ACUTE MYOCARDIA INFARCTION ISCHEMIA MI Draz MY

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myocardial ischemia infarction stent MI coronary atherosclerosis stsemi ECG egypt Draz MY 2009

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  • In-stent restenosis is a proliferative disease disorder that leads to the phenomenon of late loss. In stetnting, a late loss of between .00 and 1 mm usually occurs. This leads to a significant reduction of luminal area of a stent. Late loss can result in up to a 56% reduction in the cross-sectional area in the average 3 mm vessel. In smaller vessels, the area obstruction is more severe with late loss contributing up to a 75% reduction in cross sectional area.
  • Algorithms can be used to detail the appropriate therapies in practice. The guidelines use the same basic algorithm. The process is very dynamic and all aspects need to be considered. Evaluate the patient Determine if the patient has ACS or possible ACS Interpret the ECG and bio-markers Observe the patient Repeat measurements Some patients may present as troponin negative but over time become troponin positive without any other symptoms.
  • ACUTE MYOCARDIA INFARCTION ISCHEMIA MI Draz MY

    1. 1. بسم اللله الرحمن الرحيم ACUTE CORONARY SYNDROME SIMPLE NOTES Draz MY , Egypt 2008 Mb. Bch (Tanta), D. Sc (Al azhar) .,M. Sc (Cairo) ,M. Sc (Ain shams). Surgeon ,Internist, Emergency Registrar. [email_address]
    2. 2. Atherosclerosis <ul><li>One of the most common diseases in U.S.A. </li></ul><ul><li>50% of U.S. Deaths are attributed to MI </li></ul><ul><li>Atherosclerosis is the Principal cause of Death in Western World (Braunwald) </li></ul><ul><li>Atherosclerosis begins in childhood and advances throughout life </li></ul>
    3. 3. RISK FACTORS AND PATHOGENESIS OF ATHEROMATOUS LESIONS OF ARTERIES.
    4. 10. V.TACH.,ASYSTOLE,MASSIVE MI SUDDEN DEATH ALTERED CONDUCTION DUE TO ISCH.OR INFARCTION ARRYTHMIA MYOCARDIAL DYSFUNCTIONDUE TO INFARCTION OR ISCH. HEART FAILURE MYONECROSIS DUE TO ACUTE ISCH. MI DYNAMIC CORONARY OBSTRUCTION UNSTABLE ANGINA FIXED CORONARY ATHEROMATOUS LESION STABLE ANGINA CORONARY HEART DISEASE : CLINICAL MANIFESTATIONS AND PROBLEMS
    5. 11. Myocardial Ischemia <ul><li>Spectrum of presentation </li></ul><ul><ul><li>silent ischemia </li></ul></ul><ul><ul><li>exertion-induced angina </li></ul></ul><ul><ul><li>unstable angina </li></ul></ul><ul><ul><li>acute myocardial infarction </li></ul></ul>
    6. 16. ACC/AHA 2002 GUIDLINES
    7. 17. ACC/AHA 2002 GUIDLINES
    8. 18. ACC/AHA 2002 GUIDLINES
    9. 23. UNSTABLE ANGINA
    10. 24. Acute Coronary Syndrome Ischemic Discomfort Unstable Symptoms No ST-segment elevation ST-segment elevation Unstable Non-Q Q-Wave angina AMI AMI ECG Acute Reperfusion History Physical Exam
    11. 26. THROMBOSIS IN MYOCARDIAL INFARCTION SCORE FOR UNSTABLE AND NSTSMI
    12. 30. Unstable Angina precipitating factors <ul><li>Inappropriate tachycardia </li></ul><ul><ul><li>anemia, fever, hypoxia, tachyarrhythmias, thyrotoxicosis </li></ul></ul><ul><li>High afterload </li></ul><ul><ul><li>aortic valve stenosis, LVH </li></ul></ul><ul><li>High preload </li></ul><ul><ul><li>high cardiac output, chamber dilatation </li></ul></ul><ul><li>Inotropic state </li></ul><ul><ul><li>sympathomimetic drugs, cocaine intoxication </li></ul></ul>
    13. 31. Acute Coronary Syndrome <ul><li>*Process of resolution </li></ul><ul><ul><li>spontaneous thrombolysis </li></ul></ul><ul><ul><li>vasoconstriction resolution </li></ul></ul><ul><ul><li>presence of collateral circulation </li></ul></ul><ul><li>*Delayed or absence of resolution may lead to non-Q-wave or Q-wave myocardial infarction </li></ul>
    14. 32. Unstable Angina Therapeutic Goals <ul><li>* Therapeutic Goals </li></ul><ul><li>Reduce myocardial ischemia </li></ul><ul><li>Control of symptoms </li></ul><ul><li>Prevention of MI and death </li></ul><ul><li>* Medical Management </li></ul><ul><li>Anti-ischemic therapy </li></ul><ul><li>Anti-thrombotic therapy </li></ul>
    15. 33. Unstable Angina Medical Therapy <ul><li>Anti-ischemic therapy </li></ul><ul><ul><li>nitrates, beta blockers, calcium antagonists </li></ul></ul><ul><li>Anti-thrombotic therapy </li></ul><ul><ul><li>Anti-platelet therapy </li></ul></ul><ul><ul><ul><li>aspirin, ticlopidine, clopidogrel, GP IIb/IIIa inhibitors </li></ul></ul></ul><ul><ul><li>Anti-coagulant therapy </li></ul></ul><ul><ul><ul><li>heparin, low molecular weight heparin (LMWH), warfarin, hirudin, hirulog </li></ul></ul></ul>
    16. 34. Unstable Angina Anti-ischemic Therapy <ul><li>restrict activities </li></ul><ul><li>morphine </li></ul><ul><li>oxygen </li></ul><ul><li>nitroglycerine </li></ul><ul><ul><li>pain relief, prevent silent ischemia, control hypertension, improve ventricular dysfunction </li></ul></ul><ul><ul><li>nitrate free period recommended after the first 24-48 hours </li></ul></ul>
    17. 35. Unstable Angina Anti-ischemic Therapy <ul><li>beta-blockers </li></ul><ul><ul><li>lowering angina threshold </li></ul></ul><ul><ul><li>prevent ischemia and death after MI </li></ul></ul><ul><ul><li>particularly useful during high sympathetic tone </li></ul></ul><ul><li>calcium antagonists </li></ul><ul><ul><li>particularly the rate-limiting agents </li></ul></ul><ul><ul><li>nifedipine is not recommended without concomitant ß-blockade </li></ul></ul>
    18. 36. Unstable Angina Anti-platelet Therapy <ul><li>Thienopyridines </li></ul><ul><ul><li>ticlopidine (Ticlid; Hoffmann-La Roche) </li></ul></ul><ul><ul><li>clopidogrel (Plavix; Bristol-Myers Squibb) </li></ul></ul><ul><li>block platelet aggregation induced by ADP and the transformation of GP IIb/IIIa into its high affinity state </li></ul>
    19. 37. Unstable Angina Anti-platelet Therapy <ul><li>Clopidogrel </li></ul><ul><ul><li>CAPRIE (Clopidogrel versus Aspirin in Patients at Risk of Ischemic Events) </li></ul></ul><ul><ul><li>19,000 patients randomly assigned to clopidogrel (75 mg/d) or to aspirin (325 mg/d) </li></ul></ul><ul><ul><li>there was an 8.7% reduction in the combined incidence of stroke, MI, or death (P=.043) </li></ul></ul><ul><ul><li>patients with MI did better with aspirin </li></ul></ul><ul><ul><li>patients with PVD or stroke did better with clopidogrel </li></ul></ul>Lancet 1996;348:1329-1339 Circulation 1998;97:1107
    20. 38. Unstable Angina Anti-platelet Therapy <ul><li>GP IIb/IIIa inhibitors </li></ul><ul><ul><li>abciximab (monoclonal antibody) </li></ul></ul><ul><ul><li>eptifibatide (peptidic inhibitor) </li></ul></ul><ul><ul><li>lamifiban and tirofiban (non-peptides) </li></ul></ul><ul><li>direct occupancy of the GP IIb/IIIa receptor by a monoclonal antibody or by synthetic compounds mimicking the RGD sequence for fibrinogen binding prevents platelet aggregation </li></ul>
    21. 39. Unstable Angina Anti-platelet Therapy <ul><li>Tirofiban (Aggrastat; Merk & Co.) </li></ul><ul><ul><li>PRISM (Platelet Receptor Inhibition for Ischemic Syndrome Management) </li></ul></ul><ul><ul><li>3,200 patients with unstable angina were treated with either heparin or tirofiban </li></ul></ul><ul><ul><li>At 48 hours, there was significant risk reduction (5.9% to 3.6%) in the rate of death, MI, or refractory ischemia. The benefit was lost at 30 days. </li></ul></ul>N Engl J Med 1998;338:1498-505
    22. 40. Unstable Angina Anti-coagulant Therapy <ul><li>Low-molecular-weight heparin advantages over heparin: </li></ul><ul><ul><li>better bio-availability </li></ul></ul><ul><ul><li>higher ratio (3:1) of anti-Xa to anti-IIa activity </li></ul></ul><ul><ul><li>longer anti-Xa activity, avoid rebound </li></ul></ul><ul><ul><li>induces less platelet activation </li></ul></ul><ul><ul><li>ease of use (subcutaneous - qd or bid) </li></ul></ul><ul><ul><li>no need for monitoring </li></ul></ul>
    23. 41. NSTSMI
    24. 42. <ul><li>MYOCARDIAL PROTEINS </li></ul>Myoglobin Actin, Myosin Troponin LDH CK, AST
    25. 43. <ul><li>MYOFIBER STRUCTURE </li></ul>TnI Actin Tropomyosin TnC TnT
    26. 49. STSEMI
    27. 68. In-stent Restenosis in small vessels treated with rotational atherectomy
    28. 69. Stents <ul><li>Coronary stents have </li></ul><ul><li>revolutionized the field </li></ul><ul><li>of coronary angioplasty </li></ul><ul><li>due to their ability to </li></ul><ul><li>prevent abrupt closure of </li></ul><ul><li>the artery after </li></ul><ul><li>angioplasty and also by </li></ul><ul><li>reducing restenosis </li></ul>
    29. 71. Late Loss <ul><li>In- stent restenosis is a proliferative disease disorder </li></ul><ul><li>Late loss of between 0.8–1.0mm occurs in bare stents </li></ul><ul><li>Lumen area reduction </li></ul>
    30. 72. Definite ACS Possible ACS (–) ECG; Normal biomarkers Observe; repeat ECG, markers at 4-8 hrs No recurrent pain; (–) follow-up studies Recurrent pain; (+) follow-up studies Stress test;  LV function if ischemia (–) test: outpt follow-up (+) test Admit, Use Acute Ischemia Pathway ST  Use MI Guidelines No ST  ST-T  ’s, chest pain,  markers Symptoms Suggestive of ACS
    31. 73. Emergency Room Triage of Patients with Acute Chest Pain by Means of Rapid Testing for Cardiac Troponin T or Troponin I Christian W. Hamm, M.D., Britta U. Goldmann, M.D., Christopher Heeschen, M.D., Georg Kreymann, M.D., Jürgen Berger, Ph.D., and Thomas Meinertz, M.D. NEJM,Volume 337:1648-1653, Number 23 December 4, 1997 773 consecutive patients who had had acute chest pain for less than 12 hours without ST-segment elevation on their electrocardiograms, troponin T and troponin I status (positive or negative) was determined at least twice by sensitive, qualitative bedside tests based on the use of specific monoclonal antibodies.
    32. 74. Conclusions Bedside tests for cardiac-specific troponins are highly sensitive for the early detection of myocardial-cell injury in acute coronary syndromes. Negative test results are associated with low risk and allow rapid and safe discharge of patients with an episode of acute chest pain from the emergency room. 70 =22 % 44 =94 % 123 =16 % Tn.T +VE 114 =36 % 47 =100% 171 =22% Tn.I +VE 315 47 773 NO. UNSTABLE ANGINA MI.PATIENTS TOTAL PATIENTS
    33. 75. Missed Diagnoses of Acute Cardiac Ischemia in the Emergency Department. Pope ET AL. Volume 342:1163-1170, Number 16, NEJM April 20, 2000
    34. 76. Missed Diagnoses of Acute Cardiac Ischemia in the Emergency Department. Pope ET AL. Volume 342:1163-1170, Number 16, NEJM April 20, 2000 55 NON CARDIAC 21 NON ISCH.CARDIAC 6 STABLE ANGINA 9 UNSTABLE ANGINA 8 MI 17 ACUTE CARDIAC ISCH. % FROM TOTAL TOTAL NO.=10,689
    35. 77. 2.3% 22 966 UNSTABLE ANGINA 2.1% 19 889 ACUTE MI % OF TOTAL DISCHARGE FROM ED NO.
    36. 78. It appears that the incidence of missed diagnoses of acute cardiac ischemia in the emergency department may be reduced by: 1- Interpreting the electrocardiogram more accurately. 2- Addressing clinical factors or preconceptions that obscure the recognition of acute myocardial infarction and unstable angina in women and nonwhite patients. 3- Considering the possibility that acute cardiac ischemia may be present in patients with chief symptoms other than chest pain. 4- Assessing recent changes in the clinical course of angina more carefully.
    37. 79. الحمد لله رب العالمين

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