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SECTION 1 Pathophysiology and investigation ofcoronary artery disease58
)(
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(a) (b)
(c) (d)
(e
Fig.7.1.1 Normal anatomy of the left (a– d) and right (e, f) coronary arteries as depicted by coronary angiography. (a)Aright anterior oblique (RAO)
cranial view of the left coronary artery (LCA) illustrates the proximal (p), mid (m), and distal (d)segments of the left anterior descending artery (LAD)
after its takeoff from the left main coronary artery (LM). (b)An anteroposterior (AP) cranial view of the LCA shows septal (sept) and diagonal (diag)
branches of the LAD. (c)An RAO caudal view of the LCA highlights the left circumflex artery (LCx) and its obtuse marginal branch (OM), also showing
well the proximal LAD. (d)The LAO caudal view of the LCA is useful for demonstrating the bifurcation of the LM into the LAD and LCx. (e)The AP
cranial view of the dominant right coronary artery (RCA) illustrates the vessel’s terminal branching into the right posterior descending artery (RPDA) and
multiple right posterolateral arteries (RPL). (f)The LAO view of the RCA illustrates the vessel’s ‘C’- shaped course through the atrioventricular groove and
its division into proximal (p), mid (m), and distal (d)segments.
Complications ofdiagnostic
coronaryangiography
In the modern era, diagnostic coronary angiography can be accomplished with a high degree of safety. Analysis of 1.1million patients
without ST- elevation myocardial infarction undergoing diagnostic
coronary angiography in the United States from 2010 to 2011 revealed an overall adverse event rate of 1.35%. Key complications and
their incidence include bleeding (0.49% within 72 hours), vascular
complications requiring treatment (0.15%), stroke (0.17%, of which
9% were haemorrhagic), and new requirement for dialysis (0.14%).
Non- risk adjusted mortality was 0.72%.
f)
(a) (b)
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(c) (d)
7.1 Angiography 59
Fig.7.1.2 Coronary lesions as depicted by coronary angiography. Panel (a)illustrates an 80– 90% stenosis of the proximal left anterior descending
artery. Panel (b)illustrates a chronic total occlusion of the proximal right coronary artery, with distal filling via bridge collaterals. Panels (c)and
(d)illustrate a heavily calcified bifurcation lesion of the distal left main coronary artery before (c)and after (d)contrast medium injection.
Common proceduralconsiderations
Key considerations in performance of diagnostic coronary angiography include the following:
1. Choice of vascular access. In comparison with femoral access,
radial access reduces bleeding events and may improve patient
comfort and time to ambulation, but may be associated with
greater technical diculty, radiation exposure, and time, particularly for less experienced operators.
2. Avoidance of contrast- induced nephropathy. Risk factors for
contrast- induced nephropathy include hypotension, intraaortic balloon counterpulsation, congestive heart failure, age
greater than 75years, anaemia, diabetes mellitus, contrast media
volume, and baseline impairment in renal function. In addition
Limitations ofangiography
Although qualitative coronary angiography maintains its role
as the ‘gold standard’ for diagnosis of coronary artery disease,
it has several limitations. ese include signicant inter- and
intraobserver variability; unreliable prediction of functional signicance, particularly for intermediate and diuse lesions; reliance on optimal acquisition technique; spatial distortion, overlap,
and foreshortening due to compression of three- dimensional
anatomy into a two- dimensional image; reliance on comparison
to a ‘normal’ reference segment; and only indirect assessment of
vessel wall and plaque composition.
Appropriateuse
to careful patient selection, parsimony in cineangiography and
associated contrast usage is essential.
3. Minimization of radiation exposure. Both patients and oper-
ators are subject to the stochastic and deterministic risks of radiation exposure encountered during coronary angiography.
Techniques to keep exposure as low as reasonably achievable
have been published, and centre on deliberate use of uoroscopy and cineangiography, distance, shielding, angles, collimation, and dosimetry.
Formal intersociety eort has gone into development of appropriate use criteria for diagnostic cardiac catheterization, providing useful algorithms for triage to coronary angiography.
Broadly speaking, diagnostic coronary angiography tends to be
appropriate for patients with denite or suspected acute coronary
syndromes and symptomatic patients with a high pretest probability of coronary artery disease or intermediate- to high- risk
ndings on non- invasive testing.
SECTION 1 Pathophysiology and investigation ofcoronary artery disease60
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REFERENCES
1. Coronary angiography. Lancet. 1966;1(7446):1084– 5.
2. Bruschke AV, Sheldon WC, Shirey EK, Proudt WL. A half
century of selective coronary arteriography. J Am Coll Cardiol.
2009;54(23):2139– 44.
3. Moussa I, Ellis SG, Jones M, Kereiakes DJ, McMartin D,
Rutherford B, etal. Impact of coronary culprit lesion calcium
in patients undergoing paclitaxel- eluting stent implantation (a
TAXUS- IV sub study). Am J Cardiol. 2005;96(9):1242– 7.
4. Medina A, Suarez De Lezo J, Pan M. [A new classication of
coronary bifurcation lesions]. Rev Esp Cardiol. 2006;59(2):183.
5. Sianos G, Morel MA, Kappetein AP, Morice MC, Colombo
A, Dawkins K, etal. e SYNTAX Score:an angiographic
tool grading the complexity of coronary artery disease.
EuroIntervention. 2005;1(2):219– 27.
6. Dehmer GJ, Weaver D, Roe MT, Milford- Beland S, Fitzgerald S,
Hermann A, etal. A contemporary view of diagnostic cardiac
catheterization and percutaneous coronary intervention in the
United States:a report from the CathPCI Registry of the National
Cardiovascular Data Registry, 2010 through June 2011. J Am Coll
Cardiol. 2012;60(20):2017– 31.
7. Mehran R, Aymong ED, Nikolsky E, Lasic Z, Iakovou I, Fahy M, etal.
A simple risk score for prediction of contrast- induced nephropathy
aer percutaneous coronary intervention:development and initial
validation. J Am Coll Cardiol. 2004;44(7):1393– 9.
8. Chambers CE, Fetterly KA, Holzer R, Lin PJ, Blankenship JC, Balter
S, etal. Radiation safety program for the cardiac catheterization
laboratory. Catheter Cardiovasc Interv. 2011;77(4):546– 56.
9. Topol EJ, Nissen SE. Our preoccupation with coronary luminology.
e dissociation between clinical and angiographic ndings in
ischemic heart disease. Circulation. 1995;92(8):2333– 42.
10. Patel MR, Bailey SR, Bonow RO, Chambers CE, Chan PS,
Dehmer GJ, etal. ACCF/ SCAI/ AATS/ AHA/ ASE/ ASNC/ HFSA/
HRS/ SCCM/ SCCT/ SCMR/ STS 2012 appropriate use criteria
for diagnostic catheterization:a report of the American College
of Cardiology Foundation Appropriate Use Criteria Task Force,
Society for Cardiovascular Angiography and Interventions,
American Association for oracic Surgery, American Heart
Association, American Society of Echocardiography, American
Society of Nuclear Cardiology, Heart Failure Society of America,
Heart Rhythm Society, Society of Critical Care Medicine,
Society of Cardiovascular Computed Tomography, Society for
Cardiovascular Magnetic Resonance, and Society of oracic
Surgeons. J Am Coll Cardiol. 2012;59(22):1995– 2027.
depth relates inversely to it. Currently available catheters range between 20 and 45 MHz, providing an axial resolution of 100– 200
m and a penetration depth of up to 6mm. e cross- sectional
images are provided in grayscale format and key anatomical structures of the coronary artery or saphenous vein gra vessels wall
can be identied.
Trilaminar vesselstructure
In the normal coronary artery vessel, IVUS can reliably visualize the luminal border of the intima and the interface between
the media and adventitia, that is, the external elastic membrane
(EEM) (Fig. 7.2.1). e media– intima separation, which is demarcated by the internal elastic membrane, is oen not detectable by
IVUS since the elastic membrane and the inner part of the media
are very similar, thus blurring the interface. Also, it is not possible
to dierentiate between adventitial and periadventitial structures.
Luminalstenosis
To measure luminal stenosis accurately, a proximal and distal
reference segment with the least plaque burden should be identied as well as the localization of the minimum lumen area. e
lumen area stenosis is calculated as follows: reference segment
lumen cross- sectional area (CSA) (average between proximal and
distal reference lumen area) − minimum lumen CSA/ the reference
lumen CSA.
Plaque burden andremodelling
As the thickness of the media cannot be reliably measured, the convention is to measure the intima– media thickness from the lumen
border to the EEM. As for EEM CSA, the contour including the
EEM is used. e plaque- media area is calculated by subtracting
the lumen area from EEM CSA. e plaque burden is calculated by
dividing the plaque– media area by the EEM CSA. Oen, a lesion
is considered when a plaque burden is greater than 40% with a
length greater than 1.5mm. Remodelling is based on early pathological observations and includes either an increase or a decrease
in EEM during the process of atherosclerosis. When the EEM increases (i.e. as a response to an increasing plaque growth with the
lumen remaining patent), it is termed positive remodelling. When
the EEM area decreases, the term ‘negative’ remodelling is applied.
In the clinical scenario, serial IVUS acquisitions are frequently not
available and therefore, direct evidence of lesion remodelling is
lacking. e magnitude and direction of the remodelling of an individual lesion can be estimated by using the reference zone with
the least plaque burden by dividing the EEM area of the lesion by
the reference EEM area.
7.2 Intravascularultrasound
Lorenz Räber
Identification ofkey
anatomicalstructures
e resolution of intravascular ultrasound (IVUS) is directly related to the frequency of sound waves whereas the penetration
Plaquecomposition
IVUS characterizes the tissue according to its echogenicity. e
echogenicity in comparison with the adventitia is described as echodense/ hyperechoic (bright), or echolucent/ hypoechoic. e determination of plaque composition (mainly lipid vs other tissue) by
greyscale IVUS alone was previously shown to be unreliable due
to a low intra- and interobserver reproducibility. For this reason,
autoregressive spectral analysis of IVUS backscattered data has
been incorporated in conventional IVUS systems to facility image
(a) (b)
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(c) (d)
7.2 Intravascularultrasound 61
Fig.7.2.1 Saphenous vein graft 6months after implantation (a, b) compared to native coronary artery vessel (c, d) obtained with a 20 MHz
transducer. The vein graft cross- section reveals moderate thickening of the intimal layer early after implantation. Surrounding tissue is not present in
variance to the native coronary artery, where periadventitial tissue can be seen. Lumen line (red) and EEM (yellow).
interpretation as described elsewhere. IVUS is the most sensitive
and specic intravascular tool to assess calcium. Calcium appears
echo dense and causes acoustic shadowing, so that only the leading
edge of calcium can be measured. e degree of calcication can provide relevant information for the percutaneous coronary intervention (PCI) procedure. Fibrous plaques appear with an intermediate
or high echogenicity depending on the density of brous material.
High lipid content generally results in a low echogenicity and this
characteristic of the acoustic signal led to the term ‘so’ plaque as a
synonym for lipid- rich plaques. More recently, echo attenuation in
the absence of calcium was correlated with the presence of a lipid
or necrotic core. rombus is mostly localized intraluminally or
directly attached to the lumen and shows an irregular appearance.
No reliable criteria exist to dierentiate thrombus from other tissue
components by IVUS.
Differences betweensaphenous vein
grafts and native coronaryarteries
In contrast to native coronary arteries, vein gras have no side
branches and no periadventitial tissue. Vein gras undergo morphological changes that are comparable to native arteries: that
is, thickening of the intima with lipid deposition and medial
hypertrophy and measurements as described previously are similarly applicable. IVUS studies have shown that early intimal thickening occurs in angiographically normal saphenous vein gras
already in the rst year aer gra surgery, a process related to the
arterial pressure present (Fig. 7.2.1a,b). In one of the few serial
IVUS studies in saphenous vein gra patients, lumen loss could be
attributed not only to plaque growth but also negative remodelling,
a nding that underscores that saphenous vein gras undergo remodelling. Aparticular concern regarding PCI in saphenous vein
gra procedures is the no- reow phenomenon. IVUS- detected
intraluminal masses, multiple plaque ruptures, and degenerated
saphenous vein gras emerged as predictors of no reow in a sizeable cohort of 302 patients undergoing saphenous vein gra PCI.
An example of a highly degenerated saphenous vein gra lesion is
shown in Fig. 7.2.2.
Clinical applications ofintravascular
ultrasound incoronary arterylesions
Severity ofcoronary artery disease stenosis:functional
flow reserve versus IVUS- derived minimal lumenarea
Quantitative coronary analysis- derived percentage of diameter stenosis or minimal lumen diameter is inferior when compared with the
SECTION 1 Pathophysiology and investigation ofcoronary artery disease62
(a)
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d/e
b/c
(b) (c)
(d) (e)
Fig.7.2.2 Highly stenotic (a), degenerated saphenous vein graft 20years after implantation with a large eccentric plaque burden (b– e) at the site of
the minimal lumen area obtained by a 40 MhZ transducer. Asuperficial calcification with an acoustic shadowing can be seen in this mixed plaque. At a
less stenotic position of the lesion, the plaque burden is lower and arterialization of the vessel anatomy can be appreciated. Lumen contour (red) and
EEM (yellow).
Courtesy of Dr Kuramitsu and Dr Domei, Kokura Memorial Hospital, Japan.
gold standard functional ow reserve (FFR). Using IVUS to more
precisely assess the minimal lumen area could potentially increase
the diagnostic accuracy as compared to the gold standard FFR.
Several studies have indeed shown that diagnostic precision can be
improved when compared with quantitative coronary angiography,
yet improving sensitivity and specicity to greater than 80% appears impossible, so FFR testing should remain the gold standard
for intermediate coronary artery lesions. An exception to this is the
le main artery where both angiographic assessment and FFR assessment can be challenging.
IVUS- guided coronary artery diseasetreatment
e assessment of lesion length, diameter, and the degree of calcication provides helpful information for the planning of the
PCI procedure. Various parameters can be used to adequately select stent diameter by applying an aggressive approach (i.e. 80%
7.3 Fractional flowreserve 63
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of the EEM to EEM distance at the localization of the minimum
CSA) to a more conservative approach (i.e. average of proximal
7.3 Fractional flowreserve
and distal lumen diameter). Following PCI, IVUS can detect
ndings that are associated with an increased risk of restenosis
and stent thrombosis such as lesion underexpansion, stent strut
Giovanni Ciccarelli, Emanuele Barbato,
and Bernard De Bruyne
malapposition, dissections, and remaining disease burden at the
stent edge. Recently, the superiority of IVUS versus angiographyguided PCI was shown by the IVUS- XPL randomized trial in-
Definition
cluding 1400 patients treated with drug- eluting stents for long
coronary lesions. e use of IVUS resulted in a signicant reduction of major adverse cardiovascular events, a dierence that was
mainly driven by a reduction in the need for revascularizations of
the target lesion.
IVUS imaging forprediction ofclinicalevents
Plaque burden is the most relevant independent predictor for future cardiovascular events and can be assessed and calculated as described previously. In the PROSPECT natural history study, plaque
burden emerged as the most relevant independent correlate of major
adverse cardiovascular events related to non- culprit lesions in acute
coronary syndrome patients, resulting in a better discrimination as
Fractional ow reserve (FFR) is an index of the physiological signicance of a coronary stenosis, dened as the ratio of maximal
myocardial blood ow in the presence of the stenosis to the theoretically normal maximal myocardial blood ow (i.e. in the absence
of the stenosis)., is ow ratio can be calculated from the ratio of
distal coronary pressure (Pd) to central aortic pressure (Pa) during
maximal hyperaemia (Fig. 7.3.1). More practically, FFR indicates
to what extent the epicardial segment can be responsible for myocardial ischaemia and, accordingly, FFR quanties the expected
perfusion benet from revascularization by percutaneous coronary
intervention (PCI). Very limited evidence exists on the role on FFR
for coronary artery bypass gras (CABGs).
compared with minimal lumen diameter less than 4.0mm or the
nding of a thin- cap broatheroma.
REFERENCES
1. Mintz GS, Nissen SE, Anderson WD, Bailey SR, Erbel R, Fitzgerald
PJ, etal. American College of Cardiology clinical expert consensus
document on standards for acquisition, measurement and
reporting of IVUS. J Am Coll Cardiol. 2001;37(5):1478– 92.
2. Glagov S, Weisenberg E, Zarins CK, Stankunavicius R, Kolettis GJ.
Compensatory enlargement of human atherosclerotic coronary
arteries. N Engl J Med. 1987;316(22):1371– 5.
3. Pu J, Mintz GS, Biro S, Lee JB, Sum ST, Madden SP, etal. Insights
into echo- attenuated plaques, echolucent plaques, and plaques
with spotty calcication. J Am Coll Cardiol. 2014;63(21):
2220– 33.
4. Hozumi T, Yoshikawa J, Yoshida K, Akasaka T, Takagi T, Honda
Y, etal. Use of intravascular ultrasound for in vivo assessment
of changes in intimal thickness of angiographically normal
saphenous vein gras one year aer aortocoronary bypass surgery.
Heart. 1996;76(4):317– 20.
5. Hong YJ, Mintz GS, Kim SW, Lee SY, Kim SY, Okabe T, etal.
Disease progression in nonintervened saphenous vein gra
segments a serial intravascular ultrasound analysis. J Am Coll
Cardiol. 2009;53(15):1257– 64.
6. Hong YJ, Jeong MH, Ahn Y, Mintz GS, Kim SW, Lee SY, etal.
Intravascular ultrasound analysis of plaque characteristics and
postpercutaneous coronary intervention catheterization outcomes
according to the remodeling pattern in narrowed saphenous vein
gras. Am J Cardiol. 2012;110(9):1290– 5.
7. Hong SJ, Kim BK, Shin DH, Nam CM, Kim JS, Ko YG, etal.
Eect of intravascular ultrasound- guided vs angiography- guided
everolimus- eluting stent implantation. JAMA. 2015;314(20):
2155– 63.
8. Stone GW, Maehara A, Lansky AJ, de Bruyne B, Cristea E,
Mintz GS, etal. A prospective natural- history study of coronary
atherosclerosis. N Engl J Med. 2011;364(3):226– 35.
Practicalities
FFR is an invasive measurement obtained to complement coronary
angiography or as part of a PCI. Intracoronary nitrates must be
given before instrumenting the coronary arteries to alleviate epicardial vasomotor tone. Pa is typically obtained with a 5 or 6 F guide
catheter positioned in the ostium of the coronary artery. Pd is measured with a pressure monitoring guidewire. Aer equalization of the
two pressures at the tip of the guide catheter, the pressure sensor is
advanced in the distal part of the artery, at least 2cm distal to the
stenosis to be measured. Maximal microvascular vasodilation can
be obtained by intravenous infusion of adenosine (140 micrograms/
kg/ min) or by intracoronary bolus administration of adenosine (200
micrograms for the le coronary artery; 100 micrograms for the
right coronary artery). While it is important to record the baseline
pressure tracing, FFR can only be derived from the Pa and Pd at the
time of maximal hyperaemia, that is, when microvascular resistance
is minimal. Atypical example is shown in Fig. 7.3.2.
Fig. 7.3.2 presents a typical FFR recording. In this example FFR
equals 0.61 in the mid le anterior descending coronary artery
(LAD). is means that the maximal myocardial perfusion reaches
only 61% of what it should reach were the LAD normal.
Mainfeatures
• Normal value. In a healthy epicardial artery (sometimes called
conductance arteries), since the resistance to ow is absent, Pd
equals Pa. us, FFR equals 1 in each and every normal epicardial
segment. In contrast to most other metrics in medicine there is no
‘range’ of normal values.
• Ischaemic threshold. While the normal value of FFR equals 1, it
does not mean that all values below unity will be associated with
SECTION 1 Pathophysiology and investigation ofcoronary artery disease64
Fractional flow reserve is the ratio of maximal, hyperaemic myocardial flow in the presence of a lesion to the normal
maximal, hyperaemic myocardial flow in the absence of the lesion:
Maximal hyperaemia is achieved by vasodilation of the coronary vasculature; subsequently, vascular resistances ar
minimized and equal, and cancel out, while the venous pressure is negligible. The equation is finally expressed as:
FFR: fractional flow reserve,
:
hyperaemic flow in the presence of a lesion,
resistance of a territory perfused by a coronary artery with a stenosis,
perfused by a normal coronary artery.
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hyper
Q
FFR =
S
hyper
Q
N
e
P
d
P
a
hyper
hyper
hyper
R
: microvascular resistance of a territory
S
S
: microvascular
S
FFR =
Pd : coronary pressure distal to the lesion, Pv : venous pressure, Pa : aortic pressure, Q
hyper
Q
: hyperaemic flow in the absence of lesions, R
N
Fig.7.3.1 FFR, a ratio of two flows, can be derived from two pressures during maximal hyperaemia. The complete derivation of these equation can be
found in the article by Pijls etal.1 while the simplified derivation can be found in a recent review.
Source data from Xaplanteris P etal. Catheter- based functional metrics of the coronary circulation. Journal of Nuclear Cardiology, 2017;24(4):1178– 89.
stress- induced ischaemia. e ischaemic threshold for FFR is
around 0.80 with a narrow grey zone between 0.75 and 0.80. It
is very unlikely to observe myocardial ischaemia associated with
an FFR value greater than 0.80. When FFR is 0.80 or less, signs of
ischaemia can be present during maximal exercise or pharmacological stress. e latter is very likely when FFR is less than 0.75.
erefore, an FFR value of 0.80 is a widely accepted threshold
to guide clinical decision- making. is threshold has been established by a sequential multi- testing technique and its clinical
value has been largely conrmed., Embedded in this approach
is the fact that a non- invasive comparator was considered positive only if it was positive before revascularization and reversed to
3
Fig.7.3.2 Typical example of FFR measurement in a mid LAD in a 72- year- old woman. The baseline gradient is 14mmHg and increases to 33mmHg
during hyperaemia, corresponding to an FFR value of 0.61. Practically, this 0.61 value means that myocardial flow during maximal microvascular
dilatation is only 61% of what it should reach if the epicardial artery were normal. This calculation can only be obtained during maximal hyperaemia.
Also, it is interesting to notice that the increase in pressure gradient between rest and hyperaemia is relatively high, suggesting a preserved
microvascular function. This further illustrates the importance of recording both resting and hyperaemic coronary haemodynamics.
7.3 Fractional flowreserve 65
1.0
FFR
No revascularization
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negative aer revascularization. ese gures have been validated
by clinical outcome data.
• Myocardial mass. FFR specically relates the severity of the sten-
osis to the myocardial mass perfused by the coronary artery. For
an identical degree of epicardial stenosis, the larger the myocardial mass, the larger the hyperaemic ow and in turn, the larger
the gradient and the lower the FFR value.
• Microcirculation. In patients with coronary artery disease, micro-
circulatory function is presumably oen abnormal. Yet, in contrast to a general belief, the denition of FFR does not assume
that the microcirculation is normal, but it quanties the extent to
which the epicardial stenosis contributes to reduced myocardial
perfusion, regardless of the status of the microvascular function
in a given patient at a given point in time.
• Collaterals. Distal coronary pressure during maximal hyperaemia
reects both antegrade and retrograde ow according to their respective contribution. Accordingly, FFR incorporates the collateral contribution to myocardial perfusion.
• Haemodynamic. Within the ranges of blood pressure and heart
rate commonly encountered in the catheter laboratory, the value
of FFR is very little inuenced by natural variations in systemic
haemodynamics.
• Beyond invasive FFR. Calculation of FFR values as derived from
plain coronary computed tomography (FFRCT) have recently
been validated. is non- invasive approach allows for simultaneous assessment of both coronary anatomy and physiology.
Machine- learning algorithms keep improving the diagnostic
precision of FFRCT even in calcied arteries. In addition, in patients with stable chest pain, FFRCT has been shown to improve
patient selection for coronary angiography. is approach might
therefore introduce a true paradigm shi in the diagnostic workup of patients with suspected coronary artery disease.
• Recently, several resting pressure- derived indexes such as in-
stantaneous wave- free ratio, resting full- cycle ratio, and diastolic
pressure ratio have been introduced to assess the functional signicance of coronary stenosis and can be used to guide percutaneous treatment strategy in patients with coronary artery disease.
However, no data are available on the role of resting indexes in
guiding surgical revascularization.
No inducible
ischaemia
0.80
0.75
Inducible
ischemia
0.20
Ischaemia at rest
or necrosis
Fig.7.3.3 FFR cut- off values to guide revascularization strategy.
Revascularization
Multiple randomized clinical trials, corroborated the value of FFRbased decision- making. ey can be summarized as follows:
• When FFR is greater than 0.80 in stable lesions (i.e. stable pa-
tients or non- culprit stenosis of patients with unstable angina),
clinical outcome is not improved by PCIs as compared to medical
therapy. is has been conrmed in virtually all types of lesions
and patient subsets, including le main stenosis, proximal
LAD stenosis, small vessels, and bypass gras. In patients with
multivessel disease, FFR- based treatment forms the basis of func-
tionally complete revascularization as opposed to anatomically
complete revascularization.
• In patients with acute coronary syndromes, there are no data so
far supporting the safety and ecacy of FFR in the ‘culprit’ lesion.
From the presently available literature, FFR can be reasonably
advocated— even at the acute phase— in the non- culprit lesions
in patients with an acute coronary syndrome except in large STelevation myocardial infarctions (STEMIs) associated with elevated lling pressure and severely reduced ejection fraction.
Several large randomized controlled trials are underway to clarify
the role of FFR in patients with STEMIs and non- STEMIs.
• When FFR is less than 0.80 in stenoses located in proximal seg-
ments of large epicardial arteries, contemporary PCI is justied
as it has been shown to improve patient outcomes as compared to
medical therapy (Fig. 7.3.3)
Clinical outcomedata
In patients with stable chest pain, decision- making about treatment
strategy should be based on anatomical and functional information
on the coronary circulation. Nevertheless, a recent International
Survey on Interventional Strategy survey underscored that interventional cardiologists still prefer plain angiography, and its ‘50%
diameter stenosis’ criteria, for decision- making, even in the absence
of any budget and logistic constraints. Traditionally, the functional
data is obtained by non- invasive testing which aim at detecting
and localizing ‘myocardial ischaemia’. Yet, the diagnostic accuracy
of diagnostic testing is overrated in the literature so that in clinical
practice a sizable proportion of patients undergo coronary angiography and revascularization without prior useful functional information. erefore, obtaining ‘form and function’ at the same place
and at the same time by the same operator is an appealing concept.
In summary, solid clinical outcome data from randomized controlled trials have established the role of FFR for bidirectional reclassication of angiographically visible stenoses and might replace
non- invasive testing. Yet, the present data do not support the use of
FFR in the culprit stenosis of STEMI and non- STEMI or in the nonculprit lesion of very large STEMI with haemodynamic compromise.
Fractional flow reserve and coronary
artery bypassgrafting
ere are only scarce data available on the role of FFR- guidance of
surgical revascularization., FFR- guided CABG is now under intense investigation.
Recently, two small- sized randomized trials have compared
angiography- guided versus FFR- guided CABG, in multivessel disease patients with similar results. e GRAFFITI trial showed that
SECTION 1 Pathophysiology and investigation ofcoronary artery disease66
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functionally complete but anatomically incomplete CABG resulted
in a similar 12- month gra patency rate and clinical outcomes despite a markedly simplied surgical strategy. e FARGO trial randomized 100 patients to FFR- based or angiography- based CABG
and found that FFR- guided CABG had similar gra failure rates
and clinical outcomes as angiography- guided CABG. e trial was
stopped prematurely when less than 60% of the original sample size
was enrolled. Due to the high rate of lost to follow- up, FARGO is
very likely underpowered to detect even large dierences between
groups. Also, almost 65% of the gras in FARGO where venous (not
arterial) gras. In contrast, the IMPAG trial analysed 6- month functionality of 199 arterial gras in 68 patients with very high completeness of follow- up (94.1%) and no protocol deviation. In IMPAG,
FFR predicted 6- month gra function signicantly better than angiography, with a cut- o of 0.78.
FFR has proven its worth in decision- making for PCI, in multiple patient subgroups. In particular, recalculating the SYNTAX
score by only incorporating ischaemia- producing lesions (‘functional SYNTAX score’) as determined by FFR decreases the number
of higher- risk patients and better discriminates risk for adverse
events in patients with multivessel coronary artery disease undergoing PCI. Yet, larger studies are needed to understand how these
conclusions might apply to CABG and to dene the role of FFR in
guiding the treatment of patients with three- vessel coronary artery
disease. It is important to note that the expected consequences of
PCI of an FFR- insignicant lesion are very dierent from the consequences of bypass graing to a coronary artery with a non- owlimiting native stenosis. In the former, major adverse cardiac and
cerebrovascular event rates are increased, since the consequence of
failure of an ‘unnecessary’ stent is restenosis or occlusion, leading
to recurrent angina and/ or myocardial infarction. ere is no evidence of such a negative consequence for CABG in this scenario,
since the closure of an ‘unnecessary’ coronary gra is usually a clinically silent event.
Conflicts ofinterest
e Cardiovascular Center Aalst receives grant support from
Abbott, Boston Scientic, Biotronik, and St. Jude Medical and receives consulting fees on behalf of Dr De Bruyne and Dr Barbato
from St. Jude Medical, Opsens, and Boston Scientic outside of
the submitted work. Dr De Bruyne is a shareholder for Siemens,
GE, Bayer, Philips, HeartFlow, Edwards Life Sciences, Sano, and
Omega Pharma.
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calcic (low- backscattering, sharply delineated signal- poor regions), and lipid- rich plaques (signal- poor lipid pools covered with
brous cap) (Fig. 7.4.1b– d).
Haemodynamicsignificance
OCT has limited utility in assessment of haemodynamic signicance of coronary lesions. Minimal luminal area on OCT modestly
correlates with fractional ow reserve in non- le main coronary arteries, reecting additional factors beyond the degree of stenosis
that determine functional signicance. ere is a paucity of data correlating OCT- determined severity with fractional ow reserve and
clinical outcomes in the le main coronary artery.
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Optical coherence tomography incoronary
bypassgrafts
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Perioperative assessment ofbypassconduits
OCT can guide intraoperative selection of conduits for coronary artery bypass graing (CABG). Atherosclerotic lesions in radial arteries (RAs) and harvest- related injury (intimal trauma, thrombus)
can be visualized by OCT. Intimal tears and medial dissections in
RAs aer transradial coronary angiography are seen on OCT (Fig.
7.4.1e) and necessitate caution in using recently cannulated RAs for
CABG. e degree of spasm and vessel injury in RAs harvested
with dierent methods (open vs endoscopic, harmonic scalpel vs
7.4 Optical coherencetomography
Keyvan Karimi Galougahi, Tomasz Roleder,
Akiko Maehara, and Ziad A. Ali
Intravascular optical coherencetomography
Intravascular optical coherence tomography (OCT) is performed
by a breoptic probe deployed through a catheter that emits nearinfrared light and collects the reection. During acquisition, blood
is temporarily displaced by infusion of ush media, resulting in high
contrast between the lumen and vessel wall, allowing for accurate
and automated measurement of vessel dimensions, not possible by
other intravascular imaging modalities. is feature together with
automated OCT angiography co- registration facilitates rapid assessment of coronary lesions and can guide revascularization by
percutaneous coronary intervention (PCI). OCT has expanding
applications in the management of stable coronary artery disease
and acute coronary syndromes (ACS) in native coronaries and, potentially, in coronary bypass conduits.
electrocautery) can be assessed,, with signal attenuation in RAs
(reecting lipid content) independently predicting RA spasm post
CABG. Moreover, OCT is useful in assessing the distal anastomosis
quality intraoperatively (Fig. 7.4.1f). In theory, OCT may be used
prior to CABG to determine the suitability of distal coronary targets.
Postoperative assessment ofbypassgrafts
Saphenous veingraft
During the rst year post- CABG, saphenous vein gras (SVGs)
undergo lumen loss due to a combination of wall thickening and
negative remodelling. Aer 3years, thin- cap broatheroma (Fig.
7.4.1g) and adherent thrombus are evident. In older SVGs, athero-
sclerotic plaques become larger and aneurysmal dilations and calcication (Fig. 7.4.1h) may develop. Aer PCI on SVGs, in- stent
restenosis develops faster, causes higher stenosis compared to de
novo SVG lesions, and is evident earlier in drug- eluting versus baremetal stents (Fig. 7.4.1h).
Left internal thoracicartery
Ten years post CABG, le internal thoracic artery gras show
changes consistent with adaptive response to dierent ow dynamics
in the coronary circulation, manifesting with intimal thickening
and increased intima/ media ratio (Fig. 7.4.1i) and preservation of
Assessment ofnative coronary arterydisease
Morphologicalassessment
e trilaminar appearance on OCT represents the light scattering
from the layers of the normal coronary artery (Fig. 7.4.1a). In coronary artery disease, there is a loss of this normal architecture along
with common ndings of brous (high backscattering, signal rich),
endothelium- dependent vasodilation. A reduction in the thickness of the medial layer may reect the loss of vasa vasorum due to
manipulation during CABG and new ow conditions.
Radialartery
Progressive remodelling of the RA has been shown with intravascular
ultrasound but not yet with OCT (reduction in medial layer, increased
luminal diameter, preserved endothelium- dependent vasodilation).
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