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Acute coronary syndromes in Indian context

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Brief overview of acute coronary syndromes presented during Nizamabad CME

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Acute coronary syndromes in Indian context

  1. 1. ACS – INITIAL DIAGNOSIS & MANAGEMENT Dr Uday Prashant M.D D.M
  2. 2. Very Alarming Scene • India is the Diabetic capital of the world:- Highest no of diabetics in world at present • Indians have one of highest rates of CAD • Obesity in India is in rapid rise
  3. 3. Coronary Artery Disease in Indians = CADI • How is it different from western world • CADI strikes early ! • CADI strikes almost any one !!! • CADI strikes unexpectedly !!!! • Conventional RF can’t explain it away • CADI is malignant in its onslaught.
  4. 4. The CADI Volcano • We are in the middle of the wave of CAD epidemic • This CADI epidemic will peak by 2015 • 50% deaths in India are CVD deaths. • CADI will overtake Infectious diseases in morbidity too • By 2015 CADI will be six times more than the West • CADI will be 20 times more than the Chinese,
  5. 5. ACS • Spectrum of presentation – – – – Myocardial infarction ( 25% – 30%) Non Q wave MI ( 30% - 35% ) unstable angina (30% - 35%) Sudden Cardiac Death (5% - 10%) Non Q wave MI / USA compromises 2/3 rd of ACS cases 15% - 20% of USA are high risk cases.
  6. 6. Sudden Cardiac Death
  7. 7. Immediately next ECG
  8. 8. New Terminology in ACS Plaque Rupture Old term Stable Angina Unstable Angina New term Atherothrombosis Non– Q-wave MI STEMI UA/NSTEMI Daysweeks Antithrombotic Therapy Q-wave MI Minuteshours Thrombolysis Primary PCI ACS, acute coronary syndrome; MI, myocardial infarction; UA, unstable angina; NSTEMI, non–ST-segment elevation myocardial infarction; STEMI, ST-segment elevation myocardial infarction; PCI, percutaneous coronary intervention. Cannon CP. J Thromb Thrombolysis. 1995;2:205-218.
  9. 9. Acute Coronary Syndrome Ischemic Discomfort Unstable Symptoms No ST-segment elevation Unstable angina History Physical Exam ST-segment elevation Non-Q AMI Q-Wave AMI ECG Acute Reperfusion
  10. 10. Pathogenesis of ACS Vulnerable Non-Vulnerable Atherosclerotic Atherosclerotic Plaque Plaque
  11. 11. The Matrix Skeleton of Unstable Coronary Artery Plaque Fissures in the fibrous cap Davies MJ. Circulation. 1996;94:2013-2020.
  12. 12. Vulnerable plaques • Vulnerable plaques cause ACS • Depends upon inner free lipid content, thin fibrous cap, active inflammation, hemodynamic stresses. • More than one vulnerable plaques can be present which are not Rx by PCI. • Vulnerable plaques cannot be detected by routine CAG. • Can be inferred indirectly by hsCRP – Rx high dose statins
  13. 13. Chest pain with ACS • 15 -25 % of chest pain cases in ED have ACS • 2 % of ACS are missed • These are current US data • In India the percentages are far higher • For Pt mortality / for us medicolegal implications
  14. 14. Clinical Classification of Chest Pain Diamond . J Am Coll Cardiol 1983
  15. 15. Typical Angna • Cardiac symptoms: Presence of acute chest, epigastric, neck, jaw, or arm pain or discomfort or pressure without apparent noncardiac source. • Levine`s sign may be +ve. • More general, atypical symptoms, such as fatigue, nausea, vomiting, diaphoresis, faintness, and back pain, should not be used as a diagnosis of Angina
  16. 16. CHD Risk Equivalents 1. Diabetes Mellitus 2. Peripheral Vascular Disease (PVD) 3. Framingham risk score of > 20% 4. Carotid artery disease – • • Stroke, TIA > 50% Narrowing, Carotid Bruit 5. Abdominal Aortic Aneurysm (AAA) Adult Treatment Panel III. NIH publication 01-3095.
  17. 17. Epidemiological definition of MI • Typical chest pain lasting for > 30 min not relieved by nitrates • ECG showing characteristic changes of MI • Positive cardiac biomarkers of injury WHO states any of two from above three should be present.
  18. 18. Definition of Acute/Evolving/Recent MI 1) Typical rise and fall of biochemical markers of MI with atleast 1 of them • Ischaemic symptoms • ECG changes indicative of ischaemia (ST elevation or depression or LBBB) • Development of pathological Q waves in ECG • New RWMA or imaging e/o loss of viable myocardium ACC/AHA/EU/WHO Task force for redefinition of MI 2007 guidelines
  19. 19. ST elevation • Occurs in the early stages R ST P Q • Occurs in the leads facing the infarction • Slight ST elevation may be normal in V1 or V2
  20. 20. Deep Q wave • Only diagnostic change of myocardial infarction R ST • At least 0.04 seconds in duration P T Q • Depth of more than 25% of ensuing R wave
  21. 21. T wave changes • Late change R • Occurs as ST elevation is returning to normal ST P • Apparent in many leads T Q
  22. 22. Bundle branch block Anterior wall MI I II III aVR aVL aVF V1 V2 V3 Left bundle branch block V4 V5 V6 I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
  23. 23. Sequence of changes in evolving AMI R R T R ST ST P P P QS T Q 1 minute after onset Q 1 hour or so after onset A few hours after onset R ST P P T Q A day or so after onset ST T P T Q Later changes Q A few months after AMI
  24. 24. Anterior infarction Anterior infarction I II III Left coronary artery aVR aVL aVF V1 V2 V3 V4 V5 V6
  25. 25. Inferior infarction Inferior infarction I II III Right coronary artery aVR aVL aVF V1 V2 V3 V4 V5 V6
  26. 26. Lateral infarction Lateral infarction I II III Left circumflex coronary artery aVR aVL aVF V1 V2 V3 V4 V5 V6
  27. 27. Location of infarct combinations I aVR LATERAL aVL II V1 ANT POST V2 V4 ANT SEPTAL V5 ANT V3 III INFERIOR aVF V6 LAT
  28. 28. Right Ventricular Infarction V4R Modified from Wellens. N Engl J Med 1999;340:381. Clinical findings: Shock with clear lungs, elevated JVP Kussmaul sign Hemodynamics: Increased RA pressure (y descent) Square root sign in RV tracing ECG: ST elevation in R sided leads Echo: Depressed RV function Rx: Maintain RV preload Lower RV afterload (PA---PCW) Inotropic support Reperfusion
  29. 29. Diagnostic criteria for AMI • • • • • Q wave duration of more than 0.04 seconds Q wave depth of more than 25% of ensuing r wave ST elevation in leads facing infarct (or depression in opposite leads) Deep T wave inversion overlying and adjacent to infarct Cardiac arrhythmias
  30. 30. Cor pulmonale
  31. 31. MI presenting as Syncope • 60 yrs sudden onset chest pain f/b syncope • H/o associated sweating + • Afterwards no chest pain • No risk factors other than age • Dilemma whether it is arrythmogenic syncope.
  32. 32. Trop T -Ve
  33. 33. Non ischaemic causes of ST elevation • • • • • • • Early repolarization changes. Prinzmetal angina Ventricular aneurysm Pericarditis myocarditis Hyperkalemia, Hypercalcemia LVH, LBBB IC bleed mistaken as MI
  34. 34. Mistaken MI • Lingam diagnosed as AWMI • CAG revealed critical lesion LAD • Underwent successful stenting to LAD • But patient still symptomatic • Presented with Grade IV dyspneoa • ECHO showed COR PULMONALE
  35. 35. Non MI causes of pathalogical Q waves • Norma septal Q waves V1-V2, III & AVF (narrow) • Cardiomyopathies. • Severe LVH, LBBB • Dextrocardia/version. • COPD
  36. 36. Young MI • • • • • • Devender 27 yrs male Non smoker Non diabetic H/O travel to dubai, elctrician Middle class family Chest pain 3 hrs duration
  37. 37. Homocysti(e)ne • Normal value is up to 10 μ mols/L • Excess of homocystine generates oxidative stress on the cell membranes. • Folic acid 5 mg/ day + Vit. B6 and B12 are to be given on regular basis
  38. 38. Hyper-homocyst(e)inemia Blood Homocyst(e)ine Levels Classification Normal Moderate Intermediate Severe Values mmol/L 05 – 10 11 – 30 31 – 100 > 100
  39. 39. Lipid Profile in Young Indian Patients Angiographically Proven CHD Parameter with % Patients Total cholesterol >200 mg/dl 54.3 Triglyceride >200 mg/dl 56.1 HDL <35 mg/dl 59.6 Lp(a) >30 mg/dl 61.4 n=57; age <40 yrs Mishra et al (Cuttack) Indian Heart J 2001; 53: Abst 60
  40. 40. CHD Risk Factors - Makers • Modifiable – The New Six – hs-CRP – Lp(a) – sLDL – Endothelial Dysfunction – Apo B / Apo A1 ratio – Homocysteine
  41. 41. Risk Factors for Future Cardiovascular Events: WHS Lipoprotein(a) Homocysteine IL-6 TC LDL-C sICAM-1 SAA Apo B TC:HDL-C hs-CRP hs-CRP + TC:HDL-C 0 1.0 2.0 4.0 6.0 Relative Risk of Future Cardiovascular Events Ridker PM et al. N Engl J Med 2000;342:836-843.
  42. 42. Post stent MI • Mr Rathod 60 yrs male. • 1999 had ACS, uderwent stenting and not on reqular follow up • Asymptomatic since then • Presented with typical h/o of MI
  43. 43. Clinical indicators of successful reperfusion • Resolution of chest pain by > 50% • Resolution of ST elevations by > 50% • AIVR • Rapid rise and fall of cardiac enzymes • Clinically stable course
  44. 44. For Managment • ST elevation MI :- Rapid thrombolysis vs immediate revascularization (Complete occlusion of lumen by red thrombus) • Non ST elevation MI:- Antithrombotics and plaque stabilization or cooling off. Early invasive strategy is controversial (Partial occlusion of lumen by white thrombus)
  45. 45. Management of MI • All management strategies focus on faster reperfusion of culprit artery. • Spontaneous recanalization rates after MI is 40 % • But it is after 12 – 24 hrs • Permanent damage has already set in
  46. 46. Management of MI • Within 30 minutes if reperfused no damage to myocardium. • Within 2- 4 hrs of reperfusion the damages are minimal. • After 6 hrs what we save is much less than what myocardium we loose
  47. 47. Management of MI • After 12 hrs no use of repurfusion • permanent damage sets in though surrounding hibernating myocardium can be saved. • To assess for hibernating myocardium we have Presence of chest pain TMT Nuclear Scans Dobutamine Stress Echo MRI etc
  48. 48. • ITS NOT GIVING RIGHT TREATMENT THAT IS IMPORTANT IN MI MANAGEMENT BUT HOW FAST WE ADMINISTER THAT IS IMPORTANT • For every 30 min delay in reperfusion the one year risk of relative mortality increases by 8%
  49. 49. y
  50. 50. ? MI • Laksmi presented with 2 hrs duration of severe chest pain • She 35 years female • ECG not fulfilling criteria of MI • Enzymes useless • Later ECHO except mild apical hypokinesia normal • CAG Prox LAD 90% stenosis.
  51. 51. Reperfusion Options for STEMI Patients Step 2: Select Reperfusion Treatment. If presentation is < 3 hours and there is no delay to an invasive strategy, there is no preference for either strategy. Fibrinolysis generally preferred  Early presentation ( ≤ 3 hours from symptom onset and delay to invasive strategy)  Invasive strategy not an option  Cath lab occupied or not available  Vascular access difficulties  No access to skilled PCI lab  Delay to invasive strategy  Prolonged transport  Door-to-balloon more than 90 minutes  > 1 hour vs fibrinolysis (fibrin-specific agent) now
  52. 52. Reperfusion Options for STEMI Patients Step 2: Select Reperfusion Treatment. If presentation is < 3 hours and there is no delay to an invasive strategy, there is no preference for either strategy. Invasive strategy generally preferred  Skilled PCI lab available with surgical backup  Door-to-balloon < 90 minutes • High Risk from STEMI  Cardiogenic shock, Killip class ≥ 3  Contraindications to fibrinolysis, including increased risk of bleeding and ICH  Late presentation  > 3 hours from symptom onset  Diagnosis of STEMI is in doubt
  53. 53. Fibrinolysis I IIa IIb III Fibrinolytic therapy should not be administered to asymptomatic patients whose initial symptoms of STEMI began more than 24 hours earlier. I IIa IIb III Fibrinolytic therapy should not be administered to patients whose 12-lead ECG shows only STsegment depression, except if a true posterior MI is suspected.
  54. 54. Contraindications and Cautions for Fibrinolysis in STEMI • Any prior intracranial hemorrhage Absolute Contraindications • Known structural cerebral vascular lesion (e.g., arteriovenous malformation) • Known malignant intracranial neoplasm (primary or metastatic) • Ischemic stroke within 3 months EXCEPT acute ischemic stroke within 3 hours NOTE: Age restriction for fibrinolysis has been removed compared with prior guidelines.
  55. 55. Contraindications and Cautions for Fibrinolysis in STEMI • Suspected aortic dissection Absolute Contraindications • Active bleeding or bleeding diathesis (excluding menses) • Significant closed-head or facial trauma within 3 months
  56. 56. Contraindications and Cautions for Fibrinolysis in STEMI Relative • History of chronic, severe, poorly controlled Contraindications hypertension • Severe uncontrolled hypertension on presentation (SBP > 180 mm Hg or DBP > 110 mm Hg) • History of prior ischemic stroke greater than 3 months, dementia, or known intracranial pathology not covered in contraindications • Traumatic or prolonged (> 10 minutes) CPR or major surgery (< 3 weeks)
  57. 57. Contraindications and Cautions for Fibrinolysis in STEMI Relative • Recent (< 2 to 4 weeks) internal bleeding Contraindications • Noncompressible vascular punctures • For streptokinase/anistreplase: prior exposure (> 5 days ago) or prior allergic reaction to these agents • Pregnancy • Active peptic ulcer • Current use of anticoagulants: the higher the INR, the higher the risk of bleeding
  58. 58. Choice of Thrombolytic • Underuse:- 50 – 70% of cases only given thrombolytics. • tPA: • • Less allergic reactions • • Less fibrinogen depletion (“clot selective”) • • Faster thrombolysis • • Slightly lower overall mortality • • • • 2) Streptokinase (SK): • Less expensive ($300 vs $2500) • Lower stroke rate (0.3% vs 0.8%) • Can’t use again secondary to antibody formation
  59. 59. Thrombolysis • 90 minute patency better with rt-PA than SK (70% vs 55% in Euro CoopStudy and 70% vs 43% in TIMI-1) • Patency at 24 hours roughly equal between tPA and SK • ISIS-3 – mortality identical in head to head comparison of tPA and SK • Many studies favor tPA over SK
  60. 60. Primary PTCA • Gangasagar 52 yrs male • H/O Diabetes • Chest pain for 4 hrs
  61. 61. Classification of USA Class I:- New onset angina or 7.1% accelerated angina. Class II:- Angina at rest but not within 48 hrs. 10.3% Class III:- Angina at rest within 48 hrs. 10.9% A:- Secondary angina(14%), B:- Primary angina ( 8.5%), C:- Post infarct angina (18.5%) Adapted from Braunwald E. Circulation 1989;80:410-4
  62. 62. Medical Management of Unstable Angina • • • • • • • Nitrates:- ISIS 4 Beta Blockers:- HINT Aspirin:- Cohen, RISC, Theroux et al Clopidogrel:- CURE, CREDO, CAPRIE Heparin Or LMWH:- ESSENCE, TIMI 11B, FRIC, GP2b3a inhibitors:- PRISM, EPIC PURSUIT, CAPTURE, PARAGON • Statin:- LIPID, PROVE IT TIMI 18, TNT, A to Z • ACE:- SAVE, SOLVD
  63. 63. Death, myocardial infarction, and major bleeds at 30 days in randomized trials of glycoprotein IIb/IIIa inhibitors (filled bars) vs. control (open bars) in a conservative strategy Authors/Task Force Members, et al. Eur Heart J 2007 28:1598-1660; doi:10.1093/eurheartj/ehm161
  64. 64. SHOCK Trial • Early invasive strategy was first proved beneficial in high risk MI patients by SHOCK trail than No role for Wait & Watch & Intervene Primary PCI is better than thrombolysis PAMI, DINAMI, etc – 24 RCT`s
  65. 65. Does same apply for USA management? Answer is:- NO 1) Plaque volume (constant) & vulnerability. 2) Type of Thrombus differs (white vs red) 3) Patent lumen
  66. 66. New Terminology in ACS Plaque Rupture Old term Stable Angina Unstable Angina New term Atherothrombosis Non– Q-wave MI STEMI UA/NSTEMI Daysweeks Antithrombotic Therapy Q-wave MI Minuteshours Thrombolysis Primary PCI ACS, acute coronary syndrome; MI, myocardial infarction; UA, unstable angina; NSTEMI, non–ST-segment elevation myocardial infarction; STEMI, ST-segment elevation myocardial infarction; PCI, percutaneous coronary intervention. Cannon CP. J Thromb Thrombolysis. 1995;2:205-218.
  67. 67. Risk Stratification Tools • Clinical Assessment • Standard ECG and Non-standard ECG leads • Markers – Other: IMA, BNP, CRP • Non-Invasive Studies – Echocardiogram – Exercise testing – Technetium-99m-sestamibi – MR angio, CT angio
  68. 68. Multimarker Strategy in ACS Myocyte Necrosis Troponin Inflammation hs-CRP, CD40L HbA1c Blood glucose Accelerated Atherosclerosis Morrow DA, et al. Circulation. 2003;108:250-252. Hemodynamic Stress BNP, NT-proBNP Ischaemia IMA
  69. 69. Short-Term Risk of Death or Nonfatal Myocardial Infarction in Patients With Unstable Angina Braunwald E et al.: Unstable angina: diagnosis and management. AHCPR Publication No 94-0602
  70. 70. Risk of Death or Myocardial Infarction According to Treatment Strategy and cTnI: TACTICS TIMI 18 Morrow DA et al. JAMA 2001;286:2405-12
  71. 71. TIMI Risk Score for UA/NSTEMI: 7 Independent Predictors – ≥3 CAD risk factors – Aged ≥65 years – Prior CAD (stenosis >50%) – Aspirin in last 7 days – >2 anginal events in ≤24 hours – ST deviation – Elevated cardiac markers (CK-MB or troponin) TIMI, thrombosis in myocardial infarction; UA, unstable angina; NSTEMI, non–ST-segment elevation myocardial infarction; CAD, coronary artery disease. Antman EM, et al. JAMA. 2000;284:835-842.
  72. 72. Global Registry of Acute Coronary Events (GRACE) risk score • The GRACE risk score (on a scale of 1 to 372, with higher scores indicating greater risk) is derived from readily available hospital admission variables, - including age, - heart rate, - systolic blood pressure, - creatinine level, - Killip class, - cardiac arrest at admission, - presence of ST-segment deviation, and - elevated cardiac biomarkers. Values for these variables can be entered into the GRACE risk calculator
  73. 73. GRACE Prediction Score Card and Nomogram for All-Cause Mortality From Discharge to 6 Months Anderson, J. L. et al. J Am Coll Cardiol 2007;50:e1-e157
  74. 74. Indications for early invasive strategy • Recurrent rest angina • Elevated troponin • New ST changes • LVF • Positive stress test • EF<40% • Haemodynamic instability • Malignant arrhythmias • PCI<6 months • CABG
  75. 75. Timing of Invasive strategy in Non ST Elevation MI
  76. 76. What is early and late • Early intervention is < 24 - 48 hours of presentation. • Late intervention is >36 - 48 hours of presentation
  77. 77. ISAR COOL • Early treatment reduces long term MI, mortality. • However procedure complications increase. • To offset it “cool off” or plaque pacifying strategy using prolonged antithrombotic & GP2b3a inhibitors.
  78. 78. ISAR COOL
  79. 79. SYNERGY Trial (Circulation. 2007;116:2669-2677.)
  80. 80. Conclusions SYNERGY Trial • High-risk patients with NSTE ACS who received earlier coronary angiography had a decreased risk of death/MI through 30 days.
  81. 81. Decision-making algorithm for the management of patients with non-ST-elevation acute coronary syndrome Authors/Task Force Members, et al. Eur Heart J 2007 28:1598-1660; doi:10.1093/eurheartj/ehm161
  82. 82. Case of USA • • • • Mr Sheik Ahhmed 45 yrs male Chronic smoker Labourer For past 2 months not able to work due to chest pain • Somebody has to hit him in back for relief of pain • Increasing frequency & duration of pain
  83. 83. y
  84. 84. Wallen`s Warning
  85. 85. Care of IHD patients • Primary prevention • Secondary prevention
  86. 86. The Progressive Development of Cardiovascular Disease Intervene here } Risk Factors Endothelial Dysfunction Atherosclerosis CAD Myocardial Ischemia Coronary Thrombosis Myocardial Infarction Arrhythmia & Muscle Loss Remodeling Ventricular Dilation Congestive Heart Failure End stage Heart Disease
  87. 87. Public Awareness A survey of people with Diabetes • Findings – 68% do not consider cardiovascular disease to be complication of diabetes – 50%+ don’t feel risk for heart condition or stroke – 60% don’t feel at risk for high blood pressure or cholesterol – Awareness lowest among elderly, minorities 2
  88. 88. Why is CAD becoming so rampant • Is it people are living longer? • Is it increasing habits like smoking cocaine? • Is it raise in Diabetes? • Is it food we eat? • Or is it all in the genes?
  89. 89. With in no time !!
  90. 90. Where are we heading ? ? 20000 B.C. 2004 Paleolithic sup. age Neolithic age Hunting-gathering subsistence High level of physical activity Thrifty genotype 19th century 21st century Processed foods ­ Animal fats and glucides ¯ Dietary fibre Sedentary life Susceptibility genotype Journal of internal medicine 2003:254(2):114-25
  91. 91. This is how we take our dog to walk!
  92. 92. Secondary Prevention of CAD
  93. 93. Secondary prevention • The above drugs are minimum for post MI/USA patients • If diabetic then OHA`S 1 + 2 drugs • If severe LV dysfunction diuretics, digoxin • If PVD or BPH or OA or ED – extra drugs • Post stent tripple antiplatelets common • Antacids, vitamins, calcium etc
  94. 94. Hippocrates said …. Let your FOOD be your Medicine – Lest, Your Medicines will replace your Food !!
  95. 95. THANK YOU 5/98 MedSlides.com 146

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