(Circulation. 1998;97:1424-1425.)
© 1998 American Heart Association, Inc.
How Should We Define Inadequate Coronary Arterial Remodeling?
Toshihiko Nishioka, MD
Division of Cardiology,
Self-Defense Forces Central Hospital,
Tokyo, Japan
Hans Berglund, MD;
Huai Luo, MD;
Tomoo Nagai, MD;
; Robert J. Siegel, MD
Division of Cardiology,
Cedars-Sinai Medical Center,
Los Angeles, Calif
To the Editor:
After our report1 showing the contribution
of "inadequate compensatory enlargement" to the development of
coronary narrowing, Mintz et al2 in their
recently published report confirmed this concept in a larger study
population by using a different definition of "inadequate
arterial remodeling." However, the assessment of the
relative importance of "inadequate arterial remodeling"
is highly dependent on the definition used.
As pointed out by Mintz et al, the assessment of the true effect
of vessel remodeling on the progression of coronary narrowing
would require serial or longitudinal intravascular ultrasound studies
(IVUS) over a long time period. However, such longitudinal, serial
studies are time consuming and impractical. Consequently, we compared
the size of the external elastic lamina (EEL) area (the area within the
outer border of the sonolucent zone considered to represent
EEL) at the lesion site with those at the reference sites. The proximal
and distal reference sites were defined as the sites with minimal
narrowing by angiography and the largest lumen area and <50% area
stenosis as determined by IVUS. In our
study,1 the EEL area of all arteries was larger
at the proximal reference sites than at the distal reference sites, and
"inadequate compensatory enlargement" was defined when there was a
smaller EEL area at the lesion site than at the distal reference site.
This definition is based on two factors: (1 ) nonatherosclerotic
coronary arteries taper from the proximal to the distal portion
of the coronary artery and (2 ) "adequate arterial
remodeling" at the lesion site should result in the same or more
prominent compensatory enlargement of the vessel compared with the
distal reference site that has less luminal narrowing. Our definition
resulted in a frequency of "inadequate compensatory enlargement" of
26% or approximately 1 in 4 patients.
Mintz et al defined "inadequate arterial remodeling" as
a ratio of the lesion EEL area over the proximal reference EEL area
0.78 and found that 15% of the lesions they studied met this
criteria.2 By applying these criteria to our
study population, we found that 14% of the coronary lesions (1
in 7 patients) had "inadequate arterial remodeling,"
which reflects an excellent agreement between our studies. Hence the
apparent discrepancy between the studies (1 in 4 [26%] versus 1 in 7
[14%]) concerning the relative importance of "inadequate
arterial remodeling" seems to be due to different
definitions. We, like Pasterkamp et al,3 Mintz et
al, and others, hypothesize that a substantial proportion of
arterial stenoses are due to not only plaque
accumulation but also to the failure to develop compensatory
arterial enlargement. In this context we believe that it is
essential to carefully assess the rationale behind the definitions of
this new entity. Mintz et al based their definition of normal tapering
of the coronary artery on their previous study, in which among
146 coronary arteries with focal,
hemodynamically significant stenoses, no artery
developed EEL area tapering exceeding 21% over a 10-mm
arterial length4 from the proximal to
the distal reference site. However the proximal and the distal
reference sites used for the definition of normal tapering also had
atherosclerosis and exhibited an area stenosis
of 
50%, and these "normal sites," as pointed out by the
authors, may be affected by a variable type and degree of vessel
remodeling. Moreover, the significant lesion located between both
reference sites may have also influenced coronary remodeling at
the reference sites. Hence the prevalence of "inadequate
coronary arterial remodeling," suggested by the
data presented by Mintz et al are hampered by the fact that
they did not use "ideal" reference segments in their definition.
Our definition is not based on idealized segments either; rather, we
use the coronary artery being imaged as its own "control."
Our criteria use on-line assessment and require no complex calculations
or assumptions. IVUS imaging is used to directly assess whether
"inadequate compensatory enlargement" at the lesion site is
present in the specific coronary artery being assessed for
intervention. Should "inadequate compensatory enlargement" have an
impact on which coronary interventions are preferable in a
given clinical situation, we believe our definition may serve as an
appropriate and practical tool for the coronary
interventionalist.
References
1.
Nishioka T, Luo H, Eigler NL, Berglund H, Kim CJ, Siegel
RJ. Contribution of inadequate compensatory enlargement to development
of human coronary artery stenosis: an in vivo
intravascular ultrasound study. J Am Coll Cardiol. 1996;27:1571–1576.[Abstract]
2.
Mintz GS, Kent KM, Pichard AD, Satler LF, Popma JJ, Leon MB.
Contribution of inadequate arterial remodeling to the
development of focal coronary artery stenoses: an
intravascular ultrasound study. Circulation. 1997;95:1791–1798.[Abstract/Free Full Text]
3.
Pasterkamp G, Wensing PJ, Post MJ, Hillen B, Mali WP, Borst C.
Paradoxical arterial wall shrinkage may contribute to
luminal narrowing of human atherosclerotic femoral arteries.
Circulation. 1995;91:1444–1449.[Abstract/Free Full Text]
4.
Javier SP, Mintz GS, Popma JJ, Pichard AD, Kent KM, Satler LF,
Leon MB. Intravascular ultrasound assessment of the magnitude and
mechanism of coronary artery and lumen tapering. Am
J Cardiol. 1995;75:177–180.[Medline]
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Response
Gary S. Mintz, MD;
; Martin B. Leon, MD
Intravascular Ultrasound Imaging and Cardiac
Catheterization Laboratories,
Washington Hospital Center,
Washington, DC
The reports from Nishioka et al,1
Pasterkamp et al,2 and our
laboratory3 all confirm that inadequate
arterial remodeling contributes importantly to the process
of atherosclerotic stenosis formation in some lesions.
We agree with Nishioka and colleagues that the definition used in our
report required a number of assumptions and was, perhaps, cumbersome.
However, all of the studies (including ours) had flaws. Either the
sample size was small,1 2 the results were
potentially biased by lesion selection,1 2 3 or
the prevalence was definition dependent.1 2 3
In the report by Nishioka et al,1 the lesion was
compared with a distal reference segment.1 This
comparison also has limitations. First, the ultrasound catheter must be
advanced far enough past the lesion into the distal vessel to identify
a distal reference segment, something not always possible. Second, the
authors did not define the axial distal between their lesion image
slice and their distal reference segment. (Because vessels taper,
distal reference segment selection will also affect identification of
inadequate remodeling.) Third, it has been our experience that crossing
a stenosis with the ultrasound catheter, especially a tight
stenosis (ie, stenoses most likely to require
intervention), causes the distal vessel to become underperfused, (1 )
making identification of the distal reference segment difficult and (2 )
causing the cross-sectional measurements to be unreliably small.
Fourth, the distal reference must contain enough of a plaque burden
with positive remodeling.
We believe that remodeling is a spectrum and that many stenoses
fitting none of the definitions in these three studies may also have an
element of inadequate remodeling. Also, none of these studies
adequately address whether these findings are present during the
early stages of lesion formation in some vessels or whether plaque and
arterial shrinkage are late events.
Finally, we believe that the pathologic concepts outlined in all three
of these studies are more important than the exact prevalence of the
findings and the definitions used.
References
1.
Nishioka T, Luo H, Eigler NL, Berglund H, Kim CJ, Siegel
RJ. Contribution of inadequate compensatory enlargement to development
of human coronary artery stenosis: an in vivo
intravascular ultrasound study. J Am Coll Cardiol. 1996;27:1571–1576.
2.
Pasterkamp G, Wensing PJ, Post MJ, Hillen B, Mali WP, Borest C.
Paradoxical arterial shrinkage may contribute to luminal
narrowing of human atherosclerotic femoral arteries.
Circulation. 1995;91:1444–1449.
3.
Mintz GS, Kent KM, Pichard AD, Satler LF, Popma JJ, Leon MB.
Contribution of inadequate arterial remodeling to the
development of focal artery stenoses: an intravascular
ultrasound study. Circulation. 1997;95:1791–1798.
