JACC: CARDIOVASCULAR INTERVENTIONS
© 2012 BY THE AMERICAN COLLEGE OF CARDIOLOGY FOUNDATION
PUBLISHED BY ELSEVIER INC.
VOL. 5, NO. 5, 2012
ISSN 1936-8798/$36.00
DOI: 10.1016/j.jcin.2012.03.012
Pathology of Transcatheter Valve Therapy
Fabian Nietlispach, MD,*† John G. Webb, MD,* Jian Ye, MD,‡ Anson Cheung, MD,‡
Samuel V. Lichtenstein, MD, PHD,‡ Ronald G. Carere, MD,* Ronen Gurvitch, MB, BS,*
Christopher R. Thompson, MD,* Avi J. Ostry, MD,§ Lise Matzke, MSC,§储
Michael F. Allard, MD§储
Vancouver, British Columbia, Canada; and Bern, Switzerland
Objectives This study sought to report on the pathology of transcatheter aortic valves explanted at
early and late time points after transcatheter aortic valve implantation.
Background Information on pathological findings following transcatheter aortic valve implantation
is scarce, particularly late after transcatheter aortic valve implantation.
Methods This study included 20 patients (13 men, median age 80 years [interquartile range: 72 to
84] years) with previous transcatheter aortic valve implantation with a valve explanted at autopsy
(n ⫽ 17) or surgery (n ⫽ 3) up to 30 months after implantation (10 transapical and 10 transfemoral
procedures).
Results Structural valve degeneration was not seen, although fibrous tissue ingrowth was observed
at later time points with minimal effects on cusp mobility in 1 case. Minor alterations in valve configuration or placement were observed in up to 50% of cases, but they were not accompanied by
substantial changes in valve function or reliably associated with chest compressions. Vascular or
myocardial injury was common, especially within 30 days of transcatheter aortic valve implantation
(about 69%), with the latter associated with left coronary ostial occlusion by calcified native aortic
valve tissue in 2 cases. Mild to severe myocardial amyloidosis was present in nearly 33% of cases
and likely played a role in the poor outcome of 3 patients. Endocarditis, migration of the valve, and
embolization during the procedure led to surgical valve removal.
Conclusions Structural degeneration was not seen and minor alterations of valve configuration or
placement did not affect valve function and were not reliably caused by chest compressions. Vascular or myocardial injury is very common early after transcatheter aortic valve implantation and myocardial amyloidosis represents a relatively frequent potentially significant comorbid condition.
(J Am Coll Cardiol Intv 2012;5:582–90) © 2012 by the American College of Cardiology Foundation
From the *Division of Cardiology, St. Paul’s Hospital, Vancouver, British Columbia, Canada; the †Swiss Cardiovascular Center,
Bern University Hospital, Bern, Switzerland; ‡Division of Cardiac Surgery, St. Paul’s Hospital, Vancouver, British Columbia,
Canada; §Department of Pathology and Laboratory Medicine, University of British Columbia/St Paul’s Hospital, Vancouver,
British Columbia, Canada; and the 储University of British Columbia James Hogg Research Centre, St. Paul’s Hospital, Vancouver,
British Columbia, Canada. Drs. Nietlispach, Webb, Ye, and Cheung have received consulting fees from Edwards Lifesciences. Dr.
Nietlispach also has received unrestricted grants from the Swiss National Science Foundation and the Cardiovascular Research
Foundation (Basel, Switzerland). All other authors have reported that they have no relationships relevant to the contents of this
paper to disclose.
Manuscript received January 10, 2012; revised manuscript received March 26, 2012, accepted March 28, 2012.
Nietlispach et al.
Transcatheter Valve Pathology
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Transcatheter aortic valve implantation (TAVI) has been
established as an effective treatment for patients with severe
aortic valve stenosis who are not suitable for open-heart
surgery (1) or as an alternative treatment to open-heart
surgery in high-risk patients (2).
Mortality occurring ⬍30 days after TAVI reflects mostly
procedure-related mortality (3,4), whereas later mortality
occurring from 30 days to 1 year after TAVI is mostly
caused by either progression of heart failure or the natural
course of comorbid conditions (3,5,6). Procedure-related
mortality decreases with increasing operator and center
experience (3). Later mortality, by contrast, decreases by
performing the procedure in lower-risk populations with
fewer comorbid conditions (5).
Very little information is currently available on the
pathological findings following TAVI (7). Post-mortem
studies in humans consist of 2 case reports (8,9) and a single
series of 7 post-mortem cases (10). These prior reports
primarily demonstrate findings early after valve implantation with only 1 reported case with late follow-up at 425
days (9). In this report, we describe pathological findings in
20 valves explanted at early, intermediate, and late time
points following TAVI.
Methods
Patients. All patients with prior TAVI who died and
underwent a post-mortem examination or who had a valve
surgically explanted at our institution were reviewed. Written permission for pathological examination was obtained in
each case.
Valves and procedural approach. The Cribier-Edwards
valve (Edwards Lifesciences, Irvine, California), the prototypic balloon-expandable prosthetic implant (11), is constructed of a stainless steel frame with attached equine
pericardial leaflets and a fabric-sealing cuff. This was subsequently replaced with the Edwards Sapien valve (Edwards
Lifesciences) with bovine pericardial leaflets and a longer
fabric sealing cuff (12). The prosthetic valve is crimped onto
a balloon catheter and introduced through a large sheath in
the femoral artery (transarterial) (13) or directly through the
left ventricular apex using an intercostal incision (transapical) (14). The prosthesis is placed inside the diseased native
aortic valve and the balloon expanded, displacing the native
cusps.
Pathological analysis. Entire hearts (in case of an autopsy)
or the explanted transcatheter valves (in case of surgical
removal) were fixed in 10% buffered formalin and examined
by a cardiovascular pathologist (M.F.A.). Autopsy hearts
were examined by a stepwise approach to identify and
evaluate structural and nonstructural changes in the prosthesis, changes associated with the prosthesis or the procedure, and other cardiac or vascular findings, in accordance
with accepted approaches for traditional prosthetic valves
583
(15) or recommendations for transcatheter valves (16).
Surgically excised transcatheter valves were examined in a
similar fashion.
For microscopic analysis, paraffin-embedded myocardium
was sectioned at 4 m and stained with hematoxylin and
eosin, Masson trichrome (to identify fibrosis) (Ventana
Medical Systems, Tucson, Arizona), Prussian blue (to
identify iron) (Ventana Medical Systems), and Congo red
(Ventana Medical Systems) and sulfated Alcian blue (to
identify amyloid) (Acros Organics, Geel, Belgium, Fisher
Scientific, Ottawa, Ontario, Canada). In selected patients
with relevant rhythm disturbances and/or unexplained
death, the region of the atrioventricular node and the bundle
branches within the interventricular septum were microscopically examined. Valve cusps, when examined, were
sectioned at 4 m and stained with hematoxylin and eosin,
Movat pentachrome (Fisher Scientific; Sigma-Aldrich,
Oakville, Ontario, Canada; Acros Organics), and microbiological stains, if appropriate.
Statistics. Statistical analyses were done using R Statistical Computing for Mac OS (The R Foundation for Statistical Computing, Vienna, Austria). Data are presented as medians and interquartile ranges, unless otherwise indicated. For each valve and
cardiac findings groups (structural
Abbreviations
and nonstructural changes/dysand Acronyms
function; prosthesis/procedurerelated changes; and other cardiac
CPR ⴝ cardiopulmonary
changes), group comparison was
resuscitation
performed using Kruskal-Willis
TAVI ⴝ transcatheter aortic
valve implantation
test. Significance was taken at
p ⫽ 0.05 level for all analyses.
Results
Patient characteristics. A total of 17 valves were examined
at autopsy (median age: 78 years, 10 men), including 6
Cribier-Edwards valves and 11 Edwards Sapien valves.
Access for implantation was nearly equivalent, either apical
(n ⫽ 9) or transarterial (n ⫽ 8), for the entire group. Three
valves were removed from patients at the time of open-heart
surgery (median age: 82 years, all men).
Time after implantation and cause of death. Of the 17
autopsy patients, median post-procedural survival was 5
days (interquartile range: 2 to 25 days, range: 0 to 943 days).
Patients were stratified into 3 temporal categories (16,17):
immediate-early (⬍7 days); intermediate (7 to 29 days); and
late (ⱖ30 days). Death occurred in 9 patients ⬍7 days after
implantation and was due to: cardiac causes (heart failure,
major arrhythmia, rupture of adjacent structures, left main
occlusion) in 5; cerebrovascular accident in 1; major bleeding in 2; and sepsis in 1. In the intermediate group, cause of
death was cardiac in 3 and sepsis in 1. After 30 days, 1
patient died because of an intracerebral bleed (on warfarin
for atrial fibrillation) and 3 because of progressive heart and
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Table 1. Patient Characteristics and Pathological Findings of
Autopsy Cases
Time to Death
Age (Yrs) After Implantation
Pathological Findings
Access Route
Men
78
3 days
Recent myocardial injury
Recent brain injury
Apical
87
5 days
Coronary ostial occlusion
Recent myocardial injury
Arterial
57
5 days
Heavily calcified bicuspid
aortic valve
Recent brain injury
Apical
65
5 days
Cuspal thrombosis
Recent myocardial injury
Arterial
80
6 days
Recent myocardial injury
Recent brain injury
Apical
76
2 weeks
Amyloidosis
Arterial
77
28 days
Possible hypertrophic
cardiomyopathy
Apical
73
1 month
89
20 months
Fibrous tissue ingrowth
Amyloidosis
Arterial
85
24 months
Fibrous tissue ingrowth
Recent brain injury
Arterial
84
⬍1 day
Vascular injury
Recent myocardial injury
Apical
58
⬍1 day
Vascular injury
Recent myocardial injury
Apical
81
⬍1 day
Partial coronary ostial occlusion
Recent myocardial injury
Apical
80
5 days
Recent myocardial injury
Amyloidosis
Apical
71
10 days
Recent myocardial injury
Ischemic bowel
Apical
81
6 weeks
Amyloidosis
Apical
99
30 months
Fibrous tissue ingrowth
Amyloidosis
Arterial
Arterial
Women
16 cases showed some degree of coronary artery disease (mild to severe); 13 cases had mitral
annular calcification; all 17 cases showed myocardial hypertrophy.
renal failure. All 3 surgically excised transcatheter valves
were removed more than 30 days after implantation, ranging from 108 to 336 days after implantation (Table 1).
Structural and nonstructural prosthesis changes. The most
common structural change observed was a less than round
configuration that ranged from slightly oval to almost
D-shaped (Figs. 1 and 2). This finding occurred across all
temporal categories and, in some instances, was accompanied by an apparent malalignment or malapposition of valve
cusps (cuspal tautness, laxity, and/or poor coaptation).
There were no macroscopic signs of cuspal degeneration
(calcifications or cuspal tears), or any evidence of fracture or
disruption of the metallic stent in any valve.
Fibrous tissue ingrowth was found in valves from patients
dying late after TAVI (Fig. 3) and ranged from minimal to
extensive where a thin layer of filmy fibrous tissue covered
approximately 80% to 90% of the inner aspect of the
metallic stent (Fig. 4). Localized fibrous tissue ingrowth
onto the basal aspects of the cusps mildly reduced cuspal
mobility in 1 case (Fig. 1).
A probe-patent paravalvular defect was another relatively
frequent observation that spanned all temporal categories
(Fig. 3). Minor degrees of prosthesis malposition, using
relation of the inferior aspect of the prosthesis stent frame to
the insertion of the anterior leaflet of the mitral valve as a
guide, were also observed in several cases.
Small amounts of recent thrombotic material on the
ventricular and aortic aspects of the cusps (preferentially
near the commissural regions) and metallic stent were found
in 1 case in the immediate-early group. Histologically, the
thrombotic material was composed largely of fibrin and
platelets. Notably, echocardiography at the time of valve
implantation suggested thrombus on the guidewire and
possibly on the valve despite heparinization. There was no
evidence of thromboembolism at the time of autopsy,
however. Vegetations were not seen in any of the prostheses
from cases examined at autopsy.
Functional consequences of structural and nonstructural
prosthesis changes. Most patients demonstrated paravalvu-
lar aortic regurgitation, as assessed by echocardiography,
ranging from trivial to moderate in severity. Structural and
nonstructural prosthesis changes do not readily explain the
paravalvular regurgitation observed. Transvalvular aortic
regurgitation was not seen in the valve with fibrous tissue
ingrowth that mildly reduced cuspal mobility. Based on
cases with well-documented use of chest compressions
during cardiopulmonary resuscitation (CPR) (n ⫽ 8), an
equal number of cases with chest compressions were found
to be associated with altered valve shape (n ⫽ 4) as
compared to those that were not (n ⫽ 4). However,
dramatic changes in shape that were accompanied by
tautness of 1 valve cusp and laxity of others (Fig. 2B) did not
demonstrate significant alterations in valve function during
life.
Prosthesis- or procedure-associated changes. Most of these
findings occurred primarily in immediate-early or intermediate periods after implantation with a more frequent
occurrence in the immediate-early time frame (Fig. 5) (p ⫽
0.03). Myocardial injury in the form of contraction band
change in isolated or clusters of cardiac myocytes or areas of
coagulative necrosis of myocardium was observed in more
than 50% of all cases with the greatest frequency of
occurrence seen in patients dying in the immediate-early
period (Fig. 5). In select cases, acute injury of the conducting myocardium, especially the left bundle branch, was
observed with evidence that both ischemic and direct
traumatic injury played a role. Most likely, any injuries
observed arose from the valve or delivery system rather than
from the guidewire.
Sections of healing transapical access sites showed evidence of injured myocytes, accumulation of mesenchymal
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585
Figure 1. Bar Graph Illustrating Relative Frequency of Structural Prosthesis Changes According to Time After Implantation
Expressed as percentages. n ⫽ 4 to 9 per group.
cellular elements, hemorrhage, and small amounts of fibrous
connective tissue deposition.
Apparent obstruction of coronary ostia was observed
relatively frequently at autopsy examination, providing an
explanation for some of the myocardial injury observed
(Fig. 5). The most severe obstruction was observed in 2
cases in which a calcified and thickened native aortic valve
cusp caused complete or near complete obstruction of the
left coronary ostium. This was accompanied by hypotension
and showed significant ischemic myocardial injury in both.
The distance from the aortic annulus to the left coronary
ostium was relatively short in both patients: 8.5 and 9.5 mm,
respectively. The left sinuses of Valsalva were of normal size
and not particularly shallow.
Procedural-related injuries to vascular or other cardiac
structures were seen in a small number of cases (Fig. 5) that
when present resulted in catastrophic effects and rapidly led
to very poor outcomes. Traumatic disruption of the annular
region of the aorta occurred in 1 patient in whom the
smallest available prosthesis (23-mm diameter) was significantly larger than the relatively small (18 mm) and heavily
calcified annulus. In a second patient with severe mitral
annular calcification and substantially reduced leaflet mobility, a 2-cm tear involving the basal aspects of the anterior
mitral leaflet and adjacent outflow tract (Fig. 6) was created
during the procedure that resulted in communication between the left ventricle and atrium and hemodynamic
collapse. Transapical access was associated with massive
bleeding followed by death due to multiorgan failure at day
5 in another patient.
Other cardiac and vascular findings. All patients had evidence of increased cardiac mass or hypertrophy. Many
patients also had coronary atherosclerosis and its manifestations, including healed myocardial infarction and procedures such as coronary artery bypass surgery and/or percutaneous coronary intervention. Mitral annular calcification
was also a common finding whose severity potentially played
a role in some of the deleterious outcomes described
previously. Myocardial amyloidosis was present in nearly
one-third of all autopsy cases (5 cases, age 60 to 99 years)
and ranged in severity from relatively mild to extensive and
severe. Less severe involvement by amyloid was likely an
incidental finding in 2 patients, but where it was severe, it
may have contributed to death due to progressive heart
failure leading to death at 40, 608, and 943 days after
surgery.
Findings in surgically excised transcatheter valves. Reasons
for surgical valve explantation were: embolization at the
time of the procedure with the valve deployment in the
aortic arch and definitive surgical open-heart aortic valve
replacement with explantation of the embolized valve (at
day 108); low implantation with gradual migration to the
left ventricular outflow tract resulting in severe aortic
regurgitation (at day 109); and endocarditis (at 336 days). In
the latter case, the patient developed Streptococcus angiosus
endocarditis of mitral and transcatheter aortic valves 6
586
Nietlispach et al.
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A
B
Figure 2. Altered Transcatheter Aortic Valve Configuration
Noncircular configuration of a transcatheter valve removed from the heart
at autopsy (A) and cuspal malalignment (tautness of one cusp, arrow) in a
transcatheter valve with dramatic alterations in configuration (B).
weeks after a dental procedure that took place without
endocarditis prophylaxis. The endocarditis spread to the
mitral valve at the contact point of the aortic valve prosthesis
with the anterior mitral leaflet leading to a perforation and
regurgitation.
Discussion
As a relatively new interventional procedure, detailed pathological examination of autopsy or surgical material from
patients undergoing transcatheter implantation is critical to
the ongoing evolution and improvement of this approach to
treatment of aortic valve disease. Results of the present
investigation provide important insights into the changes in
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the transcatheter valves, mechanisms, and functional consequences of changes observed in the prostheses; emphasize
key pathologies related to the transcatheter valve implantation procedure; and serve to highlight the potential significance of comorbidities in this patient population.
Structural and nonstructural prosthesis changes. Current
surgical bioprostheses are relatively durable, although structural degeneration and failure can be anticipated to occur 5
to 20 years after implantation (18,19) with minimal histological degeneration seen up to 6 years after implantation
(20). In surgical bioprostheses, the major cause of failure is
related to calcification and tears of valve cusps, resulting in
regurgitation or stenosis (15,21). It is reassuring that we did
not observe significant structural valve failure in any case,
even up to 943 days after implantation. Variable degrees of
fibrous tissue ingrowth were observed late after implantation
with some localized involvement of valve cusps resulting in
a mild reduction in cuspal mobility but had no impact on
measurable valve function. Given its well-recognized occurrence in surgical bioprosthesis (15), it is highly likely that
more extensive fibrous tissue ingrowth will occur over time
in some prostheses and lead to prosthesis dysfunction,
which most likely can be treated by valve-in-valve implantation (22).
A less than round configuration of the stent frame was a
relatively common observation, and the degree of noncircular configuration varied substantially. We cannot speculate
on the reason for stent eccentricity, except for CPR with
chest compressions as a possible explanation in patients
dying after transcatheter valve implantation. However, a
consistent and significant relationship between a noncircular
configuration of the stent frame and CPR with chest
compressions was not observed. This does not rule out the
possibility that CPR with chest compressions may cause
deformation in selected patients. The finding of deformed
stent frames in this post-mortem study stands in contrast to
our finding on computed tomography scans, on which
circular stents were found, 3 years or more after transcatheter valve implantation (23). Chest compressions during
CPR might explain this discrepancy in part but only in
selected cases. Whether such deformed stent frames, even
when mild, increase shear stress, thereby accelerating structural valve degeneration needs further investigation (24,25).
Thrombosis and thromboembolic complications occur
less often in association with bioprostheses as compared to
mechanical valves (26). Thrombus was uncommon in our
series, with significant thrombus evident in only 1 patient in
whom intraprocedural heparinization may have been subtherapeutic. Nevertheless, post-procedural thromboembolic
stroke remains a concern, and most groups use long-term
aspirin and clopidogrel for 1 to 6 months (27). The ideal
antithrombotic regimen is yet to be determined (28).
Surgical bioprostheses are said to be associated with a 4%
10-year risk for endocarditis (29). Mechanical valves are most
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587
Figure 3. Bar Graph Illustrating Relative Frequency of Nonstructural Prosthesis Changes According to Time After Implantation
Expressed as percentages. n ⫽ 4 to 9 per group. AMVL ⫽ anterior mitral valve leaflet.
often associated with localization of infection at the sewing
ring, whereas infection of bioprosthetic valves is more often
localized on the valve cusps (15). Infection of our single
transcatheter valve was rather diffuse, involving the sewing skirt
as well as the valve cusps and was accompanied by infection
and perforation of the mitral leaflet (30). Piazza et al. (31)
reported a similar case in a low implanted CoreValve prosthesis
(Medtronic, Inc., Minneapolis, Minnesota).
Figure 4. Fibrous Tissue Ingrowth
Photograph showing fibrous tissue ingrowth on the stent frame of a transcatheter valve (arrow).
Functional consequence of prosthesis changes. Mild to
moderate paravalvular aortic regurgitation after TAVI is
common, as was observed in patients in our study, although
the clinical relevance of this degree of paravalvular regurgitation is uncertain (32–34). Despite a significantly higher
incidence of trivial to moderate paravalvular leaks in patients
after transcatheter valve implantation as compared to surgical patients, transcatheter valve patients have significantly
better hemodynamics and improvement of left ventricular
function (35–37). Whether paravalvular leaks after TAVI
result in (clinically relevant) hemolysis (as described from
surgical collectives (38)) needs further investigation.
Of interest is the finding that the presence of a noncircular shape of the stent frame, mild degrees of malalignment
or malposition of the transcatheter valve, or presence of a
probe patent paravalvular defect had no significant or
consistent association with severity of transvalvular or paravalvular aortic regurgitation during life. Thus, mild alterations in configuration or placement of transcatheter prosthetic aortic valves, as observed at autopsy, do not appear to
adversely affect function.
Prosthesis- and procedure-associated findings. Recent myocardial injury was a relatively frequent observation in our
series of patients, especially in those dying in the
immediate-early time period after implantation. Left
coronary ostial obstruction was likely causative in 2
patients and was associated with low origins of the left
coronary artery and bulky, calcified native cusps in both
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Figure 5. Bar Graph Illustrating Relative Frequency of Procedure-Associated Changes According to Time After Implantation
Expressed as percentages. n ⫽ 4 to 9 per group. AVN ⫽ atrioventricular node; BB ⫽ bundle branch; IVS ⫽ interventricular septum; PB ⫽ penetrating bundle.
cases (Fig. 7). Another known risk factor for coronary
ostial obstruction is a narrow aortic root with shallow
aortic sinuses (39). This complication has been described
in 0.6% of cases in a recent large registry (27), suggesting
that multimodality screening (40) may be important.
Obstruction of coronary arteries can be predicted during
balloon valvuloplasty with aortography during balloon
inflation. If coronary obstruction occurs during implantation, early clinical signs include hypotension and severe
hypokinesis on echocardiography (41). Management in-
cludes prompt cardiopulmonary support, coronary angiography, and, in most cases, urgent coronary revascularization (39,42,43).
New onset of heart block can occur following transcatheter valve implantation. The incidence of heart block is
reportedly lower with the balloon-expandable Edwards
valve, used in this series, as compared to the self-expanding
CoreValve (3,27,44). Based on findings in select cases where
the conduction system was examined, it appears that a
combination of direct traumatic effects to the bundle branch
Figure 6. Mitral Valve Injury With Left Ventricle and
Left Atrial Communication
Figure 7. Left Coronary Ostial Obstruction
Defect (arrow) in the anterior leaflet of a mitral valve with severe calcification of its annulus (double arrow) that led to a communication between
the left ventricle and the left atrium.
Photograph showing a bulky, calcified native valve cusp filling the sinus
region of the aorta (arrow) to cause obstruction of the left coronary
ostium.
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system and ischemic injury occurring because of pressureinduced alterations of flow in coronary septal arteries in the
interventricular septum are potential contributing factors.
Other cardiac and vascular findings. One accompanying
finding that warrants special mention is myocardial amyloidosis, which occurred in nearly one-third of all cases
studied. Senile systemic amyloidosis is very common in
elderly people, reportedly present in 25% of individuals over
the age of 80 years, and often goes unrecognized (45).
Whereas patients with cardiac amyloidosis can successfully
undergo surgical procedures, operative and post-operative
problems associated with anesthesia are well described
(46 – 48). As such, recognition of the possible presence of
the condition and involvement of anesthetists familiar with
cardiac anesthesia in this setting are important. Moreover,
the transcatheter valve approach, as compared to open-heart
valvular replacement with cardiopulmonary bypass, may be
the technique of choice in this patient population.
Conclusions
Significant structural degeneration of transcatheter valves
does not occur up to 30 months after implantation, and
minor alterations in valve configuration or placement do not
appear to be associated with substantial changes in function
of the valves during life when assessed by echocardiography.
Chest compressions during CPR may cause alterations in
configuration of valves but only in a minority of cases.
Myocardial injury is common early after the implantation
procedure with coronary ostial obstruction by a thick,
calcified native aortic valve cusp in the setting of a shallow
coronary sinus, narrow aortic root, and/or low origin of the
ostium likely a causative factor in some. Finally, myocardial
amyloidosis is common in this patient population and
warrants recognition because of its potential to have deleterious effects.
Acknowledgments
The authors wish to thank Jing Dong for her assistance with
statistical analysis and Varun Saran for his assistance with
production of figures and images.
Reprint requests and correspondence: Dr. Michael F. Allard,
University of British Columbia, G105-2211 Westbrook Mall,
Vancouver, British Columbia V6T 2B5, Canada. E-mail:
mike.allard@pathology.ubc.ca.
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Key Words: autopsy 䡲 long-term follow-up 䡲 pathology 䡲
stent deformation 䡲 tissue overgrowth 䡲 transcatheter aortic
valve replacement.