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Transcript
16
Reviews
Echocardiographic evaluation of cardiac function
response to removal of aortic stenosis: Surgical
and trans-catheter aortic valve implantation (TAVI)
Ying Zhao MD PhD1, Yi-hua He MD PhD1
Department of Ultrasound, Beijing Anzhen Hospital, Capital Medical University,
Beijing, China
Acknowledgement: Dr Zhao is supported by National natural science foundation of China (Grant No. 81200166), and 2013 Beijing
Science and Technology Foundation for Selected Overseas Chinese Scholar
Introduction
Aortic stenosis (AS) is the commonest valve disease in the
West, with a prevalence varying between 0.02% in adults
under 44 years and 3-9% in those over 80 years of age 1, 2. The
disease may remain “silent” and hence unnoticed for years,
particularly in the elderly with naturally limited exercise. With the
development of symptoms, patients may carry a mortality of
36-52%, 52-80% and 80-90% at 3, 5 and 10 years, respectively
if left untreated, with a potential high risk of sudden death 3.
Surgical aortic valve replacement (SAVR) used to be the only
effective treatment for severe AS, being the second indication
for open heart surgery after coronary artery bypass grafting
(CABG) 4. Trans-catheter aortic valve implantation (TAVI) is a
recently developed procedure which aims at non-surgical AVR
in patients with severe, symptomatic and calcified AS who
are at high surgical risk because of either poor left ventricular
(LV) function, ejection fraction (EF) <50%, or other significant
co-morbidities e.g. age >80 years, previous CABG surgery and/
or aorta or other heart valve surgery, impaired kidney function,
chronic obstructive pulmonary disease (COPD) or pulmonary
hypertension 5. Currently, this technique is not recommended
in bicuspid AS patients due to the risk of incomplete and
suboptimal deployment of the aortic prosthesis [6]. TAVI
avoids open heart surgery and hence is likely to protect
myocardial function. The purpose of this paper is to review the
echocardiographic evaluation of LV, right ventricular (RV), and
left atrial (LA) function response to SAVR and TAVI for AS.
1. Cardiac function after SAVR
1.1 LV function
Left ventricular hypertrophy (LVH) regression: AVR decreases
the LV afterload, resulting in regression of cavity hypertrophy. LV
mass regression predominantly occurs within the first 6 months
of surgery, late regression is slow and might not become
significant on long-term. Studies reported controversial results
regarding the effect of age and gender on LV hypertrophy
regression 7, however, a systematic review has shown no
statistical association between age and sex with the rate of LV
mass regression and change in EF 8.
LV function: LVEF may remain normal in more than 90% of
AS patients. However, the long-axis systolic function has been
shown to be significantly reduced in AS patients with normal
LVEF as assessed by M-mode and Pulsed tissue Doppler
velocities 9, 10. LV early diastolic filling and wall thinning rates
are also significantly depressed in AS patients, despite being
negatively correlating with age, LV peak systolic pressure and
wall thickness 11. During the cardiac cycle, the myocardial
fibre function changes are not only in the longitudinal
direction, but also in the radial and circumferential direction.
Analysis of the changes in these three directions, in AS, gives
profound information on LV function performance. The new
echocardiographic techniques e.g. tissue Doppler Imaging (TDI)
and speckle tracking echocardiography (STE) provide accurate
evaluation of LV global and segmental myocardial motion
(velocity and displacement) as well as deformation (strain and
strain rate), respectively. In AS patients, the longitudinal velocity,
strain and strain rate (SR) are significantly decreased even in
mild AS and deteriorate further as it becomes severe, similar
to the previously reported M-mode and Pulsed TDI findings.
The reduction in long-axis function is related to the extent
of LV hypertrophy 12, 13 and the severity of AS 9, 14. The radial
and circumferential strain and SR changes usually occur later
than the longitudinal function, which may remain normal in
mild AS, but decrease in moderate and severe AS 15. This has
been shown by Delgado et al who demonstrated significantly
decreased radial and circumferential strain and SR in severe
AS with preserved LVEF 16. While another study showed
supernormal circumferential strain in patients with normal EF
and decreased function when LV systolic dysfunction is present,
suggesting that the high circumferential strain may serve as
an initial compensatory mechanism for maintaining normal
LVEF 17. The differential changes in longitudinal, radial and
circumferential fibers reflect the myocardial dysfunction starting
at the subendocardium in mild AS and progressing to mid-wall
and eventually transmural impairment in severe AS.
After SAVR and immediate drop of LV overload rapid increase
of LV myocardial velocities, strain and SR in all three directions
occur, as early as 1 week of surgery before global systolic
function and LV mass regression 18-20. These improvements
may be due to the increased coronary reserve secondary
to increased valve effective orifice area, resulting in a more
effective myocardial blood supply 21. During mid-term and
long-term follow-up, the strain and SR in all directions increase
gradually and eventually normalize 16, 21, 22. Such functional
recovery in radial and circumferential directions is usually earlier
than that in the longitudinal direction. However, even with full LV
function recovery at rest, the exercise capacity of these patients
remain limited after AVR 23.
LV twist function: The heart normally rotates along its longaxis forming a wringing (twisting) motion during the cardiac
cycle. Looking from the apex, the LV base rotates clockwise
and the apex rotates counter-clockwise, resulting in a wringing
motion. The net rotation difference between apex and base is
called twist. During isovolumic relaxation, the rapid untwisting
occurs before cavity filling. Studies using magnetic resonance
17
Reviews
imaging (MRI) in AS with preserved LVEF demonstrated an
increased apical rotation and delayed LV twist and untwist
compared to normals 24, 25. Furthermore, the increased apical
rotation and LV twist correlate with the severity of AS 26. These
changes are considered as compensatory mechanisms for
the increased intracavitary pressure and the subendocardial
ischemia 26. Another explanation is the potentially rearranged
fiber architecture in AS which may alter the torsional
deformation of the heart 25. LV twist has also been shown to
increase significantly in women with congenital AS and further
increase during pregnancy 27 confirming its sensitivity to loading
conditions 18. However, this compensatory mechanism is lost in
patients with severe LV dysfunction 17. After surgery, the twist
function may normalize 28.
1.2 RV function
In AS, the RV function is already abnormal before surgery, even
in the absence of secondary pulmonary hypertension. The RV
cavity is enlarged, the overall function is reduced although the
intrinsic RV myocardial function (measured by SR) remains
preserved 29. Despite successful AVR, the preoperative RV
dysfunction remains unchanged. These findings suggest an
organic remodeling of the RV before surgery that persists
afterwards. Furthermore, AVR is known to affect RV function
with reduced amplitude of the free wall motion, clinically
described as RV long axis function or tricuspid annulus peak
systolic excursion (TAPSE), the exact explanation of such
disturbance has not been successfully established. Some
suggestions for potential mechanisms have been reported
including right atrial cannulation, suboptimal RV myocardial
preservation or sternal opening 30, 31. However, none of these
hypotheses has yet proved a satisfactory explanation. A recent
study showed that the reduced TAPSE is related to the reversed
septal motion after AVR 30, 32. With the reversed septal motion
after AVR, the time to peak septal displacement become
delayed, in contrast to the LV lateral wall which is early and its
amplitude exaggerated 33, suggesting a cross talk between LV
and RV that allows maintaining global function.
1.3 LA function
One of the hemodynamic consequences of AS is pressure
overload which leads to LA dilatation. In AS, the LA peak
systolic (reservoir function), early diastolic (conduit function),
and late diastolic (active function) longitudinal strain rate are
all reduced as well as the LA longitudinal strain [34]. LA late
diastolic SR has been shown to be independently related to
aortic valve area. After SAVR, the global peak atrial longitudinal
strain increases relative to trans-aortic mean gradient and aortic
valve area changes[35] .
2. Cardiac function after TAVI
2.1 LV function
TAVI has proved very useful in alleviating symptoms and
improving survival of AS patients. In addition, the procedure
has significant effect on LV function. The LV function changes
after TAVI are of the same nature as those after SAVR, LVH
significantly regresses although not complete after 1 year
follow-up 36. Although together with the significant drop of transvalvular gradient, early improvement of EF and posterior wall
myocardial thickening and thinning velocities occur, recovery
of strain and SR have been reported as early as after 24 hours
of the procedure 37. Eight weeks after procedure, TAVI resulted
in similar increase of LV lateral wall longitudinal amplitude
and myocardial velocity compared to SAVR 38. Meanwhile,
similar to SAVR, the decreased longitudinal systolic strain and
SR in severe AS increase after 1 month of TAVI, irrespective
of changes in EF. The unchanged radial and circumferential
strain and SR reported after procedure may be due to the
near-normal values before TAVI 39. It seems that the changes
of LV myocardial motion and deformation after TAVI or SAVR
are more dependent on the baseline patients’ characteristics
than the procedure itself since they both decrease the afterload
immediately. So far, the effect of TAVI on LV twist function
remains to be thoroughly studied.
2.2 RV function
In contrast to SAVR, TAVI has proved to have no negative effect
on RV function with TAPSE remaining well preserved and RV
free wall systolic velocity increased compared with gender,
age and LV function matched SAVR patients after 8 weeks of
procedure 32, 38.
2.3 LA function
Early after TAVI, the LA reservoir and conduit function improve
but LA systolic function remain unchanged, indicating early
partial recovery of LA function 40. The LA systolic function
recovery may need longer time.
Conclusion
In severe aortic stenosis and normal EF, the three cardiac
chambers, LV, RV and LA are disturbed and respond differently
to removal of afterload. The LV longitudinal, radial and
circumferential strain and SR are reduced and twist is increased,
all recover after SAVR and TAVI. In AS, RV cavity is enlarged and
its function compromised, but these abnormalities remain up to
6 months of SAVR, which further reduces TAPSE in contrast to
TAVI which does not. The LA strain and SR are reduced in AS
patients, and improve after successful SAVR and TAVI.
Correspondence address
Professor Yi-hua He
Department of Ultrasound, Beijing Anzhen Hospital, Capital
Medical University, Beijing, China
Email: [email protected]
Tel: 86-010-64456349
References
1. Nkomo VT, Gardin JM, Skelton TN, Gottdiener JS, Scott CG, EnriquezSarano M. Burden of valvular heart diseases: a population-based study.
Lancet. 2006;368:1005-11.
2. Iung B, Vahanian A. Epidemiology of valvular heart disease in the adult. Nat
Rev Cardiol. 2011;8:162-72.
3. Rajamannan NM, Bonow RO, Rahimtoola SH. Calcific aortic stenosis: an
update. Nat Clin Pract Cardiovasc Med. 2007;4:254-62.
4. Bridgewater B, Kinsman R, Walton P, Gummert J, Kappetein AP. The 4th
European Association for Cardio-Thoracic Surgery adult cardiac surgery
database report. Interact Cardiovasc Thorac Surg. 2011;12:4-5.
5. Vahanian A, Alfieri O, Al-Attar N, Antunes M, Bax J, Cormier B, et al.
Transcatheter valve implantation for patients with aortic stenosis: a position
statement from the European Association of Cardio-Thoracic Surgery
(EACTS) and the European Society of Cardiology (ESC), in collaboration
with the European Association of Percutaneous Cardiovascular
Interventions (EAPCI). Eur Heart J. 2008;29:1463-70.
6. Zegdi R, Ciobotaru V, Noghin M, Sleilaty G, Lafont A, Latremouille C, et
al. Is it reasonable to treat all calcified stenotic aortic valves with a valved
stent? Results from a human anatomic study in adults. J Am Coll Cardiol.
2008;51:579-84.
7. Villa E, Troise G, Cirillo M, Brunelli F, Tomba MD, Mhagna Z, et al. Factors
affecting left ventricular remodeling after valve replacement for aortic
stenosis. An overview. Cardiovasc Ultrasound. 2006;4:25.
8. Sharma UC, Barenbrug P, Pokharel S, Dassen WR, Pinto YM, Maessen JG.
Systematic review of the outcome of aortic valve replacement in patients
with aortic stenosis. Ann Thorac Surg. 2004;78:90-5.
9. Takeda S, Rimington H, Smeeton N, Chambers J. Long axis excursion in
aortic stenosis. Heart. 2001;86:52-6.
18
Reviews
pressure overload due to aortic stenosis. Circulation. 1999;100:361-8.
10.Bruch C, Stypmann J, Grude M, Gradaus R, Breithardt G, Wichter T. Tissue
Doppler imaging in patients with moderate to severe aortic valve stenosis:
clinical usefulness and diagnostic accuracy. Am Heart J. 2004;148:696702.
26.van Dalen BM, Tzikas A, Soliman OI, Kauer F, Heuvelman HJ, Vletter WB,
et al. Left ventricular twist and untwist in aortic stenosis. Int J Cardiol.
2011;148:319-24.
11.Fifer MA, Borow KM, Colan SD, Lorell BH. Early diastolic left ventricular
function in children and adults with aortic stenosis. J Am Coll Cardiol.
1985;5:1147-54.
27.Tzemos N, Silversides CK, Carasso S, Rakowski H, Siu SC. Effect of
pregnancy on left ventricular motion (twist) in women with aortic stenosis. Am
J Cardiol. 2008;101:870-3.
12.Cramariuc D, Gerdts E, Davidsen ES, Segadal L, Matre K. Myocardial
deformation in aortic valve stenosis: relation to left ventricular geometry.
Heart. 2010;96:106-12.
28.Sandstede JJ, Johnson T, Harre K, Beer M, Hofmann S, Pabst T, et al.
Cardiac systolic rotation and contraction before and after valve replacement
for aortic stenosis: a myocardial tagging study using MR imaging. AJR Am J
Roentgenol. 2002;178:953-8.
13.Dinh W, Nickl W, Smettan J, Kramer F, Krahn T, Scheffold T, et al. Reduced
global longitudinal strain in association to increased left ventricular mass
in patients with aortic valve stenosis and normal ejection fraction: a hybrid
study combining echocardiography and magnetic resonance imaging.
Cardiovasc Ultrasound. 2010;8:29.
14.Miyazaki S, Daimon M, Miyazaki T, Onishi Y, Koiso Y, Nishizaki Y, et al.
Global longitudinal strain in relation to the severity of aortic stenosis: a twodimensional speckle-tracking study. Echocardiography. 2011;28:703-8.
15.Ng AC, Delgado V, Bertini M, Antoni ML, van Bommel RJ, van Rijnsoever
EP, et al. Alterations in multidirectional myocardial functions in patients with
aortic stenosis and preserved ejection fraction: a two-dimensional speckle
tracking analysis. Eur Heart J. 2011;32:1542-50.
16.Delgado V, Tops LF, van Bommel RJ, van der Kley F, Marsan NA, Klautz RJ,
et al. Strain analysis in patients with severe aortic stenosis and preserved
left ventricular ejection fraction undergoing surgical valve replacement. Eur
Heart J. 2009;30:3037-47.
17.Carasso S, Cohen O, Mutlak D, Adler Z, Lessick J, Aronson D, et al.
Relation of myocardial mechanics in severe aortic stenosis to left
ventricular ejection fraction and response to aortic valve replacement. Am
J Cardiol. 2011;107:1052-7.
18.Carasso S, Cohen O, Mutlak D, Adler Z, Lessick J, Reisner SA, et al.
Differential effects of afterload on left ventricular long- and short-axis
function: insights from a clinical model of patients with aortic valve stenosis
undergoing aortic valve replacement. Am Heart J. 2009;158:540-5.
19.Iwahashi N, Nakatani S, Kanzaki H, Hasegawa T, Abe H, Kitakaze M. Acute
improvement in myocardial function assessed by myocardial strain and
strain rate after aortic valve replacement for aortic stenosis. J Am Soc
Echocardiogr. 2006;19:1238-44.
20.Becker M, Kramann R, Dohmen G, Luckhoff A, Autschbach R, Kelm M, et
al. Impact of left ventricular loading conditions on myocardial deformation
parameters: analysis of early and late changes of myocardial deformation
parameters after aortic valve replacement. J Am Soc Echocardiogr.
2007;20:681-9.
21.Rost C, Korder S, Wasmeier G, Wu M, Klinghammer L, Flachskampf FA, et
al. Sequential changes in myocardial function after valve replacement for
aortic stenosis by speckle tracking echocardiography. Eur J Echocardiogr.
2010;11:584-9.
22.Lindqvist P, Bajraktari G, Molle R, Palmerini E, Holmgren A, Mondillo S, et al.
Valve replacement for aortic stenosis normalizes subendocardial function in
patients with normal ejection fraction. Eur J Echocardiogr. 2010;11:608-13.
23.Zhao Y, Henein MY, Morner S, Gustavsson S, Holmgren A, Lindqvist P.
Residual compromised myocardial contractile reserve after valve replacement
for aortic stenosis. Eur Heart J Cardiovasc Imaging. 2012;13:353-60.
24.Nagel E, Stuber M, Burkhard B, Fischer SE, Scheidegger MB, Boesiger P, et
al. Cardiac rotation and relaxation in patients with aortic valve stenosis. Eur
Heart J. 2000;21:582-9.
25.Stuber M, Scheidegger MB, Fischer SE, Nagel E, Steinemann F, Hess OM, et
al. Alterations in the local myocardial motion pattern in patients suffering from
29.Calcutteea A, Holmgren A, Lindqvist P, Henein MY. Organised right ventricular
remodelling in aortic stenosis even after valve replacement. Int J Cardiol.
2013.
30.Lindqvist P, Holmgren A, Zhao Y, Henein MY. Effect of pericardial repair after
aortic valve replacement on septal and right ventricular function. Int J Cardiol.
2012;155:388-93.
31.Reynolds HR, Tunick PA, Grossi EA, Dilmanian H, Colvin SB, Kronzon I.
Paradoxical septal motion after cardiac surgery: a review of 3,292 cases. Clin
Cardiol. 2007;30:621-3.
32.Zhao Y, Lindqvist P, Nilsson J, Holmgren A, Naslund U, Henein MY. Transcatheter aortic valve implantation--early recovery of left and preservation of
right ventricular function. Interact Cardiovasc Thorac Surg. 2011;12:35-9.
33.Zhao Y, Lindqvist P, Holmgren A, Henein MY. Accentuated left ventricular
lateral wall function compensates for septal dyssynchrony after valve
replacement for aortic stenosis. Int J Cardiol. 2013;164:339-44.
34.O’Connor K, Magne J, Rosca M, Pierard LA, Lancellotti P. Impact of aortic
valve stenosis on left atrial phasic function. Am J Cardiol. 2010;106:1157-62.
35.Lisi M, Henein MY, Cameli M, Ballo P, Reccia R, Bennati E, et al. Severity of
aortic stenosis predicts early post-operative normalization of left atrial size
and function detected by myocardial strain. Int J Cardiol. 2012.
36.Tzikas A, Geleijnse ML, Van Mieghem NM, Schultz CJ, Nuis RJ, van Dalen
BM, et al. Left ventricular mass regression one year after transcatheter aortic
valve implantation. Ann Thorac Surg. 2011;91:685-91.
37.Bauer F, Eltchaninoff H, Tron C, Lesault PF, Agatiello C, Nercolini D, et al.
Acute improvement in global and regional left ventricular systolic function
after percutaneous heart valve implantation in patients with symptomatic
aortic stenosis. Circulation. 2004;110:1473-6.
38.Forsberg LM, Tamas E, Vanky F, Nielsen NE, Engvall J, Nylander E. Left
and right ventricular function in aortic stenosis patients 8 weeks posttranscatheter aortic valve implantation or surgical aortic valve replacement.
Eur J Echocardiogr. 2011.
39.Grabskaya E, Becker M, Altiok E, Dohmen G, Brehmer K, Hamada-Langer
S, et al. Impact of transcutaneous aortic valve implantation on myocardial
deformation. Echocardiography. 2011;28:397-401.
40.Spethmann S, Dreger H, Baldenhofer G, Stuer K, Saghabalyan D, Muller E,
et al. Short-term effects of transcatheter aortic valve implantation on left atrial
mechanics and left ventricular diastolic function. J Am Soc Echocardiogr.
2013;26:64-71 e2.