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Interventional Management of ACS
18th Myanmar Internal Medicine Conference 2017
Melia Hotal
29th September 2017
Prof Kyaw Soe Win
Mandalay General Hospital
Spectrum of Pathologic and Clinical ST-Segment Elevation Acute Myocardial Infarction (STEMI)
and Non-STEMI Acute Coronary Syndromes.
Anderson JL, Morrow DA. N Engl J Med 2017;376:2053-2064
Spectrum of (STEMI)
and Non-STEMI
Acute Coronary
Syndromes.
STEMI
ACS Classification and Hospitalizations
Acute Coronary Syndromes
Unstable angina
TIMI flow grade 2/3
in culprit artery
NSTEMI
- Troponin + Troponin + Troponin
TIMI flow grade 0/1
in culprit artery
Gibson CM et al. Presented at: 2008 AHA Scientific Sessions. New Orleans, LA.
Go AS et al. Heart Disease and Stroke Statistics – 2013 update. Circulation. 2013;1127:e6-e245
0.81 million admissions per year 0.33 million admissions per year
Shared pathophysiology; Shared core treatment targets
Presentation
Emergency
Department
In-hospital
6-24hrs
Aim of Treatment for ACS
To re-establish the epicardial flow before irreversible
damage occurs:
• Pharmacological intervention
• Antiplatelets- oral/ parentral
• Anticoagulants
• Fibrinolytics
• Mechanical intervention
• Coronary Angiogram
• PCI
• CABG
Real World Interventional Cardiology Practice for CAD
Intervention treatment has prognostic benefit in STEMI and
High Risk NSTE-ACS
Optimal medical therapy is essential for stable CAD and low
risk NSTE-ACSintervention treatment has no prognostic
benefit
The important thing is Timing of intervention
•?Immediate
•?Early
•?Delayed
•?Elective
Acute STEMI
15 minutes 2 hours 6 hours
% necrosis 0% 50% 90%
Occlusive thrombus on a plaque of
atheroma
Goals in Reperfusion in Acute STEMI
 Rapid
 Complete - TIMI III - Epicardial artery
 Integrity Of Microcirculation - Myocardial Perfusion
 Sustained
“TIME IS MUSCLE!”
Thrombolytic
Therapy Primary PCI
Total occlusion of proximal RCA
from TIMI -0 to TIMI -3 after PPCI
0
2
4
6
8
10
12
M
o
r
t
a
l
i
t
y
%
p = 0.003 vs TIMI 0/1
p < 0.0001 vs TIMI 0/1
P < 0.0001 vs TIMI 2
9.3%
6.1 %
3.7 %
TIMI Flow grade and mortality in Acute STEMI
90-Minute Coronary Patency: PAMI vs GUSTO
FLOW GRADE PTCA (PAMI) tPA (GUSTO)
TIMI 0-1 (no flow) 6% 19%
TIMI 2 (slow flow) -- 27%
TIMI 3 (brisk flow) 94% 54%
 Only 35% of 241,000 AMI pts were treated with lytics.
 These lytic patients frequently needed other procedures:
 70.7% underwent cath later before discharge
 30.3% “ PTCA
 13.3% “ CABG
LYTICS (35%) NO LYTICS (65%)
Mortality 5.9% 13.0%
Major bleeding 2.8% 0.5%
National Registry of Myocardial Infarction (NRMI)
Pooled data from 10 randomized trials (n=2,606):
Primary PCI is Superior to
Thrombolytic Therapy for Acute M.I.
Primary PTCA tPA p value
Mortality 4.4 % 6.5 % 0.02
Death or Reinfarction 7.2 % 11.9 % <0.001
Total Stroke 0.7 % 2.0 % 0.007
Hemorrhagic Stroke 0.1 % 1.1 % <0.001
Weaver, JAMA 1997;278:2093
Primary PCI is Superior to
Thrombolytic Therapy for Acute M.I.
pooled data from 21 randomized trials (n=7,739):
Primary PCI Lytic Rx p value
Mortality 6.9 % 9.3 % 0.0002
Reinfarction 2.4 % 6.8% <0.0001
Total Stroke 1.0 % 2.0 % 0.0004
Hemorrhagic Stroke 0.05 % 1.1 % <0.0001
Combined 8.2 14.3 <0.0001
Keeley, Lancet 2003;361:13-20
Primary PCI in Lytic Eligible Pts that are
High Risk (MITRA Registry)
(%)
O’Neill, J Invasive Cardiol 1998:10 Suppl A:4A-10A
High Risk Patients: Age >70, Anterior M.I., Heart Rate > 100
Death Reinfarction Death or Stroke
9.8%
6.7%
15.6%
3.6%
3.2%
1.4%
4.1%
0.5%
0
4
8
12
16 PCI Lytics
Death Reinfarction Death or Stroke
Re-MI
၂၀၁၅ တြင္ ကုထုုံးအလုက္ ႏ ႏလုုံးေႏတ ုံးေႏၾကာပြူ နာာ်ားာုံး
ေႏဆုံးရုတြင္ ေႏ ဆုုံး်ားႈႏႈ ႈႏႈာ္ႏုံး
0
100
200
300
400
500
600
700
129 133
431
693
18 6
79 103
ကု ်ားႈႏႈခယူႏ ခင္ႏုံး ေႏ ဆုုံး ႈႏႈာ္ႏုံး
14.8%
18.4%
4.5%13.9%
ေႏတ ုံးေႏၾကာပပင္ႏေႏအာင္ ကု ်ားႈႏႈ်ားရရေႏ ာ လူာာ်ားာုံးတြင္ ေႏ ဆုုံး်ားႈႏႈ
အ ်ားင္ႏဆုုံးႏ ဖစ္သည္
 Can be used in virtually all infarct patients.
 Produces TIMI-3 flow over 90% of the time, not 54%.
 Does not cause intracranial bleeding.
 Reduces need for subsequent procedures (cath, PCI).
 Provides important angiographic information: patients who need
urgent surgery can be detected early.
 Opens vessels as fast or faster.
 Can improve prognosis in cardiogenic shock.
 a five-fold reduction in mortality in high-risk STEMI pts compared to
thrombolytics.
Advantages of Primary PCI
Mortality rates with primary PCI as a function
of PCI-related time delay
P = 0.006
0 20 40 60 80 100
PCI-Related Time Delay (door-to-balloon - door-to-needle)
AbsoluteRiskDifferenceinDeath(%)
-5051015
Circle sizes = sample size of the
individual study.
Solid line = weighted meta-regression.
Nallamothu BK, Bates ER. Am J Cardiol. 2003;92:824-6
62 min Benefit
Favors PCI
Harm
Favors Lysis
Relationship Between Door-to-Balloon Time
Intervals and Mortality in NRMI
Cannon JAMA 2000
P = 0.35
P = 0.29
P = 0.01
P < 0.001
P < 0.001
0.6
0.8
1
1.2
1.4
1.6
1.8
2
2.2
0-60 61-90 91-120 121-150 151-180 > 180
Time (minutes)
Multvariate-adjustedOdds
ofIn-hospitalMortality
Challenges for STEMI system of care in Myanmar
• PCI is the GOLD standard, yet remains unaccessible to majority of patients.
• Primary PCI is available to <10% STEMI patients in Myanmar.
• 1.Lack of awareness
• 2.Lack of transfer facilities.
Unavailability of hospital with PCI facility.
• 3.Casualty/ED –to cath lab
Finance problem
Obtaining consent
Unavailability of cardiologist round the clock.
• Patient awareness and education for early symptom identification.
• Education required for General Practitioners /Physicians to implement early time dependent
STEMI management.
Total Ischemic Time 2013-2016
0
50
100
150
200
250
300
2013 2014 2015 2016
226.02 237.54
297.81
189.96
93.79 89.89
73.21
56.75
Patient delay System delay
01/19/2017 25How PPCI Program was started in Myanmar
Ischaemic time according to mode of admission (2016)
371
300
338
271
33 30
0
50
100
150
200
250
300
350
400
Through ERC Through Network
Total ischaemic time
Pain to CCU
Door to balloon
Note: Data including are describing the time in Minutes
Why it has to be stressed much regarding this approach ?
• Time is Myocardium.
• For each 30 min delay in treatment in STEMI patient,1 yr mortality increases by 7.5%.
• Mortality benefit with primary PCI is lost if PCI related delay exceeded 60 min.
Nallamothu et al ,Am J Cardiol,2004;94:772-774
• Practically, early fibrinolytic therapy can compensate for PCI related delay.
• Proportional mortality reduction was significantly higher in patients treated within 2 hrs
with fibrinolytics..
Circulation 2004;109:1223-1225
But… Fibrinolytics Still important
• Many patients present to hospitals without PCI capability
• Even so… PCI often cannot realistically occur within 90 minutes
• In NRMI 2006 Database, 27.6% of patients received fibrinolytic
therapy
Nallamothu BK, et al. Circulation 2005;111:761
Bates ER, et al. Circulation 2008;118:567
Antman EM, et al. JACC 2008;51:210
Gibson CM, et al. AHJ 2008;156:1035
How best to combine the two strategies?
• Can we improve on Primary PCI with concomitant (co-
administered) fibrinolytics?
• Immediate/Facilitated Approach
• Should all fibrinolytic patients go to PCI?
• Pharmacoinvasive approach
• Deferred approach
• Should only fibrinolytic “failures” get PCI?
• Rescue approach
STEMI Management
• What are the options?
•Primary PCI
•Primary Fibrinolytic Therapy
•Rescue PCI (fibrinolytic failures only)
•Immediate/Facilitated PCI (<3 hours)
•Pharmacoinvasive PCI (within 3-24 hours)
•Deferred PCI (> 24 hours)
Immediate/Facilitated PCI
• Definition: PCI immediately (< 3 hours) after fibrinolytics
• You may combine fibrinolytics with 2b/3a receptor inhibitors
• Theory:
Both PCI and Lytics
=
Rapid Early Reperfusion + Sustained Reperfusion
Immediate/Facilitated PCI
Why did it fail?
• Early period post-lytics (within 3 hours) carries the highest
risk of bleeding
• Early period paradoxically is also pro-thrombotic due to
degradation products
• Immediate PCI may increase bleeding and also paradoxically
increase ischaemic endpoints
• 2b/3a inhibitors may reduce the thrombotic complications
but at a cost of excess bleeding
Pharmaco-Invasive Strategy
Pharmcologic reperfusion therapy (lytics or half dose lytics +
IIb/IIIa) followed by transfer to a PCI hospital for urgent
cath/PCI (within 3-24 hours)
Options for Reperfusion Therapy at Non-PCI
hospitals
Transfer for Primary PCI is better than…
Pharmaco-invasive strategy which is better than…
Fibrinolysis alone
What specific ACS strategies to NSTE-ACS
• Timing of invasive strategy? ASAP? Depending on risk group?
• Clopidogrel use: When? In Whom? How much?
• GPIIb/IIIa receptor antagonist: When? Upstream? At catheterization?
Routine? Provisional?
• Enoxaparin? Heparin? DTI(bivalirudin)? Xa inhibitor (Fondaparinux)?
Managing non-ST-segment elevation ACS by early
invasive therapy improves long-term survival and
reduces late myocardial infarction and
rehospitalization for unstable angina
Bavry AA, et al. J Am Coll Cardiol 2006;48:1319–1325
Invasive and Ischemia-Guided Intervention Categories in Patients with Non-STEMI Acute
Coronary Syndromes.
Anderson JL, Morrow DA. N Engl J Med 2017;376:2053-2064
1. The concept of “risk” in the STEMI and NSTE-ACS patient
applies only to ischemic events.
2. For primary PCI, it is all about door-to-balloon time:
Antithrombin therapy doesn’t matter….
• Recurrent ischemic events are associated with worse survival.
• This is true for patients with ACS and those undergoing PCI.
BUT…
• The risk appears limited to the 30 days after the index event.
• What about the bleeding events?
SYNERGY
LMWH
ESSENCE
1994 1995 1996 1997 1998 1999 2000 2002 2003 2004 2005 20062001
CURE
Clopidogrel
Bleeding risk
Ischemic risk
GP IIb/IIIa
blockers
PRISM-PLUS
PURSUIT
ACUITYTACTICS TIMI-18
Early invasive
PCI ~ 5% stents ~85% stents Drug-eluting stents
ISAR-REACT 2
Milestones in ACS Management
OASIS-5
[ Fondaparinux ]
Anti-Thrombin Rx
Anti-Platelet Rx
Treatment Strategy
Heparin
Aspirin
Conservative
ICTUS
Bivalirudin
REPLACE 2
Adapted from and with the courtesy of Steven Manoukian, MD.
1992 1995 1998 2001 2004 2007
1997 1999
UFH
LMWH TIMI 11B
2004
SYNERGY
Bivalirudin
2003
REPLACE 2
ASA
IIb/IIIa
antagonists
1995
2001
1998
EPISTENT
PURSUIT
2001
ESPRIT
GUSTO 4
2004
ISAR REACT
Clopidogrel CURE
2000
Anti-thrombotic agents
Anti-platelet agents
Evolving ACS Therapies and Patterns of Antithrombotic Use*
ACUITY
2006
ISAR-REACT 2
* Width of bar represents approximate degree of use of antiplatelet or anticoagulants at a particular time
• Clinical trials with GP IIb/IIIa inhibitors show reductions in recurrent
ischemic events in risk-stratified subsets when they are added to
unfractionated heparin.
BUT…
• Bleeding risks are clearly higher with GPI.
• GPIs have never been shown to improve survival in the modern era of
PCI or ACS management.
• A strategy of bivalirudin appears at least as good as UFH + GPI in the
ACS patients across the entire risk spectrum.
• Major bleeding (with or without blood product
transfusions) has emerged as a powerful
independent predictor of early and late mortality in
pts with NSTEMI, STEMI and in those undergoing PCI
Time from Randomization in Days
Cumulative%Mortality
With MI 5.7%
Without major bleed 2.0%
Impact of Major Bleed and MI
after Elective and Urgent PCI
1-Year Mortality (N=6,012)
Without MI 1.9%
With major bleed 8.8%
Stone GW. J Inv Cardiol 2004;16(suppl G):12–17.
Variable Groups O.R. (95% CI) p-value
Creatinine clear. <30 mL/min 7.21 (2.53–20.51)
<0.000130–60 mL/min 3.34 (1.92–5.78)
60–90 mL/min 1.57 (0.96–2.57)
CHF Yes 4.38 (2.83–6.78) <0.0001
Major Bleeding Yes 3.26 (1.78–5.96) 0.0001
MI @30day Yes 2.77 (1.62–4.75) 0.0002
Urg Revasc @30d Yes 2.77 (1.15–6.71) .024
Hx angina Yes 2.18 (1.25–3.81) 0.006
Prior MI Yes 1.81 (1.09–3.03) 0.023
Diabetes Yes 1.64 (1.10–2.44) 0.015
Predictors of 1-year Mortality
after Elective and Urgent PCI
Stone GW. J Inv Cardiol 2004;16(suppl G):12–17.
Mehran RM et al. In press EHJ
Influence of Major Bleeding and MI in the First 30 Days on
Risk of Death Over 1 Year
Cox model adjusted for 36 baseline predictors, with MI and major bleeding
(non-CABG) as time-updated covariates
Of 13,819 enrolled pts, 524 (3.8%) died within 1 year
Myocardial infarction 2.51 (1.95-3.25) <0.0001
Major bleeding without or before
transfusion 2.00 (1.30-3.06) <0.0001
Major bleeding after transfusion 3.93 (2.95-5.24) <0.0001
HR ± 95% CI P-valueHR (95% CI)
Mehran RM et al. In press EHJ
Influence of Major Bleeding and MI in the First 30 Days on
Risk of Death Over 1 Year
Cox model adjusted for 36 baseline predictors, with MI and major bleeding
(non-CABG) as time-updated covariates
Of 13,819 enrolled pts, 524 (3.8%) died within 1 year
Myocardial infarction 2.51 (1.95-3.25) <0.0001
Major bleeding without or before
transfusion 2.00 (1.30-3.06) <0.0001
Major bleeding after transfusion 3.93 (2.95-5.24) <0.0001
HR ± 95% CI P-valueHR (95% CI)
Attributable
deaths
51.5*
66.5**
Attributable deaths = N deaths
among pts with the time updated
event (attribute) X (adj. HR – 1)/adj. HR
*9.8% of all deaths
**12.7% of all deaths
HR (95% CI) P-value
Attributable
deaths
MI Day 0-1 17.6 (10.8 to 28.7) <0.001 21
Days 2-7 8.2 (5.0 to 13.6) <0.001 19
Days 8-30 2.9 (1.6 to 5.3) 0.001 12
Days 31+ 1.4 (0.9 to 2.1) 0.12 25
Major bleed Day 0-1 5.5 (2.7 to 11.0) <0.001 9
(non CABG) Days 2-7 5.8 (3.5 to 9.7) <0.001 18
Days 8-30 5.6 (3.5 to 8.8) <0.001 24
Days 31+ 2.4 (1.7 to 3.3) <0.001 42
Transfusion Day 0-1 6.7 (3.1 to 14.7) <0.001 7
Days 2-7 8.1 (4.6 to 14.1) <0.001 15
Days 8-30 6.4 (3.7 to 10.9) <0.001 17
Days 31+ 3.1 (2.1 to 4.5) <0.001 31
Influence of MI, Major Bleed and Transfusion in the First 30 Days
on the Risk of Death Over 1 Year
Mehran RM et al. In press EHJ
0.5 1 2 4 8 16 32
Hazard ratio (95% CI)
Attributable deaths = N deaths
among pts with the time updated
event (attribute) X (adj. HR – 1)/adj. HR
Associations with Mortality
(Re)-MI  Mortality
 (Re)-MI ??  Mortality
Bleeding  Mortality
 Bleeding  Mortality??
Considerations in the Modern Era of ACS/PCI
• 55-year-old male with 3 hours
of chest pain
●Hx of HTN,  lipids
●Marked ST-segment
depression leads II, III, aVL
●Elevated serum troponin T,
CKMB 4 X ULN
●Normal renal function
• 86-year-old female with 3 hours
of chest pain
●Hx of DM, HTN,  lipids
●ECG non-specific (no prior
study for comparison)
●Elevated troponin, normal
CKMB
●Est. GFR 45 ml/min
ACS-related Bleeding—Relevant Questions
• Who bleeds? Can we risk stratify?
• Should bleeding risk affect upstream antithrombotic care? If so, how?
• Is bleeding bad or a necessary evil?
• Can blood transfusion “correct” risks associated with bleeding?
• Does bleeding affect resource use?
Independent
predictors of
major bleeding
in marker- positive
acute coronary
syndromes
Moscucci, GRACE Registry, Eur Heart J. 2003 Oct;24(20):1815-23.
Predictors of Major Bleeding in ACS
• Older Age
• Female Gender
• Renal Failure
• History of Bleeding
• Right Heart Catheterization
• GPIIb-IIIa Antagonists
26,452 patients from PURSUIT, PARAGON A, PARAGON B, GUSTO IIb NST
Bleeding severity and adjusted hazard of death
*p<0.0001
Bleeding and Outcomes in NSTE-ACS
Rao SV, et al. Am J Cardiol. 2005 Nov 1;96(9):1200-6. Epub 2005 Sep 12.
Bleeding Severity 30d Death 30d Death/MI 6 mo. Death
Mild* 1.6 1.3 1.4
Moderate* 2.7 3.3 2.1
Severe* 10.6 5.6 7.5
*Bleeding as a time-dependent covariate
• Bleeding is associated with adverse short- and long-term outcomes
among patients with ACS and those undergoing PCI
● Mortality rates are higher among those who bleed
● MI rates are higher among those who bleed
• Worse bleeding associated with worse outcomes
• This relationship is persistent after robust statistical adjustment for
confounders
Bleeding and Outcomes in ACS
30-Day Survival By Transfusion Group
Rao SV, et. al., JAMA 2004;292:1555–1562.
Transfusion in ACS
N=24,111
30-Day Survival By Transfusion Group
• Blood transfusion is independently associated with worse short
and long-term outcomes including death and recurrent MI
• Transfusion does not correct the adverse impact bleeding and is
associated with increased mortality in ACS patients
• Blood transfusion is best avoided in ACS patients whenever
possible and is associated with increased mortality in ACS
patients
Blood Transfusion in ACS
Bleeding Among Patients with ACS
• There are several therapeutic pathways for ACS care
• Choices for therapy must take into account:
● Ischemic complications
● Bleeding complications
• The risk for bleeding and ischemia increases from NSTE-ACS to STEMI
White HD et al. JACC 2008;51:1734-41.
Switching in ACUITY
Reducing (re)MI—Effect on mortality
Therapy Reduces mortality?
Clopidogrel Modestly in STEMI
GP IIb/IIIa No
UFH No
Enoxaparin No
Yusuf S. et. al. NEJM 2001
Boersma E. et. al Lancet 2002
SYNERGY Investigators. JAMA 2004
Switching Antithrombins: A Practical Strategy for the ACS Network
SYNERGY ACUITY UVM Registry
Antithrombin comparison Enoxaparin vs. UFH
UFH/Enoxaparin vs.
Bivalirudin
UFH/Enoxaparin vs.
Bivalirudin
N 9978 7104 728
Pre-randomization
antithrombin treatment
76% 59% 44%
Switch (%) 35% 29% 44%
Consistent Therapy vs.
Switched (%)
Does Not Favor
Switching
Favors
Switching
Neutral
Death or MI 14.2% vs. 22.0%* 7.4% vs. 6.9% 8% vs. 7%
Bleeding 15.1 % vs. 35.1* 5.8% vs. 2.8%+ 2% vs. 2%^
Ischemic
Complications
► Death
► MI
► Urgent TVR
Evolving Paradigm for Evaluating ACS
Management Strategies
Composite Adverse Event Endpoints
Ischemic
Complications
Hemorrhage
HIT
► Death
► MI
► Urgent TVR
► Major Bleeding
► Minor Bleeding
► Thrombocytopenia
Composite Adverse Event Endpoints
Evolving Paradigm for Evaluating
ACS Management Strategies
Periprocedural
Complications
Clinical
Benefit
► Death
► Major Disability
► Cost
► Ease of Use
► Duration of
Therapy
► Accounting for
Bleeding and
Ischemic
Endpoints
Composite Adverse Event Endpoints
Evolving Paradigm for Evaluating ACS
Management Strategies
• a balance must be struck between ischemia reduction and bleeding.
• Both ischemic complications and bleeding are associated with increased
costs.
• Escalation of therapy for ischemia in this setting is associated with increased risk
of bleeding
• This “price to be paid” has generally been accepted and tolerated, especially in
patients at high ischemic risk, who benefit disproportionately from advanced
therapy
• Enox superior to UFH in patients with higher TIMI Risk Scores
• Clopidogrel + ASA superior to ASA alone in patients with higher TIMI Risk Scores
• GP IIb/IIIa receptor antagonists benefit troponin positive patients more than troponin
negative patients
Changing the Calculations for
Assessing Guidelines Adherence
Anderson HV, Bach RG, J Am Coll Cardiol 2005;46:1488-9.
“We need to invert the current equation to calculate an opportunity score for
ACS patients rather than a risk score. Patients with higher baseline risks, such as
the elderly, would have higher opportunity scores for benefit, even allowing for
some of the greater risks from the treatment.”
Balancing Efficacy and Safety
• Current guidelines emphasize reduction of ischemic risk in NSTE ACS—
especially for upstream therapy
• Updated guidelines are expected to include data on the harm that
bleeding events cause, diminishing ischemic efficacy in some patients
• Most of physicians are comfortable with the goal of reducing ischemic
risk . . . and traditionally have left concern over bleeding to “downstream
providers”
• “balanced” pharmacotherapy will require multidisciplinary
collaboration, pathways, anticipation of consistent care (especially time
from ED to cath), and individualized patient assessment
ZONE 2- ်ား ႏေႏလုံးေအေတထေတထရာဂါကုေႏဆုံးရုၾကုံး၊ ႏ ႏလုုံးေႏတ ုံးေႏၾကာခ ်ဲ႕ဌာာ ု (၁ - ၂)
ာာရအတြင္ႏုံးေႏရာက္ႏ ႏႏုင္ ( ေအရုံးေႏပၚ ႏလုုံးေႏတ ုံးေႏၾကာခ ်ဲ႕ကုေ ပုံးႏ ခင္ႏုံး )
ZONE 3- ်ား ႏေႏလုံးေအေတထေတထရာဂါကုေႏဆုံးရုၾကုံး၊ ႏ ႏလုုံးေႏတ ုံးေႏၾကာခ ်ဲ႕ဌာာ ု (၃)
ာာရအတြင္ႏုံးေႏရာက္ႏ ႏႏုင္ ( ႏ ႏလုုံးေႏတ ုံးေႏၾကာပပင္ႏေႏဆုံးတ င္ႏုံးကုေ ပုံးႏ ခင္ႏုံး နင
ႏ ႏလုုံးေႏတ ုံးေႏၾကာခ ်ဲ႕ဌာာ ုလူာာလႊႏ်ဲႏ ခင္ႏုံး )
What have we learned and what can be done to
improve the process of PPCI?
1. Patients’ delays: Public awareness of heart attacks
2. System Delays:
1. Late Arrival in the ER
2. Delay in the diagnosis at ER
3. Delay in the referral to CCU
01/19/2017 83How PPCI Program was started in Myanmar
• single call activation to engage the cath lab
• Bypass the ER
• Develop prehospital alert and ECG transmission
using Smartphone applications and cathlab
activation before patient arrived to CCU
• avoid delay to activate the team outside working
hours
• complete coverage for PPCI irrespective of the
financial status
1st March 2015
MGH STEMI Network laughed on the day
of celebration of second year anniversary
of PPCI and Heart Attack Awareness Week
Key To Improving STEMI Care: STEMI network
01/19/2017 84How PPCI Program was started in Myanmar
01/19/2017 85How PPCI Program was started in Myanmar
Zone 1- 30 mins to MGH Cath lab lab
01/19/2017 86How PPCI Program was started in Myanmar
Zone 2- 1hr to MGH cath lab
Zone 3- 3hr to MGH cath lab
01/19/2017 87How PPCI Program was started in Myanmar
Family
Doctors
ERC
GP and
Physicians
ER MGH
IDEAL STEMI care system
01/19/2017 88How PPCI Program was started in Myanmar
Family
Doctors
ERC
GP and
Physicians
ER MGH
x
x x
x
Our Aim
01/19/2017 89How PPCI Program was started in Myanmar
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Call us and send ECG by Viber
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ERC
ER MGH
x
xCall us and send ECG by Viber
09-259898661
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01/19/2017 91How PPCI Program was started in Myanmar
Total Ischemic Time 2013-2016
0
50
100
150
200
250
300
2013 2014 2015 2016
226.02 237.54
297.81
189.96
93.79 89.89
73.21
56.75
Patient delay System delay
01/19/2017 92How PPCI Program was started in Myanmar
Ischaemic time according to mode of admission (2016)
371
300
338
271
33 30
0
50
100
150
200
250
300
350
400
Through ERC Through Network
Total ischaemic time
Pain to CCU
Door to balloon
Note: Data including are describing the time in Minutes

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Intervention treatment for acs

  • 1. Interventional Management of ACS 18th Myanmar Internal Medicine Conference 2017 Melia Hotal 29th September 2017 Prof Kyaw Soe Win Mandalay General Hospital
  • 2.
  • 3. Spectrum of Pathologic and Clinical ST-Segment Elevation Acute Myocardial Infarction (STEMI) and Non-STEMI Acute Coronary Syndromes. Anderson JL, Morrow DA. N Engl J Med 2017;376:2053-2064 Spectrum of (STEMI) and Non-STEMI Acute Coronary Syndromes.
  • 4. STEMI ACS Classification and Hospitalizations Acute Coronary Syndromes Unstable angina TIMI flow grade 2/3 in culprit artery NSTEMI - Troponin + Troponin + Troponin TIMI flow grade 0/1 in culprit artery Gibson CM et al. Presented at: 2008 AHA Scientific Sessions. New Orleans, LA. Go AS et al. Heart Disease and Stroke Statistics – 2013 update. Circulation. 2013;1127:e6-e245 0.81 million admissions per year 0.33 million admissions per year Shared pathophysiology; Shared core treatment targets Presentation Emergency Department In-hospital 6-24hrs
  • 5. Aim of Treatment for ACS To re-establish the epicardial flow before irreversible damage occurs: • Pharmacological intervention • Antiplatelets- oral/ parentral • Anticoagulants • Fibrinolytics • Mechanical intervention • Coronary Angiogram • PCI • CABG
  • 6. Real World Interventional Cardiology Practice for CAD Intervention treatment has prognostic benefit in STEMI and High Risk NSTE-ACS Optimal medical therapy is essential for stable CAD and low risk NSTE-ACSintervention treatment has no prognostic benefit
  • 7. The important thing is Timing of intervention •?Immediate •?Early •?Delayed •?Elective
  • 8. Acute STEMI 15 minutes 2 hours 6 hours % necrosis 0% 50% 90% Occlusive thrombus on a plaque of atheroma
  • 9. Goals in Reperfusion in Acute STEMI  Rapid  Complete - TIMI III - Epicardial artery  Integrity Of Microcirculation - Myocardial Perfusion  Sustained “TIME IS MUSCLE!” Thrombolytic Therapy Primary PCI
  • 10. Total occlusion of proximal RCA from TIMI -0 to TIMI -3 after PPCI
  • 11. 0 2 4 6 8 10 12 M o r t a l i t y % p = 0.003 vs TIMI 0/1 p < 0.0001 vs TIMI 0/1 P < 0.0001 vs TIMI 2 9.3% 6.1 % 3.7 % TIMI Flow grade and mortality in Acute STEMI
  • 12. 90-Minute Coronary Patency: PAMI vs GUSTO FLOW GRADE PTCA (PAMI) tPA (GUSTO) TIMI 0-1 (no flow) 6% 19% TIMI 2 (slow flow) -- 27% TIMI 3 (brisk flow) 94% 54%
  • 13.  Only 35% of 241,000 AMI pts were treated with lytics.  These lytic patients frequently needed other procedures:  70.7% underwent cath later before discharge  30.3% “ PTCA  13.3% “ CABG LYTICS (35%) NO LYTICS (65%) Mortality 5.9% 13.0% Major bleeding 2.8% 0.5% National Registry of Myocardial Infarction (NRMI)
  • 14. Pooled data from 10 randomized trials (n=2,606): Primary PCI is Superior to Thrombolytic Therapy for Acute M.I. Primary PTCA tPA p value Mortality 4.4 % 6.5 % 0.02 Death or Reinfarction 7.2 % 11.9 % <0.001 Total Stroke 0.7 % 2.0 % 0.007 Hemorrhagic Stroke 0.1 % 1.1 % <0.001 Weaver, JAMA 1997;278:2093
  • 15. Primary PCI is Superior to Thrombolytic Therapy for Acute M.I. pooled data from 21 randomized trials (n=7,739): Primary PCI Lytic Rx p value Mortality 6.9 % 9.3 % 0.0002 Reinfarction 2.4 % 6.8% <0.0001 Total Stroke 1.0 % 2.0 % 0.0004 Hemorrhagic Stroke 0.05 % 1.1 % <0.0001 Combined 8.2 14.3 <0.0001 Keeley, Lancet 2003;361:13-20
  • 16. Primary PCI in Lytic Eligible Pts that are High Risk (MITRA Registry) (%) O’Neill, J Invasive Cardiol 1998:10 Suppl A:4A-10A High Risk Patients: Age >70, Anterior M.I., Heart Rate > 100 Death Reinfarction Death or Stroke 9.8% 6.7% 15.6% 3.6% 3.2% 1.4% 4.1% 0.5% 0 4 8 12 16 PCI Lytics Death Reinfarction Death or Stroke Re-MI
  • 17.
  • 18. ၂၀၁၅ တြင္ ကုထုုံးအလုက္ ႏ ႏလုုံးေႏတ ုံးေႏၾကာပြူ နာာ်ားာုံး ေႏဆုံးရုတြင္ ေႏ ဆုုံး်ားႈႏႈ ႈႏႈာ္ႏုံး 0 100 200 300 400 500 600 700 129 133 431 693 18 6 79 103 ကု ်ားႈႏႈခယူႏ ခင္ႏုံး ေႏ ဆုုံး ႈႏႈာ္ႏုံး 14.8% 18.4% 4.5%13.9% ေႏတ ုံးေႏၾကာပပင္ႏေႏအာင္ ကု ်ားႈႏႈ်ားရရေႏ ာ လူာာ်ားာုံးတြင္ ေႏ ဆုုံး်ားႈႏႈ အ ်ားင္ႏဆုုံးႏ ဖစ္သည္
  • 19.  Can be used in virtually all infarct patients.  Produces TIMI-3 flow over 90% of the time, not 54%.  Does not cause intracranial bleeding.  Reduces need for subsequent procedures (cath, PCI).  Provides important angiographic information: patients who need urgent surgery can be detected early.  Opens vessels as fast or faster.  Can improve prognosis in cardiogenic shock.  a five-fold reduction in mortality in high-risk STEMI pts compared to thrombolytics. Advantages of Primary PCI
  • 20. Mortality rates with primary PCI as a function of PCI-related time delay P = 0.006 0 20 40 60 80 100 PCI-Related Time Delay (door-to-balloon - door-to-needle) AbsoluteRiskDifferenceinDeath(%) -5051015 Circle sizes = sample size of the individual study. Solid line = weighted meta-regression. Nallamothu BK, Bates ER. Am J Cardiol. 2003;92:824-6 62 min Benefit Favors PCI Harm Favors Lysis
  • 21. Relationship Between Door-to-Balloon Time Intervals and Mortality in NRMI Cannon JAMA 2000 P = 0.35 P = 0.29 P = 0.01 P < 0.001 P < 0.001 0.6 0.8 1 1.2 1.4 1.6 1.8 2 2.2 0-60 61-90 91-120 121-150 151-180 > 180 Time (minutes) Multvariate-adjustedOdds ofIn-hospitalMortality
  • 22. Challenges for STEMI system of care in Myanmar • PCI is the GOLD standard, yet remains unaccessible to majority of patients. • Primary PCI is available to <10% STEMI patients in Myanmar. • 1.Lack of awareness • 2.Lack of transfer facilities. Unavailability of hospital with PCI facility. • 3.Casualty/ED –to cath lab Finance problem Obtaining consent Unavailability of cardiologist round the clock. • Patient awareness and education for early symptom identification. • Education required for General Practitioners /Physicians to implement early time dependent STEMI management.
  • 23. Total Ischemic Time 2013-2016 0 50 100 150 200 250 300 2013 2014 2015 2016 226.02 237.54 297.81 189.96 93.79 89.89 73.21 56.75 Patient delay System delay 01/19/2017 25How PPCI Program was started in Myanmar
  • 24. Ischaemic time according to mode of admission (2016) 371 300 338 271 33 30 0 50 100 150 200 250 300 350 400 Through ERC Through Network Total ischaemic time Pain to CCU Door to balloon Note: Data including are describing the time in Minutes
  • 25. Why it has to be stressed much regarding this approach ? • Time is Myocardium. • For each 30 min delay in treatment in STEMI patient,1 yr mortality increases by 7.5%. • Mortality benefit with primary PCI is lost if PCI related delay exceeded 60 min. Nallamothu et al ,Am J Cardiol,2004;94:772-774 • Practically, early fibrinolytic therapy can compensate for PCI related delay. • Proportional mortality reduction was significantly higher in patients treated within 2 hrs with fibrinolytics.. Circulation 2004;109:1223-1225
  • 26. But… Fibrinolytics Still important • Many patients present to hospitals without PCI capability • Even so… PCI often cannot realistically occur within 90 minutes • In NRMI 2006 Database, 27.6% of patients received fibrinolytic therapy Nallamothu BK, et al. Circulation 2005;111:761 Bates ER, et al. Circulation 2008;118:567 Antman EM, et al. JACC 2008;51:210 Gibson CM, et al. AHJ 2008;156:1035
  • 27. How best to combine the two strategies? • Can we improve on Primary PCI with concomitant (co- administered) fibrinolytics? • Immediate/Facilitated Approach • Should all fibrinolytic patients go to PCI? • Pharmacoinvasive approach • Deferred approach • Should only fibrinolytic “failures” get PCI? • Rescue approach
  • 28. STEMI Management • What are the options? •Primary PCI •Primary Fibrinolytic Therapy •Rescue PCI (fibrinolytic failures only) •Immediate/Facilitated PCI (<3 hours) •Pharmacoinvasive PCI (within 3-24 hours) •Deferred PCI (> 24 hours)
  • 29. Immediate/Facilitated PCI • Definition: PCI immediately (< 3 hours) after fibrinolytics • You may combine fibrinolytics with 2b/3a receptor inhibitors • Theory: Both PCI and Lytics = Rapid Early Reperfusion + Sustained Reperfusion
  • 30. Immediate/Facilitated PCI Why did it fail? • Early period post-lytics (within 3 hours) carries the highest risk of bleeding • Early period paradoxically is also pro-thrombotic due to degradation products • Immediate PCI may increase bleeding and also paradoxically increase ischaemic endpoints • 2b/3a inhibitors may reduce the thrombotic complications but at a cost of excess bleeding
  • 31.
  • 32. Pharmaco-Invasive Strategy Pharmcologic reperfusion therapy (lytics or half dose lytics + IIb/IIIa) followed by transfer to a PCI hospital for urgent cath/PCI (within 3-24 hours)
  • 33.
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  • 35.
  • 36.
  • 37.
  • 38.
  • 39.
  • 40.
  • 41. Options for Reperfusion Therapy at Non-PCI hospitals Transfer for Primary PCI is better than… Pharmaco-invasive strategy which is better than… Fibrinolysis alone
  • 42.
  • 43.
  • 44.
  • 45.
  • 46. What specific ACS strategies to NSTE-ACS • Timing of invasive strategy? ASAP? Depending on risk group? • Clopidogrel use: When? In Whom? How much? • GPIIb/IIIa receptor antagonist: When? Upstream? At catheterization? Routine? Provisional? • Enoxaparin? Heparin? DTI(bivalirudin)? Xa inhibitor (Fondaparinux)?
  • 47. Managing non-ST-segment elevation ACS by early invasive therapy improves long-term survival and reduces late myocardial infarction and rehospitalization for unstable angina Bavry AA, et al. J Am Coll Cardiol 2006;48:1319–1325
  • 48. Invasive and Ischemia-Guided Intervention Categories in Patients with Non-STEMI Acute Coronary Syndromes. Anderson JL, Morrow DA. N Engl J Med 2017;376:2053-2064
  • 49. 1. The concept of “risk” in the STEMI and NSTE-ACS patient applies only to ischemic events. 2. For primary PCI, it is all about door-to-balloon time: Antithrombin therapy doesn’t matter….
  • 50. • Recurrent ischemic events are associated with worse survival. • This is true for patients with ACS and those undergoing PCI. BUT… • The risk appears limited to the 30 days after the index event. • What about the bleeding events?
  • 51. SYNERGY LMWH ESSENCE 1994 1995 1996 1997 1998 1999 2000 2002 2003 2004 2005 20062001 CURE Clopidogrel Bleeding risk Ischemic risk GP IIb/IIIa blockers PRISM-PLUS PURSUIT ACUITYTACTICS TIMI-18 Early invasive PCI ~ 5% stents ~85% stents Drug-eluting stents ISAR-REACT 2 Milestones in ACS Management OASIS-5 [ Fondaparinux ] Anti-Thrombin Rx Anti-Platelet Rx Treatment Strategy Heparin Aspirin Conservative ICTUS Bivalirudin REPLACE 2 Adapted from and with the courtesy of Steven Manoukian, MD.
  • 52. 1992 1995 1998 2001 2004 2007 1997 1999 UFH LMWH TIMI 11B 2004 SYNERGY Bivalirudin 2003 REPLACE 2 ASA IIb/IIIa antagonists 1995 2001 1998 EPISTENT PURSUIT 2001 ESPRIT GUSTO 4 2004 ISAR REACT Clopidogrel CURE 2000 Anti-thrombotic agents Anti-platelet agents Evolving ACS Therapies and Patterns of Antithrombotic Use* ACUITY 2006 ISAR-REACT 2 * Width of bar represents approximate degree of use of antiplatelet or anticoagulants at a particular time
  • 53. • Clinical trials with GP IIb/IIIa inhibitors show reductions in recurrent ischemic events in risk-stratified subsets when they are added to unfractionated heparin. BUT… • Bleeding risks are clearly higher with GPI. • GPIs have never been shown to improve survival in the modern era of PCI or ACS management. • A strategy of bivalirudin appears at least as good as UFH + GPI in the ACS patients across the entire risk spectrum.
  • 54. • Major bleeding (with or without blood product transfusions) has emerged as a powerful independent predictor of early and late mortality in pts with NSTEMI, STEMI and in those undergoing PCI
  • 55. Time from Randomization in Days Cumulative%Mortality With MI 5.7% Without major bleed 2.0% Impact of Major Bleed and MI after Elective and Urgent PCI 1-Year Mortality (N=6,012) Without MI 1.9% With major bleed 8.8% Stone GW. J Inv Cardiol 2004;16(suppl G):12–17.
  • 56. Variable Groups O.R. (95% CI) p-value Creatinine clear. <30 mL/min 7.21 (2.53–20.51) <0.000130–60 mL/min 3.34 (1.92–5.78) 60–90 mL/min 1.57 (0.96–2.57) CHF Yes 4.38 (2.83–6.78) <0.0001 Major Bleeding Yes 3.26 (1.78–5.96) 0.0001 MI @30day Yes 2.77 (1.62–4.75) 0.0002 Urg Revasc @30d Yes 2.77 (1.15–6.71) .024 Hx angina Yes 2.18 (1.25–3.81) 0.006 Prior MI Yes 1.81 (1.09–3.03) 0.023 Diabetes Yes 1.64 (1.10–2.44) 0.015 Predictors of 1-year Mortality after Elective and Urgent PCI Stone GW. J Inv Cardiol 2004;16(suppl G):12–17.
  • 57. Mehran RM et al. In press EHJ Influence of Major Bleeding and MI in the First 30 Days on Risk of Death Over 1 Year Cox model adjusted for 36 baseline predictors, with MI and major bleeding (non-CABG) as time-updated covariates Of 13,819 enrolled pts, 524 (3.8%) died within 1 year Myocardial infarction 2.51 (1.95-3.25) <0.0001 Major bleeding without or before transfusion 2.00 (1.30-3.06) <0.0001 Major bleeding after transfusion 3.93 (2.95-5.24) <0.0001 HR ± 95% CI P-valueHR (95% CI)
  • 58. Mehran RM et al. In press EHJ Influence of Major Bleeding and MI in the First 30 Days on Risk of Death Over 1 Year Cox model adjusted for 36 baseline predictors, with MI and major bleeding (non-CABG) as time-updated covariates Of 13,819 enrolled pts, 524 (3.8%) died within 1 year Myocardial infarction 2.51 (1.95-3.25) <0.0001 Major bleeding without or before transfusion 2.00 (1.30-3.06) <0.0001 Major bleeding after transfusion 3.93 (2.95-5.24) <0.0001 HR ± 95% CI P-valueHR (95% CI) Attributable deaths 51.5* 66.5** Attributable deaths = N deaths among pts with the time updated event (attribute) X (adj. HR – 1)/adj. HR *9.8% of all deaths **12.7% of all deaths
  • 59. HR (95% CI) P-value Attributable deaths MI Day 0-1 17.6 (10.8 to 28.7) <0.001 21 Days 2-7 8.2 (5.0 to 13.6) <0.001 19 Days 8-30 2.9 (1.6 to 5.3) 0.001 12 Days 31+ 1.4 (0.9 to 2.1) 0.12 25 Major bleed Day 0-1 5.5 (2.7 to 11.0) <0.001 9 (non CABG) Days 2-7 5.8 (3.5 to 9.7) <0.001 18 Days 8-30 5.6 (3.5 to 8.8) <0.001 24 Days 31+ 2.4 (1.7 to 3.3) <0.001 42 Transfusion Day 0-1 6.7 (3.1 to 14.7) <0.001 7 Days 2-7 8.1 (4.6 to 14.1) <0.001 15 Days 8-30 6.4 (3.7 to 10.9) <0.001 17 Days 31+ 3.1 (2.1 to 4.5) <0.001 31 Influence of MI, Major Bleed and Transfusion in the First 30 Days on the Risk of Death Over 1 Year Mehran RM et al. In press EHJ 0.5 1 2 4 8 16 32 Hazard ratio (95% CI) Attributable deaths = N deaths among pts with the time updated event (attribute) X (adj. HR – 1)/adj. HR
  • 60. Associations with Mortality (Re)-MI  Mortality  (Re)-MI ??  Mortality Bleeding  Mortality  Bleeding  Mortality??
  • 61. Considerations in the Modern Era of ACS/PCI • 55-year-old male with 3 hours of chest pain ●Hx of HTN,  lipids ●Marked ST-segment depression leads II, III, aVL ●Elevated serum troponin T, CKMB 4 X ULN ●Normal renal function • 86-year-old female with 3 hours of chest pain ●Hx of DM, HTN,  lipids ●ECG non-specific (no prior study for comparison) ●Elevated troponin, normal CKMB ●Est. GFR 45 ml/min
  • 62. ACS-related Bleeding—Relevant Questions • Who bleeds? Can we risk stratify? • Should bleeding risk affect upstream antithrombotic care? If so, how? • Is bleeding bad or a necessary evil? • Can blood transfusion “correct” risks associated with bleeding? • Does bleeding affect resource use?
  • 63. Independent predictors of major bleeding in marker- positive acute coronary syndromes Moscucci, GRACE Registry, Eur Heart J. 2003 Oct;24(20):1815-23. Predictors of Major Bleeding in ACS • Older Age • Female Gender • Renal Failure • History of Bleeding • Right Heart Catheterization • GPIIb-IIIa Antagonists
  • 64. 26,452 patients from PURSUIT, PARAGON A, PARAGON B, GUSTO IIb NST Bleeding severity and adjusted hazard of death *p<0.0001 Bleeding and Outcomes in NSTE-ACS Rao SV, et al. Am J Cardiol. 2005 Nov 1;96(9):1200-6. Epub 2005 Sep 12. Bleeding Severity 30d Death 30d Death/MI 6 mo. Death Mild* 1.6 1.3 1.4 Moderate* 2.7 3.3 2.1 Severe* 10.6 5.6 7.5 *Bleeding as a time-dependent covariate
  • 65. • Bleeding is associated with adverse short- and long-term outcomes among patients with ACS and those undergoing PCI ● Mortality rates are higher among those who bleed ● MI rates are higher among those who bleed • Worse bleeding associated with worse outcomes • This relationship is persistent after robust statistical adjustment for confounders Bleeding and Outcomes in ACS
  • 66. 30-Day Survival By Transfusion Group Rao SV, et. al., JAMA 2004;292:1555–1562. Transfusion in ACS N=24,111 30-Day Survival By Transfusion Group
  • 67. • Blood transfusion is independently associated with worse short and long-term outcomes including death and recurrent MI • Transfusion does not correct the adverse impact bleeding and is associated with increased mortality in ACS patients • Blood transfusion is best avoided in ACS patients whenever possible and is associated with increased mortality in ACS patients Blood Transfusion in ACS
  • 68. Bleeding Among Patients with ACS • There are several therapeutic pathways for ACS care • Choices for therapy must take into account: ● Ischemic complications ● Bleeding complications • The risk for bleeding and ischemia increases from NSTE-ACS to STEMI
  • 69. White HD et al. JACC 2008;51:1734-41. Switching in ACUITY
  • 70. Reducing (re)MI—Effect on mortality Therapy Reduces mortality? Clopidogrel Modestly in STEMI GP IIb/IIIa No UFH No Enoxaparin No Yusuf S. et. al. NEJM 2001 Boersma E. et. al Lancet 2002 SYNERGY Investigators. JAMA 2004
  • 71. Switching Antithrombins: A Practical Strategy for the ACS Network SYNERGY ACUITY UVM Registry Antithrombin comparison Enoxaparin vs. UFH UFH/Enoxaparin vs. Bivalirudin UFH/Enoxaparin vs. Bivalirudin N 9978 7104 728 Pre-randomization antithrombin treatment 76% 59% 44% Switch (%) 35% 29% 44% Consistent Therapy vs. Switched (%) Does Not Favor Switching Favors Switching Neutral Death or MI 14.2% vs. 22.0%* 7.4% vs. 6.9% 8% vs. 7% Bleeding 15.1 % vs. 35.1* 5.8% vs. 2.8%+ 2% vs. 2%^
  • 72. Ischemic Complications ► Death ► MI ► Urgent TVR Evolving Paradigm for Evaluating ACS Management Strategies Composite Adverse Event Endpoints
  • 73. Ischemic Complications Hemorrhage HIT ► Death ► MI ► Urgent TVR ► Major Bleeding ► Minor Bleeding ► Thrombocytopenia Composite Adverse Event Endpoints Evolving Paradigm for Evaluating ACS Management Strategies
  • 74. Periprocedural Complications Clinical Benefit ► Death ► Major Disability ► Cost ► Ease of Use ► Duration of Therapy ► Accounting for Bleeding and Ischemic Endpoints Composite Adverse Event Endpoints Evolving Paradigm for Evaluating ACS Management Strategies
  • 75. • a balance must be struck between ischemia reduction and bleeding. • Both ischemic complications and bleeding are associated with increased costs.
  • 76. • Escalation of therapy for ischemia in this setting is associated with increased risk of bleeding • This “price to be paid” has generally been accepted and tolerated, especially in patients at high ischemic risk, who benefit disproportionately from advanced therapy • Enox superior to UFH in patients with higher TIMI Risk Scores • Clopidogrel + ASA superior to ASA alone in patients with higher TIMI Risk Scores • GP IIb/IIIa receptor antagonists benefit troponin positive patients more than troponin negative patients
  • 77. Changing the Calculations for Assessing Guidelines Adherence Anderson HV, Bach RG, J Am Coll Cardiol 2005;46:1488-9. “We need to invert the current equation to calculate an opportunity score for ACS patients rather than a risk score. Patients with higher baseline risks, such as the elderly, would have higher opportunity scores for benefit, even allowing for some of the greater risks from the treatment.”
  • 78. Balancing Efficacy and Safety • Current guidelines emphasize reduction of ischemic risk in NSTE ACS— especially for upstream therapy • Updated guidelines are expected to include data on the harm that bleeding events cause, diminishing ischemic efficacy in some patients • Most of physicians are comfortable with the goal of reducing ischemic risk . . . and traditionally have left concern over bleeding to “downstream providers” • “balanced” pharmacotherapy will require multidisciplinary collaboration, pathways, anticipation of consistent care (especially time from ED to cath), and individualized patient assessment
  • 79.
  • 80. ZONE 2- ်ား ႏေႏလုံးေအေတထေတထရာဂါကုေႏဆုံးရုၾကုံး၊ ႏ ႏလုုံးေႏတ ုံးေႏၾကာခ ်ဲ႕ဌာာ ု (၁ - ၂) ာာရအတြင္ႏုံးေႏရာက္ႏ ႏႏုင္ ( ေအရုံးေႏပၚ ႏလုုံးေႏတ ုံးေႏၾကာခ ်ဲ႕ကုေ ပုံးႏ ခင္ႏုံး ) ZONE 3- ်ား ႏေႏလုံးေအေတထေတထရာဂါကုေႏဆုံးရုၾကုံး၊ ႏ ႏလုုံးေႏတ ုံးေႏၾကာခ ်ဲ႕ဌာာ ု (၃) ာာရအတြင္ႏုံးေႏရာက္ႏ ႏႏုင္ ( ႏ ႏလုုံးေႏတ ုံးေႏၾကာပပင္ႏေႏဆုံးတ င္ႏုံးကုေ ပုံးႏ ခင္ႏုံး နင ႏ ႏလုုံးေႏတ ုံးေႏၾကာခ ်ဲ႕ဌာာ ုလူာာလႊႏ်ဲႏ ခင္ႏုံး )
  • 81. What have we learned and what can be done to improve the process of PPCI? 1. Patients’ delays: Public awareness of heart attacks 2. System Delays: 1. Late Arrival in the ER 2. Delay in the diagnosis at ER 3. Delay in the referral to CCU 01/19/2017 83How PPCI Program was started in Myanmar • single call activation to engage the cath lab • Bypass the ER • Develop prehospital alert and ECG transmission using Smartphone applications and cathlab activation before patient arrived to CCU • avoid delay to activate the team outside working hours • complete coverage for PPCI irrespective of the financial status
  • 82. 1st March 2015 MGH STEMI Network laughed on the day of celebration of second year anniversary of PPCI and Heart Attack Awareness Week Key To Improving STEMI Care: STEMI network 01/19/2017 84How PPCI Program was started in Myanmar
  • 83. 01/19/2017 85How PPCI Program was started in Myanmar
  • 84. Zone 1- 30 mins to MGH Cath lab lab 01/19/2017 86How PPCI Program was started in Myanmar
  • 85. Zone 2- 1hr to MGH cath lab Zone 3- 3hr to MGH cath lab 01/19/2017 87How PPCI Program was started in Myanmar
  • 86. Family Doctors ERC GP and Physicians ER MGH IDEAL STEMI care system 01/19/2017 88How PPCI Program was started in Myanmar
  • 87. Family Doctors ERC GP and Physicians ER MGH x x x x Our Aim 01/19/2017 89How PPCI Program was started in Myanmar
  • 88. Family Doctors GP and Physicians Call us and send ECG by Viber 09-259898661 09-259898662 01/19/2017 90How PPCI Program was started in Myanmar
  • 89. ERC ER MGH x xCall us and send ECG by Viber 09-259898661 09-259898662 01/19/2017 91How PPCI Program was started in Myanmar
  • 90. Total Ischemic Time 2013-2016 0 50 100 150 200 250 300 2013 2014 2015 2016 226.02 237.54 297.81 189.96 93.79 89.89 73.21 56.75 Patient delay System delay 01/19/2017 92How PPCI Program was started in Myanmar
  • 91. Ischaemic time according to mode of admission (2016) 371 300 338 271 33 30 0 50 100 150 200 250 300 350 400 Through ERC Through Network Total ischaemic time Pain to CCU Door to balloon Note: Data including are describing the time in Minutes