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Acute coronary syndrome(STEMI GUIDELINES AND RECENT ADVANCES)
1. FUTURE STRATEGIES AND 2013
ACCF/AHA GUIDELINES FOR
THE MANAGEMENT OF STEMI
PRESENTER: DR ADITYA
MODERATOR: (PROF) DR. ANITA SHARMA
2. EPIDEMIOLOGY
• In 2009, nearly 683,000 patients were discharged
from U.S. hospitals with a diagnosis of ACS.
• Incidence rates for STEMI have declined over the
past decade, whereas those for non–ST-elevation
ACS have increased.
• At present, STEMI comprises approximately 25%
to 40% of MI presentations.
6. (Adapted from CW Hamm et al: Lancet 358:1533, 2001, an MJ Davies: Heart
83:361, 2000)
7. STEMI
• Diagnostic ST elevation in the absence of left
ventricular (LV) hypertrophy or left bundle-branch
block (LBBB) is defined by the ESC/ACCF/AHA for
the Universal Definition of MI as:
new ST elevation at the J point in at least 2 contiguous
leads of 2 mm (0.2 mV) in men or 1.5 mm (0.15 mV) in
women in leads V2–V3 and/or of 1 mm (0.1 mV) in other
contiguous chest leads or the limb leads.
8. • The majority of patients will evolve ECG evidence
of Q-wave infarction.
• New LBBB at presentation interfere with ST-
elevation analysis, and not a diagnostic criteria of
AMI in isolation.
11. REGIONAL SYSTEMS OF STEMI CARE,
REPERFUSION THERAPY, AND TIME-TO-
TREATMENT GOALS
All communities should create and maintain a
regional system of STEMI care.
I IIa IIb III
Performance of a 12-lead ECG by EMS
personnel at the site of FMC is recommended
in patients with symptoms consistent with
STEMI.
I IIa IIb III
12. Reperfusion therapy should be administered to
all eligible patients with STEMI with symptom
onset within the prior 12 hours.
Primary PCI is the recommended method of
reperfusion when it can be performed in a
timely fashion by experienced operators.
I IIa IIb III
EMS transport directly to a PCI-capable
hospital for primary PCI is the recommended
triage strategy for patients with STEMI with an
ideal FMC-to-device time system goal of 90
minutes or less.*
I IIa IIb III
I IIa IIb III
13. Immediate transfer to a PCI-capable hospital
for primary PCI is the recommended triage
strategy for patients with STEMI who initially
arrive at or are transported to a non–PCI-
capable hospital, with an FMC-to-device time
system goal of 120 minutes or less.
In the absence of contraindications, fibrinolytic
therapy should be administered to patients
with STEMI at non–PCI-capable hospitals when
the anticipated FMC-to-device time at a PCI-
capable hospital exceeds 120 minutes.
I IIa IIb III
I IIa IIb III
14. When fibrinolytic therapy is indicated or
chosen as the primary reperfusion strategy, it
should be administered within 30 minutes of
hospital arrival.
Reperfusion therapy is reasonable for patients
with STEMI and symptom onset within the
prior 12 to 24 hours who have clinical and/or
ECG evidence of ongoing ischemia.
I IIa IIb III
I IIa IIb III
18. I IIa IIb III
Primary PCI should be performed in patients
with STEMI and ischemic symptoms of less
than 12 hours’ duration.
Who have contraindications to fibrinolytic
therapy, irrespective of the time delay from
FMC.
I IIa IIb III
19. I IIa IIb III Primary PCI should be performed in patients
with STEMI and cardiogenic shock or acute
severe HF, irrespective of time delay from MI
onset.
20. Primary PCI is reasonable in patients with
STEMI if there is clinical and/or ECG evidence
of ongoing ischemia between 12 and 24 hours
after symptom onset.
I IIa IIb III
PCI should not be performed in a non-infarct
artery at the time of primary PCI in patients
with STEMI who are hemodynamically stable
I IIa IIb III
Harm
22. REPERFUSION AT A PCI-
CAPABLE HOSPITAL
2) ASPIRATION THROMBECTOMY
AND RECENT ADVANCES
23. ASPIRATION THROMBECTOMY
Current ACCF/AHA guidelines recommend routine
thrombus aspiration before primary PCI in STEMI
(Class IIa) based on the available evidence
supporting this therapy.
I IIa IIb III
24. • The TASTE trial enrolled 7244 patients with STEMI
randomized them to routine thrombus aspiration
or no thrombus aspiration before primary PCI*.
• There were no differences in all cause mortality at
the end of 30 days (2.8% vs. 3.0%; P = 0.63).
• There was a trend towards a reduction in
hospitalizations for recurrent myocardial infarction
and incidence of stent thrombosis.
* Fröbert O, Lagerqvist B, Olivecrona GK et al: Thrombus aspiration during ST-segment
elevation myocardial infarction. N Engl J Med 2013, 369:1587-97
25. REPERFUSION AT A PCI-
CAPABLE HOSPITAL
3) USE OF STENTS IN PATIENTS WITH STEMI
AND RECENT ADVANCES
26. Placement of a stent (BMS or DES) is useful in
primary PCI for patients with STEMI.
I IIa IIb III
BMS* should be used in patients with high
bleeding risk, inability to comply with 1 year of
DAPT, or anticipated invasive or surgical
procedures in the next year.
I IIa IIb III
27. DES should not be used in primary PCI for
patients with STEMI who are unable to
tolerate or comply with a prolonged course
of DAPT because of the increased risk of
stent thrombosis with premature
discontinuation of one or both agents.
I IIa IIb III
Harm
28. • There has been debate regarding the use of drug
eluting stents (DES) in patients with STEMI.
• While DES have been shown to have superior
efficacy as compared to bare metal stents (BMS),
there have been concerns regarding safety with
DES due to incomplete endothelialization and
inflammation eventually leading to a potentially
higher risk of stent thrombosis.
29. • Second generation EVEROLIMUS ELUTING
XIENCE V stents were associated with a lower
incidence of stent thrombosis, target vessel
revascularization and major adverse cardiac
events as compared to BMS and older
SIROLIMUS ELUTING STENTS after PCI in
patients with acute myocardial infarction.
[Sabate M, Cequier A, Iñiguez A, Serra A et al:Everolimus-eluting stent versus bare-
metal stent in ST-segment elevation myocardia infarction (EXAMINATION): 1 year results
of a randomise controlled trial. Lancet 2012, 380:1482-90]
30. • Newer second generation ZOTAROLIMUS eluting
resolute stents are also undergoing trials. [A,B]
A)Park KW, Lee JM, Kang S, et al: Safety and efficacy of second-generation everolimus-
eluting Xience V stents versus zotarolimus-eluting resolute stents in real-world practice:
patient-related and stent-related outcomes from the multicenter prospective EXCELLENT
and RESOLUTE-Korea registries. J Am Coll Cardiol 2013, 61:536-44
B) Birgelen C von, Basalus MWZ, Tandjung Ket al: Arandomized controlled trial in second-
generation zotarolimus eluting Resolute stents versus everolimus-eluting Xience V stents
in real-world patients: theTWENTE trial. J Am Coll Cardiol 2012, 59:1350-61
31. • DES with biodegradable polymers have also
emerged and were compared with BMS in 1,161
patients with AMI in the COMFORTABLE trial.
• The primary endpoint (composite of cardiac
death, target vessel re-infarction and ischemia
driven target lesion revascularization) was lower in
the biolimus stent, driven mostly by a substantial
reduction of 80% in the incidence of target vessel
reinfarction.
• There is a trend towards a lower rate of stent
thrombosis in patients with biolimus DES.
Räber L, Kelbæk H, Ostojic M et al: Effect of biolimus-eluting stents with biodegradable polymer
vs baremetal stents on cardiovascular events among patients with acute myocardial infarction:
the COMFORTABLE AMI randomized trial. JAMA 2012, 308:777-87
32. REPERFUSION AT A PCI-
CAPABLE HOSPITAL
4) ANTIPLATELET THERAPY TO SUPPORT
PRIMARY PCI FOR STEMI AND RECENT
ADVANCES
33. Aspirin 162 to 325 mg should be given before
primary PCI.
After PCI, aspirin should be continued
indefinitely.
I IIa IIb III
I IIa IIb III
34. A loading dose of a P2Y12 receptor inhibitor
should be given as early as possible or at time
of primary PCI to patients with STEMI:
• Clopidogrel 600 mg; or
I IIa IIb III
• Prasugrel 60 mg; or
• Ticagrelor 180 mg
35. P2Y12 inhibitor therapy should be given
for 1 year to patients with STEMI who
receive a stent (BMS or DES) during
primary PCI using the following
maintenance doses:
• Clopidogrel 75 mg daily; or
I IIa IIb III
• Prasugrel 10 mg daily; or
• Ticagrelor 90 mg twice a day*
*The recommended maintenance dose of aspirin to
be used with ticagrelor is 81 mg daily.
36. It is reasonable to use 81 mg of aspirin per day
in preference to higher maintenance doses
after primary PCI.
I IIa IIb III
37. It is reasonable to start treatment with an intravenous GP
IIb/IIIa receptor antagonist at the time of primary PCI
(with or without stenting or clopidogrel pretreatment) in
selected patients with STEMI who are receiving UFH.
• Double-bolus EPTIFIBATIDE: 180 mcg/kg IV bolus,
then 2 mcg/kg/min; a 2nd 180-mcg/kg bolus is
administered 10 min after the 1st bolus.
• ABCIXIMAB: 0.25 mg/kg IV bolus, then 0.125
mcg/kg/min (maximum 10 mcg/min); or
• High-bolus-dose TIROFIBAN: 25 mcg/kg IV bolus,
then 0.15 mcg/kg/min; or
I IIaIIb III
I IIaIIb III
I IIaIIb III
38. It may be reasonable to administer
intravenous GP IIb/IIIa receptor antagonist in
the precatheterization laboratory setting to
patients with STEMI for whom primary PCI is
intended.
It may be reasonable to administer
intracoronary abciximab to patients with
STEMI undergoing primary PCI.
I IIa IIb III
I IIa IIb III
Continuation of a P2Y12 inhibitor beyond 1
year may be considered in patients
undergoing DES placement.
I IIa IIb III
39. Prasugrel should not be administered to
patients with a history of prior stroke or
transient ischemic attack.
I IIa IIb III
Harm
40. PRASUGREL
• It was compared to clopidogrel in a randomized trial
(TRITON–TIMI 38) for ACS patients who were
scheduled to undergo PCI.
• Based on the promising results from this trial
(superior efficacy, albeit with a higher bleeding risk),
the agent was approved for patients with ACS
scheduled to undergo PCI.
41.
42. • A large proportion of patients with NSTEMI/ UA
grouped under NSTE-ACS were however managed
medically and didn’t receive early
revascularization.(TRILOGY ACS trial).
• This study randomized 9,326 patients with NSTE–
ACS to receive either prasugrel or clopidogrel. At a
median follow up of 1.7 years, the results were
neutral with similar efficacy and comparable
bleeding risk with both agents.
Roe MT, Armstrong PW, Fox KAA, White HD et al Prasugrel versus clopidogrel for
acute coronary syndromes without revascularization. N Engl J Med 2012, 367:1297-309
43. TICAGRELOR
• Reversible P2Y12 receptor blocker that provides a
rapid, consistent and more effective antiplatelet
effect than clopidogrel.
• It was initially compared with clopidogrel in
patients with ACS in the PLATO trial, results of
which demonstrated improved efficacy outcomes
(including reduced mortality) with similar rates of
major bleeding.
Wallentin L, Becker RC, Budaj A,et al: Ticagrelor versus clopidogrel in patients with
acute coronary syndromes. N Engl J Med 2009, 361:1045-57
44. • Pre-specified subgroup analysis from the PLATO trial
in medically managed patients with ACS
demonstrated similar results to the overall cohort
with a reduction in mortality (6.1% vs. 8.2%; P =
0.01) and a slightly higher incidence of major
bleeding (11.9% vs. 10.3%; P = 0.08) using ticagrelor
compared to clopidogrel.
James SK, Storey RF, Khurmi Nset al: Ticagrelor versus clopidogrel in patients with acute
coronary syndromes and a history of stroke or transient ischemic attack. Circulation 2012,
125:2914-21.
45. VORAPAXAR
• Vorapaxar is a oral PAR-1 antagonist that inhibits
thrombin induced platelet activation,
• a mechanism that is entirely different from those of
other available antiplatelet agents.
• Vorapaxar was tested as an adjunctive agent in
patients with NSTE–ACS in the TRACER trial.
Leonardi S, Tricoci P,White HD, Armstrong PW et al: Effect of vorapaxar on myocardial
infarction in the thrombin receptor antagonist for clinical event reduction in acute
coronary syndrome (TRA·CER) trial. Eur Heart J 2013, 34:1723-31
46. • This study randomized 12,944 patients with NSTE–
ACS to receive vorapaxar or placebo along with
routine therapy.
• Over a median follow up period of over 500 days,
there was no significant reduction in primary
endpoint (death, myocardial infarction and stroke)
but there was a substantial increase in major
bleeding events (7.2%vs. 5.2%; P<0.001) and
intracranial hemorrhage (1.1% vs. 0.2%; P<0.001)
with vorapaxar when compared to placebo
47. ABCIXIMAB
• Intravenous glycoprotein (GpIIb/IIIa) inhibitors.
• A meta-analysis on upstream abciximab (a GpIIb/IIIa
inhibitor) use in patients with NSTE–ACS (n = 46,374
patients) revealed only minor improvements in
outcomes at the risk of increased bleeding .
• Current guidelines recommend use of this agent only
in high-risk patients who have a high thrombus
burden in primary PCI.
Tricoci P, Newby LK, Hasselblad V, et al: Upstreamuse of small-molecule glycoprotein iib/ iiia
inhibitors in patients with non-ST-segment elevation acute coronary syndromes: a systematic
overview of randomized clinical trials. Circ Cardiovasc Qual Outcomes 2011, 4:448-58.
48. • Even in patients with STEMI, there is a great deal of
uncertainty about the preferred route of abciximab
administration (intracoronary vs. intravenous).
• The AIDA STEMI randomized trial compared the two
routes of abciximab in 2,065 patients presenting
within 12 hours of STEMI.
• Intracoronary and intravenous abciximab resulted in
a similar rate of the primary combined endpoint of
death, reinfarction, or congestive heart failure at 90
days of follow up.
Thiele H, Wöhrle J, Hambrecht R, et al: Intracoronary versus intravenous bolus abciximab
during primary percutaneous coronary intervention in patients with acute ST-elevation
myocardial infarction: a randomised trial. Lancet 2012, 379:923-31
49. • Statistically fewer patients in the intracoronary
group had new congestive heart failure (2·4% vs.
4·1%; P = 0·04).
• The results confirmed that, although
intracoronary abciximab resulted in a significant
improvement in myocardial perfusion without any
excess of major bleeding, there was no clear
mortality benefit with this strategy.
Kubica J, Koziński M, Navarese EP, et al: Updated evidence on intracoronary abciximab in ST-
elevation myocardial infarction: a systematic review and meta-analysis of randomized
clinical trials. Cardiol J 2012, 19:230-42
50. REPERFUSION AT A PCI-
CAPABLE HOSPITAL
5) ANTICOAGULANT THERAPY TO SUPPORT
PRIMARY PCI AND RECENT ADVANCES
51. For patients with STEMI undergoing primary PCI, the
following supportive anticoagulant regimens are
recommended:
• UFH, with additional boluses administered
as needed to maintain therapeutic
activated clotting time levels,
• Bivalirudin with or without prior
treatment with UFH.
I IIa IIb III
I IIa IIb III
52. It is reasonable to use bivalirudin
monotherapy in preference to the
combination of UFH and a GP IIb/IIIa receptor
antagonist.
Fondaparinux should not be used as the sole
anticoagulant to support primary PCI because
of the risk of catheter thrombosis.
I IIa IIb III
I IIa IIb III
Harm
53. ADJUNCTIVE ANTITHROMBOTIC
THERAPY TO SUPPORT
REPERFUSION WITH PRIMARY PCI
*The recommended maintenance dose of aspirin to be used with ticagrelor is 81 mg daily.
54. ADJUNCTIVE ANTITHROMBOTIC THERAPY TO
SUPPORT REPERFUSION WITH PRIMARY PCI
(CONT.)
*The recommended maintenance dose of aspirin to be used with ticagrelor is 81 mg daily.
†Balloon angioplasty without stent placement may be used in selected patients. It might be reasonable to provide P2Y12
inhibitor therapy to patients with STEMI undergoing balloon angioplasty alone according to the recommendations listed for
BMS. (LOE: C).
57. UNFRACTIONATED HEPARIN VS.
BIVALIRUDIN
• Previously published results from randomized
trials (HORIZONS– AMI in STEMI) have consistently
demonstrated a reduced risk of bleeding and
improved overall outcomes with bivalirudin rather
than unfractionated heparin (UFH) in ACS
patients, giving bivalirudin a CLASS 1B
RECOMMENDATION (from ACCF/AHA) as an
adjunctive therapy in patients with ACS
undergoing primary PCI.
O’Gara PT, Kushner FG, Ascheim DD et al.: 2013 ACCF/AHA guideline for the management of
ST-elevationmyocardial infarction: a report of the American College of Cardiology
Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol
2013, 61:e78-140
58. • The benefits of bivalirudin are mainly in its ability
to reduce bleeding risk.
• Retrospective analysis from Sweden’s SCAAR
database (41,537 consecutive NSTE–ACS patients
none of whom received GP IIb/III inhibitors)
revealed no benefits from using bivalirudin rather
than heparin.
• Head to head trials comparing bivalirudin with
unfractionated heparin (VALIDATE–SWEDEHEART,
HEAT–PPCI) are currently underway.
Swedish registry questions superiority of bivalirudin over heparin in patients undergoing PCI
for NSTE-ACS. [http://www.escardio.org/about/press/press-releases/pr-13/Pages/europcr-
day1.aspx - registry].
59. RESIDUAL RISK AND USE OF ORAL
ANTICOAGULANTS
• Patients with ACS remain at a significant risk of
recurrent ischemic events after initial
revascularization despite optimal medical therapy
including DAPT and aggressive risk factor
modification.
• 1 in 10 patients experiences a significant
atheroembolic event (cardiac death, myocardial
infarction or stroke) within a year of the first ACS
episode.
Go AS, Mozaffarian D, Roger VL, et al.: Heart disease and stroke statistics–2013 update: a
report from the American Heart Association. Circulation 2013, 127:e6-e245
60. • This is felt to be secondary to a persistent
thrombogenic state that extends well beyond the
initial ACS event.
• New oral anticoagulants have emerged in the last
decade with the potential to minimize residual risk.
61. RIVAROXABAN
• Rivaroxaban is a direct factor Xa inhibitor that
ultimately leads to decreased generation of
thrombin.
• Safety and efficacy of rivaroxaban in different
doses (5–20 mg) was initially tested in a phase II
dose finding trial (ATLAS ACS TIMI–46) that
revealed a dose-dependent increase in the rate of
bleeding and a reduction in ischemic events in
patients with ACS.
Mega JL, Braunwald E, Mohanavelu S et al : Rivaroxaban versus placebo in patients with
acute coronary syndromes (ATLAS ACS-TIMI 46): a randomised, double-blind, phase II trial.
Lancet 2009, 374:29-38
62. • Subsequently, a larger phase III trial (the ATLAS
ACS TIMI–51) was launched that randomized over
15,000 patients with ACS to receive either
rivaroxaban (2.5 or 5 mg twice daily) or placebo in
addition to standard medical therapy.
Mega JL, Braunwald E,Wiviott SD, Bassand J et al: Rivaroxaban in patients with a recent acute
coronary syndrome. N Engl J Med 2012, 366:9-19.
63. • Over a mean follow up of 13 months, there was a
16% reduction in primary efficacy endpoint (cardiac
death, myocardial infarction or stroke) with
RIVAROXABAN as compared to placebo.
• However, there was a threefold increase in the risk
of major bleeding and intracranial hemorrhage.
This risk was lower with a reduced dose (2.5 mg)
with relatively maintained efficacy.
64. • Overall there was a 36% reduction in all causes of
death with low dose RIVAROXABAN as compared
to placebo, which largely derived from a reduction
in sudden cardiac deaths. Results were similar in a
prespecified subgroup analysis in patients with
STEMI.
Mega JL, Braunwald E, Murphy SA et al: Rivaroxaban in patients stabilized after a ST-segment
elevation myocardial infarction: results from the ATLAS ACS-2-TIMI-51 trial (Anti-Xa Therapy to
Lower Cardiovascular Events in Addition to Standard Therapy in Subjects with Acute Coronary
Syndrome-Thrombolysis In Myocardial Infarction-51). J Am Coll Cardiol 2013, 61:1853-9
65. • A 2.5 mg twice daily dose of RIVAROXABAN was
recently approved for the same indication by the
European Commission
• Although no new data for other new oral
anticoagulants (DABIGATRAN, APIXABAN,
BETRIXABAN, DAREXABAN) were presented last
year.
http://press.healthcare. bayer.com/en/press/news-details-page.php/15050/2013-0292
66. REPERFUSION AT A NON–PCI
CAPABLE HOSPITAL
1) FIBRINOLYTIC THERAPY WHEN THERE IS AN
ANTICIPATED DELAY TO PERFORMING PRIMARY
PCI WITHIN 120 MINUTES OF FMC
67. Fibrinolytic therapy should be given to patients
with STEMI and onset of ischemic symptoms
within the previous 12 hours when it is
anticipated that primary PCI cannot be
performed within 120 minutes of FMC.
Fibrinolytic therapy is reasonable for patients
with STEMI if there is clinical and/or ECG
evidence of ongoing ischemia within 12 to 24
hours of symptom onset and a large area of
myocardium at risk or hemodynamic instability.
I IIa IIb III
I IIa IIb III
70. REPERFUSION AT A NON–
PCI CAPABLE HOSPITAL
2) ADJUNCTIVE ANTITHROMBOTIC
THERAPY WITH FIBRINOLYSIS
71. Aspirin (162- to 325-mg loading dose) and
clopidogrel (300-mg loading dose for patients
≤75 years of age, 75-mg dose for patients >75
years of age) should be administered to
patients with STEMI who receive fibrinolytic
therapy.
I IIa IIb III
72. • aspirin should be continued indefinitely
and
In patients with STEMI who receive fibrinolytic
therapy:
I IIa IIb III
• clopidogrel (75 mg daily) for at least 14
days
• and up to 1 year
I IIa IIb III
I IIa IIb III
73. ADJUNCTIVE ANTIPLATELET
THERAPY WITH FIBRINOLYSIS
It is reasonable to use aspirin 81 mg per day
in preference to higher maintenance doses
after fibrinolytic therapy.
I IIa IIb III
74. REPERFUSION AT A NON–
PCI-CAPABLE HOSPITAL
3) ADJUNCTIVE ANTICOAGULANT THERAPY WITH
FIBRINOLYSIS
75. I IIa IIb III
Patients with STEMI undergoing reperfusion
with fibrinolytic therapy should receive
anticoagulant therapy for a minimum of 48
hours, and preferably for the duration of the
index hospitalization, up to 8 days or until
revascularization if performed.
76. a. UFH adm. as a weight-adjusted intravenous
bolus and infusion to obtain an aPTT time of
1.5 to 2.0 times control, for 48 hours or until
revascularization;
b. Enoxaparin adm. a/c to age, weight, and
creatinine clearance, given as an i.v bolus,
followed in 15 min. by s/c inj. for the
duration of the index hospitalization, up to 8
days or until revascularization; or
I IIa IIb III
I IIa IIb III
Recommended regimens include:
77. • Fondaparinux administered with initial i.v dose,
followed in 24 hrs by daily s/c inj. if the
estimated creatinine clearance is greater than
30 mL/min, for the duration of the index
hospitalization, up to 8 days or until
revascularization.
I IIa IIb III
80. Cardiac catheterization and coronary angiography with
intent to perform revascularization should be performed
after STEMI in patients with any of the following:
a. Cardiogenic shock or acute severe HF that
develops after initial presentation;
b. Intermediate- or high-risk findings on
predischarge noninvasive ischemia testing;
or
c. Myocardial ischemia that is spontaneous
or provoked by minimal exertion during
hospitalization.
I IIa IIb III
I IIa IIb III
I IIa IIb III
81. • Coronary angiography with intent to perform
revascularization is reasonable for patients with
evidence of failed reperfusion or re-occlusion after
fibrinolytic therapy.
• Angiography can be performed as soon as
logistically feasible.
• Coronary angiography is reasonable before hospital
discharge in stable patients with STEMI after
successful fibrinolytic therapy.
• Angiography can be performed as soon as
logistically feasible, and ideally within 24 hours, but
should not be performed within the first 2 to 3
hours after administration of fibrinolytic therapy.
I IIa IIb III
I IIa IIb III
82. INDICATIONS FOR CORONARY ANGIOGRAPHY IN
PATIENTS
WHO WERE MANAGED WITH FIBRINOLYTIC
THERAPY OR WHO DID NOT RECEIVE
REPERFUSION THERAPY
84. Urgent CABG is indicated in patients with
STEMI and coronary anatomy not amenable
to PCI who have ongoing or recurrent
ischemia, cardiogenic shock, severe HF, or
other high-risk features.
CABG is recommended in patients with
STEMI at time of operative repair of
mechanical defects.
I IIa IIb III
I IIa IIb III
85. The use of mechanical circulatory support is
reasonable in patients with STEMI who are
hemodynamically unstable and require
urgent CABG.
Emergency CABG within 6 hours of symptom
onset may be considered in patients with
STEMI who do not have cardiogenic shock
and are not candidates for PCI or fibrinolytic
therapy.
I IIa IIb III
I IIa IIb III
86. Timing of Urgent CABG in
Patients With STEMI in
Relation to Use of Antiplatelet
Agents
87. Aspirin should not be withheld before urgent
CABG.
Short-acting intravenous GP IIb/IIIa receptor
antagonists should be discontinued at least 2
to 4 hours before urgent CABG.
Clopidogrel or ticagrelor should be
discontinued at least 24 hours before urgent
on-pump CABG, if possible.
I IIa IIb III
I IIa IIb III
I IIa IIb III
88. Abciximab should be discontinued at least 12
hours before urgent CABG.
Urgent off-pump CABG within 24 hours of
clopidogrel or ticagrelor administration might
be considered,
Urgent CABG within 5 days of clopidogrel
or ticagrelor administration or within 7
days of prasugrel administration might be
considered,
I IIa IIb III
I IIa IIb III
I IIa IIb III
90. Oral ẞblockers should be initiated in the first
24 hours in patients with STEMI who do not
have any of the following:
signs of HF, evidence of a low output state,
increased risk for cardiogenic shock,* or
other contraindications to use of oral beta
blockers.
Beta blockers should be continued during
and after hospitalization for all patients with
STEMI and with no contraindications to their
use.
I IIa IIb III
I IIa IIb III
91. Patients with initial contraindications to the
use of beta blockers in the first 24 hours after
STEMI should be re-evaluated to determine
their subsequent eligibility.
It is reasonable to administer i.v beta blockers
at the time of presentation to patients with
STEMI and no contraindications to their use
who are hypertensive or have ongoing
ischemia.
I IIa IIb III
I IIa IIb III
94. An ACE inhibitor should be administered
within the first 24 hours to all patients with
STEMI with anterior location, HF, or EF less
than or equal to 0.40, unless contraindicated.
An ARB should be given to patients with
STEMI who have indications for but are
intolerant of ACE inhibitors.
I IIa IIb III
I IIa IIb III
95. An aldosterone antagonist should be given to
patients with STEMI and no contraindications
who are already receiving an ACE inhibitor
and beta blocker and who have an EF less
than or equal to 0.40 and either symptomatic
HF or diabetes mellitus.
ACE inhibitors are reasonable for all patients
with STEMI and no contraindications to their
use.
I IIa IIb III
I IIa IIb III
98. High-intensity statin therapy should be
initiated or continued in all patients with
STEMI and no contraindications to its use.
It is reasonable to obtain a fasting lipid profile
in patients with STEMI, preferably within 24
hours of presentation.
I IIa IIb III
I IIa IIb III
101. MONOCLONAL ANTIBODIES:
INCLACUMAB
• SELECT–ACS trial examined P-selectin monoclonal
antibody, in patients with NSTE–ACS undergoing PCI .
• 544 NSTEMI patients scheduled for PCI to a placebo
infusion or to either a 5 mg/kg or 20mg/kg infusion
of INCLACUMAB.
• There were reductions in troponin I levels at 24
hours after the 20 mg/kg infusion as compared to
placebo, suggesting potential for reducing myocardial
damage.
Tardif J, Tanguay J, Wright SS, et al: Effects of the P-selectin antagonist inclacumab on myocardial
damage after percutaneous coronary intervention for non-ST-segment elevation myocardial
infarction: results of the SELECT-ACS trial. J Am Coll Cardiol 2013, 61:2048-55
102. STEM CELL THERAPY
• The use of stem cells derived from bone marrow
or myocardium to improve cardiac function has
been promising.
• The phase 1 CADUCEUS trial enrolled 30 patients
with recent MI and reduced ejection fraction
(25%–45%) and randomized them in a 2:1 ratio to
receive autologous cardiac stem cells derived from
endomyocardial biopsy (within 1.5–3 months after
myocardial infarction) or placebo.
Makkar RR, Smith RR, Cheng K et al: Intracoronary cardiosphere-derived cells for heart
regeneration after myocardial infarction (CADUCEUS): a prospective, randomised phase 1 trial.
Lancet 2012, 379:895-904
103. • Although there were no improvements in ejection
fraction at 12 months but there was a significant
decrease in myocardial scar tissue and an increase in
viable myocardium (based on cardiac MRI) in the
intervention group, as compared to placebo.
• The TIME trial randomized 120 subjects with
myocardial infarction and impaired ventricular
function that underwent PCI to receive either
autologous bone marrow cells or placebo.
Traverse JH, Henry TD, Pepine CJ et al.: Effect of the use and timing of bone marrow
mononuclear cell delivery on left ventricular function after acute myocardial infarction: the
TIME randomized trial. JAMA 2012, 308:2380-9
104. • The patients were randomized to one of four
groups: day 3 stem cell (after myocardial infarction);
day 3 placebo; day 7 stem cell; day 7 placebo
infusions.
• At 6 months follow up there were no differences in
changes in cardiac function (ejection fraction)
among any of the groups.
105. • Two trials—the ALLSTAR (allogenic cardiac stem cells)
and BAMI (autologous bone marrow cells)—are
currently enrolling patients and are underway.
107. • Utilization of intra-aortic balloon pump (IABP)
counterpulsation to support high-risk PCI.
• Even though there has been a lack of convincing
evidence of improvement in outcomes, IABP
support continues to be routinely utilized for high-
risk patients with myocardial infarction and
cardiogenic shock, and international guidelines
had given it a Class I indication.
108. • To this effect, the IABP–SHOCK II randomized trial
was launched to support the routine use of IABP
in patients with cardiogenic shock.
• The investigators randomized 600 patients with
acute myocardial infarction (AMI) and cardiogenic
shock to IABP or no IABP support.
• Surprisingly, there were no differences in
outcomes across the groups after a 30-day follow
up period (no difference in mortality, length of
hospital stay, renal function, and vasopressor use).
Thiele H, Zeymer U, Neumann F et al: Intraaortic balloon support for myocardial infarction
with cardiogenic shock. N Engl J Med 2012, 367:1287-96
109. • The PRAMI trial was a non-blinded trial which
randomized 465 patients presenting with STEMI to
either primary PCI in an infarct-related artery
alone or primary PCI and “preventive” PCI in a non
infarct artery with >50% stenosis.
Wald DS, Morris JK, Wald NJ et al: Randomized trial of preventive angioplasty in myocardial
infarction. N Engl J Med 2013, 369:1115-23
110. • There was a significant reduction in the primary
endpoint, a composite of cardiac death,
myocardial infarction and refractory angina in the
preventive PCI group when followed over 2 years
(9% vs. 23%; HR: 0.35).
• There was a trend towards a reduction in
mortality although it was not statistically
significant.
CREATE Registry: 2010 hat there have been approx. 28000 number of patients with the diagnosis of the acs
A recommendation with Level of Evidence B or C does not imply that the recommendation is weak. *Data available from clinical trials or registries about the usefulness/ efficacy in different subpopulations, such as sex, age, history of diabetes, history of prior myocardial infarction, history of heart failure, and prior aspirin use.†For comparative effectiveness recommendations (Class I and IIa; Level of Evidence A and B only), studies that support the use of comparator verbs should involve direct comparisons of the treatments or strategies being evaluated.
IN ACS. Following disruption of a vulnerable plaque, patients experience ischemic discomfort result in from a reduction of flow through the affected epicardial coronary artery. The flow reduction may be caused by a complete occlusive thrombus (right) or subtotally occlusive thrombus (left). Patients with ischemic discomfort may present with or without ST-segment elevation. Of patients with ST-segment elevation, the majority (wide red arrow) ultimately develop a Q-wave on the ECG (QwMI), while a minority (thin red arrow do not develop Q-wave and in older literature where said to have sustained a non-Q-wave MI (NQMI). Patients who present without ST-segment elevation are suffering from either unstable angina or a non-ST-segment elevation MI (NSTEMI) (wid green arrows), a distinction that is ultimately made on the presence or absence of a serum cardiac marker such as CK-MB ora cardiac troponin detected in the blood. The majority of patients presenting with NSTEMI do not develop a Q-wave onthe ECG; a minority develop a QwMI (thin green arrow).Explain nstmi.
Remember 50% of patients with history of LBBB do not present with chest pain in addition to difficult ECG interpretation patient with LBBB is difficult to diagnose and manage and should have low threshold for acute MI in these patients.
Any absence of q wave does not rule out myocardial infarction.
Potential complications of primary PCI include problems with the arterial access site; adverse reactions to volume loading, contrast medium, and antithrombotic medications; technical complications; and reperfusion events. The “no-reflow” phenomenon refers to suboptimal myocardial perfusion despite restoration of epicardial flow in the infarct artery and has been attributed to the combined effects of inflamma-tion, endothelial injury, edema, atheroembolization, vasospasm, and myocyte reperfusion injury. No-reflow is associated with a reduced survival rate. Treatment and prevention strategies have included use of the GP IIb/IIIa antagonist abciximab, vasodilators (nitroprusside, verapamil, adenosine), and inhibitors of various metabolic pathways (nicorandil, pexelizumab), albeit without consistent effect. Manual thrombus aspiration at the time of primary PCI results in improved tissue perfusion and more complete ST resolution.
Being done in india: mumbai KEM, LEELAVATI and in delhi MAXX FORtis
TASTE:Thrombus Aspiration in ST–Elevation Myocardial InfarctionLong term trial results are awaited..
*Balloon angioplasty without stent placement may be used in selected patients.
FIRST GENERATION STENT:
In india it is available as ETERNIA Excellent Flexibility and radial strength2. Trackability as never before3. verolimus drug coated4. Reduces artery Injury5. Next generation strut design offering excellent performance6. Immensely thin struts to minimize the focal injury of vessel wall7. Awesome surface finish
PRASUGREL: Prasugrel is a member of the thienopyridine class of ADP receptor inhibitors, compared to clopidogrel, prasugrel inhibits adenosine diphosphate–induced platelet aggregation more rapidly, more consistentlyTRITON–TIMI 38:TRial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet InhibitioN with Prasugrel–Thrombolysis In Myocardial Infarction
TRILOGY ACS :TaRgeted platelet Inhibition to cLarify the Optimal strateGy to medicallY manage Acute Coronary Syndromes
PLATO trial:Platelet Inhibition and Patient Outcomes.
Indian brand name BRILINTA: 2 tab of 90 mg loading dosed followed by 90 mg maintenance dose 700 rs per stripSide effect: Difficulty in breathing, headache, cough, dizziness, nausea, abnormal heart rhythm, high blood pressure, chest pain, diarrhea, back pain, low blood pressure, fatigue and chest pain
Protease activated receptor-1 (PAR-1) is a primary receptor for thrombin on platelets and is also present on vascular endothelium and smooth muscle cells. TRACER trial:thrombin receptor antagonist for clinical event reduction in acute coronary syndrome
Has some issues with the approval and fda due to its potential bleeding risk. But now fda has approved the drug, in india it is still not present in the market we will get this drug by the end of this year or beginning of 2015.
AIDA:Abciximabi.v. Versus i.c. in ST-elevation Myocardial Infarction
1) , taking into account whether a GP IIb/IIIa receptor antagonist has been administered; or
1) In patients with STEMI undergoing PCI who are at high risk of bleeding,
HORIZONS– AMI :Harmonizing Outcomes with RevascularIZatiON and Stents in Acute Myocardial InfarctionBivaluridin (angiomax or gioloc) 7800 rs vial of 250 mg
Sweden’s SCAAR :Swedish Coronary Angiography and Angioplasty Register)
ATLAS ACS:Anti-Xa Therapy to Lower cardiovascular events in Addition to Standard therapy in subjects with Acute Coronary Syndrome–Thrombolysis In Myocardial Infarction
Avail. In india as xarelto 10 mg 725 rs per strip
1) In the absence of contraindications, 2) In the absence of contraindications, when PCI is not available
except when a true posterior (inferobasal) MI is suspected or when associated with ST elevation in lead aVR.
Lmwx of 250rs from abbot Clexane of .2/.6/.8 250-1120 rs
*Although individual circumstances will vary, clinical stability is defined by the absence of low output, hypotension, persistent tachycardia, apparent shock, high-grade ventricular or symptomatic supraventricular tachyarrhythmias, and spontaneous recurrent ischemia.
GP IIb/IIIa receptor antagonists (eptifibatide, tirofiban)
2) And 3) , especially if the benefits of prompt revascularization outweigh the risks of bleeding.
*Risk factors for cardiogenic shock are age >70 years, systolic BP <120 mm Hg, sinus tachycardia >110 bpm or heart rate <60 bpm, and increased time since onset of symptoms of STEMI.Beta blocker c/i:(PR interval >0.24 seconds, second- or third-degree heart block, active asthma, or reactive airways disease).
P selectin (a cell-adhesion molecule expressed on endothelial cells and platelets)
CADUCEUS: CArdiosphere-Derived aUtologous stem CElls to reverse ventricUlardySfunction trial
The TIME (Transplantation in Myocardial Infarction) trial:
SWISS–AMI trial:SWissMulticenter Intracoronary Stem Cells Study in Acute Myocardial Infarction
ALLSTAR: Allogeneic Heart Stem Cells to Achieve Myocardial Regeneration BAMI: Bone Marrow Cells in Acute Myocardial Infarction
high-risk PCI:
Intraaortic Balloon Pump in Cardiogenic Shock (IABP-SHOCK) trial,
PRAMI: Preventive Angioplasty in Myocardial Infarction