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FIGURE 13.2 Coronary angiogram and optical coherence tomography (OCT) in 57-year-old female with ST-elevation myocardial infarction.
(A and B) Angiography revealed patent left anterior descending artery and mild ostial stenosis with haziness, in the absence of definite images of
intracoronary thrombus. (CeF) OCT (C7 Dragonfly, LightLab Imaging, Inc., Westford, MA, USA) depicted the presence of a ruptured plaque with a large
lipidic core and intraluminal protruding material, compatible with red thrombus. This example highlights the ability of OCT to identify intracoronary
thrombus over angiography and to characterize the different features of coronary plaque in acute coronary syndromes.
FIGURE 13.3 The role of optical coherence tomography (OCT) in the assessment of large thrombus burden lesions. (A) Angiography revealed
stent thrombosis of a previously implanted Cypher 3 28 mm (white arrows) on obtuse marginal before (top) and after manual thrombus aspiration
(bottom). (B) A closer look by OCT confirmed a very large thrombus burden involving the stent lumen and large areas of stent malapposition (top). The
final OCT (bottom) showed a complete apposition and expansion of self-expanding stent, with low appreciable residual thrombus.
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and the total number of high-intensity signals showed a poor correlation with myocardial damage [28]. In this regard,
Limbruno et al. [29], in a pathologic analysis of embolized debris, demonstrated that the dimensions of debris appear to be
of paramount relevance in predicting arteriolar occlusion: the larger the thrombus burden at culprit lesion, the larger the
dimensions of debris collected in the filters. Tak en together, these observations suggest that thrombus and plaque
embolization occur during revascularization of STEMI, and AVDE is only the tip of the iceberg of a phenomenon that
actually exists in almost all patients, though not angiographically detectable. Nonetheless, the burden of this phenomenon,
and perhaps its clinical hazard, strongly depends on the amount of thrombus: the larger the thrombus amount, the greater
the probability of large embolization, and the highest the probability of occluded arteriol es. According to these observations, patients presenting with LTB tended to have larger necrosis even when DE was not angiographically detected,
confirming that LTB exerts its detrimental impact on myocardial damage by both macro- and microembolization [30].
To better evaluate the impact of thrombus burden on myocardial and microvascular damage and how the latter may
reflect worse clinical outcomes, a clear definition of LTB becomes a crucial step. According to our previous experience,
LTB is defined according to the presence of one or more of the following (Fig. 13.4): (1) presence of cutoff pattern of IRA
occlusion, (2) RVD of occluded IRA of 3.5 mm, and (3) TTS 3 in the case of a patent IRA [15,31]. In particular, in
occluded IRAs (TIMI 0), LTB lesions are defined according to the presence of a cutoff pattern of the occlusion and/or
RVD 3.5 mm, whereas the tapered pattern of occlusion as well as RVD < 3.5 mm defined no LTB. In patent IRAs
(TIMI 1, 2, or 3), LTB lesions are defined according to TTS 3.
LTB, DE, and myocardial damage are highly interconnected phenomena, even if some special considerations should be
performed. DE occurs more often in the presence of specific angiographic features, identifying a subset of lesions at higher
risk of embolization. As mentioned earlier, it is important to emphasize that TTS represents a major determinant of DE, but
also other angiographic features are related to hazard of embolization, including the pattern of IRA occlusion, large IRA
diameter, and lesion length. In fact, TTS represents a practical and useful angiographic tool in thrombus grading, but its
value is limited in the presence of thrombotic occlusions, where it assumes the highest degree and gives no information
about the amount of either atheroma or superimposed thrombus. Interestingly, we have previously demonstrated that,
excluding patients with patent IRA, TTS did not remain an independent predictor of DE, sugges ting that in the presence of
a thrombotic occlusion the value of TTS in predicting DE is weak and that other angiographic tools could predict DE [15].
In this scenario, since the rate of occluded IRA in STEMI has been reported in up to 75% of cases [32], the recognition of
these angiographic features may play a crucial role in understanding the thrombus amount in the setting of coronary
occlusion [21]. Moreover, it is important to remark that plaque components other than thrombus may compose the
FIGURE 13.4 Angiographic and morphologic features of large thrombus burden lesions (LTBLs). LTBLs are defined according to the presence of
one or more of the following: (1) presence of cutoff pattern of IRA occlusion, (2) RVD of occluded IRA of 3.5 mm, and (3) TTS 3 in the case of a
patent IRA. In particular, in occluded IRAs (TIMI 0), LTBLs are defined according to the presence of a cutoff pattern of the occlusion and/or
RVD 3.5 mm, whereas the tapered pattern of occlusion as well as RVD < 3.5 mm defined no LTBL. In open IRAs (TIMI 1, 2, or 3), LTBLs are defined
according to TTS 3. IRA, infarct-related artery; RVD, reference vessel diameter; TIMI, thrombolysis in myocardial infarction; TTS, TIMI thrombus
score. Reproduced by permission of Elsevier in Napodano M, et al. Thrombus burden and myocardial damage during primary percutaneous coronary
intervention. Am J Cardiol May 1, 2014;113(9):1449e56.
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FIGURE 13.5 Angiographic determinants of distal embolization risk score (DERS) and risk classes stratification. (A) DERS is composed by four
readily available angiographic features: baseline angiographic cutoff pattern of IRA occlusion, TTS 2e4, RVD of occluded IRA 3.5 mm, and lesion
length 20 mm. (B) Assigning 0 to þ2 points to each determinant, three different risk classes can be distinguished: a low- (score 0e1), intermediate(score 2e4), and high-risk class (score 5e7), with a significant incremental rate of DE. IRA, infarct-related artery; RVD, reference vessel diameter; TIMI,
thrombolysis in myocardial infarction; TTS, TIMI thrombus score.
embolization debris [33], thus explaining the independent role of large IRA diameter and lesion length in predicting DE
[34] and suggesting a complex interplay between vessel, plaque burden, and DE.
However, because proper assessment of the relative thrombus burden in the context of STEMI lesions is not
straightforward, a new integer-based risk score has been developed to predict the risk of DE [35]. The distal embolization
risk score (DERS) is composed by four readily available angiographic variables: baseline angiographic cutoff pattern of
IRA occlusion, TTS 2e4, RVD of occluded IRA 3.5 mm, and lesion length 20 mm (Fig. 13.5A). Assigning 0 to þ2
points to each determinant, three different risk classes can be distinguished: a low- (score 0e1), intermediate- (score 2e4),
and high-risk-class (score 5e7), with a significant incremental rate of DE (Fig. 13.5B). In a large STEMI cohort [35], when
stratifying patients in integer groups according to the presence of distinct angiographic variables, a statistically significant
incremental risk of DE was observed: DE rate ranged from 3.9% in integer group 0 to 55.6% in group 7. The distribution of
risk score categories and corresponding probability of DE are shown in Fig. 13.6.
Interestingly, most patients (62%) are in the intermediate-risk category, carrying a DE risk of approximately 12%e15%.
These data appear to be in accordance with the DE rate historically reported in the literature [26,27],reflecting the reli-
ability of this risk stratification. Hazard of DE is as low as 6%e7% in the low-risk category; in contrast, patients in the
high-risk category carry a more than twofold and fourfold increase in risk of DE with respect to intermediate-risk and
low-risk groups. As regards clinical implications, the DERS seems not only able to discriminate the hazard of DE during
PPCI, but also capable of stratifying clinical outcomes throughout the hospitalization: higher risk score is associ ated with
worse clinical outcome.
IMPACT OF DISTAL EMBOLIZATION ON MYOCARDIAL DAMAGE AND CLINICAL
OUTCOMES
The negative results of large trials testing mechanical adjunctive devices during PPCI have raised concerns not only about
the effectiveness of such devices, but also, and more interestingly, about the impact of DE on myocardial reperfusion and
infarct size [36e39]. Although experimental and clinical studies have shown that DE may affect myocardial reperfusion,
enhancing myocardial necrosis [26,27], the impact of this phenomenon may be difficult to address in a clinical setting,
because myocardial reperfusion represents a complex process and the impairment of microcirculation is multifactorial in
etiology [40]. Moreover, the effectiveness of myocardial reperfusion seems largely time dependent, with myocardial
necrosis enhancing as time to treatment increases [41,42]. In this scenario, the impact of DE may be fairly different
according to time to treatment, having only limited or no relevance on reperfusion and infarct size in the latecomers, among
whom many patients have already developed transmural infarction at the time of IRA reopening [42]. Accordingly, while
the occurrence of DE seems to be not time dependent, its impact on both epicardial flow and microvascular reperfusion is
time dependent, with DE impairing myocardial reperfusion in the first 6 h after symptom onset, but having no additional
effect on microvascular damage beyond this time. Furthermor e, among patients treated within 3 h, those having DE had not
only worse myocardial reperfusion, but also larger necrosis and higher in-hospital mortality, surprisingly higher than
expected in this group [43]. This reflects the detrimental effect of DE on jeopardized myocardium when occurring early
and, at the same time, the absence of additional effect on myocardial damage when occurring late in the reperfusion
process. Examples of contrast-enhanced cardiac magnetic resonance (CE-CMR) findings in terms of myocardial and
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FIGURE 13.6 Distribution of integer risk score and corresponding probability of DE. (A) Distribution of the integer risk score. (B) Incidence of DE
by integer risk score: the C-statistic for the risk score model was 0.67 (P < .0001). (C) Distribution of low-, intermediate-, and high-risk categories. (D)
Incidence of DE by risk category: the C-statistic for the risk score model was 0.70 (P < .0001). DE, distal embolization. Reproduced by permission of
Elsevier in Napodano M, et al. Development and validation of a distal embolization risk score during primary angioplasty in ST-elevation myocardial
infarction. Am J Cardiol October 15, 2015;116(8):1172e8.
microvascular damage in patients with and without DE according to time to treatment are represented in Figs. 13.7
and 13.8. These findings could partially explain some of the disappointing results of mechanical adjunctive device use on
infarct size, coming from large randomized trials in which patients were enrolled even beyond the first 3 h from symptom
onset. Furthermore, it seems very important to speculate on the discrepancy we observed in our previous study [15] with
regard to the time window of the impact of DE on reperfusion and myocardial damage: while DE worsened myocardial
reperfusion in the first 6 h, the infarct size was affected by DE within 3 h. These observations are consistent with previous
experimental and clinical data, showing that both reperfusion and infarct size are time dependent, and that microvascular
damage lagged behind myocardial necrosis [41,42]. Moreover, these data emphasize that, even if the detrimental effect of
DE on myocardial necrosis is strictly confined to the first hours after symptom onset, left-ventricular function seems to be
affected beyond this time, showing a dissociation between myocardial necrosis and residual ventricular function and
highlighting that the extent of necrosis is not the only determinant of ventricular function after reperfused STEM I [44 e 46].
Other relevant factors affecting the impact of DE on myocardial reperfusion and damage in reperfused STEMI are
represented by thrombus burden and by the area of myocardium at risk. In fact, investigating the impact of LTB on
myocardial and microvascular damage in reperfused STEMI, using CE-CMR, we found that the presence of LTB may lead
not only to more embolization of macroscopic debris, but also to greater myocardial damage, regardless of detectable
embolization [30]. Thus, LTB seems to exert its detrimental effect on myocardium by both macro- and microembolization.
Moreover, LTB has been related to the absence of preinfarction angina in patients undergoing PPCI [47]. Interestingly, the
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FIGURE 13.7 Contrast-enhanced cardiac magnetic resonance (CE-CMR) findings in the “early comers” (<3 h) according to distal embolization.
When distal embolization occurred in patients treated early after symptoms onset (within 3 h), it was significantly related to transmural necrosis and
microvascular damage. (A) Patient with 120 min of pain-to-balloon delay, final TIMI flow grade 3, complicated by distal embolization in the left anterior
descending artery; the corresponding CE-CMR shows transmural necrosis with evidence of severe microvascular damage. (B) Pain-to-balloon time
135 min, final TIMI flow grade 3, without distal embolization; CE-CMR shows nontransmural necrosis without microvascular damage. TIMI, thrombolysis in myocardial infarction. Reproduced by permission of Elsevier in Napodano M, et al. Time-dependent detrimental effects of distal embolization on
myocardium and microvasculature during primary percutaneous coronary intervention. JACC Cardiovasc Interv November 2012;5(11):1170e7.
FIGURE 13.8 CE-CMR findings in the “latecomers” (>3 h) according to distal embolization. (A) Pain-to-balloon time was 240 min, final TIMI
flow grade 3, with distal embolization; the corresponding CE-CMR shows transmural necrosis with severe microvascular damage. (B) Pain-to-balloon
time was 300 min, final TIMI flow grade 3, without angiographic distal embolization; CE-CMR shows transmural necrosis with severe microvascular
damage. CE-CMR, contrast-enhanced cardiac magnetic resonance; TIMI, thrombolysis in myocardial infarction. Reproduced by permission of Elsevier in
Napodano M, et al. Time-dependent detrimental effects of distal embolization on myocardium and microvasculature during primary percutaneous
coronary intervention. JACC Cardiovasc Interv November 2012;5(11):1170e7.
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culprit plaques of patients without preinfarction angina contain a larger necrotic core and more often plaque rupture,
favoring the exposure of more thrombogenic substrates and larger thrombus formation [48,49]. This evidence suggests that
LTB may exert its effect on myocardial damage not only by thrombus or plaque embol ization, but also by lack of
myocardial preconditioning. The amount of myocardium at risk, in the co ntext of STEMI, represents another key factor
influencing the extent of final infarct size and thus prognosis. Previous experimental and clinical data have shown that both
reperfusion and infarct size are not only time dependent, but also related to myocardium at risk [41,42]: the larger the
jeopardized myocardium, the greater the extent of necrosis as ischemic time is prolonged. However, the occurrence of DE
during PPCI reduces or even nullifies myocardial salvage, resulting in transmural extent of necrosis and large microvascular damage. In this scenario, the impact of this complication may have limited influence on small jeopardized
myocardium, but also a remarkable impact on larger risk area, as anterior infarction. Indeed, larger myocardium at risk
generally subtends proximal coronary lesions, in which the amount of thrombus may be larger.
In conclusion, the impact of DE on myocardial damage involves multiple physiopathological factors, including LTB,
myocardial preconditioning, but also, and more interestingly, ischemic time, as well as the extent of jeopardized
myocardium. These observations provide the proof of concept in agreement with the evidence that every pharmacological
or mechanical therapy aimed to reduce the extent of myocardial damage in the setting of myocardial reperfusion should
take these factors into account.
ROLE OF MECHANICAL ADJUNCTIVE DEVICES IN THROMBUS REMOVAL AND
MYOCARDIAL DAMAGE
Mechanical thrombectomy and distal protection devices have been developed to reduce intracoronary thrombus burden and
to prevent DE and its consequences on microvascular damage. The rationale was strong and these devices were greeted
with enthusiasm by interventional cardiologists in the early phase, because of positive results coming from small registries
and single-center randomized trials [50e54]. However, these studies mostly evaluated surrogate end points of myocardial
reperfusion and were not powered to investigate clinical outcomes. Indeed, in the majority of them, independent
assessment of outcomes was lacking. After the initial enthusiasm derived from these studies, disappointing results have
been yielded in more recent larger scale trials [36,37,55e57],influencing a downgrade of routine thrombus aspiration in
current guidelines from reasonable (class IIa, level of evidence B) to no benefit of treatment (class III, level of evidence A)
[58]. In fact, two randomized controlled trials (TAST E and TOTAL trials), aiming to investigate the impact of thrombus
aspiration on clinical end points, enrolled to this purpose a very large number of subjects [36,37]: in both studies no
significant impact of thrombus aspiration on clinical end points was found. Particularly, in the TASTE trial [36], a total of
7244 patients were randomly assigned to manual thrombus aspiration followed by PCI or PCI alone. Deat h from any cause
was comparable between groups, while recurrent myocardial infarction and stent thrombosis showed a trend to lower
events in patients assigned to thrombus aspiration. In the TOTAL trial [37], including more than 10,000 patients, no
treatment effect of manual thrombus aspiration was found on cardiovascular death, recurrent myocardial infarction, heart
failure, or cardiogenic shock. It is important to emphasize that in both studies, the results were consistent across all major
prespecified subgroups, including those defined according to thrombus burden. Nonetheless, in these studies thrombus
burden was graded just according to TIMI thrombus grade, without additional scoring. Interestingly, as an ancillary finding
of the TOTAL trial, an increased rate of stroke within 30 days was associated with thrombus aspiration, ascribed as a
primary mechanism to embolization of thrombus and/or air to the brain during the procedure. However, the additional
finding of a continued increase in the rate of stroke between 30 and 180 days, observed in the same study, cannot be easily
explained, and it cannot completely rule out the play of chance as the explanation for these fi ndings with respect to stroke.
A recent meta-analysis [59], including more than 18,000 patients with STEMI randomized to routine thrombus aspiration
versus PPCI alone, revealed no reduction in cardiovascular mortality with any differences about incidence of cerebrovascular events. Some interesting data concern patients with LTB, defined as TTS 3. In this subgroup thrombus aspiration was associated with a significant reduction in cardiovascular death and all-cause mortality [59]. These results appear
biologically reasonable, since the risk benefit ratio of thrombus aspiration could be favorable in LTB lesions, characterized
by a higher hazard of DE and no reflow. However, the clinical benefit was partly offset by an increased rate of stroke. This
could be attributed to technical issues, both operator and device related. These include catheter-induced embolization of
thrombus debris into the systemic vasculature, aggressive guiding catheter manipulation required to advance the aspiration
catheter and displacing aortic atheroma, and air embolization into the systemic vasculature by bulky devices introduced in
guiding catheters [60]. Thus, the risk of systemic embolization could be reduced with improved technique. On the other
hand, one of the major limitations of current thrombus aspiration devices seems to be embolization of thrombus debris
downstream in the coronary circulation. This risk could be remarkable with large and organized thrombi. Moreover,
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another limitation of thrombus aspiration on STEMI outcomes is related to the effectiveness of current manual aspiration
devices. Interestingly, in a large real-world cohort of patients who underwent thrombus aspiration in STEMI, manual
devices did not cross the lesion in about 10% and were not able to aspirate in 27%: thus in about one-third of patients
manual thrombus aspiration could not be successfully performed [61]. More complex and bulkier devices, such as rheolytic
thrombectomy devices, might be more effective in extracting atherothrombotic debris from the coronary arteries [62], even
if no consistent clinical benefit has been shown with these devices over PCI alone [63,64]. However, the role of these
devices in LTB has not been adequately evaluated.
In addition to the proper evaluation of LTB lesions, ischemic time represents another relevant factor affecting thrombus
aspiration device effectiveness. Indeed, in the setting of PPCI, we have previously described how the detrimental impact of
DE on myocardial damage reduces according to ischemic time [31]. These observations are consistent with those reported
by Desch and coworkers [65], who demonstrated that in latecomer patients with STEMI, routine thrombus aspiration did
not improve myocardial damage, compared with conventional PCI alone. Every pharmacological or mechanical therapy
aimed at reducing the extent of myocardial damage in the setting of myocardial reperfusion may have no major effect in
these patients for two main reasons. First is the amount of myocardium at risk, which may be too small for thrombus
aspiration to affect myocardial and microvascular damage. Second, thrombus composition plays a prominent role. As
mentioned earlier, “fresh” thrombi are platelet rich, with low fibrin content, and relatively soft. As ische mic time increases,
platelet content decreases with concurrent rise of fibrin and erythrocytes, which leads to more organized and tighter
thrombi. As result, in latecomer STEMI, manipulation with the catheter might dislodge organized thrombotic material (less
suited to aspiration) with potential embolizat ion into the microcirculation, increasing the extent of myocardial necrosis.
These findings could partially explain the disappointing results of thrombus aspiration devices on infarct size, coming from
large randomized trials in which patients were enrolled even beyond the first hours from symptom onset [15]. To this
regard, it is important to highlight the results from the Intracoronary Abciximab Infusion and Aspiration Thrombectomy in
Patients Undergoing Percutaneous Coronary Intervention for Anterior ST-Segment Elevation Myocardial Infarction
(INFUSE-AMI) trial [66], in which patients with short ischemic delay (<4 h) and large jeopardized myocardium (anterior
infarction) had benefit in terms of infarct size from combining mechanical and pharmacological adjunctive therapy.
In conclusion, these observations, derived from the literature since the early 2000s, suggest that, using current devices,
routine thrombus aspiration during PPCI does not result in substantial clinical benefit and, in some situations, might be
potentially harmful. On the other hand, thrombus aspiration may be helpful only in highly selected patients and lesions,
including LTB in early comers with large area at risk. Finally, future improvement and development of novel devices able
to maximize the effectiveness of aspiration and mitigate stroke risk, as well as more appropriate selection of candidates,
will be likely to yield a more favorable riskebenefit ratio of thrombus aspiration in STEMI patients.
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