Download Echocardiographic Variables After Left Ventricular Assist Device

Echocardiographic Variables After Left Ventricular Assist
Device Implantation Associated With Adverse Outcome
Yan Topilsky, MD; Tal Hasin, MD; Jae K. Oh, MD; Daniel D. Borgeson, MD;
Barry A. Boilson, MD; John A. Schirger, MD; Alfredo L. Clavell, MD; Robert P. Frantz, MD;
Rayji Tsutsui, MD; Mingya Liu, MD; Simon Maltais, MD; Sudhir S. Kushwaha, MD;
Naveen L. Pereira, MD; Soon J. Park, MD
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Background—Operative mortality after left ventricular assist device (LVAD) implantation is heavily influenced by patient
selection and the technical difficulty of surgery. However, how we treat our patients and LVAD setting may affect the
patient outcome beyond this period. We postulated that the presence of echocardiographic variables 1 month after
surgery suggesting appropriate degree of LV unloading and an adequate forward flow would be important in
determining clinical outcomes after the initial successful LVAD implantation.
Methods and Results—We retrospectively analyzed various variables in echocardiographic examinations performed 30
days after LVAD implant in 76 consecutive patients receiving continuous flow device for their association with a
compound end point (90-day mortality, readmission for heart failure, or New York Heart Association class III or higher
at the end of the 90-day period). The echocardiographic associations examined included estimated LVAD flow, with and
without native LV contribution, interventricular septal position, the status of aortic valve opening, an estimated left atrial
pressure (ELAP), the mitral flow E-wave deceleration time, and the ratio of deceleration time to E-wave velocity (mitral
deceleration index [MDI]). Four patients died during the 30- to 90-day period, 6 patients were readmitted for heart
failure, and 25 patients were considered to have New York Heart Association class III or higher at the end of the 90-day
period. Variables associated with adverse outcome included increased ELAP (odds ratio, 1.30 [1.16 –1.48]; P⬍0.0001),
MDI ⬍2 ms/[cm/s] (odds ratio, 4.4 implantation [1.22–18]; P⫽0.02) and decreased tricuspid lateral annulus velocity
(odds ratio, 0.70 implantation [0.48 – 0.95]; P⫽0.02). A leftward deviation of interventricular septum was associated
with a worse outcome (odds ratio, 3.03 implantation [1.21–13.3]; P⫽0.01).
Conclusions—Mortality and heart failure after LVAD surgery appear to be predominantly determined by echocardiographic evidence of inefficient unloading of the left ventricle and persistence of right ventricular dysfunction. Increased
estimated LA pressure and short MDI are associated with worse mid term outcome. Leftward deviation of the septum
is associated with worse outcome as well. (Circ Cardiovasc Imaging. 2011;4:648-661.)
Key Words: left ventricular assist device 䡲 echocardiography
L
unloading may be associated with failure to improve heart
failure symptoms after LVAD surgery. Furthermore, other
factors, especially those related to right ventricle (RV) function,
may have a strong influence as well, as RV performance is the
limiting factor of total cardiac output after LVAD implantation.
We retrospectively examined various echocardiographic and
clinical variables 30 days after LVAD implantation for their
association with lack of improvement in heart failure 3 months
after discharge from hospital.
eft ventricular assist devices (LVAD) are designed for
mechanical support for patients with severe systolic heart
failure and provide effective long term circulatory support.1– 4
In most cases, axial flow pumps have replaced pulsatile
LVADs because of improved survival and less device failure.5,6 Postoperative transthoracic echocardiography (TTE) has
a major role in the treatment of LVAD patients. It is frequently
used to evaluate native heart and LVAD function and for
troubleshooting possible device malfunctions.7–11 Although continuous LVAD therapy has been in clinical use for a number of
years, a comprehensive analysis of post operative echocardiographic variables associated with failure of therapy has not been
reported to date. Because LVAD therapy is supposed to improve
cardiac output and unload the left cardiac chambers, we postulated that variables estimating total or LVAD output, as well as
those estimating the efficiency of left ventricular or left atrial
Clinical Perspective on p 661
Methods
Patient Population, LVAD Pump Setting, and
Study Design
The study cohort included 76 consecutive patients (62 males, 14
females) undergoing LVAD (HeartMate II) implantation in our
Received March 22, 2011; accepted August 15, 2011.
From the Division of Cardiovascular Diseases (Y.T., T.H., J.K.O., D.D.B., B.A.B., J.A.S., A.L.C., R.P.F., R.T., M.L., S.S.K., N.L.P.) and the Division
of Cardiovascular Surgery (S.M., S.J.P.), Mayo Clinic, Rochester, MN.
Correspondence to Soon J. Park, MD, FACC, Mayo Clinic, St Marys Hospital, 2nd St SW GO-138SE, Rochester, MN 55902. E-mail [email protected]
© 2011 American Heart Association, Inc.
Circ Cardiovasc Imaging is available at http://circimaging.ahajournals.org
648
DOI: 10.1161/CIRCIMAGING.111.965335
Topilsky et al
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institution between February 2007 and August 2010. Our practice of
patient selection, surgical techniques, preoperative and postoperative
treatments, and follow-up care remained constant over time. Transesophageal echocardiography was routinely utilized in all patients to
help us with the revolutions per minute (rpm) setting in the operating
room. The initial pump speed was selected to provide an adequate
forward flow (cardiac index measured by Swan-Ganz catheter ⬎2.2
L/min/m2), while ensuring the absence of LV collapse under TEE
guidance. Subsequently, the patients were discharged home after
optimizing their LVAD settings so that pump speed was 0 – 400 rpm
below the rpm in which their aortic valve remained closed during the
entire systole. We retrospectively analyzed different variables in
echocardiographic examinations performed 1 month after LVAD
implantation for their association with the composite end point of
persistence of New York Heart Association (NYHA) class III or
higher, readmission for heart failure during the 30- to 90-day period
or death at 90 days as the primary aim of the study. Only variables
obtained at 1 month after LVAD implantation were used for our
analysis. The LVAD speed was maintained between discharge and
the 1 month evaluation in all patients. However, during the subsequent 3 months of follow-up, the rpms were changed in some of the
patients with heart failure symptoms and echocardiographic evidence
of inefficient LV unloading. Any patient with symptoms of heart
failure during the follow-up period, with or without rpm increased,
was included in the adverse outcome group.
LV and Valvular
Echocardiographic Measurements
Two-dimensional transthoracic echocardiography was performed in
a standard manner using Sonos 5500 (Philips Medical Systems,
Andover, MA), Sequoia 512 (Siemens, Mountainview, CA), or
Vivid 7 (GE Medical Systems, Milwaukee, WI).
LV diameters and interventricular septal and posterior wall width
were measured from the parasternal short axis using 2D, or 2D
guided M-Mode echocardiogram of the LV at the papillary muscle
level using the parasternal short-axis view from the trailing edge of
the septum to the leading edge of the posterior wall as recommended.12 Ejection fraction was calculated by the Quinones
method13 assuming an akinetic apex, and LV mass was calculated by
the method proposed by Devereux and associates,14 using the same
LV dimensions made with M-mode or 2D as described above.
Valvular regurgitation was qualitatively assessed using color
Doppler according to the guidelines of the American Society of
Echocardiography (normal/trivial⫽1, mild⫽2, moderate⫽3,
severe⫽4).15
RV Echocardiographic Measurements
RV chamber size and function was measured according to the
guidelines of the American Society of Echocardiography.12 RV size
and systolic function were evaluated by measuring the RV end-diastolic area (4-chamber view), RV end-systolic area (4 chamber
view), tricuspid annulus end systolic diameter (4-chamber view), and
calculating the RV fractional area change. RV function was qualitatively graded using a 4-scale grading system (normal, mild,
moderate, severe) using all apical views, RV inflow, parasternal
long-axis, parasternal short-axis, and subcostal views. Care was
taken to obtain a true nonforshortened apical or para-apical
4-chamber view, oriented to obtain the maximum RV dimension
before making the RV estimation.12 RV function was then assessed
by 3 other methods: 2D lateral tricuspid annular motion,16 the timing
interval between the cessation and the onset of tricuspid regurgitation
flow corrected for heart rate (TRDc), using the formula TRDc⫽TR
flow time/公RR,17 a surrogate for early systolic equalization of RV
and right atrial pressure and the RV index of myocardial performance (RIMP), as previously described by others.18,19 Mean pulmonary artery pressure was estimated using the modified Bernoulli
formula (4⫻TRVmax2)⫹RAP, where TR Vmax is the peak systolic
tricuspid regurgitation velocity at end expiration, and RAP is the
right atrial pressure.
Post-LVAD Echo Variables
649
LVAD Echocardiographic Variables
Measurements of the LVAD components were performed, including
the inflow cannula, outflow graft flow velocities, and variables
estimating the LVAD flow and efficiency of left sided chamber
unloading17,20,21 (Figures 1, 2, 3, and 4).
Inflow Cannula
The inflow cannula and its orientation within the left ventricular apex
was visualized on the apical 4- and 2-chamber views, and sometimes
required off-axis imaging as well.21,22 Doppler assessment of the
inflow cannula was done in the 4- and 2-chamber views as well, as
they are usually aligned with the central axis of a properly positioned
inflow cannula. Continuous or pulsed Doppler was used for measurement of the maximal velocity along the inflow pathway from the
ventricle to the LVAD (Figure 1).
Outflow Cannula
Interrogation of the outflow cannula was performed from the high
left parasternal long-axis view, which shows the end-to-side anastomosis of the outflow cannula to the mid ascending aorta, and the
right parasternal view, which shows the long axis of the outflow
cannula traversing from the pump toward the right aspect of the
ascending aorta.21 Color flow, PW, and CW Doppler was used to
evaluate flow patterns of the outflow cannula. To measure flow
velocity the PW sample volume was positioned at least 1 cm
proximal to the aortic anastomosis and the flow was recorded away
or toward the transducer, depending on the transducer position. For
the right parasternal view, the patient was positioned on his right
side, and the image recorded with the transducer immediately
rightward to the sternum (Figure 1).
LVAD Output
The product of a pulsed-wave spectral Doppler velocity-time integral
(VTI) from the outflow cannula and its cross-sectional area equals
the flow volume created by the pump. This technique is well known
and was recently validated with the Heart Mate II in a wellconducted in vitro study.23 The same method was applied here to
calculate the LVAD minute flow rate. LVAD outflow cannula
diameter was measured in the right parasternal view, and outflow
TVI was measured using the right parasternal view or the high left
parasternal view, depending on which view afforded the lowest
Doppler angle of interrogation.21
Total Cardiac Output
The RVOT VTI was measured from pulse-wave Doppler, and RVOT
diameter was measured from the parasternal short axis at the level of
the great arteries. Total RV output (which is the sum of LVAD
output and the flow ejected through the LVOT) was calculated using
the formula (RV outflow diameter/2)2⫻␲⫻RV outflow TVI.12
Right Atrial Pressure Estimation
Right atrial (RA) pressure was estimated by the inferior vena cava
diameter as well as its response to inspiration as previously described.24 Briefly, expiratory and inspiratory inferior vena cava
(IVC) diameters and percent collapse were measured in subcostal
views within 2 cm of the right atrium. IVC diameter ⬍2.1 cm that
collapsed ⬎50% with a sniff suggested a normal RA pressure
(assigned as 5 mm Hg), whereas an IVC diameter ⬎2.1 cm that
collapsed ⬍50% with a sniff suggested a high RA pressure
(15 mm Hg). In patients with IVC diameter ⬍2.1 cm and no collapse
(⬍20%) with a sniff, RA pressure was upgraded to 20 mm Hg. In
indeterminate cases in which the IVC diameter and collapse did not
fit this paradigm, secondary indices of elevated RA pressure were
integrated. If uncertainty remained, RA pressure was left as intermediate value of 10 mm Hg.
Efficiency of LV Unloading
Several echocardiographic variables have been evaluated for the
assessment of optimal unloading of left-sided chambers. These
include the following:
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Figure 1. A, Interrogation of the inflow cannula. The inflow cannula and its orientation within the left ventricular (LV) apex visualized on
the apical 4-chamber view, aligned with the LV inflow tract, not touching any wall. B, Pulsed Doppler assessment showing laminar, low
velocity forward flow without regurgitation with a pulsatile inflow pattern because the pump inflow originates from the beating LV,
resulting in periodic changes in flow throughout the cardiac cycle, reaching a maximum during systole (S), and minimum during diastole
(D). The difference between systolic to diastolic inflow velocities is related to LV contraction in a geometry-independent way. C, Interrogation of the outflow cannula in the high left parasternal long-axis view showing the end-to-side anastomosis of the outflow cannula to
the mid ascending aorta. D, Interrogation of the outflow cannula in the mid right parasternal view as it transverses upward toward the
ascending aorta. In the mid sternum the cannula is parallel to the transducer and its diameter can be easily measured. E, We follow the
outflow cannula to the high parasternal area. The flow will change direction away from the transducer (blue) bending toward the
ascending aorta. F, This is usually the best view to measure flow velocity with the PW sample (the angle of interrogation will be optimal) positioned at least 1 cm proximal to the aortic anastomosis, the flow moving away from the transducer. AO indicates ascending
aorta; OC, outflow cannula.
(1) Left ventricular dimension in end diastole (LVEDD) and end
systole (LVESD),25 and the change in both calculated as
(LVEDD pre LVAD⫺LVEDD post LVAD)/LVEDD pre
LVAD or (LVESD pre LVAD⫺LVESD post LVAD)/
LVESD pre LVAD, respectively.
(2) Preserving a neutral position of the interventricular septum,
not shifting to the right or to the left26 (Figure 2).
(3) Degree of aortic valve opening (closed, opens intermittently
every 1:3 cycles, opens every cycle).26,27
We assessed novel variables for proper unloading of left-sided
chambers. These included:
(1) Estimation of the mean left atrial (LA) pressure by a multistep process including the following: First we estimated the
mean right atrial pressure by the inferior vena cava diameter
as well as its response to inspiration.24 Second we checked the
interatrial position at diastole using the left parasternal shortaxis view and/or 4-chamber views and defined it as deviated
to the right, neutral, or deviated to the left. The interatrial
septum (IAS) is a thin membranous structure between the left
and right atria, and its configuration is altered by minor
changes of up to 5 mm Hg in the interatrial pressure gradient.28 –30 When LA pressure is higher than the right, the IAS
configuration is convex toward the right atrium and if right
atrial pressure is higher than the left, the IAS is convex toward
the left atrium. Thus, we arbitrarily estimated the mean LA
pressure as LA pressure⫽RA pressure if inter atrial septum
was neutral, LA⫽RA pressure⫺5 mm Hg if interatrial position was deviated to the left and LA pressure⫽RA pressure⫹5 mm Hg if inter atrial position was deviated to the
right (Figure 3).
(2) Mitral inflow deceleration time is negatively related to left
ventricular filling pressure.31,32 For any given rate of deceleration of early mitral inflow, a higher E-wave velocity is
associated with increased deceleration time.33 To correct for
this potential artifact, we indexed the deceleration time for
peak E-wave velocity (mitral deceleration index [MDI]) as
previously described,33,34 and hypothesized that it may be a
useful marker of LV unloading in patients with continuous
LVAD (Figure 4).
Echocardiographic Determinants of Outcome
The associations used as potential determinants of outcome included
left ventricular diastolic diameter (mm), left ventricular systolic
diameter (mm), color Doppler qualitative grading of mitral regurgitation, aortic regurgitation and tricuspid regurgitation (TR), vena
contracta of TR, tricuspid regurgitation velocity (m/s), tricuspid
lateral annulus velocity, qualitatively estimated RV function, RIMP,
RV end-diastolic and end-systolic area, RV fractional area shortening, total cardiac output, LVAD output, inflow and outflow cannula
velocities, mitral inflow deceleration time, mitral inflow deceleration
time divided by E-wave velocity (MDI), interventricular septal
position, interatrial septal position, aortic valve opening status,
estimated RA pressure, estimated LA pressure (ELAP), and the
change in LV end diastolic and end-systolic diameters from the
baseline measurements performed before LVAD implantation.
Tricuspid and Aortic Valve Procedures
Candidates for LVAD implantation are evaluated by echocardiography to assess native tricuspid valve regurgitation (TR) and aortic
regurgitation (AR). Those with at least moderate TR (jet area/right
atrial area ⱖ20%, or vena contracta ⬎4.5 mm) underwent tricuspid
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Figure 2. Apical 4-chamber view assessing the
interventricular septal position in different patients
after left ventricular assist device (LVAD) implantation. A, Inefficient left ventricular (LV) unloading
with interatrial and interventricular septa deviated
to the right, suggesting high left atrial (LA) and LV
pressure. B, Interventricular septum deviated to
the left, suggesting markedly unloaded LV that can
be associated with adverse outcomes, right ventricular (RV) dysfunction, and functional TR. C,
Interventricular septum is neutral suggesting efficient LV decompression. Note that the interatrial
septum is deviated to the left as opposed to the
interventricular septum. This is because the interatrial septum is thinner than the thick muscular
interventricular septum and the relation between
the interatrial position and the pressure difference
between the right atrium and the left atrium is
much tighter than between the right and left ventricles. A patient is shown before (D) and after (E)
increasing the pump’s speed. D, The patient was
admitted due to persistent heart failure. On echo
examination, both interatrial (large arrow) and
interventricular septa (small arrows) were deviated
to the right suggesting inefficient unloading of left
chamber. Note the significant functional mitral regurgitation. E, After optimization of pump’s speed
the interatrial septum is deviated to the left (large
arrow) but the interventricular septum maintains a
neutral position (small arrows), suggesting optimal unloading of left chambers. Note the functional mitral regurgitation has improved considerably, as did the patient’s symptoms.
valve repair or replacement. Those with aortic insufficiency due to
significant structural defects in the aortic valve underwent aortic
valve replacement or patch closure of the valve. However, the
majority of the patients with aortic insufficiency were corrected with
a simple coaptation stitch placed at the central portion of the aortic
cusps as previously described.35,36
Interobserver and Intraobserver Variability
Interobserver variability was assessed by comparing the readings
made by another independent echocardiographer in 10 randomly
selected patients. Intraobserver variability was determined by having
the first observer who measured the data in all patients remeasure the
velocities in 10 patients at least 3 month apart. Interobserver and
intraobserver variability were assessed by the correlation coefficient
(r value) between the matched parameters, paired t test to evaluate
the difference between these measurements (P⬍0.05 for a significant
difference) the Bland-Altman method and by the within-subject
coefficient of variation. The within-subject coefficient of variation
(calculated as ratio of the standard deviation of the measurement
difference to the mean value of all measurements) provides a
scale-free unitless estimate of variation expressed as a percentage.
We measured the intra- and interobserver reproducibility for the
deceleration time, the MDI, and estimated LA pressure, and expressed them using the coefficient of variation.
Statistical Analysis
Data were checked visually looking for heavy tails or outliers and
analyzed using the Shaprio-Wilk test for normality. Continuous
normally distributed variables were presented as mean⫾SD and
compared using the Student t test. Ordinal and/or nonnormally
distributed data were presented by median, 1st and 3rd quartiles and
compared using the nonparametric Wilcoxon rank sum test. Categorical data were compared between groups using the ␹2 or Fisher
exact test, as appropriate.
To analyze potential factors that are associated with the adverse
combined 90-day outcome individual-predictor analyses based on
logistic regression were performed on various variables (clinical and
echocardiographic). The associations between wedge pressure and
ELAP or MDI in 8 patients in which an invasive right heart
catheterization was performed simultaneously with the echocardiographic examination were assessed using the Pearson correlation
coefficient. All probability values were 2-sided, and values of ⬍0.05
were considered to indicate statistical significance. All data were
analyzed with the JMP System software version (SAS Institute, Inc,
Cary, NC). All authors participated in designing the study, collecting
and analyzing data, and drafting and revising the manuscript. The
authors had full access to and take full responsibility for the integrity
of the data. All authors have read and agreed to the manuscript as
written.
Results
Baseline Characteristics
Table 1 shows the baseline characteristics (before LVAD
implantation) of the patients enrolled, divided into 2 groups,
those (30 patients) with adverse LVAD outcomes 90 days
after surgery (mortality or admission for heart failure during
the 90-day period, or persistence of NYHA class III or higher
at the end of the period), and those (46 patients) considered to
have normal 90-day outcome. The patients’ mean age was
63.2⫾12 years, and 80.0% were men. The most common
etiology for heart failure was ischemic heart disease (51%)
followed by dilated cardiomyopathy (38%). Eleven percent of
patients (8 patients) had restrictive cardiomyopathy as the
indication for LVAD surgery.35 Most patients (65%) were
implanted for destination therapy. Most patients were Caucasian, 39% had hypertension and 27% had diabetes. We
have calculated and included the clinical score proposed by
Lietz-Miller37 for all patients (Table 1).
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Figure 3. A through C, A patient was readmitted for persistent heart failure 30 days after left ventricular assist device (LVAD) surgery.
A, M-mode examination of the aortic valve affirms permanent closure of the valve suggesting efficient decompression of the left ventricle. B, Short-axis view on the level of great arteries shows an interatrial septum deviated to the right, suggesting that the left atrial
pressure is higher than right atrial pressure. C, Subcostal view showing a dilated inferior vena cava with a less than 50% change during
inspiration. The right atrial pressure was estimated to be 15 mm Hg, suggesting that left atrial pressure is even higher. D, The pump’s
speed was increased by 600 rpm, resulting in a left atrial septum deviated to the left. E, Four-chamber view showed that the interventricular septum is not deviated to the left. F, Echo performed 24 hours after the change in pump’s speed showed that the right atrial
pressure has decreased (the inferior vena cava is not dilated and collapses during inspiration). The interatrial septum was neutral, suggesting normally decompressed left atrium estimated to be 5 mm Hg.
The pre LVAD echocardiographic variables associated
with worse outcome included a smaller LV end-systolic
diameter, lower TR velocity, shorter TRDc, and lower hemoglobin. Variables estimating LV systolic function, and LV
filling pressures before LVAD surgery were not different
between the groups. These results are consistent with our
previous report assessing pre LVAD echocardiographic predictors of adverse outcome after LVAD surgery.17
Ninety-Day Post-LVAD Adverse Outcomes
Table 2 compares the echocardiographic, functional, laboratory, and pump variables measured 30 days after surgery
between patients with and without the compound 90-day
adverse outcome. We divided the echocardiographic variables
into those assessing the native left ventricle, valves, right
ventricle, LV unloading, and pump flows. Four patients died
between days 30 to 90 after surgery. The causes of deaths
included uncontrolled right heart failure and multiorgan failure
in 3 and intracerebellar bleeding in 1. Six patients were readmitted for heart failure, 25 patients were considered to have
NYHA class III or higher at the end of the 90-day period.
None of the variables assessing the valve function, native
left ventricle function, or size at the 30 days examination
showed significant association with 90-day outcome. Patients
with adverse outcome 90 days after surgery had significantly
lower tricuspid lateral annular motion, increased prevalence of
RV dysfunction (⬎moderate, qualitatively estimated), suggesting worse RV function. Patients with adverse outcome had
increased ELAP, higher prevalence of MDI ⬍2 m/[cm/s]),
higher prevalence of inter atrial septum deviated to the right, all
suggesting inefficient LV unloading. Of note, patients with
worse outcome had increased prevalence of inter ventricular
septum deviated to the left. There was no significant difference
in the status of aortic valve opening, pump speed (rpm), pump
flow (estimated by the controller or echocardiography), or pulse
index between the groups. We have evaluated the clinical
characteristics, as well as laboratory variables at the time of the
echo (30 days after surgery) and presented them in Table 2. The
patients with adverse 90-day outcome were clinically worse at
30 days as evidenced by significantly more patients in NYHA III
or IV functional class, higher creatinine, higher BUN and a trend
for increased NT-BNP.
Patients with adverse outcome had lower 6-minute walk
distance 3 months after surgery, as expected.
Thirty-Day Post-LVAD Echocardiographic Variables
Associated With 90-Day Adverse Outcome
Individual-predictor analyses for prediction of the 90-day
combined outcome (Table 3) revealed no significant associ-
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Figure 4. A and B, A patient was readmitted for persistent heart failure 30 days
after left ventricular assist device (LVAD)
surgery. A, Mitral inflow PW interrogation
showing a markedly short deceleration
time (red arrow), E-wave velocity of 0.86
m/s (yellow arrow), and a very steep
slope of mitral valve deceleration index
(MDI) calculated as 1.37 ms/[cm/s] (white
arrow). The pump’s speed was increased
by 400 rpm. C, M-mode examination of
the aortic valve shows that the aortic
valve is now permanently closed. D,
Mitral inflow PW interrogation showing
prolongation of the deceleration time (red
arrow), E-wave velocity of 0.79 m/s (yellow arrow), and a milder slope of MDI
calculated as 2.17 ms/[cm/s] (white
arrow). The patient’s symptoms improved
considerably, and NT-BNP decreased a
few days after the change in rpm.
ation with the compound outcome measure for the variables
related to the valvular function, left ventricle function or size
or pump flows, and output. The only variables assessing RV
function that were significantly associated with worse 90-day
outcome were a lower tricuspid lateral annulus velocity and
an interventricular septum deviated to the left, suggesting that
the RV flow is not rapid enough to fill the left ventricle. We
have recently shown that the most significant predictor of
outcome using the pre LVAD echocardiographic examination
was the decreased timing interval between the cessation and
the onset of TRDc.17 Surprisingly, TRDc measured 30 days
after LVAD implantation was not associated with adverse
outcome (P⫽0.8). Patients with NYHA class III/IV at 30
days were more likely to have adverse 90-day outcome, with
a RR of 12.0 (4.1–39.9; P⬍0.0001).We have analyzed
whether NT-BNP (evaluated 30 days after LVAD implantation) is associated with the adverse outcome at 90 days. We
found that 30 day NT-BNP is associated with increased risk
for adverse outcome at the 90-day period by a risk ratio of
1.18 (0.98 –1.56) for every increase in NT-BNP by 1 ng/mL,
with marginal statistical significance (P⫽0.08). When we
log-transformed the 1-month NT-BNP data it became nonsignificant as a predictor of outcome (P⫽0.3). The decrease
(%) in NT-BNP from baseline (before LVAD) to 30 days
after LVAD implantation was significantly associated with
the 90-day adverse outcome (RR, 0.6 [0.21– 0.96]; P⫽0.02
for 1% change). When we log transformed the NT-BNP
change from baseline to one month it became nonsignificant
as a predictor of outcome as well (P⫽0.6) (Table 3).
Most of the variables suggesting non efficient LV unloading were associated with worse outcome. These included
MDI ⬍2 m/[cm/s], higher ELAP (using the multistep process
described in the methods section) and an atrial septum
deviated to the right.
To analyze the significance of ELAP, deceleration time
and MDI we compared them to the wedge pressure in 8
patients in which the echocardiographic and hemodynamic
evaluation were performed simultaneously. The ELAP was
positively and significantly correlated to the wedge pressure
(r⫽0.74; P⫽0.03). Both deceleration time (r⫽⫺0.69;
P⫽0.056) and MDI (r⫽⫺0.72; P⫽0.04) were negatively
correlated to the wedge pressure but the correlation was better
when the deceleration time was corrected for the E-wave
velocity.
Intraobserver and Interobserver Variability
Comparison of intraobserver timing intervals showed good
agreement between measurements: estimated LA pressure
(mean difference, ⫺1.0⫾3.1 mm Hg; r⫽0.93; P⫽0.34), Deceleration time (mean difference, 5.0⫾12.9 ms; r⫽0.96;
P⫽0.25), and MDI (mean difference, 0.04⫾0.25 ms/[cm/s];
r⫽0.98; P⫽0.62). The Bland-Altman plot showed a random
scatter of points around 0, indicating no systematic bias or
measurement error proportional to the measurement value.
Measurement variability (within-subject coefficient of variation and 95% confidence interval of the Bland-Altman
method) for measurements for intraobserver differences was
as follows: estimated LA pressure 27.4% and ⫾1.0 mm Hg,
Deceleration time 7.1% and ⫾4.1 ms and MDI 9.4% and
⫾0.08 ms/[cm/s] Comparison of interobserver timing intervals showed good agreement as well: estimated LA pressure
(mean difference, ⫺0.1⫾3.2 mm Hg; r⫽0.88; P⫽0.92), deceleration time (mean difference, 4.9⫾12.2 ms; r⫽0.97;
P⫽0.24), and MDI (mean difference, ⫺0.02⫾0.25 ms/[cm/s];
r⫽0.98; P⫽0.84). The Bland-Altman plot showed a random
scatter of points around 0, indicating no systematic bias or
measurement error proportional to the measurement value.
Measurement variability (within-subject coefficient of variation and 95% confidence interval of the Bland-Altman
method) for measurements for interobserver differences was
as follows: estimated LA pressure, 26.6% and ⫾3.2 mm Hg;
deceleration time, 6.7% and ⫾12.2 ms; and MDI, 9.6% and
⫾0.25 ms/[cm/s].
654
Circ Cardiovasc Imaging
November 2011
Table 1. Baseline Characteristics (Before LVAD Implant) for
Patients Divided Into Groups With and Without Adverse 90-Day
Outcome (Mortality, Hospitalization for Heart Failure, NYHA
Class III or Higher)
Characteristic
Age, y
Sex, male, %
Race, %
No Adverse
Outcome (n⫽46)
61.9⫾14
Adverse 90-Day
Outcome (n⫽30)
63.9⫾11
P Value
0.5
Continued
No Adverse
Outcome (n⫽46)
Adverse 90-Day
Outcome (n⫽30)
P Value
VO2 max, mL/kg per min㛳
10.3⫾2.5
10.0⫾3.2
0.7
Left ventricular diastolic
diameter, mm*
69.3⫾8
64.8⫾11
0.06
63.2⫾7
58.2⫾11
0.05
Characteristic
75
90
0.3
Left ventricular systolic
diameter, mm*
Caucasian, 96
Caucasian, 94
0.4
Ejection fraction, %*
18.8⫾7
22.7⫾11
0.1
African
American, 2
African
American, 3
Left atrial volume index,
mL/m2*
65.7⫾28
67.2⫾18
0.8
E/e⬘ ratio*
0.9
Downloaded from http://circimaging.ahajournals.org/ by guest on May 14, 2017
Asian, 2
Asian, 0
Native American,
0
Native American,
3
Hypertension, %
37
40
0.9
Diabetes, %
20
37
0.1
Chronic renal failure, %
44
63
0.1
Atrial fibrillation, %
15
20
0.6
AICD
44
37
0.4
Weight, kg
Table 1.
26.5⫾12
26.3⫾10
Tricuspid regurgitation
velocity, m/s*
3.1⫾0.6
2.8⫾0.6
0.05
Tricuspid valve lateral
annulus velocity, m/s*
0.08⫾0.03
0.08⫾0.03
0.3
63
76
0.2
Right ventricle
dysfunction ⬎MO*§
TRDc, ms
482⫾66
446⫾72
0.04
RIMP*
0.61⫾0.25
0.52⫾0.24
0.2
Mean right atrial
pressure, mm Hg*
14.4⫾5
16.3⫾8
0.3
36.6⫾10
34.5⫾8
0.3
83.7⫾19
88.2⫾21
0.4
2.0⫾0.2
2.0⫾0.2
0.6
NYHA class IV, %
44
76
0.02
Prior sternotomy, %
42
50
0.7
Mean pulmonary
pressure, mm Hg*
Preoperative IABP, %
25
40
0.2
PVR, Woods Units‡
4.6⫾3
3.8⫾3
0.3
Preoperative inotropic use
60
69
0.5
RV dP/dt*‡
502⫾208
440⫾180
0.2
0
3
0.2
Mean Wedge
pressure, mm Hg*‡
23.1⫾6
22.9⫾6
0.9
BSA
Preoperative mechanical
ventilation
Destination therapy, %
56
70
0.4
Cardiac output, L/min*‡
3.7⫾1
4.1⫾1
0.1
Type of cardiomyopathy
I (56); R (5)
I (43); R (20)
0.2
2.0⫾0.6
0.2
D (37)
Cardiac index,
L/min/m2*‡
1.9⫾0.5
D (39)
Heart rate, beats per
minute
75.5⫾15
75.5⫾13
0.9
Systolic blood
pressure, mm Hg
98.3⫾11
98.3⫾17
0.9
Diastolic blood
pressure, mm Hg
66.8⫾10
62.5⫾10
0.1
Hemoglobin†
12.5⫾2
11.4⫾12
0.02
Bilirubin†
1.23⫾0.6
1.12⫾0.8
0.5
AST
59⫾90
81⫾231
0.6
ALT
88⫾204
71⫾197
0.7
LVAD indicates left ventricular assist device; NYHA, New York Heart
Association; AICD, automatic implantable cardioverter-defibrillator; AST, aspartate aminotransferase; ALT, alanine aminotransferase; BUN, blood urea nitrogen; PT INR, prothrombin international normalized ratio; NT-BNP, N-terminal
pro-B-type naturetic peptide; ACE inhibitors, angiotensin-converting enzyme
inhibitors; BB, beta-blocker; BSA, body surface area; IABP, intra-aortic balloon
pump; I, ischemic; D, dilated; R, restrictive; MDI, mitral deceleration index;
TRDc, tricuspid regurgitation time corrected for heart rate; RIMP, right index of
myocardial performance; and PVR, pulmonary vascular resistance.
*Last echocardiographic measurement before LVAD implantation.
†Variables measured or calculated before LVAD implantation.
‡Last hemodynamic study before transplant.
§Right ventricle dysfunction greater than moderate by the qualitative
assessment.
㛳VO2 max measured in 10 patients in the adverse outcome group and 30
patients in the no adverse outcome group; 6-minute walk assessed in 6
patients in the adverse outcome group and 15 patients in the no adverse
outcome group.
BUN†
28⫾13
30⫾14
0.6
Creatinine†
1.5⫾0.8
1.6⫾0.6
0.5
PT INR
1.4⫾0.4
1.4⫾0.4
0.9
6567⫾6123
5652⫾6035
0.6
Log NT-BNP
8.4⫾0.9
8.1⫾1.1
0.4
Lietz-Miller score†
7.8⫾4
8.4⫾7
0.6
NT-BNP†
ACE inhibitors
58
53
0.3
BB
77
88
0.9
Aldospirone, %
43
47
0.5
Digoxin
65
40
0.1
Diuretics
88
96
0.3
Statins, %
63
43
0.3
322⫾83
308⫾117
6-Minute walk, m㛳
0.8
(Continued)
Long-Term Outcomes
Mean follow-up duration after surgery was 321 [186 – 602]
days. Eighteen patients (24%) died during follow-up, and
14 patients had their LVAD explanted for heart transplantation during the follow-up period. The causes of deaths in
the 14 patients surviving the 90-day period were traumatic
head trauma injury in 2, hemorrhagic stroke in 2, unexplained sudden death in 6, RV failure in 1, embolic stroke
in 1, complication of myocardial biopsy after transplant in
1, and 1 patient who decided to withdraw support due to
Topilsky et al
Post-LVAD Echo Variables
Table 2. Post-LVAD 30-Day Echocardiographic, LVAD Controller, and Laboratory and Clinical Variables
Divided Into Patients With and Without Adverse 90-Day Outcome
No Adverse Outcome
(n⫽46)
Adverse 90-Day Outcome
(n⫽30)
Left ventricular diastolic diameter, mm*
58.3⫾9
55.0⫾11
0.3
Left ventricular systolic diameter, mm*
50.2⫾10
47.4⫾13
0.4
Ejection fraction, %*
26.0⫾12
25.6⫾13
0.9
Characteristic
P Value
Native left ventricle and valves
AR ⬎trivial*
41
53
0.4
MR ⬎mild*
9
27
0.4
Right ventricle function and size
Tricuspid regurgitation velocity, m/s*
Tricuspid valve lateral annulus velocity, m/s*
Right ventricle dysfunction ⬎MO*§
2.5⫾0.4
2.4⫾0.5
0.3
0.09⫾0.03
0.07⫾0.02
0.01
Downloaded from http://circimaging.ahajournals.org/ by guest on May 14, 2017
11
46
0.03
RVEDA, cm2*
28.8⫾7
29.2⫾7
0.8
RVESA, cm2*
18.1⫾5
19.8⫾6
0.3
RV FAC, %*
38.0⫾10
32.6⫾13
0.09
TRDc, ms
412⫾60
389⫾55
0.3
RIMP
0.28⫾0.12
0.34⫾0.2
0.2
TV annulus diameter*
3.2⫾0.4
3.3⫾0.5
0.7
TR vena contracta*
3.6⫾2.4
4.4⫾2.5
0.3
E-wave velocity*
0.72⫾0.1
0.79⫾0.18
0.2
E/e⬘ ratio*
14.5⫾4
22.8⫾13
0.3
0 (29); I (12); C (59)
0 (18); I (11); C (71)
0.5
R (3); N (71); L (26)
R (24); N (51); L (25)
0.01
LV unloading
Aortic valve status, %*
Atrial septal position, %*
Atrial septal position to right, %*
Ventricular septal position, %*
Ventricular septal position to left, %*
3
R (57); N (39); L (4)
4
24
R (43); N (40); L (17)
17
0.07
0.6
Left ventricular diastolic diameter change, %*
⫺15.8⫾11
⫺13.2⫾19
Left ventricular systolic diameter change, %*
⫺20.5⫾17
⫺13.7⫾25
Estimated LA pressure*
Estimated LA pressure ⬎15 mm Hg, %*
Deceleration time*
Deceleration time ⬍150*
MDI, ms/关cm/s兴*
MDI ⬍2 m/关cm/s兴*
0.004
0.2
0.4
7.4⫾4
14.1⫾6
⬍0.0001
7
55
⬍0.0001
189⫾51
15
288⫾137
20
170⫾63
42
219⫾121
56
0.3
0.04
0.09
0.01
LVAD flows by echocardiography
Total output*
5.6⫾2
5.8⫾2
0.8
LVAD output*
5.3⫾1.3
4.7⫾1.2
0.3
LVAD output index*
2.7⫾0.7
2.4⫾0.6
0.4
Inflow velocity*
77.4⫾41
75.5⫾32
0.8
109.7⫾39
97.3⫾41
0.3
9538⫾221
9542⫾301
0.9
Pump flow†
5.5⫾0.8
5.3⫾0.7
0.5
Pump flow index†
2.6⫾0.4
2.6⫾0.4
0.8
PI†
5.0⫾0.6
4.9⫾0.8
Outflow velocity*
Controller pump parameters
Pump speed†
0.7
(Continued)
655
656
Circ Cardiovasc Imaging
Table 2.
November 2011
Continued
No Adverse Outcome
(n⫽46)
Characteristic
Adverse 90-Day Outcome
(n⫽30)
P Value
Laboratory and clinical parameters
at the day of echo
NYHA class
NYHA class III/IV, %
I (7); II (68)
I (0); II (20)
III (23); IV (2)
III (43); IV (37)
25
80
⬍0.0001
⬍0.0001
Heart rate, beats per minute
85.7⫾11
88.7⫾10
0.3
Mean blood pressure, mm Hg
88.7⫾7
87.1⫾11
0.6
Atrial fibrillation, %
NT-BNP
Log NT-BNP
Hemoglobin†
Albumin†
11
16.6
0.7
2840⫾1411
3981⫾4188
0.2
7.8⫾0.5
8.0⫾0.7
0.3
10.7⫾2
10.2⫾1
0.2
Downloaded from http://circimaging.ahajournals.org/ by guest on May 14, 2017
3.5⫾0.7
3.3⫾0.6
0.3
Creatinine†
0.94⫾0.3
1.3⫾0.7
0.02
BUN†
20.1⫾9
27.6⫾16
0.05
Bilirubin†
0.94⫾0.5
2.3⫾6.3
0.3
ACE inhibitors, %†
30
10
0.03
BB, %†
52
20
0.008
Diuretics, %†
83
92
0.3
90-Day postdischarge parameters
NYHA‡
NT-BNP‡
6-Minute walk, m‡
I (36); II (64)
I (0); II (4)
III (0); IV (0)
III (81); IV (15)
1885⫾1509
3125⫾2067
273⫾128
239⫾95
⬍0.0001
0.05
0.0009
LVAD indicates left ventricular assist device; AR, aortic regurgitation; MR, mitral regurgitation; RVEDA, right ventricle end-diastolic
area; RVESA, right ventricle end-systolic area; RV FAC, right ventricle fractional area change; TV, tricuspid valve; O, opening every
cycle; I, intermittent opening; C, permanently closed; R, deviated to the right; N, neutral position; L, deviated to the left; LA, left atrium;
ELAP, estimated left atrial pressure; MDI, mitral deceleration index; and NYHA, New York Heart Association.
*Echocardiographic measurement performed 30 days after LVAD implant.
†Variables measured 30 days after LVAD implantation.
‡Variables measured at the end of 90-day period after LVAD implantation.
§Right ventricle dysfunction greater than moderate by the qualitative assessment.
persistent RV failure and need for dialysis. The actuarial
survival rate was 83.2⫾17% and 68.0⫾8% at 1 and 2
years, respectively.
There were too few events to permit meaningful analyses
of the association between echocardiographic variables and
long term outcome.
ELAP was significantly but weakly correlated with pump
speed (r⫽⫺0.27; P⫽0.02) as well as MDI (r⫽0.24; P⫽0.04)
suggesting that increasing the speed may decrease LA pressure and lengthen the mitral deceleration time. Our experience in several different patients corroborates this assumption
(Figures 2 and 3).
Discussion
This study is one of the first to report on echocardiographic
variables after LVAD surgery associated with adverse outcome and persistence of heart failure. We found that adverse
events in the 90 days after surgery period were associated
with evidence of decreased RV contraction (lower tricuspid
lateral annulus velocity) and inadequate LV unloading
(ELAP, MDI) in the 30-day echocardiographic examination.
Deviation of the interventricular septum to the left, which
may be related to reduced RV forward flow or over decompression of the LV, was associated with adverse outcomes as
well.
RV Dysfunction
RV dysfunction is very common immediately after LVAD
surgery and was shown to contribute to the perioperative
mortality,1,3,7 as well as decreased long term survival. We
believe that postoperative RV dysfunction is comprised of 2
processes: one of secondary RV dysfunction related to LV
failure and the second due to intrinsic RV dysfunction. We do
not offer LVAD therapy in patients with primary RV dysfunction such as RV dysplasia. However, we believe that
secondary RV dysfunction usually improves with an effective
LVAD therapy in the overwhelming majority of patients with
LV dysfunction as the primary cause of heart failure. Therefore, we consider LVAD therapy in all patients with end stage
heart failure due to primary LV failure regardless of the
degree of RV dysfunction. The only variables we found to be
related to RV function in the echocardiographic examination
Topilsky et al
Table 3. Individual-Variable Analyses of Mid Term
Compound 90-Day Adverse Event in Patients Undergoing
LVAD Implantation
Table 3.
OR (95% CI)
Variable
Left ventricular diastolic
diameter, mm
0.96 (0.89 –1.03)
Left ventricular systolic
diameter, mm
0.97 (0.92–1.03)
MR
Mi/No: 0.48 (0.15–1.6)
P Value
0.3
0.4
0.5
Mo/Mi: 2.0 (0.20–23.5)
AR
Mi/No: 2.4 (0.48–15.4)
0.3
TR vena contracta
1.14 (0.91–1.44)
0.2
Tricuspid regurgitation velocity, m/s
0.46 (0.12–1.62)
0.2
0.7 (9.48–0.95)
0.02
Tricuspid lateral annulus velocity,
m/s
Downloaded from http://circimaging.ahajournals.org/ by guest on May 14, 2017
Right ventricle dysfunction
⬎moderate
RIMP, 0.1 increase
1.07 (0.57–2.0)
0.8
1.3 (0.89–1.96)
0.2
RVEDA, cm2
1.01 (0.93–1.09)
0.8
RVESA, cm2
1.05 (0.96–1.16)
0.3
RV FAC, %
0.96 (0.91–1.00)
0.07
Total output
1.07 (0.65–1.8)
0.8
LVAD output
0.67 (0.31–1.3)
0.2
LVAD output index
0.56 (0.14–1.95)
0.4
Inflow velocity
0.99 (0.98–1.01)
0.8
Outflow velocity
0.99 (0.98–1.01)
0.3
E/e⬘ ratio
1.15 (0.95–1.68)
0.2
Deceleration time
0.99 (0.98–1.0)
0.3
Deceleration time ⬍150 ms
2.04 (1.04–4.3)
0.04
MDI
0.99 (0.98–1.00)
0.07
MDI ⬍2 ms/关cm/s兴
4.4 (1.22–18.0)
0.02
ELAP
1.3 (1.16–1.48)
⬍0.0001
ELAP ⬎15 mm Hg
Atrial septal position
15.6 (4.4–73.7)
⬍0.0001
N/R: 0.18 (0.02–0.89)
0.07
L/N: 2.02 (0.69–6.05)
Atrial septal position to the right
Ventricular septal position
2.1 (1.02–5.6)
0.05
N/R: 2.25 (0.86–6.0)
0.01
L/N: 5.9 (1.12–119.1)
Ventricular septal position to the left
Aortic valve status
3.03 (1.21–13.3)
0.01
I/O: 1.09 (0.17–6.2)
0.7
C/I: 1.46 (0.32–7.8)
657
Continued
NT-BNP, 100 pg/mL
Variable
Post-LVAD Echo Variables
Log NT-BNP
OR (95% CI)
P Value
1.18 (0.98 –1.56)
0.08
1.5 (0.71–3.6)
0.3
NT-BNP change, %
0.6 (0.21–0.96)
0.02
Log NT-BNP change
0.8 (0.4–1.6)
0.6
NYHA class III or IV
12.0 (4.1–39.9)
⬍0.0001
LVAD indicates left ventricular assist device; OR, odds ratio; CI, confidence
interval; AR, aortic regurgitation; MR, mitral regurgitation; RVEDA, right
ventricle end-diastolic area; RVESA, right ventricle end-systolic area; RV FAC,
right ventricle fractional area change; TV, tricuspid valve; O, opening every
cycle; I, intermittent opening; C, permanently closed; R, deviated to the right;
N, neutral position; L, deviated to the left; LA, left atrium; ELAP, estimated left
atrial pressure; MDI, mitral deceleration index; and NYHA, New York Heart
Association.
performed 30 days after LVAD implantation associated with
the 90-day adverse outcome were decreased tissue Doppler
tricuspid valve lateral velocity and a interventricular septum
deviated to the left. This is in marked discordance with the
echocardiographic variables before LVAD surgery in which
the main variable associated with outcome was the TR
duration corrected for heart rate (TRDc). TRDc is related to
the pressure difference in mean systolic right ventricular
pressure and mean right atrial pressure.17 In other words, it
describes hemodynamic interactions between the pulmonary
vasculature (pulmonary hypertension), venous system (right
atrial pressure) and right ventricular contractility. Once an
LVAD is in place, left ventricular end-diastolic pressure, and
secondary pulmonary hypertension usually improve considerably21 and TRDc is no longer predictive of outcome. On the
other hand, the tissue Doppler tricuspid valve lateral velocity
is a sensitive measure of right ventricular contraction. In
patients with severe LV dysfunction before LVAD implantation, it was markedly reduced in all patients due to the
excessive after load imposed on the RV and could not
discriminate between patients with reversible/secondary or
irreversible/primary RV damage. After LVAD implantation,
tissue Doppler tricuspid valve lateral velocity increased considerably in the patients in which RV dysfunction was secondary to
the increased after load imposed by the failing LV but did not
improve in patients who had irreversible RV damage, making it
a sensitive indicator of RV reserve after LVAD.
LV Unloading
Left ventricular diastolic diameter
change, %
1.00 (0.96–1.06)
0.7
Left ventricular systolic diameter
change, %
1.00 (0.98–1.04)
0.5
Because LVAD therapy is supposed to increase cardiac
output and unload the left-sided chambers, we postulated that
variables estimating the cardiac output and the efficiency of
left ventricular or left atrial decompression may be predictive
of failure to improve heart failure.
Hemoglobin
0.77 (0.55–1.01)
0.06
Aortic Valve Opening Status
Bilirubin
1.09 (0.93–1.69)
0.3
Albumin
0.18 (0.03–0.61)
0.003
3.4 (0.84–19.2)
0.03
In a patient on LVAD support, the total forward blood flow in
the ascending aorta is the sum of contributions from both
LVAD and the LV. In the setting of a high LVAD pump
speed, the flow contribution by the native LV would be
minimal, the LV would not be able to generate any stroke
volume, and the entire forward flow would be from the
LVAD. On the other hand, if the LVAD pump speed settings
Laboratory and clinical parameters at
the day of echo
Creatinine
BUN
1.04 (1.01–1.1)
Platelets
0.99 (0.98–0.99)
0.04
0.04
(Continued)
658
Circ Cardiovasc Imaging
November 2011
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are low, the native LV generates a stroke volume by opening
of the native aortic valve which contributes to the overall
forward flow. Thus, we expected the status of aortic valve
opening to reflect the efficiency of LV unloading and to be
associated with outcome. Our analysis did not prove the
“aortic valve opening status” to be significantly associated
with the 90-day outcome. The status and rate of aortic valve
opening depends on the relation between LV intracavitary
pressure and aortic pressure during systole. In patients with
very poor LV contractility, the aortic valve may not open
despite inefficient LV unloading and high LV filling pressure
(Figure 2). On the other hand, when LV function recovers the
aortic valve may open with each cardiac contraction even if
the LV is unloaded because the LV effectively competes with
the LVAD. Therefore, the degree of aortic opening is influenced by the complex interaction between the native heart
and the LVAD in each patient. The lack of statistical
significance for “aortic valve opening status” does not suggest that it is not useful. Aortic valve opening may be an
important variable as it is a surrogate marker of preserved
pulse pressure, but it is important to note that there is still no
data that indicates that short or long-term outcomes are best
with intermittent AV opening. We believe that when setting
LVAD rpm, we should aim for 3 objectives: adequate cardiac
output, ameliorate congestion, and maximize pulse pressure.
Of course, it would be ideal to emulate nature as much as
possible, that is, produce near normal pulse pressure. Therefore, we aim to minimize LVAD pump speed to increase
pulse pressure as much as possible as long as we do not
compromise the first 2 objectives for the third.
Estimated LA Pressure
It has been previously shown that because the IAS is a thin
membranous structure between the left and right atria, its
configuration is altered by the interatrial pressure gradient in
normal patients, as well as in patients with mitral stenosis,
mitral regurgitation, and tricuspid regurgitation.28,29,38
In normal subjects, the IAS protrudes slightly toward the
right atrium in end-systole. However, it flattens or retracts
slightly toward the left atrium in end-diastole. These changes
in IAS position corresponded to a left-to-right pressure
gradient of 3–5 mm Hg during the peak of the “v” point with
a transient reversal of the left-to-right gradient during atrial
contraction observed in normal patients.30 Based on these
observations, suggesting that a change in inter atrial pressure
gradient of less than 5 mm Hg shifts the inter atrial septum
either to the left or to the right we have arbitrarily estimated
the mean LA pressure as LA pressure⫽RA pressure if inter
atrial septum was neutral, LA⫽RA pressure⫺5 mm Hg if
interatrial position was deviated to the left, and LA
pressure⫽RA pressure⫹5 mm Hg if interatrial position was
deviated to the right. Because estimation of RA pressure
using the inferior vena cava diameter and its response to
inspiration has been previously validated,24,39,40 we hypothesized that combining the estimated RA pressure and the
position of the interatrial septum may prove valuable in
estimating the efficiency of LA and LV unloading and LVAD
function. To try to validate our approach to assess left atrial
pressure we compared the estimated left atrial pressure by
echocardiography (ELAP) to the wedge pressure in 8 patients in
which an invasive right heart catheterization was performed
simultaneously with the echocardiographic examination. The
correlation was significant (r⫽0.74; P⫽0.03), suggesting that
the ELAP may be considered a reasonable surrogate (although
not perfect estimation) for wedge pressure.
A higher estimated LA pressure (ELAP), especially above
a cutoff of 15 mm Hg was found to be associated with
increased risk for early adverse outcome. We believe that
elevated LA pressure may reflect inefficient LV unloading,
and worse RV function (as it is influenced by RA pressure as
well), or the combination of both, making it a useful parameter for estimating proper LVAD function. Furthermore, it
may be changed using manipulation of the pump’s speed
(Figure 3), making it an attractive parameter to use during
“ramp/optimization” studies. In simple words, if a patient has
an estimated RA pressure ⱖ15 mm Hg (estimated by the
inferior vena cava diameter and its response to inspiration)
the clinician may consider increasing the pump speed to the
point the interatrial position assumes a leftward or at least
neutral position.
Mitral Deceleration Index
There is an inverse relation between the mitral inflow
deceleration time and the LV end-diastolic pressure.31,32 For
any given rate of deceleration of early mitral inflow, a higher
E-wave velocity (E) is associated with a longer deceleration
time. In patients with LVADs, E-wave velocity will represent
the complex interaction between the left atrial pressure in
early diastole and the negative pressure created by the LVAD
in the left ventricle. We postulated that deceleration time
normalized for E-velocity will better predict cardiovascular
(CV) events compared with deceleration time or E-velocity
alone, as been previously shown in patients with hypertrophic
cardiomyopathy and/or hypertension.33,34 MDI is inversely
related to the deceleration slope and positively related to the
pressure half-time.33,34 Just as in patients with mitral stenosis,
a long MDI suggests slower increase in left ventricular
pressure and slower pressure equilibration between left
atrium and left ventricle. In patients with mitral stenosis the
slow increase in ventricular pressure is related to the obstruction to inflow, but in patients with an LVAD, it is due to the
increased rate of clearance of blood out of the left ventricle.
To try to validate the association between the mitral inflow
deceleration time, or MDI and LV end-diastolic pressure, we
compared these parameters to the wedge pressure (which in
patients with no mitral stenosis can be considered a good
surrogate for LV end-diastolic pressure) in 8 patients in
which an invasive right heart catheterization was performed
simultaneously with the echocardiographic examination. We
found that both the mitral inflow deceleration time, and MDI
were negatively correlated to the wedge pressure, but the
correlation was better for the MDI. These results suggest that
the MDI is a reasonable surrogate for LV end diastolic
pressure.
A short MDI ⬍2 ms/[cm/s] was found to be associated
with early adverse outcome. We believe that a short MDI
reflects rapid rise in LV diastolic pressure, equilibrating early
with LA pressure reflecting inefficient clearance of blood by
Topilsky et al
the LVAD. The mitral deceleration index was related to pump
speed and could be increased with increasing pump speed,
suggesting it can be another parameter to use during “ramp/
optimization” studies (Figure 3), especially in patients in
which the aortic valve is already closed but still have clinical
or hemodynamic evidence of insufficient LV decompression.
In other words, if a patient has MDI ⬍2 ms/[cm/s] and
symptoms of pulmonary congestion, an increase in pump
speed until the MDI is ⬎2 ms/[cm/s] may improve outcomes.
Interventricular Septal Position
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The interventricular septum is muscular and stiffer than the
interatrial septum and thus needs higher interventricular
gradient to be shifted to the right or to the left. In patients with
an LVAD, an increase in pump speed up to the point that the
left ventricular pressure is so low that it results in leftward
shift of the ventricular septum, may represent a right ventricle
that cannot generate enough flow to “fill” the left ventricle at
the same rate as the flow created by the LVAD. The shift in
the interventricular position may impair RV output by itself,
diminishing the left ventricular cavity even further. This
worsening spiral may cause the septum to encroach on the
inflow cannula resulting in ventricular arrhythmias or drastically decreasing LVAD preload. Furthermore, this shift may
also induce tricuspid regurgitation, resulting in systemic
congestion and lower forward output.20 Of note, this is in
marked discordance with the interatrial septum, which can be
shifted to the left with smaller transatrial pressure gradients,
which may be of use when right atrial pressure is
⬎15 mm Hg. We believe that LVAD unloading to the extent
of interventricular septum shift to the left, resulting in severe
TR or potential RV dysfunction should be avoided, but,
fortunately, this occurs infrequently. In some of these patients, hemodynamic guidance with right heart catheterization
to optimize cardiac output and LA pressure during speed
adjustment may be helpful.
Echocardiographic Evaluation of LVAD
Performance and Optimization Studies
The present study is a retrospective analysis of the echocardiographic variables obtained at 1 month after LVAD implantation. LVAD settings during those echocardiographic
exams were not changed between discharge and the 1-month
evaluation. We did not perform optimization studies using the
newer variables (deceleration time, MDI, and ELAP) at the
time of our primary analysis. The concept of “optimization”
of LVAD settings, based on echocardiographic appearance
has only been formulated recently, and thus we are unable to
answer the questions of whether optimization is associated
with best short term or long-term outcomes.
Nevertheless, we find it intriguing that adverse outcomes
were associated with echocardiographic variables suggestive
of poor LV unloading or RV failure at 1 month. Based on
these findings, our present routine is to perform “optimization” echocardiographic studies in every patient that presents
with heart failure symptoms (NYHA class III or higher)
during follow-up. Because LAVD is placed to address low
cardiac output and LV congestion, we believe that speed
setting should be set to address both of these issues. At the
Post-LVAD Echo Variables
659
first step in LVAD optimization we assess RV cardiac output
(which is the total cardiac output), or LVAD output, as
described in the Methods section. LVAD speed setting should
be altered to optimize cardiac output to be compatible with
life (we use a cutoff of cardiac index ⬎2.2 L/min/m2). In
some, it may be beyond what we could achieve by LVAD
setting adjustment due to severe intrinsic RV failure, but
these patients are rare and usually have uncontrollable RV
dysfunction or are in need of an RV assist device. In the
second step, we believe echo should help to set LVAD rpm to
improve LV filling pressures by assessing mitral valve inflow
deceleration time, MDI, or by judging RA pressure and LA
pressure by using the inferior vena cava method and the
interatrial septal position, respectively. As to the “aortic valve
opening status,” it was not found to be a significant predictor
of short-term outcome. The lack of statistical significance for
“aortic valve opening status” does not suggest that it is not
useful because it may be a surrogate marker of preserved
pulse pressure. We believe that it would be ideal to preserve
near normal pulse pressure, although there is no data that
indicates that long-term outcomes are best with intermittent
AV opening. On the other hand, we should not compromise
the first 2 objectives (cardiac output and LV unloading) for
the third. We also believe that LVAD unloading to the extent
of interventricular septum shift to the left, resulting in severe
TR or potential RV dysfunction should be avoided. In some
of these patients, if intermittent AV opening, or neutral
interventricular position cannot be achieved without elevated
ELAP or shortened MDI, hemodynamic guidance with right
heart catheterization to optimize cardiac output and LA
pressure during speed adjustment may be helpful. It is
important to note that the present study was not aimed to find
one “perfect” echo variable to predict failure or success, and
we do not believe such a variable exists. For evaluating or
optimizing LVAD performance a multifaceted approach is
essential. We should estimate the 3 goals of optimal LVAD
therapy: improved cardiac output, LV unloading and preserved pulsatility. The availability of different variables
assessing these 3 objectives of LVAD function (total cardiac
output, LVAD output, aortic valve status, LV diameter,
interventricular position, MDI, ELAP) provides an internal
verification and corroboration of LVAD function, particularly
when technical or physiological conditions preclude the use
of one or the other of these indexes. The interpreter must
integrate the different variables and disregard “outlying” data,
making the best estimate of LVAD function. Finally, the
echocardiographic and Doppler data are best interpreted
within the clinical context at the time of the examination. The
different variables (aortic valve status, MDI, ELAP) may be
influenced by LVAD speed, and hemodynamic conditions
such as blood pressure, fluid status, or inotropic use. Therefore, it is essential to record the pump’s rpm and patient’s
blood pressure at the time of the study and note the patient’s
medications whenever possible.
LV Recovery
Dandel et al41 have previously reported echo variables that
were useful in predicting successful recovery, which were
mostly related to LV geometry and systolic function (LV
660
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November 2011
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diameter and ejection fraction) rather than echo hemodynamics. Their study was very different from our study in many
aspects. First, they aimed for echocardiographic predictors of
LV recovery, which is rare and would likely require a totally
different approach than support intended for a lifetime as in
our cohort. Second, they used “off-pump” echocardiographic
examinations as opposed to our exams, which were performed on full LVAD support. Third, their study involved
mostly pulsatile LVADs, whereas ours was restricted to
evaluation of continuous-flow LVADs alone. Nonetheless,
ability to assess myocardial recovery during LVAD support
would be enormously helpful. An important provision is that
both LV preload and after load need to be consistent to be
able to compare LV recovery variables over time. We
hypothesize that if we could estimate LV end diastolic
pressure, using MDI or deceleration time, concurrent with
assessment of variables of LV contractility as LV ejection
fraction, these would be reasonable variables to screen for
myocardial recovery.
Conclusion
Mortality and persistent heart failure after LVAD surgery
appear to be predominantly determined by inefficient unloading of left chambers and persistent RV dysfunction. Increased
ELAP, MDI ⬍2 ms/[cm/s], and the degree of RV dysfunction, reflected by decreased tissue Doppler tricuspid lateral
annulus velocity, or an interventricular septum deviated to the
left are all associated with worse mid-term outcome.
An appropriate combination of flow, unloading and pulse
pressure is yet to be determined for the best long-term
outcome. Our study was not designed to establish the causeand-effect relationship between “optimizing” LVAD variables and better clinical outcome, but it seems to suggest that
such a concept should be explored further in a larger
prospective study using serial changes in echo variables
during long-term support.
Study Limitations
At the present time, we lack conclusive hemodynamic evidence proving our approach to assess left atrial pressure,
which will need validation in prospective studies using
simultaneous hemodynamic and echocardiographic studies.
Because of the relatively small number of patients and events
we lacked the statistical power to predict long-term outcome
or to show associations between echo variables and individual end points (mortality, heart failure admissions) and thus
were forced to use a combined end point. Furthermore, the
same limitation may have resulted in that some potentially
important associations (aortic valve opening status, LVAD
output) did not reach significance. Results of the present
study were based on a retrospective, observational analysis
that precluded us from defining the cause and effect relationship between “optimizing” LVAD parameters and better
clinical outcome. Given the exploratory nature of the results
and the relatively limited number of patients validation in
larger patient samples will be required. There is selection bias
in that patients who died earlier than 30 days were omitted.
Patients who died had significantly lower LVAD output than
the survivors (4.6⫾0.5 L/min versus 5.2⫾0.6 L/min;
P⫽0.05), which may have resulted in the non significant
impact of calculated LVAD flow on outcome.
Acknowledgments
We thank Zhou Li for her help with statistical analyses.
Disclosures
None.
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CLINICAL PERSPECTIVE
A successful acute outcome after left ventricular assist device (LVAD) implantation depends on patient selection and the technical
difficulty of surgery. However, how we treat our patients and LVAD settings may affect the patient outcome beyond the postsurgical
period. In the present study, we retrospectively analyzed various variables in echocardiographic examinations performed 30 days after
LVAD implant for their association with a compound end point (90-day mortality, readmission for heart failure, or New York Heart
Association class III or higher at the end of the 90-day period). We found that mortality and persistent heart failure after LVAD surgery
are predominantly associated with echocardiographic variables assessing the efficiency of unloading of the left ventricle and atrium, and
those assessing right ventricular function. The only right ventricular variable significantly associated with adverse outcome was a
decreased tissue Doppler velocity of the lateral tricuspid annulus. The variables assessing LV unloading, associated with adverse
outcome were a high estimated left atrial pressure (⬎15 mm Hg) and a short mitral inflow deceleration time divided by the E wave
velocity (⬍2 ms/[cm/s]). An interventricular septum deviated to the left was associated with worse outcome as well. In conclusion,
echocardiographic variables suggestive of efficient but not excessive LV unloading are associated with favorable mid and long-term
outcome after LVAD surgery.
Echocardiographic Variables After Left Ventricular Assist Device Implantation
Associated With Adverse Outcome
Yan Topilsky, Tal Hasin, Jae K. Oh, Daniel D. Borgeson, Barry A. Boilson, John A. Schirger,
Alfredo L. Clavell, Robert P. Frantz, Rayji Tsutsui, Mingya Liu, Simon Maltais, Sudhir S.
Kushwaha, Naveen L. Pereira and Soon J. Park
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Circ Cardiovasc Imaging. 2011;4:648-661; originally published online September 21, 2011;
doi: 10.1161/CIRCIMAGING.111.965335
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