Acute Myocardial Infarction

1. Acute MyocardialInfarction Christopher Powe, PhD (c), ACNP Trauma & Surgical Critical Care University of Mississippi MedicalCenter

2. AcuteMI • Any degree of myocardial necrosis caused by myocardial ischemia and detected using a sensitive and specific preferred biomarker, such as cardiactroponin.

3. Acute MyocardialInfarction • Annual incidenceinUS: 900,000 • Mortality: 225,000 • Pre-admissionmortality:125,000

4. Acute Coronary Syndromes(ACS) Van de Werf F. Throm Haemost. 1997;78(1):210-213.

5. AcuteMI: Pathophysiology • Acute plaque fissuring andrupture • Superimposedthrombus • Transient or permanentocclusion

6. Clinical manifestations of arterialthrombosis ST MI: occlusive thrombus (platelets, red blood cells, andfibrin) UA/NQMI: Partially-occlusive thrombus (primarilyplatelets) Intra-plaque thrombus (plateletdominated) Plaquecore Intra-plaque thrombus(platelet dominated) Plaquecore SUDDENDEATH Adapted from Davies MJ. Circulation. 1990; 82 (supl II):30-46.

7. Pathophysiology ofUA/NQMI White HD. Am J Cardiol. 1997; 80 (4A):2B-10B.

8. Acute MyocardialInfarction • Lipid-rich soft plaques surrounded by a thin fibrous cap are more dangerous in terms of thrombus than collagen-rich and hard plaques.

9. Stable and VulnerablePlaques Large lipid core with thin fibrous cap, macrophages interacting withthrombus Reduced lipid core with thick fibrous cap reinforced with increased smooth musclecells Thrombus Lumen Endothelium Thick Fibrouscap Smooth Musclecells Lipid richcore Platelets Thin fibrouscap Macrophage

10. Small,vulnerableplaques are responsible for causingMI 68% 60 MI Patients (%) 40 20 18% 14% 0 <50% 50%–70% %Stenosis >70% Falk et al: Circulation1995;92:657–671

11. AcuteMI Initial Recognition andManagement • Time is of theessence • Initial evaluation ideally shouldbe • accomplished within 10minutes • Goal: treatment within 1hour after symptomonset

12. Acute MI: DiagnosticCriteria • Clinical history of ischemic-typechest • discomfort • Changes on serially obtained ECGtracings • Rise and fall in serum cardiacmarkers

13. Acute MI: ECGChanges

14. Correlation of ECGChangesand Areasof Damage

15. Acute AnteriorMI

16. Acute Anterior WallMI

17. Acute Anterior WallMI

18. Acute InferiorMI

19. Acute Inferior WallMI

20. Acute PosteriorMI

21. AcuteInferiorWall MI with PosteriorExtension

22. Right VentricularInfarction • ST segment elevation V4R highlypredictive • of RVinfarct • Higher in-hospitalmortality • Higher incidence of in-hospital complications NEJM1993(APR);328:981-8.

23. Acute Right Ventricular Wall MI Right SidedLeads

24. ChestPain Patients in the EmergencyRoom • 10% have ST-segmentelevation • 10% have non-diagnostic ECGchanges • 30% have cardiac ischemiawithout • infarction • 50% have symptoms of non-cardiacorigin • ARCH INT MED1987;147:843.

25. Acute MI: InitialECG Non-diagnosticECG’s • Normal • Subtle ST-Tchanges • Isolated T-wavechanges • NegativeU-waves • Normalization of previous abnormalST-segment • andT-waves • Conductiondefects • “Silent” areas: right,posterior

26. Acute MI: SerumMarkers

27. Acute MI: SerumMarkers

28. Acute MI: SerumMarkers

29. Acute MI: SerumMarkers

30. AcuteMI: TroponinLevels GUSTO-IIaTrial • Troponin T levels above 0.1 ng/ml were predictive of early MI/death even in patients with no ST-segment elevation or CPK elevation. NEJM1996;335:1333-41.

31. AcuteMI Treatment CurrentStandard of Care • Early sustained reperfusion of jeopardized myocardium using thrombolytic agents or primary angioplasty in appropriatepatients • Other measures to reduce myocardial damage

32. Acute MI: Outcome • Outcome after acute myocardial infarction is a function of vessel patency rate and time from occlusion to reperfusion

33. Benefitsof RapidReperfusion • Decreasedmortality • Decreasedmorbidity • Increased myocardialsalvage • Increased left ventricularfunction

34. Patients with SuspectedMI EarlyTreatment • Oxygen by nasalprongs • Sublingualnitroglycerin • Adequate analgesia (morphineor • meperidine) • Aspirin, 160 to 325mg • 12-Leadelectrocardiogram

35. 1341 JAG'C Vol. 28, No.5 November l , 1996:1328-428 RYAN ET AL MANAGEMENT OF ACUT E MYOCARDIALINFARCTION l Goal = 10minutes (£'atient with ischemic-type chestdiscomfoV Triage for rapid care Aspirin 160-325 mgchewed Obtain Baseline Serum Cardiac MarkerLevels Assess Initial 12 leadECG Normal or NondiagnosticECG ECG strongly suspicious for ischemia (ST Depression, Twinversion) ST Elevationor New orPresumably NewBBB Admit • Continue evaluation and treatment in ED or monitoredbed: • Obtain follow-up serum cardiac markerlevels • Consider 2DEcho Assesscontraindications tothrombolysis Initiate Anti-lschemicTherapy Initiate Anti-lschemicTherapy jGoal<30minutesfor Initiate ReperfusionStrategy Qvidence ofischemialinfarction""0 initiation ofthrombolysis lGoal=8-12hours and <60 minutesfor arrival in cath lab for I°PTCA YesNo Admit/ ----Initiatereperfusion strategy if ST elevationdevelops • Routine Blood Tests tobe • obtained onadmission: • •CBC • Lipid profile • Electrolytelevel Discharge

36. ThrombolyticTherapy Effecton Mortality 40 35 30 25 20 15 10 5 0 35 LivesSavedperThousand 25 19 16 0-1Hour 2-3Hour 4-6Hour 7-12Hour Lancet Ltd1994;343:311-322

37. Acute MI: Thrombolysis • Benefit greatest if therapy initiatedearly • Highly significant reduction inmortality • Benefits patients irrespective of age,gender, • and comorbidconditions • Slightly increased risk ofintracerebral hemorrhage

38. Thrombolysis Candidates • Time to therapy 12 hours orless • Acute ST-segmentelevation • Symptoms consistent with acute MIand • presence of Left Bundle BranchBlock • Patients without ST-segment elevation should not receive thrombolytictherapy

39. ThrombolyticTherapy Contraindications • Activebleeding • Recent majorsurgery • Stroke within 2months • Markedly elevated bloodpressure • Significant bleedingdiathesis

40. ThrombolyticAgents • Nonspecific agents deplete coagulationfactors • Streptokinase • Anistreplase • Urokinase • Specific agents do not depletecoagulation • factors • Alteplase(tPA) • Reteplase

41. PrimaryPTCA • Alternative to thrombolytic therapy if performed in a timely fashion by skilled individuals in high-volumecenters • Reperfusion strategy in patients with risk of bleeding contraindications to thrombolytic therapy

42. AcuteMI • Adjunctive DrugTherapy

43. Aspirin PotentialBenefits • Inhibition of tromboxane A2formation • Blockage of platelet aggregationand • thrombuspropagation • Prevention of coronary reocclusion after successfulthrombolysis

44. Aspirin ISIS-2Trial • Mortality decreased23% • Non-fatal MI decreased44% • Non-fatal stroke decreased46% • 42% reduction in mortality when addedto Streptokinase

45. Aspirin Guidelines • Chewable Aspirin ispreferred • Dose of 160 to 325 mg should be given as soon aspossibel • Contraindicated in patients with known hypersensitivity (may substitute Ticlopidine or Clopidagrel • Caution in patients with active or recent hemorrhaging, including stroke or pepticulcer disease

46. Heparin PotentialBenefits • Prevention of venousthrombosis • Decrease left ventricular muralthrombus • Decrease arterialembolization • Decrease re-infarction or extension of infarct

47. Heparin • Post thrombolytic therapy, heparin administration based more on current practice than onevidence

48. Heparin • Should be used in large AWMI or in patients with LV mural thrombus to reduce risk ofstroke • For patients with smaller MI and without thrombus, little data on benefit ofheparin

49. High Risk for SystemicEmbolization • Large or anteriorMI • Atrialfibrillation • Previousembolus • Known LVthrombus

50. Heparin Guidelines • Intravenously in patientsreceiving • alteplase/retaplase • Subcutaneously in all patients not treated with thrombolytic therapy • Intravenous form preferred in patientsat • high risk of embolicevent