KCI등재
SCIE
SCOPUS
Strategy for the Treatment of Clopidogrel Low Responsiveness in Diabetes Mellitus and Stent Implantation
저자
김장영 (연세대학교)
발행기관
학술지명
권호사항
발행연도
2009
작성언어
English
등재정보
KCI등재,SCIE,SCOPUS
자료형태
학술저널
발행기관 URL
수록면
459-461(3쪽)
KCI 피인용횟수
8
제공처
소장기관
Platelets play a central role in the pathogenesis of atherothrombosis.
1) Thus, achieving platelet inhibition is
an important part of managing patients that have experienced
an atherothrombotic event. Dual antiplatelet
therapy with clopidogrel plus aspirin has been shown to
markedly reduce ischemic events in patients undergoing
percutaneous coronary intervention (PCI) and stenting.2)
Despite its proven benefit of dual antiplatelet therapy,
diabetic patients remain at increased risk of recurrent
ischemic events when compared to non-diabetic patients.
Recent evidence suggests that diabetic patients are resistant
or partially responsive to treatments with a dual antiplatelet
effect (especially clopidogrel) which is related
to poor clinical outcomes such as stent thrombosis and
recurrent atherothrombotic events.3)4) Yang et al.5) previously
reported that triple antiplatelet therapy (dual antiplatelet
plus cilostazol) results in more potent inhibition
of adenosine diphosphase (ADP) induced platelet
aggregation than dual antiplatelet therapy in patients
with diabetes and drug-eluting stent (DES) implantation.
These results suggest that triple antiplatelet therapy is a
treatment option for amelioration of low responsiveness
to clopidogrel in diabetes mellitus (DM).
No treatments of clopidogrel low responsiveness in
DM have been reported to date. An initial approach to
clopidogrel low responsiveness was considered to be a
correctable cause of resistance, including hyperglycemia,
noncompliance, insulin resistance (metabolic syndrome)
and drug interaction.
Currently, practical strategies to overcome clopidogrel
low responsiveness include 1) addition of cilostazol, 2)
increasing the dose of antiplatelet agents, and 3) the use
of new drugs, such as prasugrel or ticagrelor.
Adding Cilostazol
Cilostazol is a potent oral antiplatelet agent with a rapid
onset of action that selectively inhibits phosphodiesterase
III and increases cyclic adenosine mono phosphate
(cAMP) levels in platelets. The increase in cAMP blocks
all activating pathways in platelets, including ADP-induced
platelet activations.6)
An OPTIMUS-2 study7) of randomized crossover platelet
function study in patients with type 2 DM and coronary
artery disease following dual antiplatelet therapy
revealed that the reduced platelet inhibition of P2Y12
signaling can be enhanced by adjunctive treatment with
cilostazol when compared with dual antiplatelet therapy.
Thus, cilostazol led to significantly increased P2Y12 platelet
inhibition, as measured by flow cytometry and light
transmission aggregometry. These findings were similar
to the results of a study conducted by Yang et al. Several
clinical studies have shown that triple antiplatelet therapy
has better clinical outcomes than dual antiplatelet
therapy in patients undergoing PCI and coronary stenting.
Lee et al.8) compared the clinical benefit undergoing
PCI between dual antiplatelet therapy (aspirin plus clopidogrel
or ticlopidine, group I, n=1,597) and triple antiplatelet
therapy (aspirin plus clopidogrel or ticlopidine
plus cilostazol, group II, n=1,415) groups. They found
that stent thrombosis within 30 days was significantly
lower in group II (0.1%) than in group I (0.5%; p=0.024).
Additionally, the independent predictors of stent thrombosis
were found to be primary stenting {hazard ratio
(HR) 7.9, 95% confidence interval (CI) 2.0 to 30.8, p=
○ cc This is an open-access article distributed under the terms of the Creative
Commons Attribution License, which permits unrestricted use, distribution,
and reproduction in any medium, provided the original work is properly cited.
Refer to the page 462-466
460·Clopidogrel Low Responsiveness in DM and DES
0.003} and triple therapy (HR 0.12, 95% CI 0.015 to
0.98, p=0.048). They concluded that triple antiplatelet
therapy more effectively prevented thrombotic complications
after stenting without an increased risk o...
Platelets play a central role in the pathogenesis of atherothrombosis.
1) Thus, achieving platelet inhibition is
an important part of managing patients that have experienced
an atherothrombotic event. Dual antiplatelet
therapy with clopidogrel plus aspirin has been shown to
markedly reduce ischemic events in patients undergoing
percutaneous coronary intervention (PCI) and stenting.2)
Despite its proven benefit of dual antiplatelet therapy,
diabetic patients remain at increased risk of recurrent
ischemic events when compared to non-diabetic patients.
Recent evidence suggests that diabetic patients are resistant
or partially responsive to treatments with a dual antiplatelet
effect (especially clopidogrel) which is related
to poor clinical outcomes such as stent thrombosis and
recurrent atherothrombotic events.3)4) Yang et al.5) previously
reported that triple antiplatelet therapy (dual antiplatelet
plus cilostazol) results in more potent inhibition
of adenosine diphosphase (ADP) induced platelet
aggregation than dual antiplatelet therapy in patients
with diabetes and drug-eluting stent (DES) implantation.
These results suggest that triple antiplatelet therapy is a
treatment option for amelioration of low responsiveness
to clopidogrel in diabetes mellitus (DM).
No treatments of clopidogrel low responsiveness in
DM have been reported to date. An initial approach to
clopidogrel low responsiveness was considered to be a
correctable cause of resistance, including hyperglycemia,
noncompliance, insulin resistance (metabolic syndrome)
and drug interaction.
Currently, practical strategies to overcome clopidogrel
low responsiveness include 1) addition of cilostazol, 2)
increasing the dose of antiplatelet agents, and 3) the use
of new drugs, such as prasugrel or ticagrelor.
Adding Cilostazol
Cilostazol is a potent oral antiplatelet agent with a rapid
onset of action that selectively inhibits phosphodiesterase
III and increases cyclic adenosine mono phosphate
(cAMP) levels in platelets. The increase in cAMP blocks
all activating pathways in platelets, including ADP-induced
platelet activations.6)
An OPTIMUS-2 study7) of randomized crossover platelet
function study in patients with type 2 DM and coronary
artery disease following dual antiplatelet therapy
revealed that the reduced platelet inhibition of P2Y12
signaling can be enhanced by adjunctive treatment with
cilostazol when compared with dual antiplatelet therapy.
Thus, cilostazol led to significantly increased P2Y12 platelet
inhibition, as measured by flow cytometry and light
transmission aggregometry. These findings were similar
to the results of a study conducted by Yang et al. Several
clinical studies have shown that triple antiplatelet therapy
has better clinical outcomes than dual antiplatelet
therapy in patients undergoing PCI and coronary stenting.
Lee et al.8) compared the clinical benefit undergoing
PCI between dual antiplatelet therapy (aspirin plus clopidogrel
or ticlopidine, group I, n=1,597) and triple antiplatelet
therapy (aspirin plus clopidogrel or ticlopidine
plus cilostazol, group II, n=1,415) groups. They found
that stent thrombosis within 30 days was significantly
lower in group II (0.1%) than in group I (0.5%; p=0.024).
Additionally, the independent predictors of stent thrombosis
were found to be primary stenting {hazard ratio
(HR) 7.9, 95% confidence interval (CI) 2.0 to 30.8, p=
○ cc This is an open-access article distributed under the terms of the Creative
Commons Attribution License, which permits unrestricted use, distribution,
and reproduction in any medium, provided the original work is properly cited.
Refer to the page 462-466
460·Clopidogrel Low Responsiveness in DM and DES
0.003} and triple therapy (HR 0.12, 95% CI 0.015 to
0.98, p=0.048). They concluded that triple antiplatelet
therapy more effectively prevented thrombotic complications
after stenting without an increased risk of side effects
when compared to dual antiplatelet. These bench
and clin...
분석정보
연월일 | 이력구분 | 이력상세 | 등재구분 |
---|---|---|---|
2023 | 평가예정 | 해외DB학술지평가 신청대상 (해외등재 학술지 평가) | |
2020-01-01 | 평가 | 등재학술지 유지 (해외등재 학술지 평가) | KCI등재 |
2011-01-01 | 평가 | 등재학술지 유지 (등재유지) | KCI등재 |
2009-01-01 | 평가 | 등재학술지 유지 (등재유지) | KCI등재 |
2008-05-15 | 학회명변경 | 한글명 : 대한순환기학회 -> 대한심장학회영문명 : The Korean Society Of Circulation -> The Korean Society of Cardiology | KCI등재 |
2007-01-01 | 평가 | 등재학술지 유지 (등재유지) | KCI등재 |
2005-08-02 | 학술지등록 | 한글명 : Korean Circulation Journal외국어명 : Korean Circulation Journal | KCI등재 |
2004-01-01 | 평가 | 등재학술지 선정 (등재후보2차) | KCI등재 |
2003-01-01 | 평가 | 등재후보 1차 PASS (등재후보1차) | KCI후보 |
2001-07-01 | 평가 | 등재후보학술지 선정 (신규평가) | KCI후보 |
기준연도 | WOS-KCI 통합IF(2년) | KCIF(2년) | KCIF(3년) |
---|---|---|---|
2016 | 1.13 | 0.34 | 0.71 |
KCIF(4년) | KCIF(5년) | 중심성지수(3년) | 즉시성지수 |
0.45 | 0.36 | 0.52 | 0.12 |
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