นายแพทย เกร ยงไกร เฮงร ศม ห วหน ากล มงานอาย รศาสตร ห วใจ สถาบ นโรคทรวงอก นนทบ ร

Transcription

1 Acute Coronary syndrome นายแพทย เกร ยงไกร เฮงร ศม ห วหน ากล มงานอาย รศาสตร ห วใจ สถาบ นโรคทรวงอก นนทบ ร

2 New Pathogenesis of ACS J Am Coll Cardiol. 2013;61(1):1-11. doi: /j.jacc

3 Patho-physiology <> 3

4 Differential Diagnosis Aortic dissection Pneumothorax Pulmonary embolism 4

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6 Evolution of EKG in STEMI 6

7 ST Elevation Localizing Infarcts on the 12 Lead ECG Lateral - Cx Ant sep - LAD Anterior - LAD Inferior - RCA Lateral - Cx Ant sep - LAD Lateral - Cx Inferior - RCA Inferior - RCA Anterior - LAD Lateral - Cx 7

8 Posterior Myocardial Infarction Clinical Significance Posterior infarction accompanies 15-20% of STEMIs, usually occurring in the context of an inferior or lateral infarction. Isolated posterior MI is less common (3-11% of infarcts). Posterior extension of an inferior or lateral infarct implies a much larger area of myocardial damage, with an increased risk of left ventricular dysfunction and death. Isolated posterior infarction is an indication for emergent coronary reperfusion. However, the lack of obvious ST elevation in this condition means that the diagnosis is often missed. 8

9 The ACC/AHA 2013 guidelines makes these changes, which we've covered before, to the identification of STEMI: "New or presumed new" Left Bundle Branch Block is no longer an indication for a STEMI. Providers should use Sgarbossa's criteria to diagnose STEMI in the presence of LBBB. (Editor's Note: we're going to go ahead and add that our readers should take this one step further and utilize Smith's modification to Sgarbossa's criteria.) Isolated ST-depression in V1-V4 is an indication of a posterior STEMI. Widespread ST-depression with ST-elevation in avr is an indication of proximal LAD or LMCA occlusion. (Editor's Note: the evidence points more towards this being an indication of 3-vessel disease or near occlusion of the LAD/LMCA.) Hyperacute T-waves, e.g. de Winter ST/T-wave changes, are an early indicator of a STEMI. 9

10 UA/NSTEMI 9/00 UA/NSTEMI THREE PRINCIPAL PRESENTATIONS Rest Angina* Angina occurring at rest and prolonged, usually > 20 minutes New-onset Angina Increasing Angina New-onset angina of at least CCS Class III severity Previously diagnosed angina that has become distinctly more frequent, longer in duration, or lower in threshold (i.e., increased by > 1 CCS) class to at least CCS Class III severity. * Pts with NSTEMI usually present with angina at rest. Braunwald Circulation 80:410; 1989

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12 Cardiac markers Troponin ( T, I) Very specific and more sensitive than CK Rises 4-8 hours after injury May remain elevated for up to two weeks Can provide prognostic information Troponin T may be elevated with renal dz, poly/dermatomyositis CK-MB isoenzyme Rises 4-6 hours after injury and peaks at 24 hours Remains elevated hours Positive if CK/MB > 5% of total CK and 2 times normal Elevation can be predictive of mortality False positives with exercise, trauma, muscle dz, DM, PE 12

13 Elevations of Troponin in the absence of an Acute Coronary Syndrome Congestive heart failure - acute and chronic Renal Failure Tachy or bradyarrhythmias, or heart block Acute neurological disease, including stroke, or subarachnoid haemorrhage Pulmonary embolism, severe pulmonary hypertension Cardiac contusion, ablation, pacing, cardioversion, or endomyocardial biopsy Infiltrative diseases, e.g., amyloidosis, haemochromatosis, sarcoidosis, and scleroderma White HD Lancet

14 Elevations of Troponin in the absence of an Acute Coronary Syndrome Inflammatory diseases, e.g., myocarditis, myocardial extension of endocarditis Drug toxicity, e.g., adriamycin, 5-fluorouracil, herceptin, capecitabine Aortic dissection, aortic valve disease, hypertrophic cardiomyopathy Hypothyroidism Phaeochromocytoma Takosubo cardiomyopathy Burns affecting >30% of body surface area Rhabdomyolysis with cardiac injury Critically ill patients with respiratory failure, or sepsis Snake bites White HD Lancet

15 Time is muscle Muscle = Survival Aims: to prevent death to minimize patient s discomfort and distress to limit the extent of myocardial damage Strategy: Re-establish myocardial reperfusion before irreversible damage occurs: mechanically (Percutaneus coronary intervention) pharmacologically (induction of thrombolysis by fibrinolytic agent) 15

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17 Morphine to relief pain Oxygen if oxygen saturation < 94% NTG or ISDN to relief pain (no history of sildenafril within 24 hours) Antiplatelets Statin Beta blocker ACEI or ARB 17

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19 Indications for Fibrinolytic Therapy When There Is a >120-Minute Delay From FMC to Primary PCI 19

20 (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 Dose 1.5 MU in min Up to 100 mg in 90 min (based on weight) 10 U? 2 (30 min apart) each over 2 min mg based on weight Bolus administration No No Yes Yes Antigenic Yes No No No Allergic reactions hypotension most common Systemic fibrinogen depletion 90-min patency rates (%) Yes No No No Marked Mild Moderate Minimal TIMI grade 3 flow (%) Cost per dose (Rs) 2500 ACS (50mg) -KK 20

21 Indications for Transfer for Angiography After Fibrinolytic Therapy *Although individual circumstances will vary, clinical stability is defined by the absence of low output, hypotension, persistent tachycardia, apparent shock, high-grade ventricular or symptomatic supraventricular tachyarrhythmias, and spontaneous recurrent ischemia. 21

22 Primary PCI in STEMI 22

23 Adjunctive Antithrombotic Therapy to Support Reperfusion With Fibrinolytic Therapy 23

24 Adjunctive Antithrombotic Therapy to Support Reperfusion With Fibrinolytic Therapy (cont.) 24

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30 UA/NSTEMI 9/00 RISK STRATIFICATION IN EMERGENCY DEPARTMENT HIGH RISK-FEATURES (RISK RISES WITH NUMBER) History Clinical findings ECG Cardiac markers Prolonged ischemic discomfort (>20 min), ongoing rest pain, accelerating tempo of ischemia Pulmonary edema; S 3 or new rales New MR murmur Hypotension, bradycardia, tachycardia Age >75 years Rest pain with transient ST-segment changes > 0.05 mv; new bundle-branch block, new sustained VT Elevated (e.g. TnT or TnI>0.1 ng/ml)

31 High risk UA or NSTEMI-ACS Severe chest pain (prolong, ongoing, recurrent chest pain > 2 within 24 hours) Unstable hemodynamic (hypotension, new tachyarrhythmia,bradycardia, heart block), Cardiogenic shock Heart failure, LVEF < 40% New MR murmur Dynamic ischemic ST-T changes with chest pain, sustained ventricular tachycardia Elevated troponin T หร อ troponin I > 0.1 ng/ml อาย มากกว า 75 ป Prior PCI ภายใน 6 เด อน Prior CABG DM Mild to moderate renal dysfunction 31 ACS High 2013 risk -KK score (Grace risk score > 140)

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34 Risk stratification before discharge ทาในราย low หร อ Intermediate risk ท ไม ม เจ บแน นหน าอก ไม ม ภาวะ ห วใจล มเหลว เป นเวลาอย างน อย ช วโมง (Class I;C) ว ธ ทดสอบข นก บ resting ECG สภาพผ ป วยและความชานาญหร อเทคโนโลย ท ม อย ของแต ละโรงพยาบาล (Class I;C) ควรใช Cardiac imaging สาหร บการทา risk stratification ในรายท resting ECG ม ST segment depression 0.1 mv, left ventricular hyperyrophy, intraventricular conduction defects, paced-rhythm, pre-excitation (WPW syndrome) ผ ป วยท ได ร บยา digoxin และม ข อจาก ดทางกายภาพ เช น severe COPD, peripheral vascular disease โรคข อเข าเส อม (Class I;B) 34

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37 Topics STE-ACS, NSTE-ACS,UAP Diagnosis EKG & markers (tropnin T & I) Management -Drugs, -Fibrinolytics vs PPCI in STE-ACS, 37 -Early invasive stratergy vs. Conservative stratergy in NSTE-ACS or UAP - Risk stratification - Cardiac rehabiliatation - Secondary prevention

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40 การให ยากล บบ านในผ ป วย ACS Antiplatelets ASA Clopidogrel or Ticagrelor Antiangina Beta blocker Nitrate ± CCB Antiatheros clerosis ACEI or ARB Statin 40 AA in pts. with poor LVEF, Influenza vaccine