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European Heart Journal (2000) 21, 92–94
Article No. euhj.1999.1892, available online at http://www.idealibrary.com on
Editorials
Intravascular ultrasound guided PTCA: a way to escape
stent mania?
See page 137 for the article to which this Editorial
refers
In 1995, a total of 278 982 percutaneous coronary
interventions were carried out in Europe alone[1]. In
the United States, the corresponding figure for the
same period was approximately 500 000, and these
figures continue to increase worldwide, year after
year. To date, plain old balloon angioplasty remains
the strategy of choice in the majority of cases, even
though a myriad of different devices have been conceived,
developed and tested in percutaneous coronary
interventions. However, up to now, no other
single device has seen the same spectacular explosion
on the market as the stent, and none has managed to
oust the angioplasty balloon from its position at the
top of the polls.
Introduced in 1986, stents spread relatively slowly
until the publication of large multicentre trials demonstrating
the efficacy of this device in the prevention
of restenosis[2,3]. Since then, stents have spread like
wildfire, and their diffusion has been all the more
encouraged by improvements in the prevention of
subacute occlusions. In 1997, the average rate of
stenting in Europe was 51%, with figures ranging
from 25% in Eastern Europe to more than 60% in
Western European nations[4]. Since this report was
compiled, the rate of stenting has continued to grow,
and is probably around 70% now.
The most common indications for stenting are
abrupt vessel closure, suboptimal result defined by
residual stenosis >30%, coronary dissection of grade
C or higher and treatment of restenosis on a native
artery, not to mention the very broad indications for
stenting in veinous bypass grafts. Without a doubt,
stenting makes it possible to control abrupt occlusions
and to optimize the result of the conventional
angioplasty procedure. In short, the stent has made
angioplasty safer and easier, with improved immediate
results. However, it is worth noting that all these
indications for stenting are based on observational
studies only. The only indication in which the efficacy
of stents has been proven is still complied with
relatively rarely, namely the prevention of restenosis
in STRESS-BENESTENT-type lesions, i.e. in lesions
less than 15 mm in length, and in arteries with a
diameter >2·8 mm and <3·5 mm[4].
Furthermore, it would appear that stenting is
becoming systematic in certain centres, irrespective of
vessel size —large or small, irrespective of the final
result after conventional angioplasty, and the aspect
of the lesion site —dissected or not, dissection with
limited or non-limited flow. Direct stenting is the
other representative example of growing stent-mania.
This consists in deliberate stent deployment as the
primary treatment, without previous dilation of the
vessel, in the hope of reducing both the risk of vessel
trauma and of dissection.
All in all, the attitude of extensive stenting prevails
today despite the fact that it has never been demonstrated
that stenting reduces immediate complications
after angioplasty[2,3]. In particular, stents have never
been shown to reduce the rate of post-procedure
minor enzyme release, the prognosis of which is
uncertain[5]. Widespread stenting persists, despite the
considerable cost induced by their mass use, and
despite the risk of intra-stent restenosis, which is
estimated to be around 25%, and for which no
satisfactory solution has yet been found[6].
In this context, the article by Schroeder et al.[7] in
this issue, in which they analyse the immediate and
long-term evolution of arterial dissections after intravascular
ultrasound guided PTCA, provides us with
an alternative view of angioplasty in the age where
the stent is king. Does their view focus on the past, or
look to the future? One must not forget the limitations
of this paper, which presents the experience
of a single centre in a non-randomized study. Intravascular
ultrasound represents a major advance in
coronary imaging because it allows a very precise
picture of the exact size of the lumen, and also of the
vessel structure, plaque burden and presence of calcification.
So far, intravascular ultrasound imaging
has been principally used to optimize stent deployment[
8–10], and to demonstrate the reality of arterial
remodelling post-angioplasty[11]. It has now become
an indispensable tool for the analysis of the intimal
mechanisms of endoluminal coronary interventions.
0195-668X/00/020092+12 $35.00/0
2000 The European Society of Cardiology
Moreover, recent studies would tend to prove that
intravascular ultrasound allows for a physiological
approach to coronary flow[12]. Furthermore, Abizaid
et al. have shown that a stenosis is not haemodynamically
significant when the cross-sectional area
of the narrowing is >4 mm2[13]. Using intravascular
ultrasound to guide angioplasty offers the possibility
of optimizing balloon size by adapting it to the real
diameter of the artery as measured from external
elastic lamina to external elastic lamina, and not
according to the vascular lumen size as is the case in
quantitative angiography. This results in a balloon/
artery ratio considerably greater than 1, and is probably
one of the reasons why residual stenosis of <30%
at the end of the procedure, a so-called ‘stent like
result’ can be more frequently obtained with intravascular
ultrasound guided PTCA than in traditional
angiography guided PTCA. Contrary to previous
reports stating that oversizing resulted in more
frequent complications, the rate of major adverse
cardiac events in this report does not seem to be
increased compared to conventional balloon angioplasty
without oversizing[14]. Finally, intravascular
ultrasound also allows for a close analysis of dissection,
and shows that these latter are in fact very
common, occurring in more than two-thirds of all
cases of angioplasty. This confirms that dissections
are an integral part of the mechanism of action of
angioplasty.
The article by Schroeder et al.[7] shows above all
that the evolution of non-stented arterial dissections,
provided they are not flow-limiting, is favourable in
the majority of cases, with the rate of major adverse
cardiac events in this series not exceeding that
attained in other series with extensive stenting. This
result seems to be achievable thanks to significant
over-sizing of the balloon compared to the
angiography-determined lumen size, resulting in
major enlargement of lumen size so that arterial
dissections do not compromise the flow. The final
result is that the rate of the stenting in this series will
probably be considered by most interventional cardiologists
as being ridiculously low, at less than 5%. In
addition, the long-term evolution indicates that a low
restenosis rate can be achieved without the use of
stents. Of course, to be validated, these results need to
be confirmed by further studies, and reproduced by
other investigators.
All in all, intravascular ultrasound is one of the
tools developed for and by angioplasty, but which did
not experience the same widespread use as some of
the other devices at the disposal of interventional
cardiologists. This lack of popularity is most likely
due to the relatively high price of the intravascular
ultrasound consoles which are necessary to operate
the probes, and of course, the price of the actual
intravascular ultrasound catheter itself, even though
this latter is still considerably cheaper than a stent.
In addition, the use of intravascular ultrasound
increases the complexity of the procedure, whereas
stent implantation results in over-simplification
of the procedure, and increased comfort for the
physician, explaining the relative lack of interest by
interventional cardiologists in this imaging technique.
In any case, this article clearly shows that angioplasty
carried out in a different way, with the choice
of balloon size guided by accurate intravascular
ultrasound measurement of vessel size, makes it
possible to achieve results which compare favourably
with systematic stenting. The time has come to carry
out further, randomized studies in this area. Some
are already ongoing in Europe. It remains to be
seen whether it is possible to escape from the
‘pense´e unique’ that coronary angioplasty must
systematically involve stent implantation.
J.-P. BASSAND
University Hospital Saint-Jacques,
Besanc¸on, France
References
[1] Windecker S, Maier-Rudolph W, Bonzel T et al. on behalf of
the Working Group Coronary Circulation of the European
Society of Cardiology. Interventional cardiology in Europe
1995. Eur Heart J 1999; 20: 484–95.
[2] Fischman DL, Leon MB, Baim DS et al. Stent Restenosis
Study Investigators. A randomized comparison of coronarystent
placement and balloon angioplasty in treatment of
coronary artery disease (STRESS trial). N Engl J Med 1994;
331: 496–501.
[3] Serruys P, De Jaegere P, Kiemenij F et al. Benestent Study
Group. A comparison of balloon-expandable-stent implantation
with balloon angioplasty in patients with coronary heart
disease. N Engl J Med 1994; 331: 489–95.
[4] Eeckhout E, Wijns W, Meier B, Goy JJ on behalf of the
members of the Working Group on Coronary Circulation of
the European Society of Cardiology. Indications for intracoronary
stent placement: the European view. Eur Heart J
1999; 20: 1014–9.
[5] Simoons ML, van den Brand M, Lincoff M et al. Minimal
myocardial damage during coronary intervention is associated
with impaired outcome. Eur Heart J 1999; 20: 1112–9.
[6] Kasaoka S, Tobis J, Akiyama T et al. Angiographic and
intravascular ultrasound predictors of in-stent restenosis.
J Am Coll Cardiol 1998; 32: 1630–5.
[7] Schroeder S, Baumbach A, Mahrholdt H. The impact of
untreated coronary dissections on the acute and long-term
outcome after intravascular ultrasound guided PTCA. Eur
Heart J 2000; 21: 137–45.
[8] Colombo A, Hall P, Nakamura S et al. Intracoronary stenting
without anticoagulation accomplished with intravascular
ultrasound guidance. Circulation 1995; 91: 1676–88.
[9] de Jaegere P, Mudra H, Figulia H et al. Intravascular Ultrasound
guided optimized stent deployment. Immediate and 6
months clinical and angiographic results from the Multicenter
ultrasound Stenting in Coronaries Study (MUSIC). Eur Heart
J 1998; 19: 1214–23.
Editorials 93
Eur Heart J, Vol. 21, issue 2, January 2000
[10] Schiele F, Meneveau N, Vuillemenot A et al. Impact of IVUS
guidance in stent deployment on 6 month restenosis rate. A
multicenter randomized study comparing two strategies, with
and without IVUS guidance. J Am Coll Cardiol 1998; 32:
320–8.
[11] Mintz GS, Popma JJ, Pichard AD et al. Arterial remodeling
after coronary angioplasty: a serial intravascular ultrasound
study. Circulation 1996; 94: 35–43.
[12] Takagi A, Tsurumi Y, Ishii Y, Suzuki K, Kawana M,
Kasanuki H. Clinical potential of intravascular ultrasound for
physiological assessment of coronary stenosis. Relationship
between quantitative ultrasound tomography and pressderived
fractional flow reserve. Circulation 1999; 100: 250–5.
[13] Abizaid A, Mintz G, Mehran R et al. Long-term follow-up
after percutaneous transluminal coronary angioplasty was
not performed based on intravascular ultrasound findings.
Importance of Lumen Dimensions. Circulation 1999; 100:
256–61.
[14] Roubin GS, Doublas JS Jr, King SB et al. Influence of balloon
size on initial success, acute complications, and restenosis
after percutaneous transluminal coronary angioplasty. A
prospective randomized study. Circulation 1988; 78: 557–65.
European Heart Journal (2000) 21, 94–96
Article No. euhj.1999.1669, available online at http://www.idealibrary.com on
Diagnosing primary diastolic heart failure
With the increasing refinement of methods to uncover
early phases of cardiac failure, we have, over the past
two decades, witnessed the emergence of diastolic
dysfunction and diastolic failure of the heart as
separate, widely recognized clinical entities. Whereas
the majority of the conditions related to diastolic
dysfunction and failure are the mere consequence of
systolic cardiac failure, there also exists a distinct
primary form of diastolic failure. Primary diastolic
failure has been commonly defined as a condition
with classic findings of congestive heart failure
with normal ventricular systolic function, but with
predominantly diastolic dysfunction. It has been
observed in a large variety of clinical conditions and
was believed to occur more commonly—at least in
the elderly population—than previously thought,
accounting for about 30% to 40% of all patients with
congestive heart failure.
In an excellent review, Vasan et al.[1] surveyed 31
studies on diastolic failure published in the period
January 1970–March 1995. From their critical analysis,
the authors were astonished to find that the
prevalence of primary diastolic heart failure, i.e.
patients with congestive heart failure and normal
ventricular systolic performance, varied widely from
13% to 74%. Despite the many possible causes, interpretations
and warnings suggested by these authors,
it is surprising that their conclusions were not taken
more seriously. Similar criticisms were recently raised
by Caruana et al.[2]. In a Letter to the Editor in
the European Heart Journal (20/5), Caruana et al.
responded to a report entitled ‘How to diagnose
diastolic heart failure’ by the European Study Group
on Diastolic Heart Failure[3]. In the Working Group’s
Report, it was stated that a diagnosis of primary
diastolic heart failure requires three obligatory conditions
to be satisfied simultaneously: (1) presence of
signs or symptoms of congestive heart failure; (2)
presence of normal or only mildly abnormal left
ventricular systolic function; (3) evidence of abnormal
left ventricular relaxation, filling, diastolic distensibility
or diastolic stiffness. Using echocardiographic
examination in patients with dyspnoea but no apparent
left ventricular systolic dysfunction, Caruana
et al. observed a prevalence of primary diastolic
dysfunction of 3–5% when using an E/A ratio in
association with deceleration time, but of 27% if
isovolumic ventricular relaxation time was used.
There was poor overlap between subjects found to be
‘abnormal’ by each of the two different criteria, with
only 2–3% when both indices were combined. From
this, the authors concluded (i) that different measures
of diastolic dysfunction give different prevalences
of primary diastolic failure, and (ii) that there is
no simple echocardiographic means of reliably
diagnosing diastolic dysfunction.
As previously stated by Vasan et al.[1], only two
reasons could possibly account for this somewhat
absurd wide variation in clinical prevalence of primary
diastolic heart failure. Either there is no agreement
of what should be considered as near-normal
systolic function and how it should be measured, or
there is no clear, generally agreed definition of diastolic
dysfunction or failure. Moreover, as many conditions
may clinically resemble primary diastolic
failure, one should first exclude all non-cardiac causes
94 Editorials

2000 The European Society of Cardiology

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