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Intervention treatment for acs

ACS

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Intervention treatment for acs

  1. 1. Interventional Management of ACS 18th Myanmar Internal Medicine Conference 2017 Melia Hotal 29th September 2017 Prof Kyaw Soe Win Mandalay General Hospital
  2. 2. 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.
  3. 3. 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
  4. 4. 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
  5. 5. 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
  6. 6. The important thing is Timing of intervention •?Immediate •?Early •?Delayed •?Elective
  7. 7. Acute STEMI 15 minutes 2 hours 6 hours % necrosis 0% 50% 90% Occlusive thrombus on a plaque of atheroma
  8. 8. 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
  9. 9. Total occlusion of proximal RCA from TIMI -0 to TIMI -3 after PPCI
  10. 10. 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
  11. 11. 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%
  12. 12.  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)
  13. 13. 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
  14. 14. 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
  15. 15. 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
  16. 16. 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
  17. 17.  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
  18. 18. 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
  19. 19. 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
  20. 20. 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.
  21. 21. 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
  22. 22. 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
  23. 23. 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
  24. 24. 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
  25. 25. 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
  26. 26. 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)
  27. 27. 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
  28. 28. 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
  29. 29. 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)
  30. 30. Options for Reperfusion Therapy at Non-PCI hospitals Transfer for Primary PCI is better than… Pharmaco-invasive strategy which is better than… Fibrinolysis alone
  31. 31. 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)?
  32. 32. 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
  33. 33. 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
  34. 34. 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….
  35. 35. • 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?
  36. 36. 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.
  37. 37. 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
  38. 38. • 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.
  39. 39. • 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
  40. 40. 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.
  41. 41. 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.
  42. 42. 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)
  43. 43. 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
  44. 44. 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
  45. 45. Associations with Mortality (Re)-MI  Mortality  (Re)-MI ??  Mortality Bleeding  Mortality  Bleeding  Mortality??
  46. 46. 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
  47. 47. 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?
  48. 48. 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
  49. 49. 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
  50. 50. • 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
  51. 51. 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
  52. 52. • 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
  53. 53. 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
  54. 54. White HD et al. JACC 2008;51:1734-41. Switching in ACUITY
  55. 55. 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
  56. 56. 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%^
  57. 57. Ischemic Complications ► Death ► MI ► Urgent TVR Evolving Paradigm for Evaluating ACS Management Strategies Composite Adverse Event Endpoints
  58. 58. Ischemic Complications Hemorrhage HIT ► Death ► MI ► Urgent TVR ► Major Bleeding ► Minor Bleeding ► Thrombocytopenia Composite Adverse Event Endpoints Evolving Paradigm for Evaluating ACS Management Strategies
  59. 59. 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
  60. 60. • a balance must be struck between ischemia reduction and bleeding. • Both ischemic complications and bleeding are associated with increased costs.
  61. 61. • 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
  62. 62. 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.”
  63. 63. 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
  64. 64. 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 )
  65. 65. 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
  66. 66. 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
  67. 67. 01/19/2017 85How PPCI Program was started in Myanmar
  68. 68. Zone 1- 30 mins to MGH Cath lab lab 01/19/2017 86How PPCI Program was started in Myanmar
  69. 69. Zone 2- 1hr to MGH cath lab Zone 3- 3hr to MGH cath lab 01/19/2017 87How PPCI Program was started in Myanmar
  70. 70. Family Doctors ERC GP and Physicians ER MGH IDEAL STEMI care system 01/19/2017 88How PPCI Program was started in Myanmar
  71. 71. Family Doctors ERC GP and Physicians ER MGH x x x x Our Aim 01/19/2017 89How PPCI Program was started in Myanmar
  72. 72. 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
  73. 73. 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
  74. 74. 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
  75. 75. 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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