Development and Validation of a Distal Embolization Risk

Score During Primary Angioplasty in ST-Elevation

Myocardial Infarction
Massimo Napodano, MDa,*, Ahmed H. Al Mamary, MDa, Filippo Zilio, MDa, Gilberto Dariol, MDa,
Anna C. Frigo, MD, PhDb, Giuseppe Tarantini, MD, PhDa, Anna Carrer, MDa,
Chiara Fraccaro, MD, PhDa, Gianpiero DAmico, MDa, and Sabino Iliceto, MDa
This study aims to develop and validate a new angiographic risk score to predict the risk of
distal embolization (DE) during primary percutaneous coronary intervention (p-PCI) for
ST-elevation myocardial infarction. Study included data from 1,200 patients who underwent
p-PCI. The cohort was randomly split into a derivation cohort (n [ 814) and a validation
cohort (n [ 386). Logistic regression was used to examine the relation between risk factors
and the occurrence of DE. To each covariate in the model was assigned an integer score
based on the regression coefcients. Variables included in the risk score, according to
multivariable analysis, were occlusion pattern of infarct-related artery, Thrombolysis In
Myocardial Infarction Thrombus Score 2 to 4, reference vessel diameter 3.5 mm, and lesion
length >20 mm. To each variable was assigned a 0- to D2-point score according to the
strength of the statistical association. Rates of DE in low-, intermediate-, and high-risk
groups were 5.6%, 15.8%, and 40% in the derivation cohort (p for trend <0.0001; C-statistic 0.70) and 7.5%, 12.1%, and 37.9% in the validation cohort (p for trend <0.0001; C-statistic
0.62), respectively. In conclusion, the individual risk of DE in patients who underwent p-PCI
can be predicted using a simple 4-variables model based on angiographic features. 2015
Elsevier Inc. All rights reserved. (Am J Cardiol 2015;116:1172e1178)

Experimental and clinical studies have shown that distal

embolization (DE) complicating primary percutaneous coronary intervention (p-PCI) may affect myocardial reperfusion, limiting myocardial salvage and worsening prognosis of
ST-elevation myocardial infarction (STEMI).1e3 Thus far,
several patient-related, lesion-related, and procedural factors
have been associated with the risk of DE during p-PCI.4e7 In
particular, p-PCI in the context of large thrombus burden
lesions is strongly associated with DE and poor myocardial
reperfusion.8,9 However, proper assessment of the relative
thrombus burden in the context of STEMI lesions is not
straightforward,10 and a systematic DE risk assessment has
not been realized at the individual patient level. A risk score
for DE during p-PCI in STEMI can be a helpful tool to
personalize risk assessment. In the present study, we aimed
to develop and validate a practical risk score for DE based on
a large data set of patients who underwent p-PCI for STEMI.
Methods
We conducted an observational analysis based on a large
registry of patients who underwent p-PCI at the
a
Cardiology Unit and bBiostatistics Unit, Department of Cardiac
Thoracic and Vascular Sciences, University of Padova, Italy. Manuscript
received April 24, 2015; revised manuscript received and accepted July 9,
2015.
See page 1178 for disclosure information.
*Corresponding
author:
Tel:
(39)
0498211844;
fax:
(39) 0498212309.
E-mail address: massimo.napodano@gmail.com (M. Napodano).

0002-9149/15/$ - see front matter 2015 Elsevier Inc. All rights reserved.
http://dx.doi.org/10.1016/j.amjcard.2015.07.027

Catheterization Laboratories of Padova University from 2006

to 2011. Data from 1,200 patients who underwent p-PCI
within 12 hours from symptom onset of STEMI at our institution were prospectively collected. Inclusion criteria for patient selection in the current analysis were continuous chest
pain for at least 20 minutes, presentation within 12 hours of
onset of pain, and ST-segment elevation
1 mm (0.1 mV) in

2 contiguous leads on the 12-lead electrocardiogram or
new-onset left bundle branch block. Exclusion criteria for the
present analysis were (1) manual or mechanical thrombus
aspiration or utilization of distal protection devices and
(2) contraindication to dual antiplatelet therapy. P-PCI was
performed with standard technique by radial approach or
femoral approach in patients unsuitable for radial catheterization. The infarct-related artery (IRA) was the only target of
the procedure, and deployment of coronary bare metal stents
or drug-eluting stents were left at operators discretion. All
patients received 250 mg acetylsalicylic acid (intravenous
bolus) before the procedure and thereafter 100 to 325 mg/day
orally; heparin (70 U/kg) was given to maintain the activated
clotting time >250 seconds during the procedure. Clopidogrel
was given as soon as possible after hospital admission at
loading dose of 600 mg orally and then at a daily dose of
75 mg. Abciximab was given as 0.25 mg/kg intravenous bolus
followed by intravenous infusion >12 hours according to
operators choice. At the time of study execution, prasugrel
and ticagrelor, and also bivalirudin, were not available in our
facility. All patients expressed written informed consent to the
procedure.
Two experienced interventional cardiologists assessed all
angiographic and procedural parameters. Both reviewers
www.ajconline.org

Coronary Artery Disease/Distal Embolization Risk Score in Primary PCI

1173

Table 1
Clinical, procedural and angiographic characteristics of derivation cohort
Variable
Age (years)
Men
Diabetes mellitus
Hypertension
Dyslipidemia
Smoker
Anterior MI
Previous angina
Previous HF
Previous MI
Previous PCI
Pain-to-balloon time (minutes)
Multivessel Coronary Disease
Infarct related artery
Left Main
Left Anterior Descending
Left Circumex
Right
SVG
TTS 2-4
Occlusion pattern
Cut-off pattern
Tapered pattern
Persistent-dye pattern
TIMI ow pre 2/3
No-ow improvement
Collateral circulation
QCA before PCI
% DS
RVD
MLD
Lesion Length
Stent deployment
Total Stent Length
Stent/ Vessel
Abciximab
Post-PCI Angiographic Data
Final TIMI ow 3
Final MBG 2/3
Angiographic No-reow
QCA after PCI
% DS
RVD
MLD

All
(N 814)
64
642
151
452
358
438
436
226
10
92
79
200
421

(54-74)
(78.9%)
(18.6%)
(55.5%)
(44.0%)
(53.8%)
(53.6%)
(27.8%)
(1.2%)
(11.3%)
(9.7%)
(140-300)
(52.0%)

No DE
(N 697)
64
557
129
385
310
380
383
192
7
80
65
195
359

(54-74)
(79.9%)
(18.5%)
(55.2%)
(44.5%)
(54.5%)
(54.9%)
(27.5%)
(1.0%)
(11.5%)
(9.3%)
(140-300)
(51.7%)

DE
(N 117)

67 (57-75)
85 (72.6%)
22 (18.8%)
67 (57.2%)
48 (41.0%)
58 (49.6%)
53 (45.3%)
34 (29.1%)
3 (2.5%)
12 (10.2%)
14 (12.0%)
212.5 (135-330)
62(53.9%)

0.05
0.07
0.91
0.62
0.52
0.36
0.05
0.69
0.16
0.72
0.36
0.60
0.66

8(1.0%)
415 (51.0%)
92(11.3%)
284 (34.9%)
15 (1.8%)
306 (37.6%)

7 (1.0%)
360 (51.6%)
79(11.3%)
236 (33.9%)
15 (2.1%)
244 (35.0%)

1
55
13
48
0
62

(0.8%)
(47.0%)
(11.1%)
(41.0%)
(0.0%)
(53.0%)

365
123
47
245
183
171

293
111
39
226
140
149

72
12
8
19
43
22

(61.5%)
(10.3%)
(6.8%)
(16.2%)
(36.7%)
(18.8%)

(44.8%)
(15.1%)
(5.8%)
(30.1%)
(22.5%)
(21.0%)

100
2.9
0.0
16.6

(96-100)
(2.5-3.3)
(0.0-0.3)
(13.0-21.7)
98.0%
18.0 (15.0-28.0)
1.0 (0.9-1.1)
276 (33.9%)

100
2.9
0.0
16.4

735 (90.3%)
469 (57.6%)
53 (6.5%)
10.0 (5.0-14.0)
3.2 (2.8-3.5)
2.9 (2.5-3.2)

(42.0%)
(15.9%)
(5.6%)
(32.4%)
(20.1%)
(21.4%)

(95-100)
(2.5-3.2)
(0.0-0.4)
(12.9 -21.6)
98.0%
18.0 (15.0-28.0)
1.0 (0.9-1.1)
212 (30.4%)

0.35

<0.001
<0.001
<0.001
<.0001
0.55

100 (100-100)
3.1 (2.7-3.6)
0.0 (0.0-0.0)
18.1 (13.2-22.1)
98.3%
18.5 (16.0-26.0)
1.0 (1.0-1.1)
64 (54.7%)

0.091
<.0001
0.06
0.52
1.00
0.52
0.57
<.0001

646 (92.7%)
430 (61.7%)
32 (4.6%)

89 (76.1%)
39 (33.3%)
21 (17.9%)

<.0001
<.0001
<.0001

10.0 (5.0-14.0)
3.1 (2.8-3.5)
2.9 (2.5-3.2)

10.0 (5.0-15.0)
3.3 (3.0-3.6)
3.0 (2.7-3.4)

0.16
0.08
0.17

DS diameter stenosis; HF heart failure; MBG myocardial blush grade; MI myocardial infarction; MLD minimal lumen diameter;
PCI percutaneous coronary intervention; QCA quantitative coronary analysis; RVD reference vessel diameter; SVG saphenous vein graft;
TIMI Thrombolysis In Myocardial Infarction; TTS TIMI thrombus score.

were blinded to clinical outcomes. Consensus was achieved

in all patients. Half of the angiograms were randomly
selected and re-analyzed by the same analysts for intraobserver variability and by a third experienced interventional
cardiologist for interobserver variability. Intracoronary
thrombus at baseline was angiographically identied and
scored in 5 according to the Thrombolysis In Myocardial
Infarction (TIMI) Thrombus Score (TTS).11 In patients with
occluded IRA at baseline angiography, TTS was reassessed
after positioning of the wire: if wire positioning restored
antegrade ow, TTS 5 was reclassied as TTS 1 to 4 according to thrombus burden; otherwise, the case was

classied as TTS 5 and associated with TTS 1 for statistical

analysis. In cases without ow restoration after wire placement, we did not take into account angiography after predilation12 to avoid the potential contribution of balloon
pre-dilation to DE. The angiographic pattern of coronary
occlusion, when present, was dened on baseline angiogram
as follows: (1) cut-off pattern, when there was an abrupt
occlusion of the epicardial vessel; (2) tapered occlusion,
when there was a vessel tapering just before the occlusion;
and (3) persistent dye pattern, when there was a dye staining
just proximally and/or distally to the occlusion.3,4 TIMI ow
and myocardial blush grade were assessed as previously

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The American Journal of Cardiology (www.ajconline.org)

Table 2
Clinical and angiographic characteristics of derivation and validation cohort

Table 3
Univariate predictors of distal embolization in the derivation cohort

Variable

Variable

Age (years)
Men
Diabetes mellitus
Hypertension
Dyslipidemia
Smoker
Anterior MI
Previous angina
Previous HF
Previous MI
Previous PCI
Pain-to-balloon
time (minutes)
IRA
Left Main
Left Anterior
Descending
Left Circumex
Right
SVG
TTS 2-4
Occlusion pattern
Cut-off pattern
Tapered pattern
Persistent-dye
pattern
TIMI ow pre 2/3
TIMI ow pre 0/1
No-ow
improvement
Collateral
circulation
Lesion length

20 mm
QCA before PCI
% DS
RVD
3.5 mm
MLD

All
(N1200)

Derivation
(N814)

Validation
(N386)

64 (57-74)
945 (78.7%)
225 (18.8%)
693 (57.7%)
534 (44.6%)
659 (54.9%)
623 (52.0%)
318 (26.5%)
13 (1.1%)
133 (11.1%)
97(8.1%)
195 (140-300)

64 (54-74)
64 (55-74)
640 (78.6%)
305 (79.0%)
148 (18.2%)
77(19.9%)
459 (56.4%)
234 (60.6%)
366 (45.0%)
168 (43.5%)
455 (55.9%)
204 (54.8%)
437 (53.7%)
186 (48.2%)
217 (26.6%)
101 (26.2%)
8 (1.0%)
5 (1.3%)
89 (10.9%)
44 (11.4%)
62(7.6%)
35(9.1%)
195 (140-300) 197.5 (140-300)

0.82
0.88
0.45
0.16
0.64
0.33
0.08
0.81
0.78
0.81
1.00
0.15

12 (1.0%)
585 (48.7%)

7 (0.9%)
410 (50.4%)

5 (1.3%)
175 (45.3%)

0.31

136
440
27
540

96
284
17
373

40
156
10
167

(11.3%)
(36.7%)
(2.2%)
(45.0%)

(11.8%)
(34.9%)
(2.1%)
(45.9%)

(10.4%)
(40.4%)
(2.6%)
(43.3%)

0.81

540 (45.0%)
181 (15.1%)
77 (6.4%)

373 (45.8%)
118 (14.5%)
52 (6.3%)

167 (43.3%)
63 (16.3%)
25 (6.5%)

0.38

351 (29.2%)
849 (70.8%)
273 (22.7%)

238 (29.2%)
576 (70.8%)
184 (22.6%)

113 (29.3%)
273 (70.7%)
89 (23.1%)

0.94
0.94
0.86

254 (21.2%)

175 (21.5%)

79 (20.5%)

0.66

394 (32.8%)

284 (34.9%)

110 (28.5%)

0.02

100 (98-100)
170 (14.2%)
0.0 (0.0-0.3)

100 (98-100)
122 (15.0%)
0.0 (0.0-0.3)

100 (95-100)
48 (12.4%)
0.0 (0.0-0.4)

0.69
0.23
0.68

DS diameter stenosis; HF heart failure; IRA infarct related artery;

MI myocardial infarction; MLD minimal lumen diameter;
PCI percutaneous coronary intervention; QCA quantitative coronary
analysis; RVD reference vessel diameter; SVG saphenous vein graft;
TIMI Thrombolysis In Myocardial Infarction; TTS TIMI thrombus
score.

reported.13,14 DE was dened as a distal lling defect with an

abrupt cutoff in
peripheral coronary branches of IRA,
distal to the PCI site.4 Angiographic no-reow was dened
as substantial coronary antegrade ow reduction (TIMI <3)
without mechanical obstruction.4 Quantitative coronary
analysis was performed at baseline and after procedure as
previously described.4
Major adverse events occurring during hospitalization,
including death, nonfatal re-infarction, heart failure, and
stroke, were collected. Diagnosis of nonfatal re-infarction
was based on typical chest pain and/or new ST-segment
changes with troponin I level re-elevation as previously
described.4,15 Heart failure was dened as development of
signs of congestion and/or hemodynamic instability. Stroke

RVD
3.5 mm
Cut-off occlusion pattern
TTS 2-4
No-ow improvement
Lesion length
20 mm
TIMI-ow 2/3 at baseline
DS, %
Anterior MI
Male gender

Odds-Ratio 95% Condence Interval

3.37
2.20
2.09
2.31
1.50
0.40
1.02
0.68
0.67

p
<.0001
<0.001
<0.001
<.0001
0.05
<0.001
0.09
0.05
0.08

2.125 - 5.361
1.473 - 3.289
1.410 - 3.107
1.520 - 3.515
1.005 - 2.252
0.241 - 0.677
0.997 - 1.039
0.458 - 1.026
0.427- 1.044

DS diameter stenosis; MI myocardial infarction; RVD reference

vessel diameter; TIMI Thrombolysis In Myocardial Infarction;
TTS TIMI thrombus score.

Table 4
Multivariate predictors of distal embolization in the derivation cohort and
corresponding integer assignment for calculation of DE risk score
Variable

OR

Cut-off occlusion pattern

RVD
3.5 mm
TTS 2-4
Lesion length
20 mm

2.40
3.25
2.70
1.55

95% CI
1.558
1.998
1.760
1.008

3.703
5.276
4.140
2.571

Points

<.0001
<.0001
<.0001
0.046

2
2
2
1

RVD reference vessel diameter; TTS TIMI thrombus score.

was dened by development of new cognitive or neurologic

impairment conrmed by computed tomography or magnetic resonance imaging.4,15
In regard to risk score development, we randomly divided
the pooled data set in a 2:1 fashion into a derivation cohort
and a validation cohort and considered the incidence of DE
for the primary analysis. Demographic, clinical, and angiographic characteristics were compared between patients with
and without DE in the derivation cohort and between derivation and validation cohort, with the Students t test for
quantitative variables and the chi-square test for categorical
variables. Univariable and multivariable analyses for prediction of DE were performed using a logistic regression
model in the derivation cohort. To prevent overtting, in the
multivariable analysis, we included covariates independently
related to DE in previous studies4e8 with a p value <0.05 in
the univariable analysis: reference vessel diameter (RVD),
occlusion pattern of the IRA, TTS, absence of ow
improvement after wire positioning, lesion length
20 mm,
TIMI 2/3 ow at baseline, diameter of stenosis, anterior
myocardial infarction, and gender; the model was built using
a backward selection procedure. Each signicant covariate in
this model was assigned an integer score based on the
regression coefcients. Risk score was calculated in each
patient by adding the points for each risk factor present. The
rate of DE within each score category was derived per
integer score and then per low-, intermediate-, or high-risk
classication. A signicant p value for trend was considered at the p <0.05 level. Overall model performance was
assessed by the C-statistic.
To test the validity of these ndings, we investigated the
association of the derived risk score with the DE rate

Coronary Artery Disease/Distal Embolization Risk Score in Primary PCI

1175

Figure 1. Distribution of integer risk score and corresponding probability of distal embolization in the derivation cohort. Distribution of the integer risk score
(A); incidence of DE by integer risk score (B): the C-statistic for the risk score model was 0.67 (p <0.0001); distribution of low-, intermediate-, and high-risk
categories (C); incidence of DE by risk category (D): the C-statistic for the risk score model was 0.70 (p <0.0001).

observed in the validation cohort. Rates of DE per risk score

category were derived and compared for trend. Overall
model performance was assessed by the C-statistic. A secondary analysis was performed with inclusion of major
adverse cardiovascular events occurring during hospitalization (death, nonfatal re-infarction, heart failure, and stroke)
in both data sets (derivation and validation) to provide information on prediction of adverse events. Clinician blinded
to angiographic and procedural data adjudicated major
adverse cardiovascular events, as previously described.4,15
All analyses were carried out using SAS 9.2 (SAS Institute Inc., Cary, North Carolina) for Windows.
Results
The study included 1,200 subjects, of whom 173 (14.4%)
had DE during p-PCI. Study population was randomly split
in a 2:1 fashion into derivation (n 814) and validation
(n 386) cohorts. Baseline characteristics of derivation
cohort are reported in Table 1. There were no signicant
differences in risk factors and clinical history between patients with and without DE. At angiographic analysis, patients in the DE group showed a higher rate of cut-off
pattern of occluded IRA and more often TIMI ow 0/1 at
baseline with no-ow improvement after wire positioning,
longer and tighter culprit lesion, and larger RVD than patients without DE. Moreover, patients with DE showed
signicant differences in effectiveness of reperfusion, as
assessed by TIMI ow and myocardial blush grade;

angiographic no-reow was also more frequent in the DE

group (Table 1). There were no differences in baseline
clinical, angiographic, and procedural data between derivation and validation cohorts except for lesion length
(Table 2).
Table 3 lists univariate correlates of DE in the derivation
cohort. At multivariate analysis, presence of cut-off occlusion
pattern of IRA at baseline angiography, TTS, RVD
3.5 mm,
and lesion length
20 mm resulted in independent predictors
of DE (Table 4). These variables entered in the risk score
calculation, by assigning a 0 to 2 points according to strength
of statistical association. Table 4 lists ORs and the corresponding integer assignments for calculation of the risk score;
risk score was calculated in each patient by adding the points
for each risk factor present. Derivation cohort risk scores
ranged from 0 to 7, with most subjects distributing in the
intermediate scores. The distribution of the integer risk score
and corresponding probability of DE are shown in Figure 1,
respectively: DE rate ranged from 3.9% in integer group 0% to
55.6% in group 7 (Figure 1), and C-statistic for the risk score
was 0.67 (p value for trend <0.0001). From observation of
these data, 3 categories of DE risk were dened: risk scores
0 to 1 were considered low risk, 2 to 4 intermediate risk, and
5 to 7 high risk. The distribution of risk score categories and
corresponding probability of DE are shown in Figure 1,
respectively: the rate of DE was 5.6% in low-risk, 15.8% in
intermediate-risk, and 40.0% in the high-risk group (p value
for trend <0.0001). C-statistic for the risk score was 0.70
(p value trend <0.0001).

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The American Journal of Cardiology (www.ajconline.org)

Figure 2. Distribution of integer risk score and corresponding probability of distal embolization in the validation cohort. Distribution of the integer risk score
(A); incidence of DE by integer risk score (B): the C-statistic for the risk score model was 0.61 (p <0.01); distribution of low-, intermediate-, and high-risk
categories (C); incidence of DE by risk category (D): the C-statistic for the risk score model was 0.62 (p <0.01).

Figure 3. Predicted (derivation cohort) versus observed (validation cohort)

distal embolization rate. DE rates in the derivation cohort (red bars) and
validation cohort (blue bars) according to low-, intermediate-, and high-risk
score group. The C-statistic for the risk score was 0.68 (p <0.0001) in the
derivation cohort and 0.64 (p <0.0001) in the validation cohort.

To validate the risk model, we computed the risk score

for each patient in the validation cohort, according to the
presence of risk factors (Table 4). The distribution of
the integer risk score and corresponding probability of DE in
the validation cohort are shown in Figure 2, respectively.
The C-statistic for DE risk score model in this cohort was
0.61 (p <0.01). Frequency distribution of categorized risk
groups, dened as low-, intermediate-, and the high-risk

group, was comparable with that observed in the derivation cohort (p ns; Figure 2). DE rate was 7.5%, 14.7%,
and 37.9% in low-, intermediate-, and the high-risk group,
respectively (C-statistic 0.62, p <0.01; Figure 2). In the
validation cohort, the observed DE rates in each risk category were comparable with those predicted in the derivation
cohort (p ns; Figure 3).
As regards clinical outcome according to risk score,
inhospital mortality was not different across the risk groups
in both derivation and validation cohort (p ns; Figure 4).
In the derivation cohort, heart failure occurred in 11.9%,
12.9%, and 17.6%, respectively, in low-, intermediate-, and
the high-risk group (p 0.03; Figure 4). Likewise, in the
derivation cohort, the incidence of composite end point of
death/heart failure/stroke signicantly increased with the
risk score (p 0.04; Figure 4). Interestingly, in the validation cohort, the same trend in clinical outcomes was
observed, although it did not reach statistical signicance
(Figure 4).
Discussion
The current analysis, in a large data set of patients with
STEMI, resulted in the development and validation of an
integer-based risk score comprising 4 readily available
angiographic variables, which was able to predict the risk of
DE. Stratifying patients in integer groups, based on the
presence or absence of distinct angiographic variables,
a statistically signicant incremental risk of DE was

Coronary Artery Disease/Distal Embolization Risk Score in Primary PCI

1177

Figure 4. Clinical outcomes according to risk score category in the derivation and validation cohorts. Incidence of death (red bars), HF (blue bars), and combined
death/HF/stroke (yellow bars) according to low-, intermediate-, and high-risk score category in derivation (A) and validation (B) cohort. HF heart failure.

observed in both the derivation and validation cohorts.

According to the integer risk score, we classied population
in 3 categories, as low-, intermediate-, and high-risk group,
showing signicant incremental rate of DE. These trends
paralleled each other in the derivation and validation
cohorts, for both integer and categorized groups. Interestingly, we found that most patients (62%) were in the
intermediate-risk category, carrying a DE risk approximately of 12% to 15%. These data appear in accordance
with DE rate historically reported in literature,1,4 reecting
the reliability of our risk stratication. Hazard of DE was as
low as 6% to 7% in the low-risk category; in contrast, patients in the high-risk category carried more than twofold
and fourfold increase in risk of DE with respect to
intermediate-risk and low-risk group, respectively.
In the matter of the determinants of DE, thus far, the
TIMI thrombus score has represented a valuable angiographic tool to assess thrombus amount and the most widely
used classication of thrombus burden in coronary
lesions.11 The TIMI classication of thrombus relies on the
angiographic assessment of the presence and size of intracoronary thrombus, using a simple score ranging from
grade 0 (no thrombus) to grade 5 (very large thrombus
content, which completely occludes vessel ow). Nevertheless, the accuracy of the highest level (grade 5) is subject
to interpretation challenges: because of total occlusion of
the vessel, in fact, the relation between the underlying
plaque burden and thrombus content is unknown, yet this
grade supposedly represents the highest thrombus load.10
Accordingly, in the present study, the highest value of
TTS did not predicted DE, suggesting the weak predictive
value of that score in case of total occlusion. We previously
reported on angiographic determinants of DE, identifying a
subset of lesions at higher risk of embolization: pattern of
occlusion of IRA, large RVD (
3.5 mm), and lesion length;
interestingly, TTS predicted DE only in patients with patent
vessel at baseline.4 Sianos et al12 provided a reclassication of TTS after antegrade ow restoration by
either guidewire positioning or undersized (2 mm) balloon
pre-dilation, to make it more reliable in case of occluded
vessels. However, to explore the potential role of baseline

angiography in predicting the hazard of DE, avoiding the

contribution of balloon pre-dilation, we did not consider
angiography after pre-dilation. Nonetheless, to overcome
these limitations, we also considered other variables known
to be related to thrombus amount in previous studies.3e7 To
this regard, it is important to emphasize that plaque
components, other than thrombus, may compose the
embolization debris.9,16 Recently, it has been shown that
ruptured plaque and large plaque burden, as assessed by
intravascular ultrasound, predict DE in acute coronary
syndromes.17,18 Moreover, thrombus composition other
than thrombus amount might affect the hazard of DE and
poor myocardial reperfusion.19
As regards clinical implications and limitations, a relevant
nding of our study is that the angiographic risk score was
not only able to discriminate the hazard of DE during p-PCI,
but it was also capable to stratify clinical outcome
throughout the hospitalization. In fact, a higher risk score
was associated with worse clinical outcome in the derivation
cohort. The same trend was observed in the validation
cohort, even if it did not reach statistical signicance; this
difference, however, is probably to be ascribed to the sample
size of this cohort, relatively small to identify signicant
differences in clinical outcome. The aim of our study was to
provide a simple risk score that can be used to determine the
risk of DE during p-PCI. Angiography offers poor sensitivity
and specicity in thrombus detection and quantication,
whereas intravascular ultrasound imaging and optical
coherence tomography seem more reliable tools to this
purpose.20 Therefore, it focuses on a practical approach to
assess DE risk using angiographic variables readily available
at the time of PCI. Despite uncertain immediate clinical
application, we believe that the development and initial
validation (albeit with low discriminatory ability in validation cohort, expressed by C-statistic 0.61) of this DE risk
score can be a useful tool particularly for future clinical
investigation and analyses of trials or registries as it can be
a simple way for risk stratication of patients during p-PCI.
Because we did not include patients who underwent
thrombus aspiration; however, the new risk score pertains
only to the hazard of embolization using conventional p-PCI

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The American Journal of Cardiology (www.ajconline.org)

(balloon and/or stent), and any inference should not be

drawn about the appropriateness or need for thrombus
aspiration according to the DE risk score. Nevertheless,
future studies could be useful to assess the impact of
thrombus aspiration according to the DE risk score.
Although our results derive from a large cohort, these are not
necessarily be generalizable to the entire population of patients with STEMI, and therefore, these ndings require
further validation in different and multicenter series. Moreover, to denitely judge the clinical relevance of the DE risk
score, further evaluations based on large populations using
longer follow-up is needed. Finally, the results of our study
should be cautiously interpreted since the introduction of the
novel antithrombotic and antiplatelets regimens.21e23
Disclosures
The authors have no conicts of interest to disclose.
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