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Current Management of  Acute Coronary Syndrome in a  Non- Interventional Center
Definition ,[object Object],[object Object],[object Object]
Acute Coronary Syndromes  Unstable Angina Ischemic Chest Discomfort No ST Elevation ST Elevation Non -ST Elevation MI ST Elevation MI ECG Cardiac markers – +
Golden Hour ,[object Object],[object Object],[object Object],[object Object]
Process of care in emergency department: 4 D’s  ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Time interval 1 Time interval 2 Time interval 3 Door To Drug time
Door to Needle time ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Reducing treatment delays ,[object Object],[object Object],[object Object],[object Object],[object Object]
Emergency Room Triage in ACS ,[object Object],[object Object],[object Object]
TRIAGE OF ACS Ischemic Chest Discomfort ST Elevation  or New LBBB ECG s/o Ischemia ST dep, T inversion Non-diagnostic  or Normal ECG Assess initial ECG Aspirin  Baseline CK, CK-MB Assess C/I to thrombolysis  Anti-ischemic therapy Reperfusion therapy [ thrombolyse or Primary PTCA ] Admit Anti-ischemic therapy Serial cardiac markers 2D Echo E/o ischemia / MI No  Yes Discharge Admit Goal  10 minutes   Goal < 30 min for STK  or < 60 min for arrival in Cath Lab for PTCA
Criteria For The Diagnosis Of  Acute Myocardial Infarction (AMI)    Biomarkers +    of the following Pathological findings of AMI Typical symptoms of AMI + one of the following Procedural myocardial damage Typical symptoms of myocardial ischemia No other findings required ST segment elevation in the ECG    cardiac biomarkers to prespecified levels; symptoms may be absent; ECG changes absent/nonspecific Q waves in the ECG   Increased levels of cardiac biomarkers   ST segment elevation or depression in the ECG       Modified from Alpert J, Thygesen K, et al: Towards a new definition of myocardial infarction for the 21st century. J Am Coll Cardiol 2000, in press.
Initial Presentation
Common Symptom History In Acute MI ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
No pain ; No gain ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Recognition of High Risk Cases ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Electrocardiogram “standard of care”
ECG Patterns Normal 38% ST  Depression 18% T Inversion 23% ST  Elevation 11% LBBB 10% Hamm et al.  NEJM 1997;337 ST Depression 57% Normal 13% T Inversion 13% ST Elevation 17% TIMI IIIb Investigators, Circulation 1994;89 In Acute Chest Pain In unstable angina
Prognostication through ECG  ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Risk of MI/Death  during 1 yr Followup  based on ECG on Admission The RISC Study Group . J.Intern.Med.1993;234
Limitations of ECG ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Pseudo-infarction on ECG ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Cardiac Markers
TABLE 35-1  -- CAUSES OF MYOCARDIAL INFARCTION WITHOUT CORONARY ATHEROSCLEROSIS  CORONARY ARTERY DISEASE OTHER THAN ATHEROSCLEROSIS Arteritis    Luetic    Granulomatous (Takayasu disease)    Polyarteritis nodosa    Mucocutaneous lymph node (Kawasaki) syndrome    Disseminated lupus erythematosus    Rheumatoid spondylitis    Ankylosing spondylitis Trauma to coronary arteries    Laceration    Thrombosis    Iatrogenic    Radiation (radiation therapy for neoplasia) Coronary mural thickening with metabolic disease or intimal    proliferative disease    Mucopolysaccharidoses (Hurler disease)    Homocysteinuria    Fabry disease    Amyloidosis    Juvenile intimal sclerosis (idiopathic arterial calcification of infancy)    Intimal hyperplasia associated with contraceptive steroids or with the postpartum period    Pseudoxanthoma elasticum    Coronary fibrosis caused by radiation therapy Luminal narrowing by other mechanisms    Spasm of coronary arteries (Prinzmetal angina with normal coronary arteries)    Spasm after nitroglycerin withdrawal    Dissection of the aorta    Dissection of the coronary artery EMBOLI TO CORONARY ARTERIES Infective endocarditis Nonbacterial thrombotic endocarditis Prolapse of mitral valve Mural thrombus from left atrium, left ventricle, or pulmonary veins Prosthetic valve emboli Cardiac myxoma Associated with cardiopulmonary bypass surgery and coronary arteriography Paradoxical emboli Papillary fibroelastoma of the aortic valve (&quot;fixed embolus&quot;) Thrombi from intracardiac catheters or guidewires CONGENITAL CORONARY ARTERY ANOMALIES Anomalous origin of left coronary from pulmonary artery Left coronary artery from anterior sinus of Valsalva Coronary arteriovenous and arteriocameral fistulas Coronary artery aneurysms MYOCARDIAL OXYGEN DEMAND-SUPPLY DISPROPORTION Aortic stenosis, all forms Incomplete differentiation of the aortic valve Aortic insufficiency Carbon monoxide poisoning Thyrotoxicosis Prolonged hypotension HEMATOLOGICAL (IN SITU THROMBOSIS) Polycythemia vera Thrombocytosis Disseminated intravascular coagulation Hypercoagulability, thrombosis, thrombocytopenic purpura MISCELLANEOUS Cocaine abuse Myocardial contusion Myocardial infarction with normal coronary arteries Complication of cardic catheterization Modified from Cheitlin M, et al: Myocardial infarction without atherosclerosis. JAMA 231:951, 1975. Copyright 1975, American Medical Association. MARKER MW (D) TIMES TO INITIAL ELEVATION (hr) MEAN TIME TO PEAK (NONTHROMBOLYSIS) TIME TO RETURN TO NORMAL RANGE MOST COMMON SAMPLING SCHEDULE hFABP 14,000-15,000 1.5 5-10 hr 24 hr On presentation, then 4 hr later Myoglobin 17,800 1-4 6-7 hr 24 hr Frequent; 1-2 hr after CP MLC 19,000-27,000 6-12 2-4 d 6-12 d Once at least 12 hr after CP cTnI 23,500 3-12 24 hr 5-10 d Once at least 12 hr after CP cTnT 33,000 3-12 12 hr-2 d 5-14 d Once at least 12 hr after CP MB-CK 86,000 3-12 24 hr 48-72 hr Every 12 hr×3     MM-CK tissue isoform 86,000 1-6 12 hr 38 hr 60-90 min after CP MB-CK tissue isoform 86,000 2-6 18 hr Unknown 60-90 min after CP Enolase 90,000 6-10 24 hr 48 hr Every 12 hr×3 LD 135,000 10 24-48 hr 10-14 d Once at least 24 hr after CP MHC 400,000 48 5-6 d 14 d Once at least >2 d after CP hFABP=heart fatty acid binding proteins; MLC=myosin light chain; cTnI=cardiac troponin I; cTnT=cardiac troponin T; MB-CK=MB isoenzyme of creatinine kinase (CK); MM-CK=MM isoenzyme of CK; LD=lactate dehydrogenase; MHC=myosin heavy chain; CP=chest pain
Appearance of Cardiac Markers in Blood  Versus  Time After Onset of Symptoms.  ,[object Object],[object Object],[object Object],[object Object]
Predictive Value of Troponin Rapid Testing ,[object Object],[object Object],[object Object]
Troponins ,[object Object]
Clinical Status   GISSI-1 (%) Killip   Definition  Incidence Control Lytic Class Mortality Mortality I No CHF 71 7.3 5.9 II S3 gallop or 23 19.9 16.1 basilar rales III Pulmonary edema 4 39.0 33.0 (rales >1/2 up) IV Cardiogenic shock 2 70.1 69.9 Killip T et al. Am J Cardiol 20:457;1967 GISSI. Lancet 1”397-401, 1986
Hospital Phase
Hospital Phase : Tools ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Hemodynamic Classification Forrester J et al. NEJM 295:1356:1976
Echocardiography ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Echocardiography ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Am J Cardiol 81(12A):13G-16G;1998
Mitral inflow patterns Normal Relaxation Defect Pseudo - Normalization Restrictive  pattern A E ,[object Object],[object Object],[object Object]
Complications ,[object Object],[object Object],Free Wall VSD Papillary muscle rupture Subepicardial  aneurysm
LV ANEURYSM MR CARDIAC RUPTURE VSD.
Complications ,[object Object],LV dilatation Papillary muscle dysfunction Papillary muscle rupture LV thrombus Pericardial effusion/tamponade RVinfarct LV outflow tract obstruction
Echo: value in ACS ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Management ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
 
Anti-Ischemic therapy for Continuing Ischemia ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Class-I Recommendations, ACC/AHA practice guidelines
Anti Ischemic Therapy ,[object Object],[object Object],[object Object]
NITRATES  IN  ACS
Beta Blockers in  ACS *  Eur H Journal 1985;6 #  Lancet 1986;ii
Calcium Ch. Blockers in  ACS Salim Yusuf, BMJ 1989; 299
Antiplatelet and Anticoagulation Therapy ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Anticoagulants  Unfractionated Heparin (UFH) ,[object Object],[object Object],[object Object]
Unfractionated Heparin (UFH) ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Low-Molecular-Weight Heparin (LMWH) ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Role of Anticoagulants in ACS
New Anti coagulants in ACS
ESSENCE Trial  (Efficacy and Safety of Subcutaneous Enoxaparin in non-Q-Wave Coronary Events Study) ,[object Object],[object Object],[object Object],[object Object]
ESSENCE Trial incidence of death, MI, or recurrent angina N Eng J Med 1997;337:447-452 heparin  enoxaparin Heparin  enoxaparin n=1564  n=1607 n=1564  n=1607 19.8% 16.6%  P=0.019 23.3% 19.8%  P=0.016 Day 14 Day 30
AntiThrombotic Tt for ACS ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Anti Platelet Tt in  ACS ,[object Object],[object Object],[object Object]
Aspirin ,[object Object]
Incidence of Ischemic Events No aspirin (early 1980s) Aspirin Aspirin + Heparin 16% 12% 9% Incidence of death and MI
[object Object],[object Object],[object Object],[object Object],[object Object]
Thienopyridines ,[object Object],[object Object],[object Object]
Aspirin & Ticlopidine in  ACS
CAPRIE  (Clopidogrel versus Aspirin in Patients at Risk of Ischemic Events) ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
 
CURE ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
 
 
 
Clopidogrel in Unstable Angina to Prevent Recurrent Ischemic Events (CURE) ,[object Object],[object Object],[object Object],[object Object],[object Object]
New Agents ,[object Object],[object Object],[object Object],[object Object],[object Object]
Thrombotic Process – Pathophysiology Platelet Aggregation Ruptured Plaque Fibrinogen VWF VWF GP  II b/ III a  Receptor GP  I b  Receptor
IV Anti-platelet Therapy ,[object Object],[object Object],[object Object],[object Object]
 
 
 
 
 
[object Object],[object Object]
Abciximab  in  ACS
 
IV GP IIb/IIIa ACS Trials  (1998-2000) ,[object Object],[object Object],[object Object]
Recommendations for Antiplatelet & Anticoagulation Therapy   ,[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object]
 
Early Conservative vs Invasive Strategies   Recommendations Class I   ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object]
CASE 1 ,[object Object],[object Object],[object Object],[object Object]
 
CASE 2 ,[object Object],[object Object],[object Object],[object Object]
 
Post discharge Care ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
POST INFARCT REMODELING Lessened  Wall stress Increased  Wall Stress No prevention LV dilation and  remodeling LV failure WALL STRESS = Pressure x Radius 2 x (wall thickness) ACE inhibition Beta-blocker LV Smaller Less failure
ACE INHIBITORS Dzau-Braunwald model RISK FACTORS Hypertension LVH Atheroma Ischemia Thrombosis Sudden Death Infarction Reinfarction Loss of muscle Remodeling LV Failure - - - - - - - = ACE inhibitor effect
Future Directions ,[object Object],[object Object],[object Object],[object Object]
INDICATIONS OF PRIMARY PTCA ,[object Object],[object Object],[object Object],[object Object]
Interventions  in  ACS ,[object Object],[object Object],[object Object],[object Object]
PTCA in  ACS ,[object Object],[object Object],Early Invasive Conservative Mortality/Reinf   6 wks  7.2 %  7.8 % 1 Yr  10.8%  12.2%
PTCA in  ACS VANQWISH  TRIAL 916 Pts. Of  UA Early  Invasive  Conservative 24 % 19% 1 yr Mortality or Reinf
PTCA in  ACS FRISC  2 2457 Pts  of ACS Early Invasive Tt  Selective Invasive Tt 9.5 % 12 % 6 Mo Death or Reinf. Procedural   1.2 %   0.4 %   Mortality
CABG  in  ACS
Future Directions ,[object Object],[object Object]
EMERGENCY ROOM PROTOCOL FOR ACUTE CHEST  PAIN
Phases & Lesion Morphology of Atherosclerosis American Heart Assn. Committee on Vascular Lesions
AMI: Parameters influencing prognosis Acute MI At Presentation In Hospital At Discharge Size of  infarct Recurrent ischemia LV systolic  dysfunction Diastolic dysfunction Mechanical complications Residual ischemia LV  dysfunction Risk of  arrhythmia Age Gender ECG features Concomitant Risk factors Clinical status
 
 
 
 
 
TIMI myocardial perfusion grade and mortality
Second International Study of Infarct Survival (ISIS-2).
Mortality differences during days 0 to 35 subdivided by presentation features in nine trials of thrombolytic therapy
TIMI Risk Score for STEMI for predicting 30-day mortality
 
 
Acute Coronary Syndromes Spectrum Acute Coronary Syndromes No ST elevation ST elevation Enzymes not   Enzymes   USA NSTEMI STEMI
 
Treatment of ACS ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Rx  of ACS ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Antithrombotic Drug Therapy Abciximab (ReoPro)  with unfractionated heparin and aspirin 0.25-mg/kg intravenous bolus followed by an infusion of 0.125 μg/kg/min for 12–24 h up to 10 mg/min Eptifibatide (Integrilin) with unfractionated heparin and aspirin 180-μg/kg bolus followed by an infusion of 2 μg/kg/min up to 72 h for intervention. Max 15 mg/h Tirofiban (Aggrastat)  with unfractionated heparin and aspirin 0.4 μg/kg/min × 30 min 0.1-μg/kg/min infusion × 48 h up to 108 h (PRISM-Plus) Enoxparin (clexane) 1 mg/kg q12 h Clopidogrel (Plavix) 300 mg initially, followed by 75 mg/d
Findings in High-Risk Patients ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Predictive  Value of Troponins in ACS
Initial Presentation : Clinical The GUSTO Pyramid: 30 Day Mortality Model Lee et al. Circulation 1995;91:1659-1668 Influence of  Clinical characteristics on 30  day  mortality in thrombolyzed patients with STEMI Age (31%) Systolic Blood Pressure (24%) Killip Class (15%) Heart Rate (12%) MI Location (6%) Prior MI (3%) Age x Killip (1.3%) Height (1.1%) Diabetes (1%) Time-to-Rx (1%) Smoker (0.8%) Weight (0.8%) Accel t-PA (0.8%) Prior CABG (0.8%) HTN (0.6%) H/o CV D (0.4%)
Initial Presentation TIMI Risk Score for STEMI Morrow et al. In TIME II substudy. Circulation 2000; 102:2031-2037 1 Yr Mortality Score 0 - 1%; Score >8 - 17%
Painful facts ,[object Object],[object Object],[object Object]
ECG : prognostication GUSTO I outcome based on ECG 6.7%    ST II, III, aVF only distal RCA or LCx br. Small inferior 10.2%    ST V 1-4  or     ST I, aVL, V 5-6 beyond / in diagonal LAD (Distal) / diagonal 12.4%    ST V 1-6 , I, aVL before diagonal LAD (Mid) 25.6%    ST V 1-6 , I, aVL, fascicular or BBB before septal LAD (Prox) 8.4%    ST II, III, aVF and  V 1 ,V 3 R,V 4 R or V 5-6  or R >S V 1-2 proximal RCA or LCX Moderate-to- large inferior (post, lat, RV) 1-Year mortality ECG Occlusion Site Category
Admission ECG   Prognostic Value for Triaging GUSTO IIb Trial Eur H. J 1997
Clinical presentation ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 

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Ac Coronary Syndrome

  • 1. Current Management of Acute Coronary Syndrome in a Non- Interventional Center
  • 2.
  • 3. Acute Coronary Syndromes Unstable Angina Ischemic Chest Discomfort No ST Elevation ST Elevation Non -ST Elevation MI ST Elevation MI ECG Cardiac markers – +
  • 4.
  • 5.
  • 6.
  • 7.
  • 8.
  • 9. TRIAGE OF ACS Ischemic Chest Discomfort ST Elevation or New LBBB ECG s/o Ischemia ST dep, T inversion Non-diagnostic or Normal ECG Assess initial ECG Aspirin Baseline CK, CK-MB Assess C/I to thrombolysis Anti-ischemic therapy Reperfusion therapy [ thrombolyse or Primary PTCA ] Admit Anti-ischemic therapy Serial cardiac markers 2D Echo E/o ischemia / MI No Yes Discharge Admit Goal 10 minutes Goal < 30 min for STK or < 60 min for arrival in Cath Lab for PTCA
  • 10. Criteria For The Diagnosis Of Acute Myocardial Infarction (AMI)  Biomarkers +  of the following Pathological findings of AMI Typical symptoms of AMI + one of the following Procedural myocardial damage Typical symptoms of myocardial ischemia No other findings required ST segment elevation in the ECG  cardiac biomarkers to prespecified levels; symptoms may be absent; ECG changes absent/nonspecific Q waves in the ECG   Increased levels of cardiac biomarkers   ST segment elevation or depression in the ECG       Modified from Alpert J, Thygesen K, et al: Towards a new definition of myocardial infarction for the 21st century. J Am Coll Cardiol 2000, in press.
  • 12.
  • 13.
  • 14.
  • 16. ECG Patterns Normal 38% ST Depression 18% T Inversion 23% ST Elevation 11% LBBB 10% Hamm et al. NEJM 1997;337 ST Depression 57% Normal 13% T Inversion 13% ST Elevation 17% TIMI IIIb Investigators, Circulation 1994;89 In Acute Chest Pain In unstable angina
  • 17.
  • 18. Risk of MI/Death during 1 yr Followup based on ECG on Admission The RISC Study Group . J.Intern.Med.1993;234
  • 19.
  • 20.
  • 22. TABLE 35-1 -- CAUSES OF MYOCARDIAL INFARCTION WITHOUT CORONARY ATHEROSCLEROSIS CORONARY ARTERY DISEASE OTHER THAN ATHEROSCLEROSIS Arteritis    Luetic    Granulomatous (Takayasu disease)    Polyarteritis nodosa    Mucocutaneous lymph node (Kawasaki) syndrome    Disseminated lupus erythematosus    Rheumatoid spondylitis    Ankylosing spondylitis Trauma to coronary arteries    Laceration    Thrombosis    Iatrogenic    Radiation (radiation therapy for neoplasia) Coronary mural thickening with metabolic disease or intimal    proliferative disease    Mucopolysaccharidoses (Hurler disease)    Homocysteinuria    Fabry disease    Amyloidosis    Juvenile intimal sclerosis (idiopathic arterial calcification of infancy)    Intimal hyperplasia associated with contraceptive steroids or with the postpartum period    Pseudoxanthoma elasticum    Coronary fibrosis caused by radiation therapy Luminal narrowing by other mechanisms    Spasm of coronary arteries (Prinzmetal angina with normal coronary arteries)    Spasm after nitroglycerin withdrawal    Dissection of the aorta    Dissection of the coronary artery EMBOLI TO CORONARY ARTERIES Infective endocarditis Nonbacterial thrombotic endocarditis Prolapse of mitral valve Mural thrombus from left atrium, left ventricle, or pulmonary veins Prosthetic valve emboli Cardiac myxoma Associated with cardiopulmonary bypass surgery and coronary arteriography Paradoxical emboli Papillary fibroelastoma of the aortic valve (&quot;fixed embolus&quot;) Thrombi from intracardiac catheters or guidewires CONGENITAL CORONARY ARTERY ANOMALIES Anomalous origin of left coronary from pulmonary artery Left coronary artery from anterior sinus of Valsalva Coronary arteriovenous and arteriocameral fistulas Coronary artery aneurysms MYOCARDIAL OXYGEN DEMAND-SUPPLY DISPROPORTION Aortic stenosis, all forms Incomplete differentiation of the aortic valve Aortic insufficiency Carbon monoxide poisoning Thyrotoxicosis Prolonged hypotension HEMATOLOGICAL (IN SITU THROMBOSIS) Polycythemia vera Thrombocytosis Disseminated intravascular coagulation Hypercoagulability, thrombosis, thrombocytopenic purpura MISCELLANEOUS Cocaine abuse Myocardial contusion Myocardial infarction with normal coronary arteries Complication of cardic catheterization Modified from Cheitlin M, et al: Myocardial infarction without atherosclerosis. JAMA 231:951, 1975. Copyright 1975, American Medical Association. MARKER MW (D) TIMES TO INITIAL ELEVATION (hr) MEAN TIME TO PEAK (NONTHROMBOLYSIS) TIME TO RETURN TO NORMAL RANGE MOST COMMON SAMPLING SCHEDULE hFABP 14,000-15,000 1.5 5-10 hr 24 hr On presentation, then 4 hr later Myoglobin 17,800 1-4 6-7 hr 24 hr Frequent; 1-2 hr after CP MLC 19,000-27,000 6-12 2-4 d 6-12 d Once at least 12 hr after CP cTnI 23,500 3-12 24 hr 5-10 d Once at least 12 hr after CP cTnT 33,000 3-12 12 hr-2 d 5-14 d Once at least 12 hr after CP MB-CK 86,000 3-12 24 hr 48-72 hr Every 12 hr×3 MM-CK tissue isoform 86,000 1-6 12 hr 38 hr 60-90 min after CP MB-CK tissue isoform 86,000 2-6 18 hr Unknown 60-90 min after CP Enolase 90,000 6-10 24 hr 48 hr Every 12 hr×3 LD 135,000 10 24-48 hr 10-14 d Once at least 24 hr after CP MHC 400,000 48 5-6 d 14 d Once at least >2 d after CP hFABP=heart fatty acid binding proteins; MLC=myosin light chain; cTnI=cardiac troponin I; cTnT=cardiac troponin T; MB-CK=MB isoenzyme of creatinine kinase (CK); MM-CK=MM isoenzyme of CK; LD=lactate dehydrogenase; MHC=myosin heavy chain; CP=chest pain
  • 23.
  • 24.
  • 25.
  • 26. Clinical Status GISSI-1 (%) Killip Definition Incidence Control Lytic Class Mortality Mortality I No CHF 71 7.3 5.9 II S3 gallop or 23 19.9 16.1 basilar rales III Pulmonary edema 4 39.0 33.0 (rales >1/2 up) IV Cardiogenic shock 2 70.1 69.9 Killip T et al. Am J Cardiol 20:457;1967 GISSI. Lancet 1”397-401, 1986
  • 28.
  • 29. Hemodynamic Classification Forrester J et al. NEJM 295:1356:1976
  • 30.
  • 31.
  • 32.
  • 33.
  • 34. LV ANEURYSM MR CARDIAC RUPTURE VSD.
  • 35.
  • 36.
  • 37.
  • 38.  
  • 39.
  • 40.
  • 41. NITRATES IN ACS
  • 42. Beta Blockers in ACS * Eur H Journal 1985;6 # Lancet 1986;ii
  • 43. Calcium Ch. Blockers in ACS Salim Yusuf, BMJ 1989; 299
  • 44.
  • 45.
  • 46.
  • 47.
  • 50.
  • 51. ESSENCE Trial incidence of death, MI, or recurrent angina N Eng J Med 1997;337:447-452 heparin enoxaparin Heparin enoxaparin n=1564 n=1607 n=1564 n=1607 19.8% 16.6% P=0.019 23.3% 19.8% P=0.016 Day 14 Day 30
  • 52.
  • 53.
  • 54.
  • 55. Incidence of Ischemic Events No aspirin (early 1980s) Aspirin Aspirin + Heparin 16% 12% 9% Incidence of death and MI
  • 56.
  • 57.
  • 59.
  • 60.  
  • 61.
  • 62.  
  • 63.  
  • 64.  
  • 65.
  • 66.
  • 67. Thrombotic Process – Pathophysiology Platelet Aggregation Ruptured Plaque Fibrinogen VWF VWF GP II b/ III a Receptor GP I b Receptor
  • 68.
  • 69.  
  • 70.  
  • 71.  
  • 72.  
  • 73.  
  • 74.
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  • 77.
  • 78.
  • 79.
  • 80.  
  • 81.
  • 82.
  • 83.
  • 84.  
  • 85.
  • 86.  
  • 87.
  • 88. POST INFARCT REMODELING Lessened Wall stress Increased Wall Stress No prevention LV dilation and remodeling LV failure WALL STRESS = Pressure x Radius 2 x (wall thickness) ACE inhibition Beta-blocker LV Smaller Less failure
  • 89. ACE INHIBITORS Dzau-Braunwald model RISK FACTORS Hypertension LVH Atheroma Ischemia Thrombosis Sudden Death Infarction Reinfarction Loss of muscle Remodeling LV Failure - - - - - - - = ACE inhibitor effect
  • 90.
  • 91.
  • 92.
  • 93.
  • 94. PTCA in ACS VANQWISH TRIAL 916 Pts. Of UA Early Invasive Conservative 24 % 19% 1 yr Mortality or Reinf
  • 95. PTCA in ACS FRISC 2 2457 Pts of ACS Early Invasive Tt Selective Invasive Tt 9.5 % 12 % 6 Mo Death or Reinf. Procedural 1.2 % 0.4 % Mortality
  • 96. CABG in ACS
  • 97.
  • 98. EMERGENCY ROOM PROTOCOL FOR ACUTE CHEST PAIN
  • 99. Phases & Lesion Morphology of Atherosclerosis American Heart Assn. Committee on Vascular Lesions
  • 100. AMI: Parameters influencing prognosis Acute MI At Presentation In Hospital At Discharge Size of infarct Recurrent ischemia LV systolic dysfunction Diastolic dysfunction Mechanical complications Residual ischemia LV dysfunction Risk of arrhythmia Age Gender ECG features Concomitant Risk factors Clinical status
  • 101.  
  • 102.  
  • 103.  
  • 104.  
  • 105.  
  • 106. TIMI myocardial perfusion grade and mortality
  • 107. Second International Study of Infarct Survival (ISIS-2).
  • 108. Mortality differences during days 0 to 35 subdivided by presentation features in nine trials of thrombolytic therapy
  • 109. TIMI Risk Score for STEMI for predicting 30-day mortality
  • 110.  
  • 111.  
  • 112. Acute Coronary Syndromes Spectrum Acute Coronary Syndromes No ST elevation ST elevation Enzymes not  Enzymes  USA NSTEMI STEMI
  • 113.  
  • 114.
  • 115.
  • 116. Antithrombotic Drug Therapy Abciximab (ReoPro) with unfractionated heparin and aspirin 0.25-mg/kg intravenous bolus followed by an infusion of 0.125 μg/kg/min for 12–24 h up to 10 mg/min Eptifibatide (Integrilin) with unfractionated heparin and aspirin 180-μg/kg bolus followed by an infusion of 2 μg/kg/min up to 72 h for intervention. Max 15 mg/h Tirofiban (Aggrastat) with unfractionated heparin and aspirin 0.4 μg/kg/min × 30 min 0.1-μg/kg/min infusion × 48 h up to 108 h (PRISM-Plus) Enoxparin (clexane) 1 mg/kg q12 h Clopidogrel (Plavix) 300 mg initially, followed by 75 mg/d
  • 117.
  • 118. Predictive Value of Troponins in ACS
  • 119. Initial Presentation : Clinical The GUSTO Pyramid: 30 Day Mortality Model Lee et al. Circulation 1995;91:1659-1668 Influence of Clinical characteristics on 30 day mortality in thrombolyzed patients with STEMI Age (31%) Systolic Blood Pressure (24%) Killip Class (15%) Heart Rate (12%) MI Location (6%) Prior MI (3%) Age x Killip (1.3%) Height (1.1%) Diabetes (1%) Time-to-Rx (1%) Smoker (0.8%) Weight (0.8%) Accel t-PA (0.8%) Prior CABG (0.8%) HTN (0.6%) H/o CV D (0.4%)
  • 120. Initial Presentation TIMI Risk Score for STEMI Morrow et al. In TIME II substudy. Circulation 2000; 102:2031-2037 1 Yr Mortality Score 0 - 1%; Score >8 - 17%
  • 121.
  • 122. ECG : prognostication GUSTO I outcome based on ECG 6.7%  ST II, III, aVF only distal RCA or LCx br. Small inferior 10.2%  ST V 1-4 or  ST I, aVL, V 5-6 beyond / in diagonal LAD (Distal) / diagonal 12.4%  ST V 1-6 , I, aVL before diagonal LAD (Mid) 25.6%  ST V 1-6 , I, aVL, fascicular or BBB before septal LAD (Prox) 8.4%  ST II, III, aVF and V 1 ,V 3 R,V 4 R or V 5-6 or R >S V 1-2 proximal RCA or LCX Moderate-to- large inferior (post, lat, RV) 1-Year mortality ECG Occlusion Site Category
  • 123. Admission ECG Prognostic Value for Triaging GUSTO IIb Trial Eur H. J 1997
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