Stemi by dr.mehelina

Stemi by dr.mehelina

1. STEMI Dr.Mehelina Hossain MD,Phase A Critical Care Medicine Dhaka Medical College Hospital

2. Universal definition of myocardial infarction A combination of criteria is required to meet the diagnosis of acute MI, namely the detection of an increase and/or decrease of a cardiac biomarker, preferably high-sensitivity cardiac troponin , with at least one value above the 99th percentile of the upper reference limit and at least one of the following: (1) Symptoms of ischaemia . (2) New or presumed new significant ST-T wave changes or left bundle branch block on 12-lead ECG. (3) Development of pathological Q waves on ECG. (4) Imaging evidence of new or presumed new loss of viable myocardium or regional wall motion abnormality. (5) Intracoronary thrombus detected on angiography or autopsy .

3. Types Type 1 MI Type 1 MI is characterized by atherosclerotic plaque rupture, ulceration, fissure, erosion or dissection with resulting intraluminal thrombus in one or more coronary arteries leading to decreased myocardial blood flow and/or distal embolization and subsequent myocardial necrosis . Type 2 MI Type 2 MI is myocardial necrosis in which a condition other than coronary plaque instability contributes to an imbalance between myocardial oxygen supply and demand. Mechanisms include coronary artery spasm, coronary endothelial dysfunction, tachyarrhythmias , bradyarrhythmias , anaemia , respiratory failure, hypotension and severe hypertension, injurious effects of pharmacological agents and toxins.

4. Continue…… Type 3 sudden cardiac death with symptoms of ischaemia,new ST elevation or LBBB or coronay thrombus Type 4a MI associated with PCI Type 4b MI associated with stent thrombosis Type 5 MI associated witH CABG

5. DEFINITION STEMI is a clinical syndrome defined by characteristic symptoms of myocardial ischemia in association with persistent electrocardiographic (ECG) ST elevation and subsequent release of biomarkers of myocardial necrosis.

6. Modifiable risk factors : Smoking Diabetes Hypertension P hysical inactivity Hyperlipidemia Obesity D epression , social isolation and lack of social support. Non-modifiable risk factors : Gender Age F amily history of premature coronary disease D iabetes

7. SIGNS Signs of sympathetic activation : Pallor,Sweating,Tachycardia Signs of vagal activation : Vomiting,Bradycardia Signs of impaired myocardial function : Hypotension,oliguria,cold periphery. Narrow pulse pressure Raised JVP Third heart sound Lung Crepitation Sign of tissue damage : Fever Complications : Murmur Pericardial rub

8. DIAGNOSIS It is based on : Clinical Findings Classical ECG Changes Rising Titre of Cardiac Enzymes The classic ECG findings:   ST segment elevation, followed by T wave inversion and Q waves.

9. ECG Diagnostic ST elevation in the absence of left ventricular (LV) hypertrophy or left bundle-branch block (LBBB) is defined as: New ST elevation at the J point in at least 2 contiguous leads of 2 mm (0.2 mV) in men or 1.5 mm (0.15 mV) in women in leads V2–V3 and/or of 1 mm (0.1 mV) in other contiguous chest leads or the limb leads.

10. The majority of patients will evolve ECG evidence of Q-wave infarction. New LBBB at presentation interfere with ST-elevation analysis, and not a diagnostic criteria of AMI in isolation.

11. LOCALISATION Category Anatomy of Occlusion ECG Findings Proximal LAD Proximal to first septal perforator ST V1-V6, I, aVL Fascicular or Bundle Branch Block Mid LAD Proximal to Large Diagonal but Distal to First Septal Perforator ST V1-V6, I, aVL Distal LAD or Diagonal Distal to Large Diagonal or Diagonal Itself ST ↑ V1–V4, or I, aVL , V5, V6 Moderate to Large Inferior (Posterior, Lateral, Right Ventricular) Proximal RCA or Left Circumflex ST ↑ II, III, aVF , and any of the following: (a) V1, V3R, V4R (b) V5, V6 (c) R > S in V1, V2 Small Inferior Distal RCA or Left Circumflex Branch ST ↑ II, III, aVF only

12. ECG???

13. ASTEMI(EXT ANT) A ASTEMI

14. ASTEMI( Inf )

15. POST. ECG

16. ASTEMI( Inf )with Post.Ext

17. Differentials for ST-Segment Elevation Myocardial Infarction Comorbid ischemia ST elevation but no ischemia Chest pain but no ischemia Aortic dissection Early repolarization Aortic dissection Systemic arterial embolism Left ventricular hypertrophy Myopericarditis Hypertensive crisis Left bundle branch block Pleuritis Aortic stenosis Hyperkalemia Pulmonary embolism Cocaine use Brugada syndrome Costochondritis Arteritis Gastrointestinal disorders

18. The Laboratory Diagnosis of STEMI is done by : Cardiac Troponin The most sensitive and specific marker of myocardial necrosis. CK-MB Myoglobin

19. Causes of Serum Troponin T and I Elevations, Including Both ACS, Non Coronary Events and Non Cardiac Events Acute Myocardial Infarction Shock of any form ( Cardiogenic , Obstructive, Distributive) Myocarditis and Myopericarditis Cardiomyopathies Acute Congestive Failure (Pulmonary Edema) Sepsis Pulmonary Embolism Renal Failure Burns Acute CNS Event Rhabdomyolysis Cardiiac Neoplasm, Inflammatory Syndromes, Infiltrative Diseases Sympathomimetic Ingestions Congenital Coronary Anomalies Extreme Physical Exertion

20. Other Investigation Cardiac Imaging : Echocardiography : Wall motion Defect LV Impairment Chest X Ray : Pulmonary edema Cardiomegaly Widened mediastinum Routine Blood Tests: U&E Lipid Profile RBS

21. Risk Stratification Five simple baseline parameters have been reported to account for > 90% of the prognostic information for 30-day mortality. These characteristics are given in descending order of importance: Age Systolic blood pressure Killip classification Heart rate Location of MI In addition, various risk models have been created to improve risk prediction.

22. TIMI Risk Model for Prediction of Short-Term Mortality in ST-Segment Elevation Myocardial Infarction Patients

23. Management Early and Emergency Medical Management : Cardiac Monitoring Oxygen IV Access and Blood for U&E, Glucose, CBC, Cardiac Enzyme Brief History and Clinical Assessment Loading Dose of Aspirin and Clopidogrel Analgesia if Continuing Pain Antiemetic and Anxiolytic if required Reperfusion Therapy / Thrombolytic Therapy

24. STEMI Management Outline

25. Reperfusion at a PCI-Capable Hospital 1. Primary PCI in STEMI: Recommendations CLASS I Primary PCI should be performed in patients with 1.STEMI and ischemic symptoms of less than 12 hours’ duration 2.STEMI and ischemic symptoms of less than 12 hours’ duration who have contraindications to fibrinolytic therapy, irrespective of the time delay from FMC 3. STEMI and cardiogenic shock or acute severe HF, irrespective of time delay from MI onset. ( Level of Evidence: B)

26. Contd.. CLASS IIa Primary PCI is reasonable in patients with STEMI if there is clinical and/or ECG evidence of ongoing ischemia between12 and 24 hours after symptom onset (94,95). ( Level of Evidence: B) CLASS IIb 1. PCI may be performed in a noninfarct artery at the time of primary PCI in patients with STEMI who are hemodynamically stable .

27. Adjunctive Antiplatelet Therapy Class I 1. Aspirin 162 to 325 mg should be given before primary PCI. ( LOE: B) 2. After PCI, aspirin should be continued indefinitely.(81 to 325 mg daily maintenance dose) ( LOE: A) 3. A loading dose of a P2Y12 receptor inhibitor should be given as early as possible or at time of primary PCI to patients with STEMI. Options include: a. Clopidogrel 600 mg ( LOE: B); or b. Prasugrel 60 mg( LOE: B); or c. Ticagrelor 180 mg. ( LOE: B)

28. Continue…. 4. P2Y12 inhibitor therapy should be given for 1 year to patients with STEMI who receive a stent (BMS or DES) during primary PCI using the following maintenance doses: a. Clopidogrel 75 mg daily ( LOE: B); or b. Prasugrel 10 mg daily ( LOE: B); or c. Ticagrelor 90 mg twice a day. ( LOE: B) Class III: Harm Prasugrel should not be administered to patients with a history of prior stroke or transient ischemic attack. ( LOE: B)

29. Adjunctive Anticoagulant Therapy : Class I 1. For patients with STEMI undergoing primary PCI, the following supportive anticoagulant regimens are recommended: a. UFH, with additional boluses administered as needed to maintain therapeutic activated clotting time levels, taking into account whether a GP IIb / IIIa receptor antagonist has been administered ( LOE: C); or b. Bivalirudin with or without prior treatment with UFH.( LOE: B)

30. Continue…….. Class IIa 1. In patients with STEMI undergoing PCI who are at high risk of bleeding, it is reasonable to use bivalirudin monotherapy in preference to the combination of UFH and a GP IIb / IIIa receptor antagonist. ( Level of Evidence: B) Class III: Harm 1. Fondaparinux should not be used as the sole anticoagulant to support primary PCI because of the risk of catheter thrombosis.304 ( Level of Evidence: B)

31. Reperfusion at a Non–PCI Capable Hospital 1) Fibrinolytic Therapy When There Is an Anticipated Delay to Performing Primary PCI Within 120 Minutes of FMC

32. Indications for Fibrinolytic Therapy When There Is a >120-Minute Delay From FMC to Primary PCI

33. FibrinoLytics

34. Contraindications and Cautions for Fibrinolytic Therapy in STEMI Absolute contraindications Any prior ICH Known structural cerebral vascular lesion ( eg , AVM ) Known malignant intracranial neoplasm (primary or metastatic) Ischemic stroke within 3 months EXCEPT acute ischemic stroke within 4.5 h Suspected aortic dissection Active bleeding or bleeding diathesis (excluding menses) Significant closed-head or facial trauma within 3 mo Intracranial or intraspinal surgery within 2 mo Severe uncontrolled hypertension (unresponsive to emergency therapy) For streptokinase, prior treatment within the previous 6 mo

35. CONTINUE….. Relative contraindications History of chronic, severe, poorly controlled hypertension Significant hypertension on presentation (SBP 180 mm Hg or DBP 110 mm Hg) History of prior ischemic stroke 3 mo Dementia Known intracranial pathology not covered in absolute contraindications Traumatic or prolonged (10 min) CPR Major surgery (3 wk ) Recent (within 2 to 4 wk ) internal bleeding Noncompressible vascular punctures Pregnancy Active peptic ulcer Oral anticoagulant therapy

36. Adjunctive Antiplatelet therapy Aspirin (162- to 325-mg loading dose) and clopidogrel (300-mg loading dose) for patients ≤75 years of age, 75-mg dose for patients >75 years of age) should be administered to patients with STEMI who receive fibrinolytic therapy.(C.O.R : IA) Aspirin should be continued indefinitely (C.O.R: IA) Clopidogrel (75 mg daily) for atleast 14 days (C.O.R. IA) And upto 1 year (C.O.R IC)

37. Adjunctive Anticoagulant Therapy Patients with STEMI undergoing reperfusion with fibrinolytic therapy should receive anticoagulant therapy for a minimum of 48 hours, and preferably for the duration of the index hospitalization, up to 8 days or until revascularization if performed. Recommended Regimen : UFH adm . as a weight-adjusted intravenous bolus and infusion to obtain an aPTT time of 1.5 to 2.0 times control, for 48 hours or until revascularization.(COR IC) Enoxaparin adm . a/c to age, weight, and creatinine clearance, given as an i.v bolus, followed in 15 min. by s/c inj. for the duration of the index hospitalization, up to 8 days or until revascularization; or

38. Continue….. Fondaparinux administered with initial i.v dose, followed in 24 hrs by daily s/c inj. if the estimated creatinine clearance is greater than 30 mL /min, for the duration of the index hospitalization, up to 8 days or until revascularization. Enoxaparin : ● If age 75 y: 30-mg IV bolus, followed in 15 min by 1 mg/kg subcutaneously every 12 h (maximum 100 mg for the first 2 doses) ● If age> 75 y: no bolus, 0.75 mg/kg subcutaneously every 12 h (maximum 75 mg for the first 2 doses) ● Regardless of age, if CrCl 30 mL /min: 1 mg/kg subcutaneously every 24 h ● Duration: For the index hospitalization, up to 8 d or until revascularization

39. Routine M edical Therapies

40. DELAYED INVASIVE MANAGEMENT Indications for Coronary Angiography in Patients Who Were Managed With Fibrinolytic Therapy or Who Did Not Receive Reperfusion Therapy

41. Complications EARLY COMPLICATION (<1 WEEK) Acute Cardiac Failure Cardiogenic Shock Arrythmias : Supraventricular Arrythmia : Sinus Tachycardia or Bradycardia Atrial Ectopic Beats Atrial Fibrillation / Flutter Ventricular Arrythmia : Ventriculat Ectopic Beats Accelerated Idioventricular Rhythm VT

42. Contd … AV Block and Intraventricular Block Mitral Regurgitation Rupture of Interventricular septum Cardiac Temponade Post-Infarct Angina Pericarditis Mural Thrombus

43. Contd.. Late Complications(>1 Week Post-MI) Post MI(Dressler’s) Syndrome LV Aneurysm Chronic Cardiac Failure

44. CARDIAC REHABILITATION A. Cardiac Rehabilitation Programme Formal rehabilitation programs which use exercise and patient education to help patients modify their lifestyles Home programme and family care. B. Lifestyle Modification : Optimal control of hypertension and diabetes Weight reduction Resumption of daily activities C.Secondary Prevention

45. Thank you All

46. SYMPTOMS THE CLASSIC SYMPTOMS INCLUDE Severe crushing substernal chest pain at rest > 2 0 minutes N ot relieved by sublingual nitrates or rest Radiation to the neck, jaw, back, shoulder, right arm and epigastrium . ASSOCIATED SYMPTOMS : Diaphoresis, Dyspnea , Fatigue, light-headedness, palpitations, acute confusion, indigestion, nausea, or vomiting. Gastrointestinal symptoms are especially common with inferior infarction. Myocardial ischemic pain localized to the epigastrium is often misdiagnosed as indigestion. Acute MI can occur without chest pain, especially among postoperative patients, the elderly, and those with diabetes mellitus.

47. Residual Risk and Use of Oral Anticoagulants Patients with ACS remain at a significant risk of recurrent ischemic events after initial revascularization despite optimal medical therapy and aggressive risk factor modification. 1 in 10 patients experiences a significant atheroembolic event (cardiac death, myocardial infarction or stroke) within a year of the first ACS episode. This is felt to be secondary to a persistent thrombogenic state that extends well beyond the initial ACS event. New oral anticoagulants have emerged in the last decade with the potential to minimize residual risk ie . Rivaroxaban

48. Electrographic Criteria For The Diagnosis of AMI In The Presence of LBBB Criteria Score ST-segment elevation > 1 mm concordant with QRS 5 ST-segment depression > 1 mm in leads V1, V2 or V3 3 ST-segment elevation > 5 mm discordant with QRS 2 Point scores for each criteria met are added. Total Point Score of # yields >90% specificity and 88% positive predictive value.

49. CK-MB Myoglobin Troponin 1. Rapid, cost-efficient, accurate assays 1. High sensitivity 1. Greater sensitivity and specificity than CK-MB 2. Ability to detect early reinfarction 2. Useful in early detection of MI 2. Detection of recent MI up to 2 weeks after onset 3.Detection of reperfusion 32. Detection of recent MI up to 2 weeks after onset 4.Most useful in ruling out MI 4. Detection of reperfusion Advantages

50. CK-MB 1. Lack of specificity with skeletal muscle disease/injury 2. Low sensitivity during early MI (<6 h) or late (>36 h) after symptom onset and for minor myocardial damage Myoglobin 1. Very low specificity with skeletal muscle injury or disease 2. Rapid return to normal Troponins 1. Low sensitivity in early phase of MI (<6 h after symptom onset) 2. Limited ability to detect late minor re-infarction Disadvantages

51. The Global Registry of Acute Coronary Events (GRACE) score

52. STEMI ST segment elevations T wave changes Q wave development Enzyme elevations Reciprocals