Fischman, David

Jasti, Babu

Kaliyadan, Antony G.

Ogilby, David

Ruggiero, Nicholas

Savage, Michael

Siu, Henry

Walinsky, Paul

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CRT-112 “Very” Very Late Stent Thrombosis: Acute Myocardial Infarction From Drug Eluting Stent Thrombosis Occurring Greater Than 5 Years Post-Implantation 

J A C C : C A R D I O V A S C U L A R I N T E R V E N T I O N S , V O L . 7 , N O . 2 S , S u p p l S , 2 0 1 4 S11
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YCRT-112
“Very” Very Late Stent Thrombosis: Acute Myocardial Infarction From Drug Eluting
Stent Thrombosis Occurring Greater Than 5 Years Post-Implantation
Antony G. Kaliyadan, Henry Siu, David Fischman, Nicholas Ruggiero, II, Babu Jasti,
Paul Walinsky, David Ogilby, Michael Savage
Thomas Jefferson University Hospital, Philadelphia, PA
Background: A serious long-term complication of drug-eluting stents (DES) is the
occurrence of very late stent thrombosis (VLST) beyond one year after implantation.
While VLST has been observed at least 3 to 5 years following the initial procedure, it
remains unknown whether DES thrombosis is a ﬁnite phenomenon which abates over
time or is a risk that persists indeﬁnitely.
Methods: A retrospective chart and angiographic review was performed to identify a
series of patients who presented to our institution with acute myocardial infarction
(MI) due to “very”, very late stent thrombosis (VVLST), deﬁned as stent thrombosis
occurring more than 5 years after DES implantation.
Results: The study group consisted of 6 patients (5 men and 1 woman), aged 32 to
70 years, who had angiographically conﬁrmed deﬁnite VVLST. Five of the patients
were active smokers and 3 were diabetic. Interval between stent implantation and
VVLST ranged from 5.6 to 7.0 years. The DES was sirolimus-eluting in 3 patients
and paclitaxel-eluting in 3 patients. None of the patients were taking clopidogrel at
the time of VVLST. The interval between clopidogrel discontinuation and VVLST
was 1 week in 2 patients, 3-6 months in 2 patients, and greater than 5 years in 2
patients. Only 2 patients were taking chronic aspirin therapy. Therefore, 4 of the 6
patients were on no antiplatelet therapy prior to VVLST. The clinical presentation
of VVLST was an acute MI in all patients, with ST segment elevation in 5 of the 6.
All patients were treated successfully by emergent repeat percutaneous coronary
intervention.
Conclusion: Risk of stent thrombosis persists beyond 5 years after implantation of
ﬁrst generation DES. These sobering ﬁndings underscore the need for clinical vigi-
lance in these patients and corroborate current PCI guidelines which recommend
continuing at least aspirin indeﬁnitely after DES.A
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s70 Male 76 SES Yes NSTEMI OM1 0 Yes [730] Yes
[1,825]Yes No No Yes 23 Prior32 Male 84 SES No STEMI LAD 0 Yes [7] Yes, [7] Yes Yes Yes Yes 58 Active54 Male 68 PES No STEMI RCA 0 No Yes [180] No Yes No Yes 29 Active48 Female 67 SES No STEMI RCA 0 No Yes [90] No No No Yes 33 Active61 Male 77 PES No STEMI LAD 0 Yes
[1,825]Yes
[1,825]Yes Yes Yes Yes 23 Active63 Male 67 PES Yes STEMI LCx 0 Yes [7] Yes [7] No Yes Yes Yes 46 ActiveCRT-113
Post-procedural Hypotension After Primary Percutaneous Coronary Intervention in
ST-Elevation Myocardial Infarction
Jee Eun Kwon, Sang-Wook Kim, Wang-Soo Lee, Joon Hwa Hong, Sharath Kumar,
Eun Young Kim, Kwang Je Lee, Chee Jeong Kim, Dai Yun Cho, Tae Ho Kim
Chung-Ang University Hospital, Seoul, Korea, Republic of
Background: The clinical signiﬁcance of post-procedural hypotension has not been
evaluated in patients with ST elevation myocardial infarction (STEMI) after successful
primary percutaneous coronary intervention (PCI).Methods: Total of 236pts with STEMI who underwent primary PCI were reviewed.
Pts who presented with cardiogenic shock before or during PCI were excluded.
Echocardiography was done within 48hrs. All pts underwent VH-IVUS imaging of
culprit lesion.
Results: Among 236pts, 54pts presented with post-procedural hypotension after
successful primary PCI without any deﬁnite cause. Pt age was 62  8 yrs in post-PCI
hypotensive STEMI vs 58  13 in normotensive STEMI (p¼0.048). The incidence
of hypertension was 41% (21/54) in post-PCI hypotensive STEMI vs 54% (98/182) in
normotensive STEMI (p¼0.105). Peak troponin-I and CK-MB were similar, and
Thrombolysis in myocardial infarction (TIMI) grade before PCI was lower in hypo-
tensive group. However, door to balloon and symptom to balloon time were longer in
hypotensive group. Ejection fraction was lower and left ventricular end-systolic
dimension was larger in hypotensive group. Minimal lumen area (MLA) was smaller
and maximal necrotic core (%) was larger in post-PCI hypotensive STEMI, but the
incidence of VH-TCFA was similar (56% vs 42%, p¼0.505). By logistic multivariate
regression analysis, the most important independent predictors of post-procedural
hypotension were longer symptom to balloon time (OR 1.012, p¼0.0093) and percent
maximal necrotic core (OR 1.244, p¼0.018). However, there were no signiﬁcant
differences in the 30days and 1yr MACCE of these two group.
Conclusion: Post-procedural hypotension after successful primary PCI was predicted
by delayed reperfusion time and prominent necrotic core of culprit lesion, although it
results in no difference of patient’s outcome.post-PCI hypotensive
STEM (n¼54)
post-PCI normotensive
STEMI (n¼182) p-value
Peak CK-MB 275.08  209.38 248.49  228.31 0.536
Peak Troponin I 314.92  274.83 298.78  405.98 0.823
Door to balloon time 100  75.36 61.21  35.96 0.004
Sx to balloon time 352.70  295.35 149.37  75.63 <0.0001
TIMI grade (0/1/2/3) 42/4/8/0 83/31/68/0 0.004EF (%) 43.17  9.66 52.82  10.56 <0.0001
Lesion length (mm) 25.44  9.14 20.92  8.76 0.009
Distal reference lumen area (mm2) 2.99  0.42 3.19  0.47 0.026
Vessel area (mm2) 12.20  4.61 12.54  5.84 0.788
Lumen area (mm2) (MLA site) 2.80  0.82 3.38  2.18 0.048
Plaque area (mm2) (MLA site) 12.82  4.78 11.94  5.50 0.464
Remodeling index (max. NC site) 1.41  0.61 1.27  0.34 0.279
Average ﬁbrotic area (%) 59.77  14.61 63.11  15.44 0.337
Average ﬁbrofatty area (%) 14.14 14.67 11.45  7.64 0.379
Average NC area (%) 19.21  13.63 18.25  12.26 0.739
Average dense calcium area (%) 6.91  9.53 7.18  7.91 0.888
% Fibrotic area (max. NC site) 50.75  13.47 63.11  15.44 <0.0001
% Fibrofatty area (max. NC site) 5.65  6.58 11.45  7.64 <0.0001
% Necrotic core area (max. NC site) 33.50  14.84 18.25  12.26 <0.0001
% Dense calcium area (max. NC site) 10.09  7.41 7.18  7.91 0.102CRT-114
Addition of Eptifibatide to Bivalirudin During St-Elevation Myocardial Infarction: Role
for Combination Therapy?
Nevin Baker, Orlando Escarcega, Michael Lipinski, Marco Magalhaes, Sa’ar Minha,
Joshua Loh, Lakshmana Pendyala, Al Fazir Omar, Hideaki Ota, Augusto Pichard,
Lowell Satler, William O. Suddath, Rebecca Torguson, Ron Waksman
MedStar Heart Institute, Washington, DC
Background: Patients presenting with ST-elevation myocardial infarction (STEMI)
represent a high risk group for in-hospital adverse events. The value of eptiﬁbatide in
addition to bivalirudin in this population for prevention of such events has not been
determined.
Methods: 1,849 STEMI patients underwent primary percutaneous coronary inter-
vention; 1,639 received bivalirudin monotherapy compared with 210 who received
bivalirudin plus provisional eptiﬁbatide. Primary endpoint was a composite of in-
hospital death, Q-wave MI, or acute stent thrombosis; adjusted for group differences.
Safety was assessed by the occurrence of thrombolysis in myocardial infarction (TIMI)


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CRT-112 “Very” Very Late Stent Thrombosis: Acute Myocardial Infarction From Drug Eluting Stent Thrombosis Occurring Greater Than 5 Years Post-Implantation

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