Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3865_Библиотеки_им_академика_М_И_Перельмана
.pdf
380 Anticoagulation Therapy
https://t.me/med1917
Controversy: Triple Antithrombotic Therapy in Patients
with PCI/Coronary Artery Stents Requiring Long-Term
Anticoagulation
•
Patients with ACS are indicated for dual antiplatelet therapy (DAPT) with aspirin
and a P2Y12 inhibitor for up to 1 year to prevent recurrent cardiovascular death,
MI, or stroke as well as stent thrombosis.
•
Data from well-designed clinical trials evaluating triple antithrombotic therapy
following PCI are scarce and limited to just two randomized trials, WOEST and
ISAR-TRIPLE.
38-42
In WOEST, 573 patients receiving a VKA and undergoing PCI were
randomized to dual therapy (DT) with VKA plus clopidogrel or triple
therapy with VKA, clopidogrel, and low-dose aspirin. At 1 year, the
DT group had lower:
Rates of all TIMI bleeding
Rates of BARC serious bleeding
Major adverse cardiac events
A recent meta-analysis confirmed similar thromboembolic but lower
bleeding risk with clopidogrel plus VKA versus triple therapy.
In ISAR-TRIPLE, patients receiving VKA therapy and aspirin (75–200
mg daily) and undergoing PCI (most had second- and third-genera
tion DES) were randomized to 6 weeks vs. 6 months of clopidogrel
therapy with INR targets around 2.
No difference in net clinical adverse effects (composite
of death, MI, definite stent thrombosis, stroke, or TIMI
major bleeding) at 9 months and no major difference in
TIMI major bleeding.
Only about one-third of patients in WOEST and ISAR TRIPLE had
ACS; therefore, little information is available to base a recommen
dation on dual versus triple therapy in this patient population.
Results from three small, observational studies reported a higher
bleeding rate with prasugrel and similar bleeding rates with ticagre
lor as part of triple therapy.
Limitations with the registries and sparse data with randomized
clinical trials have resulted in variability in professional association
guideline recommendations (Table 15-12).
European guidelines recommend focus on patients with AF and
recommend a radial approach and newer generation DES. DAPT
without oral anticoagulation may be used in patients with AF
and low risk of stroke (CHA
females). Either a DOAC or a VKA may be selected (Figure 15-4).
U.S. guidelines state:
Duration of triple therapy should be minimized.
Clopidogrel is preferred as the P2Y12 inhibitor.
Low-dose aspirin should be used as part of the triple
therapy regimen.
30,31
40
41
43-45
30,31,46-48
-Vasc score of 1 in males and 2 in
2DS2
42
40,41
47,48
-
-
-
ACUTE CORONARY SYNDROMES 381
https://t.me/med1917
Use of DOAC compared to VKA is not discussed.
PIONEER AF-PCI was released late in the publication
process of this book. For a short discussion of this trial,
see Appendix M.
TABLE 15-12: Triple Therapy
Guideline Triple Antithrombotic Therapy Recommendation
2014 ACC/AHA NSTE
31
ACS
2013 ACC/AHA STEMI
primary PCI
2014 ESC NSTE
ACS
30
46,47
(Section 5.4)
Minimize the duration of triple therapy (IC).
Use a lower intensity INR (2–2.5) (IIbC).
Add a proton pump inhibitor to minimize bleeding risk (IC for a
patient with prior GI bleeding, IIaC for all patients).
Minimize the duration of triple therapy (IC).
Use a lower intensity INR (2–2.5) (IIbC).
Avoidance of a DES (no recommendation grade).
In patients with low bleeding risk (HAS-BLED score ≤2) triple therapy
with either VKA or DOAC, clopidogrel and low-dose aspirin (75–100
mg/day) for up to 6 months, then oral anticoagulant plus single
antiplatelet therapy from 6 months to 1 year, then anticoagulant alone
after 1 year (IIaC).
In patients with high bleeding risk (HAS-BLED score ≥3) triple therapy
with either VKA or DOAC, clopidogrel and low-dose aspirin (75–100
mg/day) for 1 month, then oral anticoagulant plus single antiplatelet
therapy from 1 month to 1 year (regardless of stent type), then
anticoagulant alone after 1 year (IIaC).
Consider DAPT rather than triple therapy if high bleeding risk (HASBLED score ≥3) and low stent thrombosis risk (IIbB).
In a patient with AF taking chronic anticoagulation and having a low
CHA
2DS2
sinus rhythm with normal LV function), discontinue the DOAC and use
DAPT with low-dose aspirin and either prasugrel or ticagrelor (IIaC).
In a patient with AF on a DOAC, prefer radial access for coronary
angiography (section 5.4.1).
In a patient with AF requiring triple therapy, a DOAC may be used
in addition to aspirin and clopidogrel but use the lowest dose of the
DOAC tested in clinical trials of AF (dabigatran 110 mg bid, apixaban
2.5 mg bid, and rivaroxaban 15 daily).
Do not use prasugrel or ticagrelor as part of triple therapy with a
DOAC.
If DES, may use triple therapy (clopidogrel in regimen) for 1 month
then discontinue clopidogrel at 1 month, continue DT with aspirin
and oral anticoagulant from 1 month to 1 year, then anticoagulation
alone at 1 year.
Add a proton pump inhibitor for gastric protection.
Use radial access for PCI (IA).
For patients at low bleeding risk, new generation DES preferred over
BMS (IIaB).
For patients at high bleeding risk, individualize the choice of stent
type.
For medically managed patients (no PCI), consider 1 antiplatelet
agent plus oral anticoagulant for up to 1 year, then oral anticoagulant
alone (IIaC).
30,31,46-48
-Vasc score of 1 in males and 2 in females (especially in normal
30,31
(continued)
382 Anticoagulation Therapy
https://t.me/med1917
TABLE 15-12: (Continued)
Guideline Triple Antithrombotic Therapy Recommendation
2015 EHRA practical
guideline on the use
of DOACs in patients
48
with AF
Low-dose aspirin 75–100 mg/day as part of DT or triple therapy.
Clopidogrel rather than prasugrel or ticagrelor as part of triple
therapy.
Factors that shorten recommended durations of triple therapy:
Uncorrectable high bleeding risk (HAS-BLED score), low
atherothrombotic risk (ACS GRACE score <118).
Factors that may lengthen triple therapy:
high GRACE risk score ≥118, left main coronary artery stent, left
anterior descending artery stent, proximal bifurcating stent, recurrent
MI, AND low bleeding risk (HAS-BLED).
First-generation DES, ACS,
Scenario 1: AF patients already taking DOAC undergoing PCI
Discontinue DOAC at least 24 hr prior to elective PCI and at least 12
hr for NSTE ACS PCI if possible; restart same DOAC post-PCI at a
lower dose (dabigatran 110 mg bid, apixaban 2.5 mg bid, rivaroxaban
15 mg daily, edoxaban 30 mg daily) with at least one antiplatelet
agent; consider proton pump inhibitor for gastric protection.
Elective PCI:
DES, DOAC plus clopidogrel from 1 month to 1 year, then DOAC
alone.
ACS:
followed by DT with NOAC plus either clopidogrel or low-dose
aspirin.
1 month triple therapy for a BMS or newer generation
6 months triple therapy unless high bleeding risk then 1 month;
Scenario 2: Recent (<1 year ACS) who develops AF requiring
anticoagulation
Follow above recommendation depending on month’s post-ACS.
Scenario 3: ACS ≥1 year ago (stable CVD) who develops AF requiring
anticoagulation
Follow above recommendation for DOAC alone (i.e., discontinue all
antiplatelet agents).
ACC/AHA: American College of Cardiology/American Heart Association, ACS: acute coronary
syndrome, CABG: coronary artery bypass graft, CrCl: creatinine clearance, CVD: cardiovascular
disease, DAPT: dual antiplatelet therapy, DOAC: direct-acting oral anticoagulants, EHRA:
European Heart Rhythm Association, ESC: European Society of Cardiology, FDA: U.S. Food and
Drug Administration, NSTE: non-ST-segment elevation, PCI: percutaneous coronary intervention,
STEMI: ST-segment elevation myocardial infarction
ACUTE CORONARY SYNDROMES 383
https://t.me/med1917
*European guidelines suggest lower dose DOAC (apixaban 2.5 mg PO bid, dabigatran
110 mg PO bid, rivaroxaban 15 mg PO daily, edoxaban 30 mg PO daily);
81 mg PO daily, PCI = percutaneous coronary intervention; DES = drug-eluting stent; BMS
= bare metal stent; VKA = vitamin K antagonist; DOAC = direct-acting oral anticoagulant;
DAPT = dual antiplatelet therapy
b
low-dose aspirin
FIGURE 15-4. Triple Antithrombotic Therapy in Patients
Undergoing PCI
Source: Adapted with permission from Heidbuchel H, Verhamme P, Alings M, et al.
Updated European Heart Rhythm Association Practical Guide on the use of non-vitamin
K antagonist anticoagulants in patients with non-valvular atrial fibrillation. Europace.
2015;17(10):1467-1507.
46,47
Controversy: Duration of Dual Antiplatelet Therapy
(DAPT) for Patients with Second- and Third-Generation
Drug-Eluting Stents
•
The duration of DAPT with aspirin and a P2Y12 inhibitor following PCI with a
DES is evolving.
•
Stent platforms of newer generation DES are becoming less thrombogenic than
older DES (
TABLE 15-13: Drug-Eluting Stent Types
• First-generation (older generation): paclitaxel, sirolimus
• Second-generation: zotarolimus, everolimus
• Third-generation: biodegradable polymer (e.g., biolimus)
• Fourth-generation: bioresorbable (e.g., everolimus)
Table 15-13).
•
First-generation DES were clearly associated with a four- to five-fold increased
risk of stent thrombosis, necessitating DAPT for at least 1 year after placement.
•
More recent trials with newer generation DES have suggested similar major
adverse cardiac event rates and bleeding with 6 months, compared to 9 months
of DAPT where patients were randomized to discontinue clopidogrel at 6 months
as well as at 24 months in another trial where clopidogrel or prasugrel were
discontinued at 6 months.
49
50,51
384 Anticoagulation Therapy
https://t.me/med1917
In the recent DAPT study where the majority, but not all patients, received a
newer generation DES:
Rates of stent thrombosis (0.4% vs. 1.4%) and major cardiovascular
and cerebrovascular (4.3% vs. 5.9%) events at 24 months post-PCI
were reduced.
Moderate or severe bleeding increased when DAPT with clopidogrel
or prasugrel was continued beyond 12 months (2.5% vs. 1.6%).
•
When a duration of <12 months versus ≥12 months are compared, there is no
difference in major adverse cardiac events and an increased risk of bleeding.
•
There is no difference in CV, noncardiovascular, and total mortality with a duration
of longer than 6 months compared to a shorter duration.
•
In higher-risk patients with a history of MI at the time of PCI, DAPT for a median
of 33 months decreased ischemia events but increased major but not fatal bleeding. There was no difference in CV mortality.
•
On November 6, 2015, the U.S. Food and Drug Administration (FDA) issued
a drug safety communication stating that it had conducted a meta-analysis of
available data and found that ≥12 months of DAPT does not increase or decrease
mortality compared to less than 12 months of therapy.
•
As of April 2018, the most contemporary practice guidelines incorporating this
recent data are the European Society of Cardiology guidelines for patients with
NSTE ACS.
47
Ideally, all patients, whether PCI or medically managed, should
continue DAPT for at least 12 months (IA recommendation). Newer
generation DES is recommended over BMS for PCI (IA recommendation) unless bleeding risk is increased and then a newer generation
BMS is recommended with 30-day duration of DAPT (IIbB recommendation). For patients with NSTE ACS and a DES who develop
bleeding or an increased bleed risk, a shorter course of DAPT 3–6
months is recommended.
49
52,53
54
55
56
• Patients with stable CAD receiving newer
generation DES likely derive little benefit from
extended duration of DAPT beyond 6 months.
• Whereas in patients with ACS, the decision on
duration of DAPT should be individualized,
evaluating patient characteristics for recurrent
stent thrombosis or major adverse cardiac events
but is likely >12 months.
• A DAPT risk score has been developed to identify
patients at low risk of ischemic CV and major
bleeding events likely to derive little benefit from
continuing DAPT beyond 12 months.
57,58
If
validated in other studies, this risk score would
be a valuable clinical tool to determine a plan for
DAPT duration.
ACUTE CORONARY SYNDROMES 385
https://t.me/med1917
Step-Down Therapy of P2Y12 Inhibitors Following
Myocardial Infarction: Ticagrelor for Secondary
Prevention
•
Ticagrelor added to low-dose aspirin is now FDA-approved in a reduced dose
of 90 mg PO bid to reduce the risk of cardiovascular death, MI, or stroke for
patients who are at least 1 year post-MI without a history of prior stroke.
•
In PEGASUS TIMI-54 patients who were 1–3 years post-MI (median time 1.7
years) to either ticagrelor 90 mg PO bid or 180 mg PO bid and placebo found.
Both ticagrelor groups significantly reduced ischemic risk by about
59
15%.
Increased TIMI major bleeding (but not fatal or intracranial hemor-
rhage) more than two-fold.
No mortality benefit observed in ticagrelor-treated patients
compared to placebo.
Controversy: Bivalirudin Efficacy and Safety Compared to
Unfractionated Heparin for PCI
•
There have been conflicting data regarding the comparative efficacy and safety
of bivalirudin and UFH (with or without a glycoprotein IIb/IIIa inhibitor) in ACS
and PCI clinical trials.
major bleeding but increases the frequency of stent thrombosis with similar net
clinical benefit.
•
There has been no substantive biological plausibility as to why bivalirudin has
been found to reduce mortality in some trials but not others.
•
Until additional data are available, either anticoagulant is an acceptable choice
(as per ACC/AHA practice guidelines) and practitioners should review utilization
and patient in-hospital bleeding risk and rates.
60-64
In general, the results suggest that bivalirudin reduces
62
65
30,31
CURRENT DOAC DATA FOR SECONDARY ACS
PREVENTION
•
Rivaroxaban and apixaban added to aspirin and clopidogrel have been studied
in secondary prevention following ACS.
In ATLAS ACS2 TIMI 51, rivaroxaban 2.5 mg twice daily and 5 mg
Both doses of rivaroxaban reduced the primary composite endpoint
Patients enrolled in COMPASS did not have ACS and did not have
Most patients discontinued clopidogrel at 12 months per practice
66
twice daily started were compared to placebo in 15,526 patients
with ACS.
of cardiovascular death, MI, or stroke as well as stent thrombosis
compared to placebo.
a current indication for DAPT.
standards, and much of the benefit was seen during dual therapy
of rivaroxaban and aspirin alone.
386 Anticoagulation Therapy
https://t.me/med1917
The lower dose of 2.5 mg twice daily also reduced the rate of
cardiovascular death.
Frequency of non-CABG major bleeding was significantly increased
with both doses of rivaroxaban (1.8% and 2.4%) compared to
placebo (0.6%) as was the frequency of intracranial hemorrhage
(0.4% and 0.7% compared to 0.2%).
Rivaroxaban has failed to achieve FDA approval for this indication.
•
APPRAISE-2 was a trial of patients on apixaban 5 mg twice daily or placebo
for ACS.
67
Trial was terminated due to increased risk of TIMI major bleeding
with apixaban (2.4% vs. 0.9%) as well as increased intracranial
hemorrhage (0.6% vs. 0.2%).
Rivaroxaban with and without aspirin was more effective than aspirin alone
for secondary cardiovascular prevention in patients with stable cardiovascular
disease in the COMPASS trial.
•
27,395 patients were randomized to rivaroxaban (2.5 mg twice daily) plus aspirin
(100 mg once daily), rivaroxaban (5 mg twice daily), or aspirin (100 mg once
daily). To be eligible for the trial, patients had to have history of coronary artery
disease, peripheral arterial disease, or both.
•
The group assigned to combined rivaroxaban and aspirin had a lower incidence
of the primary outcome (composite of cardiovascular death, stroke, or myocardial
infarction) than those assigned to aspirin alone. It also lowered all-cause mortal
ity. However, the benefit came at the cost of more major bleeding, including
increased ICH, but not fatal bleeding.
•
Rivaroxaban alone did not reduce the primary endpoint when compared to
aspirin alone, but did lead to more major bleeding.
68
-
REFERENCES AND KEY ARTICLES*
1. Mozaffarian D, Benjamin EJ, Go AS, et al. Heart disease and stroke statistics—20169
update: a report from the American Heart Association Statistics Committee and Stroke
Statistics Subcommittee. Circulation. 2015 Dec 16 (Epub ahead of print).
2. Rich JD, Cannon CP, Murphy SA, et al. Prior aspirin use and outcomes in acute
coronary syndromes. J Am Coll Cardiol. 2010;56:1376-1385.
3. Thygesen K, Alpert JS, White HD, et al. Third universal definition of myocardial
infarction. Circulation. 2012;126:2020-2035.
*4. Antman EM, Cohen M, Bernink PJ, et al. The TIMI risk score for unstable angina/non-
ST elevation MI: A method for prognostication and therapeutic decision making. JAMA.
2000;284:835-842.
5. TIMI Risk Score for UA/NSTEMI. Available at: http://www.mdcalc.com/timi-riskscore-for-uanstemi/. Accessed October 21, 2015.
6. Simms AD, Reynolds S, Pieper K, et al. Evaluation of the NICE mini-GRACE risk
scores for acute myocardial infarction using the Myocardial Ischaemia National Audit
Project (MINAP) 2003–2009: National Institute for Cardiovascular Outcomes Research
(NICOR). Heart. 2013;99:35-40.
ACUTE CORONARY SYNDROMES 387
https://t.me/med1917
7. Pieper KS, Gore JM, Fitzgerald G, et al. Validity of a risk-prediction tool for hospital
mortality: the Global Registry of Acute Coronary Events. Am Heart J. 2009;157:1097-
1105.
GRACE 2.0 Risk Calculator. Available at: http://gracescore.org/WebSite/default.
8.
aspx?ReturnUrl=%2f. Accessed October 21, 2015.
9. Mehran R, Rao SV, Bhatt DL, et al. Standardized bleeding definitions for cardiovascular
clinical trials: a consensus report from the Bleeding Academic Research Consortium.
Circulation. 2011;123(23):2736-2747.
Granger CB, Hirsch J, Califf RM, et al. Activated partial thromboplastin time and
10.
outcome after thrombolytic therapy for acute myocardial infarction: results from the
GUSTO-I trial. Circulation.1996;93:870-878.
11.
Gilchrist IC, Berkowitz SD, Thompson TD, et al. Heparin dosing and outcome in acute
coronary syndromes: the GUSTO-IIb experience. Global use of strategies to open
occluded coronary arteries. Am Heart J. 2002;144:73-80.
Nallamothu BK, Bates ER, Hochman JS, et al. Prognostic implication of activated
12.
partial thromboplastin time after reteplase or half-dose reteplase plus abciximab:
results from the GUSTO-V trial. Eur Heart J. 2005;26:1506-1512.
13.
Cheng S, Morrow DA, Sloan S, et al. Predictors of initial nontherapeutic anticoagulation
with unfractionated heparin in ST-segment elevation myocardial infarction.
Circulation. 2009;119:1195-1202.
Anand SS, Yusuf S, Pogue J, et al. Relationship of activated partial thromboplastin time
14.
to coronary events and bleeding in patients with acute coronary syndromes who receive
heparin. Circulation. 2003;107:2884-2888.
15.
Newby LK, Harrington RA, Bhapkar MV, et al. An automated strategy for bedside
aPTT determination and unfractionated heparin infusion adjustment in acute coronary
syndromes: insights from PARAGON A. J Thromb Thrombolysis. 2002;14:33-42.
Becker RC, Cannon CP, Tracy RP, et al. Relation between systemic anticoagulation as
16.
determined by activated partial thromboplastin time and heparin measurements and
in-hospital clinical events in unstable angina and non-Q wave myocardial infarction.
Thrombolysis in Myocardial Ischemia III B Investigators. Am Heart J. 1996;131:421-
433.
17. Thomas MP, Mahaffey KW, Chiswell K, et al. Activated partial thromboplastin time
measurement is not associated with clinical outcomes in patients with high-risk nonST-segment elevation acute coronary syndromes treated with unfractionated heparin. J
Thromb Thrombolysis. 2012;34(1):114-119.
*18. Garcia DA, Baglin TP, Weitz JI, et al. Parenteral anticoagulants: Antithrombotic
Therapy and Prevention of Thrombosis. 9th ed. American College of Chest Physicians
Evidence-based Clinical Practice Guidelines (8th ed.). Chest. 2012;141(suppl 2):e24Se43S.
19. Olson JD, Arkin CF, Brandt JT, et al. College of American Pathologists Conference
XXI on laboratory monitoring of anticoagulant therapy: laboratory monitoring of
unfractionated heparin therapy. Arch Pathol Lab Med. 1998;122(9):782-798.
20. Harrington RA, Becker RC, Cannon CP, et al. Antithrombotic therapy for non-STsegment elevation acute coronary syndromes: Antithrombotic Therapy and Prevention
of Thrombosis. 9th ed. American College of Chest Physicians Evidence-based Clinical
Practice Guidelines. Chest. 2008;133(suppl 6):670S-707S.
388 Anticoagulation Therapy
https://t.me/med1917
21. TIMI 11A Investigators. Dose-ranging trial of enoxaparin for unstable angina: results of
TIMI 11A. The Thrombolysis in Myocardial Infarction (TIMI) 11A Trial Investigators. J
Am Coll Cardiol. 1997;29:1474-1482.
Montalescot G, Cohen M, Salette G, et al. Impact of anticoagulation levels on outcomes
22.
in patients undergoing elective percutaneous coronary intervention: insights from the
STEEPLE trial. Eur Heart J. 2008;29:462-471.
Montalescot G, Collet JP, Tanguy A, et al. Anti-Xa activity related to survival and
23.
efficacy in unselected acute coronary syndrome patients treated with enoxaparin.
Circulation. 2004;110:392-398.
*24.
Subherwal S, Bach RG, Chen AY, et al. Baseline risk of major bleeding in non-ST-
segment-elevation myocardial infarction: the CRUSADE (Can Rapid risk stratification
of Unstable angina patients Suppress ADverse outcomes with Early implementation of
the ACC/AHA Guidelines) Bleeding Score. Circulation. 2009;119(14):1873-1882.
Mathews R, Peterson ED, Chen AY, et al. In-hospital major bleeding during ST-
25.
elevation and non-ST-elevation myocardial infarction care: derivation and validation
of a model from the ACTION Registry
®
-GWTG™. Am J Cardiol. 2011;107(8):1136-
1143.
26. Flores-Rios X, Couto-Mallon D, Rodriuez-Garrido J, et al. Comparison of the
performance of the CRUSADE, ACUITY-HORIZONS, and ACTION bleeding risk score
in STEMI undergoing primary PCI: insights from a cohort of 1391 patients. Eur Heart
J Acute Cardiovasc Care. 2012;2(2):19-26.
27. Routledge H, Sastry S. Radial versus fmoral access for acute coronary syndromes. Curr
Cardiol Rep. 2015;17:117.
28. Valgimigli M, Gagnor A, Calabo P, et al. Radial versus femoral access in patients with
acute coronary syndromes undergoing invasive management: a randomized multicenter
trial. Lancet. 2015;385(9986):2465-2476.
29.
CRUSADE Bleeding Score Calculator. Available at: http://www.crusadebleedingscore.
org/. Accessed October 22, 2015.
O’Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the
*30.
management of ST-elevation myocardial infarction: a report of the American College of
Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J
Am Coll Cardiol. 2013;61(4):e78-e140.
*31. Amsterdam EA, Wenger NK, Brindis RG, et al. 2014 AHA/ACC Guideline for the
Management of Patients with Non-ST-Elevation Acute Coronary Syndromes: a report
of the American College of Cardiology/American Heart Association Task Force on
Practice Guidelines. J Am Coll Cardiol. 2014;64(24):e139-e228.
32. Smith SC Jr, Feldman TE, Hirshfeld JW Jr, et al. ACC/AHA/SCAI 2005 guideline update
for percutaneous coronary intervention: a report of the American College of Cardiology/
American Heart Association Task Force on Practice Guidelines (ACC/AHA/SCAI Writing
Committee to Update the 2001 Guidelines for Percutaneous Coronary Intervention). J
Am Coll Cardiol. 2006;47(1):e1-e121.
33. Gallo R, Steinhubl SR, White HD, et al. Impact of anticoagulation regimens on sheath
management and bleeding in patients undergoing elective percutaneous coronary
intervention in the STEEPLE trial. Catheter Cardiovasc Interv. 2009;73:319-325.
34. Cantor WJ, Mahaffey KW, Huang Z, et al. Bleeding complications in patients with acute
coronary syndrome undergoing early invasive management can be reduced with radial
ACUTE CORONARY SYNDROMES 389
https://t.me/med1917
access, smaller sheath sizes, and timely sheath removal. Catheter Cardiovasc Interv.
2007;69:73-83.
35. Angiomax (bivalirudin) for injection. Removal of the femoral artery catheter. Available
at: http://www.angiomax.com/Catheter/Default.aspx. Accessed October 20, 2009.
36. Bonaca MP, Bhatt DL, Cohen M, Long-term use of ticagrelor in patient with prior
myocardial infarction. N Engl J Med. 2015;372:1791-1800.
37. Giugliano RP, White JA, Bode C. Early versus delayed, provisional eptifibatide in acute
coronary syndromes. N Engl J Med. 2009;360:2176–2190.
Hansen ML, Sorensen R, Clausen MT, et al. Risk of bleeding with single, dual, or triple
38.
therapy with warfarin, aspirin, and clopidogrel in patients with atrial fibrillation. Arch
Intern Med. 2010;170(16):1433-1441.
39.
Lamberts M, Gislason GH, Oleson JB, et al. Oral anticoagulation and antiplatelets in
atrial fibrillation patients after myocardial infarction and coronary intervention. J Am
Coll Cardiol. 2013;62(11):981-989.
Dewilde WJ, Oirbans T, Verheugt FW, et al. Use of clopidogrel with or without
40.
aspirin in patients taking oral anticoagulant therapy and undergoing percutaneous
coronary intervention: an open-label, randomised, controlled trial. Lancet. 2013;
381(9872):1107-1115.
41. Fiedler KA, Maeng M, Mehilli J, et al. Duration of triple therapy in patients requiring
oral anticoagulation after drug-eluting stent implantation: The ISAR-TRIPLE Trial. J
Am Coll Cardiol. 2015;65(16):1619-1625.
42.
D’Ascenzo F, Taha S, Moretti C, et al. Meta-analysis of randomized controlled trials
and adjusted observational results of use of clopidogrel, aspirin, and oral anticoagulants
in patients undergoing percutaneous coronary intervention. Am J Cardiol.
2015;115(9):1185-1193.
43. Sarafoff N, Martischnig A, Wealer J, et al. Triple therapy with aspirin, prasugrel,
and vitamin K antagonists in patients with drug-eluting stent implantation and an
indication for oral anticoagulation. J Am Coll Cardiol. 2013;61:2060-2066.
44. Braun OÖ, Bico B, Chaudhry U, et al. Concomitant use of warfarin and ticagrelor as an
alternative to triple antithrombotic therapy after an acute coronary syndrome. Thromb
Res. 2015;135(1):26-30.
45. Fu A, Singh K, Abunassar J, et al. Ticagrelor in triple antithrombotic therapy: predictors
of ischemic and bleeding complications. Clin Cardiol. 2016;39:19-23.
46. Collet JP, Roffi M, Mueller C, et al. Questions and answers on antithrombotic therapy:
a companion document of the 2015 ESC Guidelines for the management of acute
coronary syndromes in patients presenting without persistent ST-segment elevation.
Eur Heart J. 2016;37:e1-e7.
*47. Roffi M, Patrono C, Collet JP, et al. 2015 ESC Guidelines for the management of acute
coronary syndromes in patients presenting without persistent ST-segment elevation:
Task Force for the Management of Acute Coronary Syndromes in Patients Presenting
without Persistent ST-Segment Elevation of the European Society of Cardiology (ESC).
Eur Heart J. 2016;37(3):267-315.
*48. Heidbuchel H, Verhamme P, Alings M, et al. Updated European Heart Rhythm
Association Practical Guide on the use of non-vitamin K antagonist anticoagulants in
patients with non-valvular atrial fibrillation. Europace. 2015;17(10):1467-1507.
Соседние файлы в папке Библиотека им академика М.И. Перельмана