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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3585_Библиотеки_им_академика_М_И_Перельмана
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1.5 Fluoroscopy andImaging Strategies
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a
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Fig. 1.34 Viewing the longitudinal axis of the target vessel on the
detector. (a) The green line depicts the axis of the ROI (dark green line).
It is assumed that the axis will appear as the red line when projected on
the anterior detector surface. The detector surface is not always parallel
with the longitudinal axis of the target vessel in the ROI.To make the
surface parallel with the axis of the vessel, the detector should be
rotated 90 degrees around the axis viewed on its surface. For example,
assuming that the angle α between the axis of the target vessel and the
vertical axis of the detector surface is 30 degrees, as shown here, the
detector should be rotated toward the LAO projection at an angle of
about 30 degrees in the CR direction or should be rotated toward the
RAO projection at an angle of about 60 degrees in the CA direction to
make it parallel with the vessel. (b) This is the result of rotating the
detector from the position shown in a at 90 degrees toward the LAO
projection and at an angle of 30 degrees in the CR direction. Since the
detector surface is parallel to the longitudinal axis of the target vessel in
a
the ROI, the longest view of the vessel is obtained in the projection
perpendicular to a plane encompassing the axis. In biplane cineangiography, the other projection is normally the AP projection (shown in a).
When using biplane imaging equipment, it is usual to search for the
optimal position of the lateral detector while keeping one detector in the
AP projection. As orthogonality of the two planes can be checked visually, it is easier to set the position of the lateral detector in this way. (c)
To make the surface of other detector parallel with the longitudinal axis
of the target vessel, the detector should be rotated at 90 degrees again in
the direction perpendicular to the longitudinal axis of the plane shown
in b. The new detector position provides a view of the target vessel in a
projection orthogonal to a plane encompassing its longitudinal axis,
thus giving the longest view of the vessel. With biplane imaging equipment, ne adjustments to the orientation of the AP detector can be made
in this way to achieve imaging in two orthogonal projections
b
Fig. 1.35 Optimal projections for viewing LCX lesions. (a) In this
patient, the longest view of the LCX encompassing the CTO is obtained
in the RAO+ CA projection, and the LAD runs horizontally in this
projection. (b) After the detector is rotated 90 degrees (LAO+CA), the
LAD runs vertically, and the LCX lesion is viewed at an angle of 90
degrees. Performing uoroscopy in two optimal projections allows
accurate detection of guidewire deviations
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cd
RAO+CAAP+CR
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1 Mitsudo’s PCI Techniques forCTO
a
LAO+CA RAO+CA
Fig. 1.36 Fluoroscopy of the LAD ostium. (a, b) In the LAO+CA
projection (a), the LAD runs upward vertically from the ostium to
Segment #6, remaining almost perpendicular to the detector surface. In
the RAO+ CA projection (b) (after rotating the detector 90 degrees
toward the RAO projection), the target vessel runs horizontally.
Rotating the detector 90 degrees in the CR direction alone (no change
to the RAO) will obtain a projection perpendicular to the longitudinal
axis of the target vessel in the ROI.However, it is difcult to clearly
distinguish between the LAD and LCX in the RAO+CR projection.
Therefore, you should use this projection (a & b) while advancing a
guidewire through the LAD ostium. After the ROI moves to Segment #6
b
of the LAD, the LAO+CA projection provides a markedly shortened
view of the target vessel. Accordingly, after the guidewire has entered
the LAD, you should move the AP detector to the RAO+ CR projection. However, none of the available biplane imaging equipment can
provide simultaneous images in two RAO planes each angled in the CA
and CR directions. (c, d) In this situation, a good solution is to rotate the
AP detector in the AP+CR direction. Since many biplane imagers do
not allow the two detectors to be set at angles that are too tight, you
need to determine the optimal uoroscopy angles compatible with the
equipment being used
AP+CRLAO+CR
1.5 Fluoroscopy andImaging Strategies
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a
AP+CA LAO+CR
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b
Fig. 1.37 Fluoroscopy of the RCA bifurcation. (a) The two optimal
projections orthogonal to the longitudinal axis of the distal part of
Segment #3 of the RCA are often the AP (RAO)+CA and LAO+CR
projections. However, it is hard to distinguish #4PD from #4AV in the
AP (RAO)+ CA projection. (b) To view the distal bifurcation of the
RCA, I use the AP+CR and LAO+CR projections that allow the two
branches to be clearly distinguished, although there is partial overlap of
the two detector surfaces
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1 Mitsudo’s PCI Techniques forCTO
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Table 1.5 Fluoroscopy projections providing the longest view of the longitudinal axis of the target vessel in the ROI
RCA LCA
ROI Projection ROI Projection
Posteroanterior Lateral Posteroanterior Lateral
RCA ostium AP+CR LAO+CA LMT ostium AP+CR (LAO)+CA
RCA (#1-#2) RAO LAO LMT to the bifurcation RAO+CR LAO+CA
RCA (#2-#3) AP+CA(RAO+CA) LAO+CR LAD (#6-#7) AP(RAO)+CA LAO+CA
RCA (#3-#4) AP+CR LAO+CR LAD (#7-#8) AP+CR
RAO+CA
LAD (#11-#13) AP(RAO)+CA LAO+CA
Column 3 Fluoroscopy Angle and Detector Surface
LL+CR
AP+CR
In this textbook, I use the uoroscopy angle and the detector surface to explain the optimal imaging strategy. The
uoroscopy angle means the angle of the projection, which can be precisely expressed as RAO, LAO, CR, CA, (and
AP, LL), or combinations supplemented with the respective angles. The longest view of a vessel is obtained when it
is viewed in the direction orthogonal to its longitudinal axis, and there will be no shortening in this projection. By
combining this projection with a second projection obtained by rotating the detector 90 degrees around the vessel
axis, two orthogonal projections of the target vessel are obtained.
At that time (or moment), the detector surface is perpendicular to the uoroscopic axis and parallel with the longitudinal axis of the target vessel. It is very difcult to manually calculate a second angle that is at 90 degrees from the
rst angle and to express this as a uoroscopy angle relative the rst angle and the direction of the vessel axis. While
computerized calculation is easy, it requires data about the direction of the target vessel on the image to be input. As I
have described in detail in the text, it is not so difcult to rotate the other detector around the axis of the target vessel in
the ROI projected on the surface of the rst detector to obtain the second projection. Whether the second detector has
been positioned correctly at 90 degrees can be checked by observing if the surfaces of the two detectors are orthogonal
to each other. While this method cannot ensure complete orthogonality of the two detector surfaces, I think that achieving approximately orthogonal projections is sufcient.
1.5.1.4 Isocenter
During all PCI procedures, including those for CTO, you
should always perform “isocentric” coronary cineangiography, i.e., imaging with the patient’s heart positioned exactly
at the center of rotation of the arms of the imager (Fig.1.38).
All of the uoroscopy equipment introduced recently has
been designed to position the focus of the X-ray tube and the
center of the detector surface on a line that passes through
the center of rotation, so positioning the patient’s heart at the
center ensures isocentric imaging.
To position the patient’s heart at the center of rotation,
you should rotate the arms laterally and adjust the height
of the examination table so that the patient’s heart is at the
center of the detector surface while checking the image.
Once adjusted, the examination table height must not be
changed when the arms are rotated. This ensures that the
patient’s heart always remains at the center of the detector
surface. Basically, you do not need to obtain test images or
adjust the examination table height to optimize the position
of the patient’s heart even after changing the direction of
projection, so this method of isocentric imaging saves time
and also reduces radiation exposure for the patient.
Isocentric imaging is even more useful when performing biplane cineangiography of the coronary arteries. Many
biplane imagers are equipped with isocentric posteroanterior and lateral arms, while some allow adjustment of the
height of the lateral arm, a function that is apparently useful but removes isocentricity. However, once the lateral arm
has been adjusted, it can be troublesome to reposition the
patient’s heart at the center of both detectors after changing the uoroscopy angles. This procedure takes time and
increases radiation exposure for the patient, so it is better not
to cancel the isocentricity of the arms, even when using an
imager with such a feature.
1.5 Fluoroscopy andImaging Strategies
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Fig. 1.38 Setting the isocentric position. Once the height of the imag-
ing table has been adjusted to position the patient’s heart at the center of
rotation of both arms of the imager, there is no need to adjust the table
height further when the projection is changed
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1.5.2 Bilateral Angiography andCollateral
Flow Angiography (Contralateral
Imaging, etc.)
Some interventionalists still perform PCI for CTO without
contralateral imaging, but I think that contralateral imaging
is basically an essential part of PCI for CTO.When PCI is
done for native coronary artery CTO, contralateral imaging
is only unnecessary if angiography can visualize the true
lumen of the target coronary artery distal to the occlusion via
an ipsilateral collateral vessel (Fig.1.39).
When you have a manual sensation that the guidewire has
entered the true lumen of the vessel distal to the occlusion,
the tip of the guidewire can actually be located (1) in the
true lumen distal to the occlusion, (2) in a very soft subintimal space distal to the occlusion, (3) in a small side branch,
or (4) outside the vessel wall but within the pericardium. In
this situation, contralateral imaging is essential to visually
conrm the exact position of the tip of the guidewire and to
navigate the guidewire (if it has deviated) into the true lumen
with reference to an appropriate landmark.
If contralateral imaging for diagnosis of in-stent occlusion
visualizes the target coronary artery distal to the occlusion,
including part of the stented region (Fig.1.40), there is no
need to repeat contralateral imaging during PCI.However,
contralateral imaging will be required during PCI if the
occlusion extends to the distal end of the stent (Fig.1.41),
because the guidewire may slip into the subintimal space
after passing through the stent in this situation.
Fig. 1.39 Ipsilateral coronary collateral vessel. If there is a well-developed ipsilateral coronary collateral, contralateral imaging is not required
because imaging of the target coronary artery provides sufcient information about the segment distal to the occlusion
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1 Mitsudo’s PCI Techniques forCTO
Fig. 1.40 In-stent occlusion in the distal RCA.Contralateral diagnos-
tic imaging has delivered contrast medium to the target vessel distal to
the stent. In this situation, you can smoothly advance a guidewire
through the distal coronary artery segment from the end of the stent.
You can also perform tip injection near the distal end of the stent to
reconrm the anatomy of the distal segment
Column 4 Rotational Angiography
Fig. 1.41 In-stent occlusion in the RCA. Contralateral diagnostic
imaging has not delivered contrast medium to the target vessel distal to
the stent. After advancing a guidewire to the distal end of the stent, you
need to nd the distal cap of the lesion, and you will have to perform
contralateral imaging to do so
Recent reports have demonstrated the benet of rotational angiography for visualizing CTO lesions during
PCI.Rotational angiography was originally used as a method for imaging examinations such as three- dimensional
assessment of the cerebral vessels. This angiographic technique has subsequently attracted attention as a method for
multidirectional observation of the coronary arteries during PCI for CTO where only monoplane imaging equipment
is available. Although rotational angiography is useful in some respects, I do not employ it for the following reasons:
Rotational angiography is not compatible with biplane imagers. When performing PCI for CTO, I always use a
biplane imager, and I do not think that rotational angiography is ever superior to simultaneous bidirectional (posteroanterior and lateral) imaging.
As mentioned in the text, to determine the optimal projections for checking whether the tip of a guidewire has
entered the subintimal space or the true lumen (plaque), you only need to set one detector parallel with the longitudinal
axis of the target vessel and then rotate the other detector at least 90 degrees around the vessel axis. Images obtained
in these projections will clearly show whether the guidewire has deviated from the true lumen.
Nonetheless, imagers only permit rotation of the detectors around the body axis, rather than around the vessel
axis. Many segments of the coronary arteries are parallel with the body axis in the vertical heart, but run at a wide
angle or perpendicular to the body axis in the horizontal heart. Rotational angiography may be most useful when
the target vessel axis is parallel with the body axis, but is virtually useless when the vessel axis is perpendicular to
the body axis. At best, vascular movement with pulsation may provide some supporting information in the latter
situation. Rotational angiography is of intermediate benet in most other cases where the target vessel axis and
body axis are at an oblique angle to each other.
1.6 Antegrade Approach
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Based on the above, rotational angiography is useful for conrming whether a guidewire is in the true lumen of
a vessel that is parallel with the body axis. On the other hand, to correct the direction of a guidewire while using
rotational angiography for guidance, it is necessary to check images obtained in the projection showing the greatest
deviation and in a second projection perpendicular to the rst, which means that you must search for the correct
guidewire route in two nonsimultaneous projections that are not always parallel with the vessel axis. If you are not
using rotational angiography, you can manipulate the guidewire while checking images obtained in two orthogonal
projections that are parallel with the longitudinal axis of the target vessel, but it is impossible to manipulate a guidewire while obtaining images by rotational angiography. In contrast, biplane cineangiography provides simultaneous
imaging of the target vessel in two orthogonal projections parallel with the longitudinal axis of the vessel, allowing
the direction of the guidewire to be corrected in a real-time manner.
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1.6 Antegrade Approach
I have always thought of antegrade PCI as the basic
interventional method for CTO, even after introduction of the
retrograde approach. Although retrograde PCI has undoubtedly led to new breakthroughs by allowing the recanalization
of CTOs that are untreatable by antegrade PCI, there are still
many CTOs that can be managed via the antegrade approach
but not the retrograde approach. Therefore, interventionalists
should rst become familiar with antegrade PCI for CTO and
should aim to develop sophisticated strategies and technical
expertise in this setting.
1.6.1 Mechanism ofCTO Formation
andChanges After Occlusion
The mechanisms underlying coronary occlusion may be
multifactorial, and occlusions that are caused by various
mechanisms may evolve into CTOs over time. How successfully a particular guidewire can be used to cross a CTO will
vary with the mechanism involved in formation of the occlusion. In addition to the underlying mechanism, the time since
occurrence of occlusion and the properties of any preexisting
plaque at the site of occlusion can inuence success in crossing the CTO with a guidewire.
Here, I will discuss the possible mechanisms underlying
the formation of coronary artery occlusion and the changes
of the occlusion over time after it develops. I will also discuss changes of the surrounding plaque before occurrence
of occlusion, in order to provide useful hints about how a
guidewire can cross the CTO and how to select and manipulate the guidewire.
1.6.1.1 Occlusion Resulting fromTight Stenosis
(Fig.1.42)
In a patient without documented myocardial infarction, a
CTO is most likely to result from gradually progression of
tight stenosis (Fig.1.42b). The nal event that leads to complete occlusion may be thrombosis or plaque proliferation.
Functional CTO is characteristically accompanied by a
relatively long tight stenosis that has progressed gradually.
With progression of a long stenosis, the perfusion pressure
in the stenosed segment may decrease until it is equal to that
in collateral vessels, resulting in loss of both antegrade and
retrograde perfusion at the site of a lesion that has not yet
reached complete occlusion. In functional CTO, development of collaterals precedes the onset of occlusion, and the
patient often remains unaware of the occurrence of occlusion since there are no or only mild symptoms. Therefore,
it is often difcult to determine when occlusion actually
occurred in patients with a CTO of this type. After occlusion, the occluded site and surrounding tissues undergo several changes over time, including (1) expansion of thrombus,
(2) hardening of thrombus and plaque, (3) calcication of
thrombus and plaque, (4) intra-thrombus/intra-plaque recanalization/angiogenesis, and (5) development of collateral circulation/arteriogenesis, and so on.
1. If there are no side branches near the site of occlusion,
thrombus will extend to involve the nearest branch. If
there is only a small amount of plaque at the nearest
branch, the thrombus will become widespread and cause
abrupt thrombotic occlusion (Figs 1.42c and 1.43). If a
side branch (even a small one) is present near the proxi-
mal end of an occlusion resulting from tapered stenosis, a
tapered type of occlusion will form (Fig.1.44).
2. The thrombus occluding the vessel hardens over time, but
remains softer than the surrounding plaque for a while.
The difference in hardness between thrombus and plaque
is particularly marked when the plaque is partially calci-
ed. However, thrombus that extends to cover a nearly
normal vessel wall may not necessarily be softer than the
wall itself.
3. After more time has elapsed, the occluding thrombus
may become brotic, organized, and sclerotic and can
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Tight stenosis
a
b
c
a
b
c
a
b
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undergo calcication. A calcied thrombus may be as
hard as or even harder than the surrounding plaque. In
particular, thrombus at the proximal end (entry) of an
occlusion is likely to undergo brosis and sclerosis due
to rheological stress.
4. The occluding thrombus may undergo local thrombolysis, leading to recanalization by a narrow channel
through the thrombus or formation of a new capillary
channel. If such recanalization or angiogenesis is visible on CAG and there is TIMI grade 1 ow, the lesion
does not meet the denition of CTO.However, if competition with a gradually developing collateral results in
loss of antegrade perfusion, such a new channel may be
invisible on CAG, and TIMI grade 0 ow will be seen
(functional CTO; Fig.1.45). Functional CTO can also
be due to a tight stenosis with no history of occlusion.
Coronary artery occlusion that persists for at least
3months basically meets the denition of CTO, but a
small channel may still be visible on bilateral angiography. Without performing bilateral angiography, it is
often difcult to determine whether there is a channel
within a lesion. I routinely perform bilateral angiography if contralateral imaging shows any collateral, and I
do not regard coronary occlusion accompanied by a visible channel as a CTO.
However, a very small channel may not be detected,
even if bilateral CAG is performed.
5. A CTO resulting from tight stenosis often has many collaterals and a clearly visible exit.
1 Mitsudo’s PCI Techniques forCTO
Fig. 1.43 Abrupt occlusion. Abrupt occlusion may occur if the occlud-
ing thrombus extends to the sites of branches (a or b) or if thrombus
forms in an abruptly narrowed vessel (c)
(Functional total occlusion)
Thrombotic occlusion
Fig. 1.42 Potential mechanisms of coronary artery occlusion (1).
Thrombus formation in a functional CTO resulting from tight stenosis:
In a vessel segment with a tight stenosis (a), thrombotic occlusion may
occur (b). If the stenotic lesion is far from the nearest side branch, there
will be no perfusion at the distal end of the occlusion, and the thrombus
may extend as far as the rst branch (c)
Expansion of thrombus
Fig. 1.44 Tapered occlusion. If a vessel is narrowed by tapered plaque
and if there is blood ow (swirling) into the proximal blind end even
after complete occlusion, thrombus will not form at the proximal end,
and the occlusion will retain a tapered shape (a). If the plaque is originally tapered and the affected vessel becomes occluded just distal to a
side branch, the occlusion will also be tapered (b)
Small plaque
a
b
c
a
b
c
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4. A recanalized channel due to thrombolysis is likely to
appear early after thrombotic occlusion and is expected to
have a relatively large diameter. In the later phase, angiogenesis may occur within the organized thrombus.
5. In many cases, collaterals are not fully developed immediately after acute thrombotic occlusion. While collaterals develop progressively over time, they are often not
large enough to create a rim at the distal cap of the occlusion or to deliver blood to the distal lumen of the occluded
vessel.
Fig. 1.45 Functional CTO (a, b, c).A vessel with a very tight stenosis (not
complete occlusion) may appear to be occluded on diagnostic CAG.This
occurs because development of collaterals reduces the pressure gradient
across the stenotic region, leading to very poor blood ow between the
proximal and distal ends of the tight stenosis. Functional CTO also includes
occlusion with recanalization or with a microchannel that is not well developed enough to be detected by CAG.I consider that any occlusion with a
channel recognizable on bilateral angiography should not be regarded as a
CTO.Since many interventionalists do not perform bilateral angiography
during PCI, the actual prevalence of functional CTO is unknown
Plaque rupture &
thrombotic occlusion
Expansion of thrombus
1.6.1.2 Acute Thrombotic Occlusion (Fig.1.46)
In patients with ST-elevation myocardial infarction, thrombotic occlusion occurs due to rupture of a plaque that has
only caused mild stenosis (Fig.1.46). In a patient with previous acute myocardial infarction or Q-wave infarction, a CTO
is likely to have been caused by development of occlusion at
such a site over time.
Fig. 1.46 Potential mechanisms of coronary artery occlusion (2).
Another mechanism of coronary artery occlusion, which is associated
with myocardial infarction, is rupture of a relatively small plaque (a)
that results in thrombotic occlusion (b). When occlusion is due to this
mechanism, the occluding thrombus often expands until it reaches the
nearest side branch (c)
1. Like CTOs with other etiologies, the occluding thrombus
expands until it reaches a branch vessel, i.e., the point
where there is some blood ow (Fig.1.46c), but thrombus
is the predominant feature of the lesion, distinguishing
this type of CTO from the others. For several months after
the occurrence of occlusion, this type of CTO has a relatively soft central core for the full length of the lesion, and
the wall of the occluded vessel is generally also soft.
2. The thrombus becomes more brotic and sclerotic over
time, with the lesion largely being composed of relatively
homogeneous tissue (Fig. 1.47). If the vessel wall also
hardens, the thrombus in the lumen remains comparatively soft (refer to Column 5– Fig.1.56. If the luminal
thrombus hardens preferentially, it becomes harder than
the vessel wall (refer to Column 5—Fig. 1.57.
3. Calcication of the thrombus/plaque may also occur,
leading to a relatively homogenous lesion.
Fig. 1.47 Histological changes over time. Unlike an occlusion com-
posed of heterogeneous tissue with a relatively small intraluminal channel (Fig.1.42), a lesion created by acute thrombotic occlusion remains
relatively homogeneous
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1 Mitsudo’s PCI Techniques forCTO
1.6.1.3 Occlusions withComplex Etiologies
Theoretically, a tight stenosis and ruptured plaque can coexist in a vessel. Therefore, thrombotic occlusion due to ruptured plaque and occlusion of the stenotic lesion may occur
either synchronously or metachronously.
1.6.2 Histological Features Before andAfter
Occlusion
The condition of the coronary artery walls may differ before
occlusion, and this can have various inuences on guidewire crossing. Important factors that need to be considered
include (1) the (extent of) tortuosity, the plaque burden, the
hardness of the vessel wall and plaque, and the plaque characteristics (e.g., lipid content and severity of calcication)
at the entry to the CTO and (2) the vessel tortuosity, plaque
burden, plaque hardness, lipid core, and extent and distribution of calcication in the lesion itself.
The following changes may occur after occlusion: (1)
thrombolytic or angiogenic recanalization; (2) brosis, sclerosis, and calcication at the entry of the occlusion; (3) brosis, sclerosis, and calcication of the lesion; and (4) brosis,
sclerosis, and calcication at the exit of the occlusion.
Among these changes, calcication can have a major
inuence on the outcome of PCI, depending on its distribution. The extent of vascular calcication varies considerably
among individuals and between anatomical regions, but it
is well-known that dialysis patients often have very severe
vascular calcication.
1.6.3 Guidewire Crossing Based
onthePresumed Mechanism ofCTO
Formation andChanges After Occlusion
The outcome of PCI for CTO can be dramatically improved
by prior knowledge of the properties of the culprit plaque,
the mechanisms involved in CTO formation, and the postocclusion changes of the lesion. However, we can only consider the possibilities before starting PCI and make the best
conjecture from the nal or interim outcome of the procedure. Information on how a guidewire was advanced through
a vessel, whether there was an inection point or whether it
was blocked during intervention, is useful for estimating the
route and the position of the tip within the occlusion. The
interventionalist should modify his/her strategy while adjusting assumptions about the etiology based on these points.
My basic guidewire crossing strategies for use in ante-
grade PCI for various types of CTO are summarized below
(the details are given later).
1. If there is a channel within the occlusion, you should slide
a guidewire along the channel or advance a guidewire while
exploring the channel (exploration strategy; Fig.1.48).
A channel may exist within an occlusion, even if it
cannot be visualized by bilateral angiography or tip
injection. Since standard coronary artery imaging has a
resolution of 100 μm, a channel with a diameter less
than 100μm may not be visible on CAG.
2. If there is no channel within the occlusion, a guidewire
must be used to penetrate it. In this case, you should
advance the guidewire while exploring for a relatively
soft point where the occlusion may be most recent
(exploration with penetration strategy [Fig. 1.49]).
3. As in ST-elevation myocardial infarction, formation of a
large thrombus after rupture of a small plaque may often
be the initial event that leads to CTO.The thrombus often
extends as far as the nearest relatively large side branch to
form a large lesion that undergoes organization and brosis over time (Fig.1.47). In this setting, the intrinsic hardness of the vessel wall as well as the extent of organization/
brosis of the thrombus can determine the difculty of
crossing the CTO through the true lumen with a guidewire. For example, in a younger patient with old myocardial infarction, the vessel walls are relatively soft, but the
occluding thrombus, if organized, will tend to block the
guidewire inside the lesion and cause it to deviate into the
subintimal space. In an older patient with arteriosclerosis
and old myocardial infarction, the occluding thrombus,
even if organized, may still be softer than the vessel wall
(intimal sclerosis), potentially facilitating advancement of
the guidewire through the true lumen.
Thus, there may be no relatively soft region of a CTO
created by acute thrombotic occlusion when the thrombus has undergone homogenous sclerosis. In such a situation, you will not nd any softer region in the lesion
compared with the surrounding vascular tissues. If the
guidewire tip enters the lesion at the center of the lumen,
it will advance through the true lumen, but it is sometimes difcult to make a clear distinction between the
intraluminal and extraluminal tissues, and the absence
of a dimple at the center of the lumen may make it difcult to nd the true lumen. In a long CTO, initial success with directing the guidewire into the true lumen
does not ensure that it will remain inside the lumen as it
is advanced. To keep the wire in the true lumen, it must
be advanced while exploring the route and checking the
position of the tip with reference to various landmarks to
verify that it has followed the presumed route of the
lumen through the lesion. If this is not done, you cannot
prevent deviation of the guidewire into the subintimal
space. In this situation, extensive exploration may actually increase the risk of the guidewire deviating outside
the true lumen. Since greater importance is placed upon
penetration than exploration, this is termed the penetration with exploration strategy (Fig.
4. If a guidewire has been blocked by hard tissue within the
lumen and has slipped into the subintimal space, you
should exchange it for another wire with a higher tip
1.50).
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