Dr. m vinod cardiologist


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Dr. m vinod cardiologist

  1. 1. Dr . M. Vinod Kumar. M.D., D.M.(Cardiology)Interventional Cardiologist
  2. 2.  Definition ,pathology and diagnosis Risk stratification Medical management Secondary prevention
  3. 3. Applying Classification of Recommendations and Level of EvidenceClass I Class IIa Class IIb Class IIIBenefit >>> Risk Benefit >> Risk Benefit ≥ Risk Risk ≥ Benefit Additional studies with Additional studies with No additional studies focused objectives broad objectives needed; needed needed Additional registry data would be helpful Procedure/TreatmentProcedure/ Treatment IT IS REASONABLE to should NOT beSHOULD be perform Procedure/Treatment performed/administeredperformed/ procedure/administer MAY BE CONSIDERED SINCE IT IS NOTadministered treatment HELPFUL AND MAY BE HARMFULLevel A: Recommendation based on evidence from multiple randomized trials or meta-analyses Multiple (3-5) population risk strata evaluated; General consistency of direction and magnitude of effectLevel B: Recommendation based on evidence from a single randomized trial or non-randomized studies Limited (2-3) population risk strata evaluatedLevel C: Recommendation based on expert opinion, case studies, or standard-of-care Very limited (1-2) population risk strata evaluated
  4. 4.  ST Elevation Myocardial infarction (STEMI) is a major public health problem in both the developed and the developing countries in the world. The incidence in the developing countries is now similar to that in the developed countries. Approximately 3-4 per cent of Indians in rural areas and 8-10 per cent in urban areas have CAD.
  5. 5.  STEMI is fatal in about one third of the patients, with 50% deaths occurring in the first hour from ventricular tachy arrhythmias. Time to thrombolysis remains a key modifiable determinant of mortality in STEMI.
  6. 6.  Rapid diagnosis and early risk stratification of patients presenting with acute chest pain constitute the pillars of success in STEMI management. An efficient regional system of care based on pre-hospital diagnosis, triage and rapid transportation to the best available facility holds the key to success of treatment and significantly improves outcome.
  7. 7. Revised Definition of Myocardial Infarction Criteria for Acute, Evolving, or Recent MI Either of the following criteria satisfies the diagnosis for acute, evolving, or recent MI:1. Typical rise and/or fall of biochemical markers of myocardial necrosis with at least one of the following: a. Ischemic symptoms b. Development of pathologic Q waves in the ECG c. Electrocardiographic changes indicative of ischemia (ST-segment elevation ) d. Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality2. Pathologic findings of an acute myocardial infarction
  8. 8. 1. Spontaneous ( primary) myocardial infarction2. Myocardial infarction secondary3. Sudden unexpected cardiac death, including cardiac arrest4a . Myocardial infarction associated with PCI4b. Myocardial infarction associated with stent thrombosis5. Myocardial infarction associated with CABG
  9. 9.  Almost all MIs result from coronary atherosclerosis. An ACS develops when the vulnerable or high-risk plaque undergoes disruption of the fibrous cap. Disruption of the plaque is the stimulus for thrombogenesis. Following disruption of a vulnerable or high-risk plaque reduction of flow through the affected epicardial coronary artery. The flow reduction may be caused by a completely occlusive thrombus leads to STEMI or subtotally occlusive thrombus leads to UA/NSTEMI.
  10. 10. Acute Coronary Syndromes. Anderson J L et al. Circulation 2011;123:e426-e579Copyright © American Heart Association
  11. 11.  Symptoms such as anginal chest pain, dyspnoe, palpitation, diaphoresis etc ECG: ST segment elevation or new onset LBBB Enzymes : CKMB, Trop T and I
  12. 12. Electrocardiogram Show 12-lead ECG results to emergency physicianI IIa IIb III within 10 minutes of ED arrival in all patients with chest discomfort (or anginal equivalent) or other symptoms of STEMI.I IIa IIb III In patients with inferior STEMI, ECG leads should also be obtained to screen for right ventricular infarction.
  13. 13. I IIa IIb III Laboratory examinations should be performed as part of the management of STEMI patients, but should not delay the implementation of reperfusion therapy.  Serum biomarkers for cardiac damage  Complete blood count (CBC) with platelets  International normalized ratio (INR)  Activated partial thromboplastin time (aPTT)  Electrolytes and magnesium  Blood urea nitrogen (BUN)  Creatinine  Glucose  Complete lipid profile
  14. 14. I IIa IIb III Cardiac-specific troponins should be used as the optimum biomarkers for the evaluation of patients with STEMI who have coexistent skeletal muscle injury. For patients with ST elevation on the 12-lead ECG andI IIa IIb III symptoms of STEMI, reperfusion therapy should be initiated as soon as possible and is not contingent on a biomarker assay.
  15. 15. 100Multiples of the URL 50 Cardiac troponin-no reperfusion 20 Cardiac troponin-reperfusion 10 CKMB- no reperfusion CKMB- reperfusion 5 2 Upper reference limit 1 0 1 2 3 4 5 6 7 8 URL = 99th %tile of Days After Onset of STEMI Reference Control Group
  16. 16.  There is risk stratification within STEMI, but in general, STEMI is high-risk. Important to select greater-risk patients who warrant more aggressive strategies for prevention of future serious events such as reinfarction or sudden death.
  17. 17.  Occurs in several stages  Initial presentation  In-hospital course (CCU, intermediate CU)  At the time of hospital discharge
  18. 18.  Prior angina pectoris  ECG Criteria Prior MI  Markedly elevated cardiac Female gender enzymes Hypertension  Elevated BUN History of CHF  Complications Hyperlipidemia  VSR/PMD-rupture Diabetes  Myocardial rupture
  19. 19.  Anterior MI/ Persisting ST elevation Q waves in multiple leads RVMI + IWMI High sum of ST elevation Reciprocal ( anterior ) ST depression Persisting ST depression Prolonged QT Conduction defects/ heart block Sinus tachycardia/atrial fibrillation
  20. 20.  TIMI GRACE killips PURSUIT best used to supplement—not replace—clinical judgment less useful in atypical presentations, but indeed validated in an ED population . . .
  21. 21. (David A et al. TIMI Risk Score for ………..: An Intravenous nPA for Treatment of Infarcting Myocardium Early II Trial Substudy. Circulation 2000, 102:2031-2037)
  22. 22. CLASS CLINICAL FINDINGS 30 DAY MORTALITY RATEClass 1 No rales, no 3rd 2.8% heart soundClass 2 Rales in <1⁄2 lung 8.8% field or presence of a 3rd heart soundClass 3 Rales in >1⁄2 lung 14.4% field–pulmonary edemaClass 4 Cardiogenic shock– 67% determined clinically
  23. 23.  The first goal for healthcare professionals is to diagnose in a very rapid manner whether the patient is having an STEMI or NSTEMI because therapy differs between the 2 types of myocardial infarction.
  24. 24.  As a general rule, initial therapy for acute myocardial infarction is directed toward restoration of perfusion as soon as possible to salvage as much of the jeopardized myocardium as possible. This may be accomplished through medical or mechanical means, such as PCI or CABG.
  25. 25.  If STEMI is present, the decision as to whether the patient will be treated with thrombolysis or primary PCI should be made within the next 10 minutes. The goal for patients with STEMI should be to achieve a door- to-drug time of within 30 minutes and a door-to-balloon time of within 90 minutes.
  26. 26.  Critical factors that weigh into the selection of a reperfusion strategy include the following: The time elapsed since the onset of symptoms The risk associated with STEMI The risk of administering a fibrinolytic The time required to initiate an invasive strategy .
  27. 27.  Further treatment is based on the following: Restoration of the balance between the oxygen supply and demand to prevent further ischemia Pain relief Prevention and treatment of any complications that may arise
  28. 28. 1. Airway, Breathing, Circulation (ABC)2. Vital signs, general observation3. Presence or absence of jugular venous distension4. Pulmonary auscultation for rales5. Cardiac auscultation for murmurs and gallops6. Presence or absence of stroke
  29. 29.  MONA  Morphine  Oxygen  Nitroglycerin  Aspirin
  30. 30.  Pain contribute to the heightened sympathetic activity Management of STEMI patients in the emergency department should aim to relieve pain.
  31. 31.  Control of cardiac pain typically uses a combination of nitrates, analgesics (e.g., morphine), oxygen, and in appropriately selected patients, beta-adrenergic blocking agents.
  32. 32.  ANALGESICS. Although a wide variety of analgesic agents has been used to treat the pain associated with STEMI, including meperidine, pentazocine, and morphine. Morphine remains the drug of choice, except in patients with well-documented morphine hypersensitivity.
  33. 33.  A dose of 4 to 8 mg intravenously. Doses of 2 to 8 mg repeated at intervals of 5 to 15 minutes Toxicity —hypotension, depression of respiration, or severe vomiting. Morphine has unequivocal beneficial effects in patients with pulmonary edema because of peripheral arterial and venous dilation .
  34. 34. Morphine sulfate (2 to 4 mg intravenously withI IIa IIb III increments of 2 to 8 mg intravenously repeated at 5 to 15 minute intervals) is the analgesic of choice for management of pain associated with STEMI.
  35. 35.  OXYGEN. Hypoxemia results from ventilation-perfusion abnormalities are sequelae of left ventricular failure. Oxygen should be administered to patients with STEMI when arterial hypoxemia is clinically evident or can be documented by measurement (e.g., Sao2 < 90%). The delivery of 2 to 4 liters/min of 100% oxygen by mask or nasal prongs for 6 to 12 hours is satisfactory for most patients with mild hypoxemia.
  36. 36.  Oxygen Arterial oxygen desaturation (SaO2 < 90%) Class I(B) Uncomplicated STEMI during the first 6 hours Class IIa(c)
  37. 37.  NITRATES. Ability to enhance coronary blood flow by coronary vasodilation Decrease ventricular preload by increasing venous capacitance.
  38. 38. I IIa IIb III Patients with ongoing ischemic discomfort should receive sublingual NTG (0.4 mg) every 5 minutes for a total of 3 doses, after which an assessment should be made about the need for intravenous NTG.I IIa IIb III Intravenous NTG is indicated for relief of ongoing ischemic discomfort that responds to nitrate therapy, control of hypertension, or management of pulmonary congestion.
  39. 39. NitroglycerinI IIa IIb III Nitrates should not be administered to patients with: • systolic pressure < 90 mm Hg or ≥ to 30 mm Hg below baseline • severe bradycardia (< 50 bpm) • suspected RV infarction.I IIa IIb III Nitrates should not be administered to patients who have received a phosphodiesterase inhibitor for erectile dysfunction within the last 24 hours (48 hours for tadalafil).
  40. 40.  Long-acting oral nitrate preparations should be avoided in the early course of STEMI because of the frequently changing hemodynamic status of the patient.
  41. 41.  In patients with a prolonged period of waxing and waning chest pain, intravenous nitroglycerin may help to control symptoms and correct ischemia, but requires frequent monitoring of blood pressure.
  42. 42.  Relieve ischemic pain, reduce need for analgesics, reduce infarct size and life-threatening arrhythmias Reduce heart rate, decrease myocardial oxyzen demand .
  43. 43.  Avoid early intravenous beta blockade in patients presenting in Killip class II or higher.
  44. 44.  Favorable effects with metoprolol, atenolol, carvedilol and timolol. Beta blockers with intrinsic sympathomimetic activity probably should not be chosen. Trial of esmolol in the presence of relative contraindications.
  45. 45. Effects of Metoprolol COMMIT (N = 45,852) Totality of Evidence (N = 52,411) Death 13% P=0.0006 ReMI 30% relative 22% increase in P=0.0002 *cardiogenic shock VF 15% P=0.002 Lancet. 2005;366:1622.*Risk factors for cardiogenic shock :heart failure, age > 70 , systolic bloodpressure < 120, sinus tachycardia > 110 or heart rate < 60, increased time sinceonset of STEMI symptoms
  46. 46. Beta-Blockers Oral beta-blocker therapy should be administered promptly to those patients without a contraindication, irrespective of concomitant fibrinolytic therapy or performance of primary PCI. contraindications 1) signs of heart failure, 2) evidence of a low output state,I IIa IIb III 3) increased risk for cardiogenic shock, or 4) relative contraindications to beta blockade  1AVB > 0.24 sec,  2nd- or 3rd-degree heart block  reactive airway disease
  47. 47.  It is reasonable to administer intravenous beta-blockers promptly to STEMI patients without contraindications, especially if a tachyarrhythmia or hypertension is present.  contraindications signs of heart failure, evidence of a low output state, increased risk for cardiogenic shock, orII IIa IIb III IIa IIb III relative contraindications to beta blockade 1AVB > 0.24 sec, 2nd- or 3rd-degree heart block reactive airway disease
  48. 48. Beta-BlockersRecommendations - Class III (A)• IV beta blockers SHOULD NOT be administered to STEMI patients who have any of the following: 1) signs of heart failure 2) evidence of a low output state 3) increased risk for cardiogenic shock 4) relative contraindications to beta blockade  1AVB > 0.24 sec,  2nd- or 3rd-degree heart block  reactive airway disease
  49. 49.  Aspirin Aspirin is useful for the primary prevention of vascular events Effective across the entire spectrum of acute coronary syndromes Part of the initial management strategy for patients with suspected STEMI.
  50. 50.  In a dose of 162 mg or more, aspirin produces a rapid clinical antithrombotic effect caused by immediate and near-total inhibition of thromboxane A2 production. ISIS-2-->ASA led to 23% reduction in mortality.
  51. 51.  Because low doses (40 to 80 mg) take several days to achieve full antiplatelet effect, at least 162 to 325 mg should be administered acutely in the emergency department. To achieve therapeutic blood levels rapidly, the patient should chew the tablet to promote buccal absorption rather than absorption through the gastric mucosa.
  52. 52. I IIa IIb III Aspirin should be chewed by patients who have not taken aspirin before presentation with STEMI. TheI IIa IIb III initial dose should be 162 mg (Level of Evidence: A) to 325 mg (Level of Evidence: C) Although some trials have used enteric-coated aspirin for initial dosing, more rapid buccal absorption occurs with non–enteric- coated formulations.
  53. 53. Aspirin A daily dose of aspirin (initial dose of 162 to 325 mgI IIa IIb III orally; maintenance dose of 75 to 162 mg) should be given indefinitely after STEMI to all patients without a true aspirin allergy.
  54. 54. ReperfusionThe medical system goal is to facilitate rapid recognition andtreatment of patients with STEMI such that door-to- needle(or medical contact–to-needle) time for initiation offibrinolytic therapy can be achieved within 30 minutes or thatdoor-to-balloon (or medical contact–to- balloon) time for PCIcan be kept within 90 minutes.
  55. 55. Reperfusion Options for STEMI Patients 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
  56. 56. Reperfusion Options for STEMI Patients 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
  57. 57. Symptom Onset to Balloon Time and Mortality in Primary PCI for STEMI 6 RCTs of Primary PCI by Zwolle Group 1994 – 2001 N = 1791 12 P < 0.0001 One-year mortality, % 10 8 6 4 RR = 1.08 [1.01 – 1.16] for each 30 min delay 2 (P = 0.04) 0 0 60 120 180 240 300 360 Symptoms to balloon inflation (minutes)DeLuca et al. Circulation 2004;109:1223.
  58. 58. PCI vs Fibrinolysis for STEMI: Short Term Clinical Outcomes 35 30 PCI P < 0.0001 Fibrinolysis Frequency (%) 25 21 20 P < 0.0001 15 P=0.0002 13 P=0.0003 P < 0.0001 P=0.032 9 8 10 7 7 7 7 P=0.0004 6 P < 0.0001 5 4.5 5 2.2 1 2 0 1 0 Death Death, Recurr. Recurr. Total Hemorrh. Major Death no MI Ischemia Stroke Stroke Bleed MI SHOCK data CVA N = 7739Keeley et al. The Lancet 2003;361:13.
  59. 59.  Fibrinolysis The principal goal of fibrinolysis is prompt restoration of full IRA patency. Promote conversion of plasminogen to plasmin, which subsequently lyses fibrin thrombi.
  60. 60.  Fibrinolysis Recanalizes thrombotic occlusion associated with STEMI Restoration of coronary flow reduces infarct size Improves myocardial function. Improves survival over the short and the long term.
  61. 61.  INTRACORONARY FIBRINOLYSIS. In current practice, patients are more likely to be treated by PCI. This has reopened the concept of delivering fibrinolytic agents via the intracoronary route, but such efforts at present are largely restricted to adjunctive use during complicated PCI procedures.
  62. 62.  INTRAVENOUS FIBRINOLYSIS Streptokinase , tPA,, TNK, rPA TNK and rPA - bolus fibrinolytics
  63. 63.  WP-4 hr. t-PA is the preferred treatment streptokinase t-PA equivalent choices -risk of death is low , and increased risk of ICH . WP-4 to 12 hr . streptokinase and t-PA are equivalent options, but streptokinase is probably preferable to t-PA because of cost considerations
  64. 64. (Antman EM et al: ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction. Circulation 110:e82, 2004.)PARAMETER STREPTOKINASE ALTEPLASE RETEPLASE TNK t-PA Up to 100 mg in 10 U ? 2 (30 min 30-50 mg basedDose 1.5 MU in 30-60 min 90 min (based on apart) each over on weight weight) 2 minBolus administration No No Yes YesAntigenic Yes No No No Allergic reactionshypotension most Yes No No NocommonSystemic fibrinogen Marked Mild Moderate Minimaldepletion90-min patency rates (%) ≈50 ≈75 ≈75 ≈75TIMI grade 3 flow (%) 32 54 60 63Cost per dose (Rs) 2500 39375 (50mg)
  65. 65. GISSI-1: Streptokinase 18% reduction in mortality at 21 dGUSTO-1: tPA. 15% reduction in 30-day mortality comparedto StreptokinaseGUSTO-3: Reteplase had no benefit over tPA but is easier touse (double bolus)ASSENT: TNKase is similar to tPA but with less non-cerebralbleeding and better mortality with symptoms>4 hrs: Singlebolus, fibrin selective, resistance to PAI-1*Overall risk of ICH is 0.7%; Strokes occurred in 1.4%
  66. 66. Fibrinolysis In the absence of contraindications, fibrinolyticI IIa IIb III therapy should be administered to STEMI patients with symptom onset within the prior 12 hours and new or presumably new left bundle branch block (LBBB).
  67. 67. Fibrinolysis In the absence of contraindications, it is reasonable toI IIa IIb III administer fibrinolytic therapy to STEMI patients with symptom onset within the prior 12 hours and 12-lead ECG findings consistent with a true posterior MI. In the absence of contraindications, it is reasonable to administer fibrinolytic therapy to patients with symptoms of STEMI beginning in the prior 12 to 24 hours who have continuing ischemic symptoms and ST elevation > 0.1 mV in ≥ 2 contiguous precordial leads or ≥ 2 adjacent limb leads.
  68. 68. FibrinolysisI 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 ST-segment depression, except if a true posterior MI is suspected.
  69. 69. Contraindications and Cautions for Fibrinolysis in STEMI Any prior intracranial hemorrhageAbsoluteContraindications 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 Suspected aortic dissection Active bleeding or bleeding diathesis (excluding menses) Significant closed-head or facial trauma within 3 months
  70. 70. Contraindications and Cautions for Fibrinolysis in STEMIRelative • History of chronic, severe, poorly controlledContraindications 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)
  71. 71. Contraindications and Cautions for Fibrinolysis in STEMIRelative • Recent (< 2 to 4 weeks) internal bleedingContraindications • 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
  72. 72.  Fibrinolytics given between 12 and 24 hours No mortality benefit - LATE and EMERAS trials Increases risk of cardiac rupture (elderly population) Preferable to restrict late fibrinolytic administration to patients younger than 65 years with ongoing ischemia, especially those with large anterior infarctions.
  73. 73.  Delays in the administration of thrombolysis often occur because of the following factors: Delay in obtaining an ECG Interpretation Lack of immediate availability of thrombolytic agents
  74. 74.  EFFECT OF FIBRINOLYTIC THERAPY ON MORTALITY. Early intravenous fibrinolysis undoubtedly improves survival. The gretest benefit when administered as early as possible. Most dramatic results when given less than 2 hours after symptoms begin. 18% - 25% reduction in short-term mortality.
  75. 75.  Hazards of fibrinolysis Stroke (0.9–1.0%) - firstday after treatment, Largely attributable to cerebral haemorrhage. Advanced age, lower weight, female gender, prior cerebrovascular disease, and systolic and diastolic hypertension on admission are significant predictors of intracranial haemorrhage. Major non-cerebral bleeds (bleeding complications requiring blood transfusion or that are life-threatening) occur in 4–13% of the patients treated.
  76. 76.  Streptokinase may be associated with hypotension, but severe allergic reactions are rare. Re-administration of streptokinase should be avoided because of antibodies, which can impair its activity, and because of the risk of allergic reactions.
  77. 77. Primary PCI for STEMI: General Considerations Patient with STEMI (including posterior MI) or MI with new or presumably new LBBB PCI of infarct artery within 12 hours of symptom onset Balloon inflation within 90 minutes of presentationI IIa IIb III Skilled personnel available (individual performs > 75 procedures per year) Appropriate lab environment (lab performs > 200 PCIs/year of which at least 36 are primary PCI for STEMI) Cardiac surgical backup available
  78. 78. Primary PCI for STEMI: Specific Considerations Primary PCI should be performed in patients less thanI IIa IIb III 75 years old with ST elevation or LBBB who develop shock within 36 hours of MI and are suitable for revascularization that can be performed within 18 hours of shock.
  79. 79. Primary PCI for STEMI: Specific Considerations Primary PCI is reasonable in selected patients 75 years orI IIa IIb III older with ST elevation or LBBB who develop shock within 36 hours of MI and are suitable for revascularization that can be performed within 18 hours of shock.
  80. 80. Primary PCI for STEMI: Specific Considerations It is reasonable to perform primary PCI for patients with onset of symptoms within the prior 12 to 24 hours and 1 or more of the following: a. Severe CHFI IIa IIb III b. Hemodynamic or electrical instability c. Persistent ischemic symptoms.
  81. 81. PCI After FibrinolysisI IIa IIb III It is reasonable to perform routine PCI in patients with left ventricular ejection fraction (LVEF) ≤ 0.40, CHF, or serious ventricular arrhythmias.I IIa IIb III It is reasonable to perform PCI when there is documented clinical heart failure during the acute episode, even though subsequent evaluation shows preserved LV function (LVEF > 0.40).I IIa IIb III Routine PCI might be considered as part of an invasive strategy after fibrinolytic therapy.
  82. 82. Assessment of ReperfusionI IIa IIb III It is reasonable to monitor the pattern of ST elevation, cardiac rhythm and clinical symptoms over the 60 to 180 minutes after initiation of fibrinolytic therapy. Noninvasive findings suggestive of reperfusion include:  Relief of symptoms  Maintenance and restoration of hemodynamic and/or electrical instability  Reduction of ≥ 50% of the initial ST-segment elevation pattern on follow-up ECG 60 to 90 minutes after initiation of therapy.
  83. 83.  Flow in the IRA angiographically Gd. 0, complete Occlussion Gd. 1, some penetration Gd.2, entire vessel with Impaired flow Gd.3, entire vessel with Normal flow
  84. 84. Rescue PCIIt is reasonable to perform rescue PCIfor patients with one or more of the following:Hemodynamic or electrical instabilityPersistent ischemic symptoms orFibrinolytic therapy has failed (ST-segment elevation < 50%, resolved after 90 minutes following initiation of fibrinolytic therapy in the lead showing the worst initial elevation),A moderate or large area of myocardium at risk (Class II; LOE -B).
  85. 85.  Coronary artery bypass graft surgery should be considered when recurrent ischemia occurs in patients with STEMI whose coronary artery anatomy is not suitable for PCI. This is a class I level b indication
  86. 86.  Coronary angiography should not be performed in patients following fibrinolytic therapy with extensive comorbidities in whom the risks of revascularization are likely to outweigh the benefits (Class III; LOE, C).
  87. 87.  Establishing & maintaining patency of IRA. For prevention of DVT pulmonary embolism ventricular thrombus cerebral embolization
  88. 88. • Anticoagulant regimens with established efficacy include: UFH Enoxaparin Fondaparinux• Patients undergoing reperfusion with fibrinolytics should receive anticoagulant therapy for a minimum of 48 hours (Class IIa; C)• Preferably for the duration of the index hospitalization, up to 8 days when using regimens other than unfractionated heparin (UFH) (Class IIa; A).
  89. 89.  Trials shown that more prolonged anticoagulant therapy is beneficial (duration of index hospitalization) in patients receiving thrombolytic therapy
  90. 90.  Recommendations for Anticoagulant TherapyANTICOAGULATION WITH FIBRINOLYSIS. A regimen of UFH bolus at 60 U/kg to a maximum of 4000 U, followed by an initial infusion of 12 U/kg/hr to a maximum of 1000 U/hr given for 48 hours. Administration of enoxaparin or fondaparinux is preferred when administration of an anticoagulant for longer than 48 hours is planned for patients with STEMI treated with a fibrinolytic.
  91. 91. ADJUNCTIVE ANTICOAGULATION FOR PRIMARY PERCUTANEOUS INTERVENTION. UFH is recommended for patients undergoing primary PCI .PATIENTS TREATED WITHOUT REPERFUSION THERAPY. In STEMI patients not receiving reperfusion therapy, fondaparinux reduces the composite of death or recurrent MI without an increase in severe bleeding as compared with placebo or UFH
  92. 92.  Recommendations for Antiplatelet Therapy During the maintenance phase of antiplatelet therapy following STEMI, the dose of aspirin should be reduced to 75 to 162 mg to minimize bleeding risk. If true aspirin allergy is present, other antiplatelet agents such as clopidogrel (loading dose, 300 to 600 mg; maintenance dose, 75 mg/day) or ticlopidine (loading dose, 500 mg; maintenance dose, 250 mg twice daily) can be substituted.
  93. 93.  The addition of a P2Y12 inhibitor to aspirin is warranted for most patients with STEMI. Based on the results of the COMMIT and CLARITY-TIMI 2 trials, Clopidogrel at 75 mg/day orally is an alternative for all patients with STEMI, regardless of whether they receive fibrinolytic therapy, undergo primary PCI, or do not receive reperfusion therapy. (Class I; lOE, B). The available data suggest that a loading dose of 300 mg of clopidogrel should be given to patients younger than 75 years of age who receive fibrinolytic therapy.
  94. 94. In patients for whom PCI is planned, clopidogrel should be startedand continued: • ≥ 1 month after bare-metal stent • ≥ 3 months after sirolimus-eluting stent • ≥ 6 months after paclitaxel-eluting stent • Up to 12 months in absence of high risk for bleeding.
  95. 95. Thienopyridines In patients taking clopidogrel in whom CABG isI IIa IIb III planned, the drug should be withheld for at least 5 days, and preferably for 7 days, unless the urgency for revascularization outweighs the risk of excessive bleeding.
  96. 96. Glycoprotein IIb/IIIa InhibitorsI IIa IIb III It is reasonable to start treatment with abciximab as early as possible before primary PCI (with or without stenting) in patients with STEMI.I IIa IIb III Treatment with tirofiban or eptifibatide may be considered before primary PCI (with or without stenting) in patients with STEMI.
  97. 97.  Favorable impact on ventricular remodeling Improvement in hemodynamics Reductions in congestive heart failure  Angiotensin-converting enzyme inhibitors  Angiotensin II receptor blockers  Aldosterone blockade
  98. 98.  For high-risk patients following STEMI EF ≤40%, clinical HF DM(Class I; lOE, A). EPHESUS trial Eplerenone, 25 mg/day titrated to 50 mg/day Mean follow-up 16 months, there was a 15% reduction in the RR of mortality.
  99. 99. ACE/ARB: Within 24 HoursI IIa IIb III An ACE inhibitor should be administered orally within the first 24 hours of STEMI to the following patients without hypotension or known class of contraindications: • Anterior infarction  Pulmonary congestion  LVEF < 0.40I IIa IIb III An ARB should be given to ACE-intolerant patients with either clinical or radiological signs of HF or LVEF < 0.40.
  100. 100. ACE/ARB: Within 24 HoursI IIa IIb III An ACE inhibitor administered orally can be useful within the first 24 hours of STEMI to the following patients without hypotension or known class contraindications:  Anterior infarction  Pulmonary congestion  LVEF < 0.40.I IIa IIb III An intravenous ACE inhibitor should not be given to patients within the first 24 hours of STEMI because of the risk of hypotension (possible exception: refractory hypotension).
  101. 101.  Immediate-release preparation of nifedipine increased risk of in- hospital mortality Verapamil & diltiazem can be given for relief of ongoing ischemia or slowing of a rapid ventricular response in AF in patients with contraindication to beta blockers. INTERCEPT trial compared 300 mg of diltiazem with placebo and Diltiazem did not reduce cardiac death, nonfatal reinfarction, during a 6-month follow-up
  102. 102.  Statins Statins should be used in the secondary prevention of patients with CAD. In addition to lowering low-density lipoprotein (LDL) cholesterol, statins also improve endothelial function, have antiplatelet effects, and reduce inflammation. Data are not clear regarding the benefits of early statin use. STEMI patients are more likely to be on statin therapy in the post MI period if treatment is initiated during the index hospitalization. An LDL goal of less than 70 mg/dL should be achieved.
  103. 103.  It is reasonable to use an insulin based regimen to achieve and maintain glucose levels less than 180 mg/dl while avoiding hypoglycemia for patients with STEMI with either a complicated or uncomplicated course Class IIa(B)
  104. 104. GENERAL MEASURES. A calm, quiet atmosphere allay anxiety and reduce sympathetic tone, ultimately leading to a reduction in hypertension, tachycardia, and arrhythmias. During the first 4 to 12 hours after admission patients should receive nothing by mouth or a clear liquid diet. The diet should be enriched in foods that are high in potassium, magnesium, and fiber but low in sodium.
  105. 105.  Haloperidol, a butyrophenone, can be used safely in patients with STEMI, beginning with a dose of 2 mg intravenously for mildly agitated patients and 5 to 10 mg for progressively more agitated patients. Hypnotics, such as temazepam, 15 to 30 mg, or an equivalent, should be provided as needed for sleep. Stool softener should be used to prevent constipation and straining.
  106. 106.  Physical Activity In the absence of complications, patients with STEMI need not be confined to bed for more than 12 hours and, unless they are hemodynamically compromised. Progression of activity should be individualized depending on the patient’s clinical status, age, and physical capacity.
  107. 107.  Myocardial dysfunction frequently occurs during the acute and subacute phases following STEMI. Cardiogenic shock complicates 6–10% of all cases of STEMI and remains a leading cause of death, with hospital mortality rates approaching 50%.
  108. 108.  Heart failure Hypotension Pulmonary congestion Low output states Cardiogenic shock The diagnosis of heart failure is based on typical symptoms such as dyspnoea, signs such as sinus tachycardia, a third heart sound or pulmonary rales, and some objective evidence of cardiac dysfunction, such as LV dilatation and reduced ejection fraction.
  109. 109.  Mechanical Causes of Heart Failure Free wall rupture. Rupture of the interventricular septum. Rupture of a papillary muscle.
  110. 110.  first day and as late as 6 weeks after STEMI Radiation of the pain to either trapezius ridge. Treatment consists of aspirin doses of 650 mg orally every 4 to 6 hours may be necessary. NSAIDs and steroids should be avoided
  111. 111.  Anticoagulation- heparin to elevate the aPTT to 1.5 to 2 times that of control, followed by a minimum of 3 to 6 months of warfarin in the following clinical situations:  An embolic event has already occurred or  The patient has a large anterior infarction whether or not a thrombus is visualized echocardiographically
  112. 112. CATEGORY ARRHYTHMIA OBJECTIVE OF TREATMENT THERAPEUTIC OPTIONS Ventricular Correction of electrolyte deficits and Potassium and magnesium premature beats increased sympathetic tone solutions, beta blocker Ventricular Prophylaxis against ventricular fibrillation, Antiarrhythmic agents; tachycardia restoration of hemodynamic stability cardioversion/defibrillationElectrical Ventricular Defibrillation; bretyliuminstability Urgent reversion to sinus rhythm fibrillation tosylate Accelerated Increase sinus rate (atropine, Observation unless hemodynamic function idioventricular atrial pacing); antiarrhythmic is compromised rhythm agents Atrial overdrive pacing; Nonparoxysmal Search for precipitating causes (e.g., antiarrhythmic agents; atrioventricular digitalis intoxication); suppress arrhythmia cardioversion relatively junctional only if hemodynamic function is contraindicated if digitalis tachycardia compromised intoxication present
  113. 113. CATEGORY ARRHYTHMIA OBJECTIVE OF TREATMENT THERAPEUTIC OPTIONS Antipyretics; analgesics; consider beta Reduce heart rate to blocker unless congestive heart failure Sinus diminish myocardial present; treat latter if present with tachycardia oxygen demands anticongestive measures (diuretics, afterload reduction)Pump failure,excessivesympathetic Verapamil, digitalis glycosides;stimulation Atrial fibrillation Reduce ventricular rate; anticongestive measures (diuretics, and/or atrial restore sinus rhythm afterload reduction); cardioversion; flutter rapid atrial pacing (for atrial flutter) Paroxysmal Vagal maneuvers; verapamil, cardiac Reduce ventricular rate; supraventricular glycosides, beta-adrenergic blockers; restore sinus rhythm tachycardia cardioversion; rapid atrial pacing
  114. 114. CATEGORY ARRHYTHMIA OBJECTIVE OF TREATMENT THERAPEUTIC OPTIONS Acceleration of heart rate only if Sinus bradycardia hemodynamic function is Atropine; atrial pacing compromisedBradyarrhythmias andconduction Acceleration of sinus rate only ifdisturbances Junctional escape loss of atrial “kick” causes Atropine; atrial pacing rhythm hemodynamic compromise Atrioventricular block and Insertion of pacemaker intraventricular block
  115. 115. At time of discharge patient should be on:  ASA unless contra-indication  Clopidogrel if PCI/NSTEMI (duration minimum1 year)  Longer duration of clopidogrel if DES in critical location or complex lesion  -blocker unless contra-indication  ACE inhibitor for CHF or LV dysfunction  All for vascular protection?  Statin for LDL to < 70mg%(minimum 50% reduction)
  116. 116.  High Risk  Complicated MI  extensive ECG changes  CHF/ flash pulmonary  anterior/ infero-posterior/ edema prior MI  shock  heart block Residual ischaemia  post MI angina  RBBB  positive TMT/ perfusion scan  sustained ventricular  non-Q MI arrhythmias  ischaemia at a distance  Anxiety/ physical labor/ young age
  117. 117.  Exercise Testing  Performed either in the hospital or early after discharge in patients not selected for cardiac catheterization and without high-risk features to assess the presence and extent of inducible ischemia Class I (B)  Exercise testing might be considered before discharge of patients recovering from STEMI to guide the post discharge exercise prescription or to evaluate the functional significance of a coronary lesion previously identified at angiography Class IIb (C)
  118. 118.  Sub maximal protocol Target workload =5 METS, 70 % MPHR or symptom limited Predictors of poor outcome Ischemic ST depression > 1 mm is inconsistent predictor of mortality poor exercise tolerance < 3 minutes doubles one year mortality ( 7% to14%) Inability to exercise or contra-indication to TMT identifies High Risk patient.
  119. 119. Late Risk Stratification - 4 to 8 weeks (Assessment of residual ischaemia) TMT Stress echocardiography Adenosine/Dipyridamole Perfusion imaging  Un-interpretable ECG  Equivocal TMT  Inability to exercise
  120. 120.  Smoking Goal: Complete Cessation  With in 2yrs risk of nonfatal MI falls to normal Blood pressure control:  Goal: < 140/90 mm Hg or <130/80 mm Hg if chronic kidney disease or diabetes Physical activity:  Minimum goal: 30 minutes 3 to 4 days per week;  Optimal daily
  121. 121.  Weight management:  Goal: BMI 18.5 to 24.9 kg/m2  Waist circumference: Women < 35 in. Men: < 40 in. Diabetes management:  Goal: HbA1c < 7% Lipid management: Primary goal: LDL-C <70mg%  Start dietary therapy in all patients (< 7% of total calories as saturated fat and < 200 mg/d cholesterol). Promote physical activity and weight management. Encourage increased consumption of omega-3 fatty acids.  Assess fasting lipid profile in all patients, preferably within 24 hours of STEMI.
  122. 122.  Hormone therapy: It is recommended that not starting hormone therapy with estrogen plus progestin after STEMI and discontinuing it in postmenopausal women after STEMI. Class III (A) Antioxidant vitamins:  Such as vitamin E and/or vitamin C supplements should not be prescribed to patients recovering from STEMI to prevent cardiovascular disease
  123. 123.  Psychosocial status of the patient should be evaluated, including inquiries regarding symptoms of depression, anxiety, or sleep disorders and the social support environment. Class I (C) Treatment with cognitive-behavioral therapy and selective serotonin reuptake inhibitors can be useful for STEMI patients with depression that occurs in the year after hospital discharge. Class IIa (A)
  124. 124. ( Yusuf, S. Two decades of progress in preventing vascular disease. Lancet 2002; 360: 2-3). RRR 2yr Event RateNone 8%ASA 25% 6% -Blockers 25% 4.5%Lipid lowering 30% 3.0%ACE-inhibitors 25% 2.3% Cumulative relative risk reduction if all four drugs are used is about 75%
  125. 125. THANK YOU