This document discusses treatment of late and very late stent thrombosis. According to studies cited, the rate of late stent thrombosis with drug-eluting stents is around 1-2% which can result in significant mortality. The BASKET-LATE trial found that for every 100 patients treated with DES, 3.3 cases of cardiac death or MI are prevented but 5 cases of target lesion revascularization are induced compared to bare-metal stents when patients discontinue clopidogrel after 1 year. Independent predictors of late stent thrombosis include premature antiplatelet therapy discontinuation, renal failure, bifurcation lesions, and diabetes. The mechanisms of late stent thrombosis are proposed to involve delayed arterial healing and re-endothelialization with
A stent is a small, expandable tube. During a procedure called angioplasty, the stent is inserted into a coronary artery and expanded using a small balloon. A stent is used to open a narrowed or clotted artery.
A drug-eluting stent is a peripheral or coronary stent placed into narrowed, diseased peripheral or coronary arteries that slowly releases a drug to block cell proliferation. This prevents fibrosis that, together with clots, could otherwise block the stented artery, a process called restenosis
A stent is a small, expandable tube. During a procedure called angioplasty, the stent is inserted into a coronary artery and expanded using a small balloon. A stent is used to open a narrowed or clotted artery.
A drug-eluting stent is a peripheral or coronary stent placed into narrowed, diseased peripheral or coronary arteries that slowly releases a drug to block cell proliferation. This prevents fibrosis that, together with clots, could otherwise block the stented artery, a process called restenosis
How to deal with CALCIFIED CORONARY ARTERY LESIONS .Coronary artery calcification (CAC) is highly prevalent in patients with coronary heart disease (CHD) and is associated with major adverse cardiovascular events. There are two recognized type of CAC—intimal and medial calcification, and each of them have specific risk factors. Several theories about the mechanism of vascular calcification have been put forward, and we currently believe that vascular calcification is an active, regulated process. CAC can usually be found in patients with severe CHD, and this asymptomatic phenomenon make early diagnosis of CAC important. Coronary computed tomographic angiography is the main noninvasive tool to detect calcified lesions. Measurement of coronary artery calcification by scoring is a reasonable metric for cardiovascular risk assessment in asymptomatic adults at intermediate risk. To date, effective medical treatment of CAC has not been identified. Several strategies of percutaneous coronary intervention have been applied to CHD patients with CAC, but with unsatisfactory results. Prognosis of CAC is still a major problem of CHD patients. Thus, more details about the mechanisms of CAC need to be elucidated in order to improve the understanding and treatment of CAC.
How to deal with CALCIFIED CORONARY ARTERY LESIONS .Coronary artery calcification (CAC) is highly prevalent in patients with coronary heart disease (CHD) and is associated with major adverse cardiovascular events. There are two recognized type of CAC—intimal and medial calcification, and each of them have specific risk factors. Several theories about the mechanism of vascular calcification have been put forward, and we currently believe that vascular calcification is an active, regulated process. CAC can usually be found in patients with severe CHD, and this asymptomatic phenomenon make early diagnosis of CAC important. Coronary computed tomographic angiography is the main noninvasive tool to detect calcified lesions. Measurement of coronary artery calcification by scoring is a reasonable metric for cardiovascular risk assessment in asymptomatic adults at intermediate risk. To date, effective medical treatment of CAC has not been identified. Several strategies of percutaneous coronary intervention have been applied to CHD patients with CAC, but with unsatisfactory results. Prognosis of CAC is still a major problem of CHD patients. Thus, more details about the mechanisms of CAC need to be elucidated in order to improve the understanding and treatment of CAC.
Bare Metal Stents: Will Their Lower Thrombosis Advantage over DES Vanish Against the CoCr-Everolimus Eluting Stents? Armando Tellez, SOLACI Congress 2012, Mexico.
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Current PCI guidelines from the American Heart Association, American College of Cardiology, and Society for Cardiovascular Angiography and Interventions, published in 2006, said that performing elective PCI at centers with off-site surgical backup is "not recommended" (a class III category), and that primary PCI at these locations "may be considered" (a class IIb category) (J. Am. Coll. Cardiol. 2006;47:216-35). Favorable outcomes for primary PCI performed in facilities without cardiac surgery backup on site have been reported The new findings reported by Dr. Kutcher warrant upgrading both of these recommendations and designating both uses of PCI at centers with off-site backup as class IIa recommendations. Dr. Michael A. Kutcher performed a study using data collected by the NCDR CathPCI registry on consecutive cases done during Jan. 1, 2004, through March 30, 2006, with 308,161 patients treated at 465 U.S. centers. This included 9,029 patients treated with off-site surgical backup at 61 centers, and 299,132 patients treated at 404 centers with on-site surgical backup.
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1. TREATMENT OF LATE AND VERY LATE
STENT THROMBOSIS
DEV PAHLAJANI MD,FACC,FSCAI
CHIEF OF INTERVENTIONAL CARDIOLOGY,
BREACH CANDY HOSPITAL,MUMBAI
2. DES increased thrombogenicity
• According to the Euro PCR-06 Daily; a 1.2% rate of late stent
thrombosis means around 30,000 people were affected,
accounting for a 45% mortality rate.
3. BMS VS DES –ADVERSE EVENTS
Incidences of serious adverse events (Death or MI)
N=878
N=870
N=1675 N=1685
4. Study Design: BASKET LATE trial
743 patients randomized in the BASKET trial and without an event during the 6 month Clopidogrel phase
Drug eluting stents(DES)
Bare metal
(pooled paclitaxel and
VISION stents (BMS)
sirolimus DES groups)
N=244
n=499
Followed for 1 year off clopidogrel
•Primary Endpoint: Composite cardiac death or nonfatal MI
•Other Endpoints: “Thrombosis-related events”
Ref: Pfisterer M et al.ACC 2006
5. BASKET LATE Trial
• “For every 100 patients treated with DES,3.3
cases of cardiac death or MI are induced for
reduction of 5 cases of TLR”
7. ARC Proposed Standard Definitions
DEFINITE (Angiographic or pathologic confirmation):
Angiographic confirmation:
1. TIMI 0 with occlusion originating in or within 5 mm of stent in the presence
of a thrombus
2. TIMI flow grade 1, 2, or 3 originating in or within 5 mm of stent in the
presence of a thrombus
3. AND 1 of the following criteria < 48 hours:
4. New acute onset of ischemic symptoms at rest (typical chest pain with
duration >20 minutes)
5. New ischemic ECG changes suggestive of acute ischemia
6. Typical rise and fall in cardiac biomarkers
Pathologic confirmation:
1. Evidence of recent thrombus within the stent determined at autopsy or via
examination of tissue retrieved following thrombectomy
PROBABLE:
1. Any unexplained death within the first 30 days
2. Any MI (related to documented acute ischemia and without another obvious cause) in
the territory of the stent
POSSIBLE: Any unexplained death >30 days
8. ARC Definitions of Stent Thrombosis - Gaps
Best Balance
Includes MI with or
without angio, but
Too Narrow not 1.5%/year Too Broad
natural history
Misses people who deaths Includes natural
have an MI but don’t history events (equal
have an angiogram in both arms) that
dilute out true ST
signal*
* Worse if you include post TLR events
• Restenotic stent can’t really develop ST
• Brachytherapy or new DES certainly can
Dr. Don Baim, TCT 2006.
• More such events occur in the BMS arm
9. Thrombosis Can Occur Any Time
Post-Stent Implantation
Very
Late ST
Late ST
SAT
Acute ST
12. Stent Thrombosis
Bern-Rotterdam
3.5
3.2
3
Percent Stent Thrombosis
Bern Cypher 2.7
Bern Taxus
2.5 2.5
Bern BMS
1.9
2
1.5 1.6
1
0.5
0
0 10 30 365 730 1095
Days
Wenaweser P. et al: EHJ 2005 26 1180-1187.
Wenaweser P. et al: ESC 2006.
Bern-Rotterdam and HCRI CEC ST definitions both require angiographic confirmation.
13. LATE STENT THROMBOSIS
STEMI
ACUTE CORONARY SYNDROME
LEFT VENTRICULAR FAILURE
CARDIOGENIC SHOCK
14. TREATMENT OF LST
MANAGE LIKE PRIMARY PCI
BALLOON DILATATION
SUPPORTIVE MEASURES
IABP IF SHOCK OR LVF
LIBERAL USE OF GPIIB/IIIA BLOCKERS
ASPIRIN AND CLOPIDOGREL IF NOT ON
THROMBUS ASPIRATION
AVOID DES PREFER BMS
15. Clinical importance of stent thrombosis
Author/Year BMS/DES ST def Death or MI Death
Cutlip 2001 BMS Angio or 70% 21%
clinical
Heller 2001 BMS Angio + AMI 100% 17 %
Iakovou 2005 DES Angio or 45 %
clinical
Ong 2005 DES Angio & 100 % 25 %
clinical
Kuchulakanti DES Angio 31 %
2006
16. ‘Real-world’ outcomes through 1 year
CYPHER (n=2067) TAXUS (n=7393)
e-CYPHER ARRIVE 1& 2
Stent P value Stent P value
Thrombosis Thrombosis
2.87 vs. 2.03 0.10
Diabetes vs. No Diabetes 1.12 vs. 0.75 0.44
3.06 vs. 1.95 0.03
2.5 mm vs. >2.5 mm 1.02 vs. 0.73 0.47
4.49 vs. 1.96 <0.0001
>28 mm vs. 28 mm 1.90 vs. 0.76 0.22
4.20 vs. 1.43 <0.0001
Multiple vs. Single stents 1.35 vs. 0.73 0.22
3.53 vs. 2.05 0.01
Multiple vs. Single Vessel 1.16 vs. 0.59 0.04
3.49 vs. 2.12 0.07
Acute MI vs. Non-AMI 0.67 vs. 0.88 1.00
17. Incidence of Late stent Thrombosis >30 days
meta-analysis of 14 randomized clinical trials 6675 pts
Am J of Medicine 2006;119, 1056-1061
18. Bern-Rotterdam Analysis: Summary
The data suggest that late stent thrombosis occurs at a steady
rate during follow-up up to three years, tends to be more frequent
with PES than with SES, and can unpredictably occur at any time
point despite antiplatelet therapy.
Late stent thrombosis complicating the use of DES seems to be a
distinct entity with pathophysiological factors that differ from
those of early stent thrombosis.
Daemen et al. Lancet. 2007 Feb 24; 369: 667 – 78.
22. STENT THROMBOSIS DES
Predictors of late stent thrombosis
2229 consecutive patients at 3 centers
Independent predictors of late ST (>30 days < 9 mo)
-premature antiplatelet therapy d/c HR=161
-renal failure HR=10.1
-bifurcation lesion HR=6.0
-diabetes HR=5.8
24. Predictors of ST after DES (SES or PES)
29/2229 pts (1.3%) at 9.3 ± 5.6 mos
Iakovou et al. JAMA 2005;293:2126-2130
Multivariate predictors of stent thrombosis:
Renal failure (OR=11.5),
Bifurcation (7.2),
Prior Brachy Rx (4.2),
Diabetes(3.4),
And Low LVEF(1.1)
Iakovou I et al JAMA. 2005;293:2126-2130
26. Impaired Re-endothelialization
Pathology findings:
Sirolimus-Eluting stents from different coronary arteries in the same patient
(delayed healing)
Cypher
16 months after
deployment
BMS
24 months after
deployment
29. Percentage of Endothelialization in Drug-eluting
Stents (DES) VERSUS Bare-metal Stents (BMS)
as a function of Time
J Am Coll Cardiol 2006
30. Granulomatous reaction seen in 12.5 and 35% of
CYPHER stents implanted for 28 & 90 days in Pig
Coronary Arteries
31. Case presented in EURO PCR-05
• A 38 year old female died suddenly, 6 months following Taxus
stent placement for AMI
No healing or inflammation observed over the 6 months
stent implantation time
32. DES failed to cross a heavily calcified lesion!!
Undamaged Severe polymer
polymer damage
Columbia University Medical Centre
Cardiovascular Research Foundation
33. Mechanisms leading to incomplete stent
apposition
Cook, S. et al. Circulation 2007;115:2426-2434
34. The protocol sequence of IVUS imaging in very late ST patients is depicted in
A, as follows: (1) After administration of nitroglycerin (0.2 mg), an
angiogram with the use of a 6F guiding catheter was performed to define
the site of thrombotic stent occlusion
Cook, S. et al. Circulation 2007;115:2426-2434
35. Clinical outcomes and Stent Thrombosis
following off-label use of drug eluting stents
36. Antiplatelets
4% to 30% of patients treated with conventional doses of
clopidogrel do not display adequate antiplatelet response
5% to 45% of patients treated with conventional doses of
aspirin do not display adequate antiplatelet response
(Nguyen TA et al.JACC 2005;45:1157-1164.
Gum PA Stone et al.JACC 2003;41:961-965)
Premature Discontinuation
Study Yes No RR (95% CI) PAR
Iakovou et 5/17 (29%) 24/2,212 27 (12, 63) 17%
al.,2005 (7) (1.0%)
Kuchulakanti et 14/310 (4.5%) 24/2,658 5 (3,10) 29%
al.,2006 (8) (0.9%)
PAR= Pr * [(RR-1)/Pr * (RR-1)+1]
CI= confidence interval; DES= drug eluting stent; PAR= population attributable risk;
Pr=prevalence of clopidogrel discontinuation; RR= relative risk
37. Clopidogrel and DES
Late clinical events after clopidogrel discontinuation may limit
the benefit of drug-eluting stents.
An observational study of DES versus BMS –BASKET-Late study
46. All-Cause Mortality and Cumulative MACCE
Rate
Chechi, T. et al. J Am Coll Cardiol 2008;51:2396-2402
47. Stent thrombosis in DM NDM
Risk factors for stent thrombosis after implantation of Sirolimus-
eluting stents in Diabetic and Nondiabetic patients.
The EVASTENT Matched-Cohort Registry
Independent predictors of stent thrombosis
Parameter QR (95% CI) p Value
Overall population
Previous stroke 3.2 (0.99-1.0) 0.052
Renal failure 3.6 (1.6-7.7) 0.001
Insulin-requiring diabetes 2.7 (1.4-5.2) 0.004
Calcified lesion 3.7 (1.8-7.7) 0.001
Lower EF (per U) 0.95 (0.93-0.97) <= 0.001
Length stented (per mm) 1.01(1.0-1.03) 0.045
48. Very Late DES Thrombosis On-Label Use
>1 Year Post Implant Pooled RCTs
49. Aalen-Nelson Estimate Curves of Cumulative
Hazard Function for Stent Thrombosis
Park, D.-W. et al. J Am Coll Cardiol Intv 2008;1:494-503
50. Kaplan-Meier Curves of Cumulative Incidence
of Stent Thrombosis
Park, D.-W. et al. J Am Coll Cardiol Intv 2008;1:494-503
51. Rates of Stent Thrombosis in Meta-analysis
Reference Year Patients Stents FU ST Rate
Moreno 2005 5,030 BMS 48% 6–12 mn SAT: 0.35% (BMS = DES)
SES 17% LST: 0.23% (BMS = DES)
PES 34%
Bavry 2005 3,817 BMS 48% 6–12 mn SAT + LST: 0.76% (PES = BMS)
PES 52%
Morice 2006 1,386 SES 51% 12 mn SAT: SES 0.4%, PES 1.0%
(REALITY) PES 49% LST: SES 0%, PES 0.3%
Kastrati 2005 3,669 SES 50% 6–13 mn SAT + LST: 1.0% (PES = SES)
PES 50%
Spalding 2007 1,748 BMS 50% 48 mn SAT: SES 0.5%, BMS 0.5%
SES 50% LST: SES 0.3%, BMS 1.3%
VLST: SES 2.8%, PES 1.7
Mauri 2007 4,545 SES 19% 48 mn SAT: SES 0.5%, BMS 0.3%
PES 31% LST: SES 0.1%, BMS 1.0%
BMS 50% VLST: SES 0.9%, BMS 0.4%
SAT: PES 0.5%, BMS 0.5%
LST: PES 0.4%, BMS 0.3%
VLST: PES 0.9%, BMS 0.6%
52. Preventive Strategies
Optimizing stent implantation
Selection of the appropriate diameter and length of stent.
Placement of excessively long DES (overstenting) should be avoided.
Residual stent marginal dissections or significant stenoses should be
treated.
Suboptimal under- or overdeployment of stent diameter should be
avoided.
IVUS may be useful in optimizing deployment results.
Some specific techniques may be associated with higher rates of ST.
Adjunctive therapy
Dual antiplatelet therapy after DES implantation is crucial.
Recently, the recommendation has been to extend this therapy for up to
12 months in patients at low risk for bleeding events.
Preliminary data suggest that “triple” antiplatelet therapy may be
associated with a reduction in MACE, including ST, and may be a
therapeutic option for patients at high risk for ST.
53. Triple Versus Dual Antiplatelet Therapy
Dual Triple p Value
(n=1597) (n= 1415)
Stent thrombosis 9 (0.596) 1 (0.196) 0.024
Acute stent occlusion 3(0.296) 0 0.252
Sub acute stent 6(0.396) 1(0.196) 0.223
thrombosis
Major cardiac events
Myocardial infarction 11(0.796) 3(0.296) 0.063
Target lesion 9(0.596) 1(0.196) 0.024
revascularization
Repeat intervention 8(0.697) 1(0.196)
Emergency bypass 1(0.02) 0
Death 5(0.396) 3(0.296) 0.730
Primary end point 13(0.896) 4(0.396) 0.085
J. Am. Coll. Cardiol. 2005;46;1833-1837