM or IHD.
DCM was dened as LV dysfunction in the
absence of signicant coronary artery disease
(70% luminal narrowing) on coronary angiogra-
phy or absence of pathological Q waves on electro-
cardiography and absence of long-standing diabetes
mellitus, valvular heart disease, myocardial disease,
or active myocarditis. IHD was diagnosed on the
basis of documented previous myocardial infarction
or signicant coronary artery disease on coronary
Exclusion Criteria
Patients with valvular heart disease, cardiac amyloido-
sis, hypertrophic cardiomyopathy, active alcoholism,
From the Department of Cardiology, St. Johns Medical
College Hospital, Bangalore, India
Address for correspondence:
Srilakshmi M. Adhyapak, DNB(Cardiology), Department
of Cardiology, St. Johns Medical College Hospital,
Bangalore 560034, India
Manuscript received May 28, 2009; revised July 24, 2009;
accepted August 7, 2009
doi: 10.1111/j.1751-7141.2009.00053.x
chronic obstructive pulmonary disease, malignancy,
advanced liver or renal disease, recent myocardial
infarction (<6 months), or unstable angina were
excluded. Patients receiving parenteral inotropes at
presentation were also excluded. Patients with atrial
brillation and RV pacing were excluded.
All patients underwent routine blood chemistry
and hematologic tests, 12-lead electrocardiography,
chest radiography, and standard 2-dimensional and
tissue Doppler echocardiography. The clinical vari-
ables are presented in Table I.
All echocardiographic measurements were obtained
on the General Electric Vivid 3 (Milwaukee, WI)
equipped with a phased array transducer of 2.5
MHz frequency. Echocardiography was performed
at entry into the study and once in 2 weeks during
the study period. Standard 2-dimensional echocardi-
ography and pulsed Doppler tissue imaging of the
tricuspid and mitral annular motion were obtained
in all patients.
The 2-dimensional measurements were per-
formed as recommended by the American Society
of Echocardiography.
All values were indexed to
body surface area. LV ejection fraction (EF) was
determined by the modied biplane Simpsons rule.
Impaired LV function was dened as LVEF 45%.
Doppler tissue measurements were performed
with the patients in the left lateral decubitus posi-
tion, during shallow respiration. The sample volume
was placed on the tricuspid annulus, with care
taken to obtain an ultrasound beam parallel to the
direction of tricuspid annular motion. Similar
recordings were obtained at the mitral annulus.
Peak systolic (Sa), peak early (Ea) and late (Aa) dia-
stolic tricuspid, and mitral annular velocities, along
with simultaneous electrocardiogram were recorded
at a speed of 50 mm s. All measurements were
obtained on 3 to 6 consecutive heart cycles, and the
mean value was calculated.
Pulsed Doppler tracings of the tricuspid inow
and RV outow were obtained simultaneously from
the apical 5-chamber view with upward tilt of the
transducer, held at the apex. The RV ejection time
(ET) was measured from onset to the end of the
RV outow Doppler velocity prole below the
baseline. The isovolumetric relaxation time (IVRT)
was measured from cessation of the RV outow to
the onset of the tricuspid inow velocity prole
above the baseline. The isovolumetric contraction
time (IVCT) was measured from the cessation of
the tricuspid inow to the onset of RV outow
velocity prole above the baseline. The RV myocar-
dial performance index (MPI) was calculated by the
formula: IVCT + IVRT ET.
Based on the values of the pulmonary artery sys-
tolic pressure (PASP) derived from the continuous
TR velocity envelope and RV function based on the
RV Sa, the study group was classied into 4 sub-
groups: group 1, normal PASP preserved RV func-
tion; group 2, normal PASP RV dysfunction; group
3, high PASP preserved RV function; and group 4,
high PASP RV dysfunction.
The mitral inow pulsed Doppler values were
also noted. The pressure gradient between right
ventricle and right atrium was calculated from the
TR velocity envelope, and 5 to 10 mm Hg was
added as right atrial pressure, depending on the dis-
tensibility of the inferior vena cava in the subxi-
phoid views. A mean pulmonary artery pressure
>25 mm Hg at rest was dened as pulmonary
hypertension. The patients with pulmonary hyper-
tension and RV dysfunction at entry into study
were subjected to high-resolution CT scans to rule
out pulmonary thromboembolism. All echocardi-
ography was performed by 2 experienced sonog-
raphers who were blinded to the results of the
Table I. Clinical Characteristics of the Study Group
Age, y 5416.9
Male female 135 12
New York Heart Association functional class
2 65
3 60
4 22
DCM 75 (51%)
IHD 72 (49%)
LVIDd 467 mm m
LVIDs 266 mm m
LVEF 39%8%
PASP 56.38.9 mm Hg
RV Sa 11.83.6 cm s
RV MPI 0.80.7
HTN 52%
DM 57%
Diuretics 100%
ACEIs 92%
Digitalis 73%
Nitrates 49%
Spironolactone 38%
b-Blockers 35%
Antiplatelets 47%
Oral anticoagulants 34%
Abbreviations: ACEI, angiotensin-converting enzyme
inhibitor; DCM, dilated cardiomyopathy; DM, diabetes
mellitus; HTN, hypertension; IHD, ischemic heart
disease; LVEF, left ventricular ejection fraction; LVIDd,
left ventricular internal diameter in diastole; LVIDs, left
ventricular internal diameter in systole; PASP, pulmonary
artery systolic pressure; RV Sa, right ventricular annular
systolic wave by tissue Doppler imaging; RV MPI, right
ventricular myocardial performance index.
The patients were followed up for cardiac mortality
and nonfatal cardiac events relating to heart failure.
Serial echocardiography was performed at 2-week
intervals. Cardiac death was dened as death due to
heart failure, myocardial infarction, malignant ar-
rhythmias, or cardiac arrest. Heart failure requiring
hospitalization was identied as exacerbation of
dyspnea, need for parenteral diuretic therapy, and
symptoms associated with left or right heart failure.
Survival was dened as freedom from cardiac-
related death. Event-free survival was dened as
freedom from combined end point (cardiac-related
death and hospitalization for heart failure).
Statistical Analysis
Continuous variables were expressed as mean
standard deviation. Categoric variables were
expressed as frequencies. The best maximum likeli-
hood estimates of the cutoffs for parameters of
interest were obtained by a receiver operating char-
acteristic curve analysis. The continuous variables
among the 4 groups were compared using analysis
of variance, and categoric variables were compared
using chi-square test. Correlations between PASP
and variables quantifying RV function were done
using linear regression analysis. Survival analysis
was performed according to the Cox regression
method. Cumulative survival was obtained accord-
ing to the presence or absence of pulmonary hyper-
tension or RV dysfunction. A P value <.05 was
considered statistically signicant. SPSS version 10.0
for windows (SPSS Inc, Chicago, IL) was used for
There were 147 patients with heart failure. There
was a male preponderance in all 4 groups studied
(Table II). There was an almost equal distribution
of hypertension (52%) and diabetes mellitus (57%)
in all 4 groups.
In group 1, the etiology of heart failure was
DCM in most cases (n=21, 84%). However, there
was an almost equal distribution of DCM and IHD
in groups 2, 3, and 4. The patients in group 1 were
youngest (mean age, 30.66.7 years) and in group
2 were oldest (mean age, 66.48 years). There
were more patients in New York Heart Association
class 3 and 4 with associated pulmonary hyperten-
sion (groups 3 and 4) (n=61) than patients with
normal pulmonary pressures (groups 1 and 2)
(n=21, P=.002). The New York Heart Association
class 3 and 4 patients were maximal in group 4.
Resting heart rate was also signicantly higher in
group 4 (98.511.5 beats min). Group 4 patients
were receiving maximal diuretics and nitrates. The
need for higher doses of diuretics and nitrates was
in patients with pulmonary hypertension. Group 1
Table II. Characteristics of Patients Grouped According to Coupling Between Pulmonary Artery Pressure and Right
Ventricular Function
Group 1
Normal PASP
Preserved RV
Group 2
Normal PASP
Group 3
Preserved RV
Group 4
n=25 n=43 n=22 n=57
Male female 23 2 40 2 19 3 53 4
Age, y 30.66.7 66.48.58 58 53.511
Etiology (DCM IHD) 21 7 14 19 14 18 26 28
NYHA class 3 or 4 9 12 22 39
HR 88.54 91.25 915.9 98.511.5
LVIDd 4.63.3 4.30.8 4.30.6 4.70.7
LVIDs 2.90.4 2.90.6 2.50.6 2.50.6
LVEF 4113 44.48.4 44.96.5 379.6
LV E A <1 6 (30%) 21 (48.8%) 10 (45.4%) 22 (37.9%)
PASP 205 24.80.4 56.86 58.98.8
RV Sa 14.62.5 8.42.7 152.8 7.61.6
LV Sa 7.70.6 6.21.1 8.31.9 6.51.5
RV MPI 0.30.3 0.40.18 0.20.6 0.50.8
Nitrates (%) 0 38% 22.2% 42.8%
Furosemide 410.9 481.2 53.28.4 78.211.6
Abbreviations: DCM, dilated cardiomyopathy; HR, heart rate; IHD, ischemic heart disease; LV, left ventricular; LVEF, left
ventricular ejection fraction; LVIDd, left ventricular internal diameter in diastole; LVIDs, left ventricular internal diameter in
systole; LV Sa, left ventricular annular systolic wave by tissue Doppler imaging; NYHA, New York Heart Association; PASP,
pulmonary artery systolic pressure; RV MPI, right ventricular myocardial performance index; RV Sa, right ventricular annular
systolic wave by tissue Doppler imaging.
patients were receiving the lowest doses of diuretics
and nitrates.
Echocardiographic Variables
RV function was assessed by Doppler variables: RV
Sa represented RV systolic function, RV Ea and RV
Aa represented RV diastolic function, and RV MPI
represented global RV function.
The RV Sa <11.5 cm s had 89% sensitivity and
94% specicity for RV systolic dysfunction. The
RV MPI of 0.5 had 82% sensitivity and 89% speci-
city for global RV dysfunction. The interobserver
variability for Doppler variables was 3.4%, and in-
traobserver variability was 6.3%.
Groups Based on RV Function and
Pulmonary Pressures
The RV Sa was signicantly lower in group 4
(Table II) (P=.002). The RV MPI was higher in
group 4 (P=not signicant). The RV Ea was signi-
cantly lower than RV Aa in the patients with
reduced RV systolic function (groups 2 and 4) (Ea,
9.22; Aa, 14.23; P=.004). The RV Ea was sig-
nicantly lower in group 4 than in group 2
(6.41.2 and 8.73.1; P=.02). There was no dif-
ference in LV dimensions among the 4 groups. The
LVEF was signicantly lower in group 4 (P=.05).
The LV systolic function as measured by LV Sa was
also signicantly lower in this group (P=.006).
Relationship Between PASP and RV Function
A signicant inverse relationship was found between
mean PASP and RV function (r
=0.66; P<.001).
The relationship was similar between patients with
DCM and IHD. The RV Sa as a measure of RV
systolic function was used to explore the coupling
of RV function and pulmonary hypertension.
Follow-Up Data
Of the 147 patients studied, 35 (23.8%) experi-
enced a cardiac event. There were 6 cardiac-related
deaths: 4 died of progressive cardiac failure, and 2
died suddenly. Twenty-nine (19.7%) had a nonfatal
cardiac event and were hospitalized for heart failure
Table II summarizes the clinical and echocardio-
graphic characteristics of the 4 groups. The median
time to death was 5 months and median time to
hospitalization for heart failure was 6 months. The
median survival of the entire group (N=147) was
13.5 months. During follow-up, 5 died and 16 were
hospitalized for heart failure in group 4 (n=57).
There were 15 hospitalizations and 1 death in
group 3 (n=22) and no hospitalizations or deaths
in groups 1 and 2 (n=25 and n=43, respectively).
Further echocardiographic studies done at 2
weekly intervals throughout the study period did
not show signicant changes in RV and LV func-
tion. The worsening of pulmonary hypertension
was observed, and the median time from entry to
study to worsening of pulmonary hypertension by
154.8 mm Hg in groups 3 and 4 (n=79) was
9.5 months. There was a signicantly earlier wors-
ening of pulmonary hypertension in group 4 (mean,
5.72.5 months; P<.001) than group 3 (mean,
121.4 months). On Cox multivariate survival
analysis, the independent prognostic predictor of
mortality was early worsening of pulmonary hyper-
tension (hazard ratio, 0.44; 95% condence inter-
val, 0.280.91; P=.024).
RV function is related to LV function by the phe-
nomenon of ventricular interdependence. Although
the right ventricle pumps the same stroke volume as
the left ventricle, it does so with 25% of the stroke
work due to low resistance of the pulmonary circu-
lation. Therefore, by Laplaces law, its free wall is
thinner and more compliant. It is linked to the left
ventricle by the shared septum, encircling epicardial
bers of the RV free wall, which is attached to the
interventricular septum anteriorly and posteriorly.
Its shape is described as a pyramid with a triangular
base. Due to this geometric complexity, its shape
cannot be explained by mathematic models. Its
shape also changes during the cardiac cycle, making
evaluation difcult by any method that relies
predominantly on visual assessment, such as
Thermodilution, radionuclide ventriculography,
and magnetic resonance imaging have been used to
assess right ventricular size and function. In most
studies, the RVEF was determined by either radio-
isotope ventriculography
or thermodilution tech-
The normal RVEF is between 40% and
45%. An RVEF <35% indicates RV dysfunction.
The tricuspid annular systolic excursions on 2-
dimensional echocardiography have been established
as a surrogate marker for RVEF.
shortening is a greater contributor to RV stroke vol-
ume than circumferential shortening.
Doppler tissue imaging enables assessment of
velocity of contraction of longitudinal myocardial
bers at the tricuspid annulus (RV Sa). As RV sys-
tole is principally determined by shortening along
longitudinal bers, this is an accurate measure of its
systolic function. The MPI evaluates global RV
function, is load-independent, and is not inuenced
by heart rate.
The possible mechanisms of RV dysfunction
occurring in association with LV dysfunction are as
An increase in LV afterload by the failing left ven-
tricle, which increases pulmonary venous and ulti-
mately pulmonary arterial pressure, a protective
mechanism against pulmonary edema
Ventricular interdependence due to septal dys-
LV dilatation in a limited pericardial compart-
ment, which may restrict RV diastolic function
Furthermore, when the right ventricle fails in
heart failure, it may be unable to maintain the ow
volume required to maintain adequate LV preload,
constituting a nal common pathway in heart fail-
ure progression. Reports of RV dysfunction in heart
failure concordantly proved increased mortality and
frequency of nonfatal cardiac events.
RV function
was found to be more depressed in DCM than
IHD, due to its involvement in the cardiomyopathic
We found no difference in RV func-
tion between patients with DCM and IHD. The
patients with IHD who presented with severe LV
dysfunction (LV Sa <7 cm s) also had RV dysfunc-
tion. Involvement of the septum in IHD can affect
RV function directly, as previously described. Over-
all RV function depends on septal contractility also,
and not solely on free wall function.
The development of pulmonary hypertension in
heart failure was an independent predictor of hemo-
dynamic deterioration and short- and long-term
mortality, irrespective of the etiology of heart fail-
Ghio and associates
explored the cou-
pling of PASP and RV function and its effect on
prognosis of patients with heart failure. In patients
with normal PASP, the assessment of RV function
did not improve the prognostic stratication (ie,
these patients did not differ in their clinical out-
come based on normal RV function or RV dysfunc-
tion). However, when PASP was high at rest, the
prognosis was strongly related to RV function.
Patients with high PASP and RV dysfunction had
worse prognosis, and those with normal RV func-
tion had similar prognosis of patients with normal
In our study, we grouped patients who presented
with heart failure on the basis of RV function and
pulmonary pressures into 4 groups (Table II). All
patients with RV dysfunction assessed by low RV
Sa also had RV diastolic dysfunction as assessed by
RV Ea <RV Aa. Global RV function as assessed by
RV MPI was also depressed.
We used RV Sa to explore the relationship
between RV dysfunction and pulmonary pressures,
as it had greater sensitivity and specicity and was
more easily reproducible than RV MPI. There was
no difference in outcomes between RV dysfunction
and normal RV function with normal pulmonary
pressures (groups 1 and 2). There was worse prog-
nosis for survival in group 4.
During follow-up, we assessed pulmonary hyper-
tension by Doppler echocardiography and found a
median time of 9.5 months to worsening of hyper-
tension. The patients with high PASP and preserved
RV function (group 3) had a signicantly later
onset of pulmonary hypertension (121.4 months)
as compared with group 4, which had high
PASP RV dysfunction (5.72.5 months; P<.001).
Early worsening of pulmonary hypertension
was the only independent predictor of mortality.
These patients were subjected to pulmonary CT
angiography, and pulmonary thromboembolism was
ruled out.
This nding demonstrates that in patients with
pulmonary hypertension and RV dysfunction, there
is early worsening of pulmonary pressures as
opposed to patients with pulmonary hypertension
and preserved RV function. Besides, the RV func-
tion was more depressed in the patients in group 4
than in group 2. This highlights that RV function
may be more afterload-dependent than the LV func-
tion, which mainly depends on contractility for
optimal function.
Although Doppler echocardiographic variables are
sensitive and relatively load-independent, they are
not exempt from potential criticism. There exists a
considerable variation in the extent of increased PASP
in response to pulmonary venous hypertension. All
our patients were not subjected to right heart cathe-
terization due to logistic and nancial constraints;
hence, this nding could not be explored.
The prognosis of patients with symptomatic heart
failure is worst in those with high PASP and RV
dysfunction, irrespective of the etiology of heart
These patients demonstrate an early worsening
of pulmonary hypertension that portends a grave
outcome. A primary reduction in RV contractility
may not affect prognosis in heart failure if accom-
panied by normal PASP. RV contractility is worse
when associated with pulmonary hypertension.
The benets of early detection, diagnosis, and
treatment of patients in heart failure with severe
pulmonary hypertension and RV dysfunction aims
mainly to prevent its consequent morbidity and
mortality. Implicit in this study is that more intense
treatment is needed in these patients. It is therefore
necessary to initiate a coordinated and detailed cas-
cade screening of all patients with heart failure to
identify this group.
Acknowledgments: The authors acknowledge Dr Rashmi Rodrigues,
lecturer in the Department of Preventive and Social Medicine, for
valuable help with statistics; Dr Amar Prabhu Desai, MD, senior
resident in the Department of Cardiology; and Nameetha Sunath, in
the Sonography Department of Cardiology for performing
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