Acute Coronary Syndrome

REFERAT PENYAKIT DALAM RSUD BANYUMAS Yusrina Adani 08/267821/KU/12737

Daftar Isi
1. Definisi

2. Epidemiologi
3. Anatomi dan Fisiologi 4. Patofisiologi

5. Manifestasi Klinis
6. Diagnosis dan Diagnosis Banding 7. Tata laksana

8. Prognosis dan Komplikasi

9. Prevensi 10. Kesimpulan

1. Definisi
Definisi Acute Coronary Syndrome (ACS)
Sindrom koroner akut adala keadaan gawat darurat jantung dengan manifestasi klinis berupa perasaan tidak enak di dada atau gejala-gejala lain sebagai akibat iskemia miokardium.

ACS Coronary Heart Disease (CHD)

 Typical anginaAll three of the following

Substernal chest discomfort Onset with exertion or emotional stress Relief with rest or nitroglycerin

Atypical angina
Meets 2 of the above characteristics

Noncardiac chest pain

Meets 1 of the typical angina characteristics

Modified from Diamond GA. A clinically relevant classification of chest discomfort. J Am Coll Cardiol. 1983;1:574.

CCS Classification
Classification System of Angina Pectoris
Class 1 Activities Triggering Chest Pain Angina only during strenuous or prolonged physical activity

2
3

Slight limitation, with angina only during vigorous physical activity

Symptoms with everyday living activities, i.e., moderate limitation

Inability to perform any activity without angina or angina at rest, i.e., severe limitation

Adapted from Braunwald E, Antman EM, Beasley JW, et al: ACC/AHA Guidelines for the management of patients with unstable angina and non-ST segment elevation myocardial infarction: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on the management of patients with unstable angina). Journal of American College of Cardiology 36:9701062, 2000

UAP
NSTEACS ACS NSTEMI

STEACS

STEMI

 Unstable Angina Non-ST-Segment Elevation MI (NSTEMI) ST-Segment Elevation MI (STEMI)

Similar pathophysiology

Similar presentation and early management rules

STEMI requires evaluation for acute reperfusion intervention

2. Epidemiologi
CHD adalah penyebab kematian nomor 1 di dunia.
450,000 kematian di U.S di tahun 2009 Setiap tahun ada 1,200,000 kasus baru atau rekurrent penyakit jantung koroner 38% dari mereka mati mendadak.

Atherothrombosis reduces life expectancy by approximately 812 years in patients aged over 60 years1
Average remaining life expectancy at age 60 (men)
20 18 16 14
-7.4 years

Atherothrombosis reduces life expectancy

Years

12 10 8 6 4 2 0

-9.2 years -12 years

Healthy

History of CV disease

History of AMI

History of stroke

1. Peeters et al. Eur Heart J 2002; 23: 458466

Analysis of data from the Framingham Heart Study AMI = Acute myocardial infarction

3. Anatomi dan Fisiologi

Heart Region and Most Likely Associated Vessels

Anteroseptal: A. Interventriku laris anterior Posterior dan inferior: a. Coronaria dextra

Anterolateral: a. circumflexa

Anteroapical: a. Interventrikularis anterior bag. distal

4. Patofisiologi
Different stages of atherosclerotic plaque development

Characteristics of the stable atherosclerotic plaque

Fibrous cap (VSMCs and matrix)
Endothelial cells Intimal VSMCs (repair phenotype)

Lipid core

Adventitia Medial VSMCs (contractile phenotype)

Weissberg, 1999

Plaque disruption
(plaque cracking, fissuring, rupture thrombosis start point)

17

5. Manifestasi Klinis
Palpitations Substernal pain (pressure, squeezing, or a burning sensation) and may radiate to the neck, shoulder, jaw, back, upper abdomen, or either arm Exertional dyspnea that resolves with pain or rest Diaphoresis from sympathetic discharge Nausea from vagal stimulation Decreased exercise tolerance Hypotension Hypertension Pulmonary edema (sign of LHF) Jugular venous distention (sign of RHF) Cool, clammy skin and diaphoresis in patients with cardiogenic shock

Faktor Resiko
MODIFIABLE RISK FACTOR
Diabetes mellitus

UNMODIFIABLE RISK FACTOR

Increasing age Age-- > 45 for male/55 for female Male sex Family history of premature CHD Event in first degree relative >55 male/65 female

Dyslipidaemia
Active and passive cigarette smoking Hypertension High-fat diet Physical inactivity Obesity/insulin resistance

6. Diagnosis
Acute Coronary Syndrome
Chest pain typically to angina/infarction

Trombosis

ECG Cardiac Enzyme Final Diagnosis

No ST Elevation Non-STEACS UAP NSTEMI

ST Elevation Non-STEACS

Unstable Angina Pectoris

Myocardial Infarction

NQwMI

Qw MI

Circulation 2001;104:365; Lancet 2001; 358:1533-1538; J Am Coll Cardiol. 2007

Diagnosis of Angina
Diagnosis:
Anamnesis Pemeriksaan fisik EKG Biormarker Non-invasive Stress Test

10 menit

Coronary angiography
Imaging (rarely done)

Anamnesis
Aid in diagnosis and rule out other causes
1. 2. 3. 4. 5. 6. 7. 8. Onset Location and radiation of pain Duration Characteristic and quality of discomfort Palliative/Provocative factors Symptoms associated with discomfort Cardiac risk factors Past medical history -especially cardiac

Reperfusion questions
1. 2. 3. 4. Timing of presentation ECG c/w STEMI Contraindication to fibrinolysis Degree of STEMI risk

Pemeriksaan Fisik
1. 2. 3. 4. 5. 6. 7. 8. ABC Vital signs, general observation Presence or absence of jugular venous distension (JVD) Pulmonary auscultation for rales Cardiac auscultation for murmurs and gallops Presence or absence of stroke Presence or absence of pulses Presence or absence of systemic hypoperfusion (cool, clammy, pale, ashen)

EKG
ST Elevation atau LBBB baru STEMI
ST Depression or dynamic T wave inversions

NSTEMI
Non-specific ECG

Unstable Angina

Normal or non-diagnostic EKG

ST Depression or Dynamic T wave Inversions

ST-Segment Elevation MI

New LBBB

LBBB criteria: - Wide QRS complex (> 0,12 ms/ 3mm) in V5-V6, I, aVL - Broad on top/ notched - Leads that overlying RV show deep S waves (V1-V4)

Cardiac Biomarkers
IDEAL MARKER:
High concentration in myocardium Myocardium specific Released early in injury Proportionate to injury Non expensive testing

Anderson JL, et al. J Am Coll Cardiol 2007;50:e1e157, Figure 5.

Prinsip ACS
1. If the initial ECG is not diagnostic of STEMI, serial ECGs (every 1530 min) or continuous ST-segment monitoring should be performed in the patient who remains symptomatic or if there is high clinical suspicion for STEMI. 2. Show 12-lead ECG results to emergency physician within 10 minutes of ED arrival in all patients with chest discomfort (or anginal equivalent) or other symptoms of STEMI.
3. In patients with inferior STEMI, ECG leads should also be obtained to screen for right ventricular infarction.

4. Lab exams should be performed as part of the management of STEMI patients, but should not delay the implementation of reperfusion therapy. Result of the lab exams should be ready in 60 min Serum cardiac biomarker CBC

Activated partial thromboplastin time (aPTT)

Electrolytes and magnesium Blood urea nitrogen (BUN) and Creatinine Glucose Complete lipid profile

5. Cardiac-specific troponins should be used as the optimum biomarkers for the evaluation of patients with STEMI who have coexistent skeletal muscle injury.
6. For patients with ST elevation on the 12-lead ECG and symptoms of STEMI, reperfusion therapy should be initiated as soon as possible and is not contingent on a biomarker assay.

Non-invasive Stress Test

When should we do the treadmill test?
The differential diagnosis of chest pain in someone whose baseline EKG is normal The evaluation of a patient who has recently had an infarction, in order to assess his or her prognosis The evaluation of individuals over 40 years of age who have risk factors for coronary artery disease Stress testing is also frequently done in patients over 40 years of age who want to start an exercise program.

Diagnosis Banding
Differential Diagnosis of STEMI: Life-Threatening Aortic dissection Pulmonary Emboli Perforating ulcer Tension pneumothorax Boerhaave syndrome (esophageal rupture with mediastinitis)
Differential Diagnosis of STEMI: Other Cardiovascular and Nonischemic Pericarditis Atypical angina

Early repolarization
Brugada syndrome Myocarditis

Hyperkalemia
Bundle-branch blocks Hypertrophic cardiomyopathy

Differential Diagnosis of STEMI: Other Noncardiac Gastroesophageal reflux (GERD) and spasm Chest-wall pain Pleurisy Peptic ulcer disease Panic attack

7. Tata Laksana
TIME = MUSCLE
Decrease amount of myocardial necrosis Preserve LV function Prevent major adverse cardiac events Treat life threatening complications

Chest discomfort suggestive of ischemia

Chest discomfort suggestive of ischemia EMS assessment and care and hospital preparation: 1. Monitor, support ABCs. Be prepared to provide CPR and defibrillation 2. Administer aspirin, & consider oxygen, NTG, and morphine if needed 3. If available, obtain 12 lead ECG; if ST elevation: -Notify receiving hospital with transmission or interpretation -Begin fibrinolytic checklist 4. Notified hospital should mobilize hospital resources to respond to STEMI

Chest discomfort suggestive of ischemia EMS assessment and care and hospital preparation: 1. Monitor, support ABCs. Be prepared to provide CPR and defibrillation 2. Administer aspirin, & consider oxygen, NTG, and morphine if needed 3. If available, obtain 12 lead ECG; if ST elevation: -Notify receiving hospital with transmission or interpretation -Begin fibrinolytic checklist 4. Notified hospital should mobilize hospital resources to respond to STEMI

Concurrent ED assessment (<10) 1. Check vital signs; evaluate oxygen saturation 2. Establish IV access 3. Obtain 12 lead ECG 4. Perform brief, targeted history, physical exam 5. Review fibrinolytic checklist, check contraindications 6. Obtain initial cardiac marker levels, initial electrolyte and coagulation studies 7. Obtain portable chest x-ray (<30 )

Immediate ED general treatment 1. If SpO2 <94%, start oxygen at 4 lpm 2. Aspirin 160-325 mg (if not given by EMS) 3. Nitroglycerin SL or spray 4. Morphine IV if pain is not relieved by NTG

Chest discomfort suggestive of ischemia EMS assessment and care and hospital preparation: 1. Monitor, support ABCs. Be prepared to provide CPR and defibrillation 2. Administer aspirin, & consider oxygen, NTG, and morphine if needed 3. If available, obtain 12 lead ECG; if ST elevation: -Notify receiving hospital with transmission or interpretation -Begin fibrinolytic checklist 4. Notified hospital should mobilize hospital resources to respond to STEMI

Concurrent ED assessment (<10) 1. Check vital signs; evaluate oxygen saturation 2. Establish IV access 3. Obtain 12 lead ECG 4. Perform brief, targeted history, physical exam 5. Review fibrinolytic checklist, check contraindications 6. Obtain initial cardiac marker levels, initial electrolyte and coagulation studies 7. Obtain portable chest x-ray (<30 )

Immediate ED general treatment 1. If SpO2 <94%, start oxygen at 4 lpm 2. Aspirin 160-325 mg (if not given by EMS) 3. Nitroglycerin SL or spray 4. Morphine IV if pain is not relieved by NTG

ECG interpretation

Chest discomfort suggestive of ischemia EMS assessment and care and hospital preparation: 1. Monitor, support ABCs. Be prepared to provide CPR and defibrillation 2. Administer aspirin, & consider oxygen, NTG, and morphine if needed 3. If available, obtain 12 lead ECG; if ST elevation: -Notify receiving hospital with transmission or interpretation -Begin fibrinolytic checklist 4. Notified hospital should mobilize hospital resources to respond to STEMI

Concurrent ED assessment (<10) 1. Check vital signs; evaluate oxygen saturation 2. Establish IV access 3. Obtain 12 lead ECG 4. Perform brief, targeted history, physical exam 5. Review fibrinolytic checklist, check contraindications 6. Obtain initial cardiac marker levels, initial electrolyte and coagulation studies 7. Obtain portable chest x-ray (<30 )
ST elevation or new or presumably new LBBB; strongly suspicious for injury STEMI

Immediate ED general treatment 1. If SpO2 <94%, start oxygen at 4 lpm 2. Aspirin 160-325 mg (if not given by EMS) 3. Nitroglycerin SL or spray 4. Morphine IV if pain is not relieved by NTG

ECG interpretation ST depression or dynamic T wave inversion; strongly suspicious for ischemia High risk UA/ NSTEMI Normal or nondiagnostic changes in ST segment/ T wave Intermediate/ low risk UA

Start adjunctive treatments (Dont delay reperfusion) - B receptor blockers - Clopidogrel - Heparin (UFH/ LMWH)

Start adjunctive treatments (Dont delay reperfusion) - B receptor blockers - Clopidogrel - Heparin (UFH/ LMWH) Time from onset of symptoms 12 hours?
12 hours

Reperfusion goals: Therapy defined by patient and center criteria - Door-to-balloon inflation (PCI) goal of 90 min -Door-to-needle (Fibrinolysis) goal of 30 min - Continue adjunctive therapies and: - ACE inh/ ARB within 24 hours of symptom onset - HMG Co A reductase inh (statin therapy)

Start adjunctive treatments (Dont delay reperfusion) - B receptor blockers - Clopidogrel - Heparin (UFH/ LMWH) Time from onset of symptoms 12 hours?
12 hours 12 hours

Admit to monitored bed Assess risk status High risk patient: -Early invasive therapy, including catheterization and revascularization for shock within 48 hours of an AMI Continue ASA, heparin, and other therapies as indicated - ACE inhibitor/ ARB - HMG CoA reductase inhibitor (statin therapy) Not at high risk: cardiology to riskstratify

Reperfusion strategy: Therapy defined by patient and center criteria - Be aware of reperfusion goals: - Door-to-balloon inflation (PCI) goal of 90 min -Door-to-needle (Fibrinolysis) goal of 30 min - Continue adjunctive therapies and: - ACE inh/ ARB within 24 hours of symptom onset - HMG Co A reductase inh (statin therapy)

Start adjunctive treatments (Dont delay reperfusion) - B receptor blockers - Clopidogrel - Heparin (UFH/ LMWH) Time from onset of symptoms 12 hours?
12 hours

Start adjunctive treatments -Nitroglycerin -B receptor blockers - Clopidogrel - Heparin (UFH/ LMWH) - Glycoprotein IIb/ IIIa inhibitor

Reperfusion strategy: Therapy defined by patient and center criteria - Be aware of reperfusion goals: - Door-to-balloon inflation (PCI) goal of 90 min -Door-to-needle (Fibrinolysis) goal of 30 min - Continue adjunctive therapies and: - ACE inh/ ARB within 24 hours of symptom onset - HMG Co A reductase inh (statin therapy)

Start adjunctive treatments (Dont delay reperfusion) - B receptor blockers - Clopidogrel - Heparin (UFH/ LMWH) Time from onset of symptoms 12 hours?
12 hours 12 hours

Start adjunctive treatments -Nitroglycerin -B receptor blockers - Clopidogrel - Heparin (UFH/ LMWH) - Glycoprotein IIb/ IIIa inhibitor Admit to monitored bed Assess risk status High risk patient: -Early invasive therapy, including catheterization and revascularization for shock within 48 hours of an AMI (Continue ASA, heparin, and other therapies as indicated) - ACE inhibitor/ ARB - HMG CoA reductase inhibitor (statin therapy) Not at high risk: cardiology to riskstratify

Reperfusion strategy: Therapy defined by patient and center criteria - Be aware of reperfusion goals: - Door-to-balloon inflation (PCI) goal of 90 min -Door-to-needle (Fibrinolysis) goal of 30 min - Continue adjunctive therapies and: - ACE inh/ ARB within 24 hours of symptom onset - HMG Co A reductase inh (statin therapy)

Start adjunctive treatments (Dont delay reperfusion) - B receptor blockers - Clopidogrel - Heparin (UFH/ LMWH) Time from onset of symptoms 12 hours?
12 hours 12 hours

Start adjunctive treatments -Nitroglycerin -B receptor blockers - Clopidogrel - Heparin (UFH/ LMWH) - Glycoprotein IIb/ IIIa inhibitor Admit to monitored bed Assess risk status High risk patient: -Early invasive therapy, including catheterization and revascularization for shock within 48 hours of an AMI (Continue ASA, heparin, and other therapies as indicated) - ACE inhibitor/ ARB - HMG CoA reductase inhibitor (statin therapy) Not at high risk: cardiology to riskstratify

Develops high risk/ intermediate risk criteria OR troponin (+)?

Reperfusion strategy: Therapy defined by patient and center criteria - Be aware of reperfusion goals: - Door-to-balloon inflation (PCI) goal of 90 min -Door-to-needle (Fibrinolysis) goal of 30 min - Continue adjunctive therapies and: - ACE inh/ ARB within 24 hours of symptom onset - HMG Co A reductase inh (statin therapy)

Start adjunctive treatments (Dont delay reperfusion) - B receptor blockers - Clopidogrel - Heparin (UFH/ LMWH) Time from onset of symptoms 12 hours?
12 hours 12 hours

Start adjunctive treatments -Nitroglycerin -B receptor blockers - Clopidogrel - Heparin (UFH/ LMWH) - Glycoprotein IIb/ IIIa inhibitor Admit to monitored bed Assess risk status High risk patient: -Early invasive therapy, including catheterization and revascularization for shock within 48 hours of an AMI (Continue ASA, heparin, and other therapies as indicated) - ACE inhibitor/ ARB - HMG CoA reductase inhibitor (statin therapy) Not at high risk: cardiology to riskstratify

Yes

Develops high risk/ intermediate risk criteria OR troponin (+)?

Reperfusion strategy: Therapy defined by patient and center criteria - Be aware of reperfusion goals: - Door-to-balloon inflation (PCI) goal of 90 min -Door-to-needle (Fibrinolysis) goal of 30 min - Continue adjunctive therapies and: - ACE inh/ ARB within 24 hours of symptom onset - HMG Co A reductase inh (statin therapy)

Start adjunctive treatments (Dont delay reperfusion) - B receptor blockers - Clopidogrel - Heparin (UFH/ LMWH) Time from onset of symptoms 12 hours?
12 hours 12 hours

Start adjunctive treatments -Nitroglycerin -B receptor blockers - Clopidogrel - Heparin (UFH/ LMWH) - Glycoprotein IIb/ IIIa inhibitor Admit to monitored bed Assess risk status High risk patient: -Early invasive therapy, including catheterization and revascularization for shock within 48 hours of an AMI (Continue ASA, heparin, and other therapies as indicated) - ACE inhibitor/ ARB - HMG CoA reductase inhibitor (statin therapy) Not at high risk: cardiology to riskstratify

Yes

Develops high risk/ intermediate risk criteria OR troponin (+)?

Reperfusion strategy: Therapy defined by patient and center criteria - Be aware of reperfusion goals: - Door-to-balloon inflation (PCI) goal of 90 min -Door-to-needle (Fibrinolysis) goal of 30 min - Continue adjunctive therapies and: - ACE inh/ ARB within 24 hours of symptom onset - HMG Co A reductase inh (statin therapy)

Start adjunctive treatments (Dont delay reperfusion) - B receptor blockers - Clopidogrel - Heparin (UFH/ LMWH) Time from onset of symptoms 12 hours?
12 hours 12 hours

Start adjunctive treatments -Nitroglycerin -B receptor blockers - Clopidogrel - Heparin (UFH/ LMWH) - Glycoprotein IIb/ IIIa inhibitor Admit to monitored bed Assess risk status High risk patient: -Early invasive therapy, including catheterization and revascularization for shock within 48 hours of an AMI (Continue ASA, heparin, and other therapies as indicated) - ACE inhibitor/ ARB - HMG CoA reductase inhibitor (statin therapy) Not at high risk: cardiology to riskstratify

Yes

Develops high risk/ intermediate risk criteria OR troponin (+)?

No

Reperfusion strategy: Therapy defined by patient and center criteria - Be aware of reperfusion goals: - Door-to-balloon inflation (PCI) goal of 90 min -Door-to-needle (Fibrinolysis) goal of 30 min - Continue adjunctive therapies and: - ACE inh/ ARB within 24 hours of symptom onset - HMG Co A reductase inh (statin therapy)

Consider admission to ED chest pain unit/ to monitored bed in ED Follow: - Serial cardiac markers (including troponin) - Repeat EKG/ continuous ST segment monitoring - Consider stress test
Yes

Develops high/ intermediate risk criteria OR troponin (+)?

No

If no evidence of ischemia/ infarction, can discharge with follow up

Absolute contraindications for Fibrinolysis

If presentation is < 3 hours, check for
5 KEPALA 1. Malignant intracranial neoplasm (primary or metastatic) 2. Ischemic stroke within 3 months EXCEPT acute ischemic stroke within 3 hours 3. Prior intracranial hemorrhage 4. Structural cerebral vascular lesion (e.g., AVM) 5. Significant closed-head or facial trauma within 3 months 1 DADA 1 DARAH

Suspected aortic dissection

Active bleeding or bleeding diathesis (excluding menses)

8. Prognosis
1. TIMI Risk Score
2. GRACE Risk Score more complex! 3. PURSUIT Risk Score

TIMI Risk Score

TIMI Risk Score
Predicts risk of death, new/ recurrent MI, need for urgent revascularization within 14 days (UA/NSTEMI) or 7 days (STEMI) Score interpretation: 3 = low risk

4-5 = intermediate risk (use IIBIIIA)

6-7 = high risk (use IIBIIIA)

Killip Classification
Killip Classification and Mortality Rate of Acute MI* Class PAO2 Clinical Description Hospital Mortality Rate

1
2 3 4

Normal
Slightly reduced Abnormal Severely abnormal

No clinical evidence of left ventricular (LV) failure Mild to moderate LV failure

Severe LV failure, pulmonary edema Cardiogenic shock: hypotension, tachycardia, mental obtundation, cool extremities, oliguria, hypoxia

35%
610% 2030% > 80%

*Determined by repeated examination of the patient during the course of illness.

Determined while the patient is breathing room air. Modified from Killip T, Kimball JT: Treatment of myocardial infarction in a coronary care unit. A two-year experience with 250 patients. The American Journal of Cardiology 20:457464, 1967.

Komplikasi
Arrythmia
Heart Failure Hypotension and cardiogenic shock Recurrent ischemia Pericarditis

9. Prevensi
SMOKING CESSATION
DIET MODIFICATION/WEIGHT CONTROL BP CONTROL LIPID MANAGEMENT EXERCISE DIABETES MANAGEMENT

10. Kesimpulan
ACS includes UA, NSTEMI, and STEMI
Management guideline focus
Immediate assessment/intervention (MONA+BAH) Risk stratification (UA/NSTEMI vs. STEMI) RAPID reperfusion for STEMI (PCI vs. Thrombolytics) Conservative vs Invasive therapy for UA/NSTEMI

Aggressive attention to secondary prevention initiatives for ACS patients

Beta blocker, ASA, ACE-I, Statin

Referensi
Rani A. et al., 2006, Perhimpunan Dokter Spesialis Penyakit Dalam Indonesia, halaman 63 Fauci A. et al., 2005, Harrisons Principles of Internal Medicine 16th edition, p1425 Kumar P and Clark M, 2006, Clinical Medicine 7th Edition, page 743 Brady W. et al. 2012, Acute Coronary Syndrome : 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care, AHA Aroney C. et al. 2006, Guidelines for the management of acute coronary syndromes 2006, National Heart Foundation of Australia.

Acute Coronary Syndromes : a national clinical guidelines, 2007, Scottish Intercollegiate Guidelines Network.
Harrisons, Prinsiples of Internal Medicine, 18th ed, Philadelphia, McGraw Hill, 2012,138797.

TERIMA KASIH
MOHON ASUPAN

Tata Laksana
Supplemental oxygen should be administered to patients with arterial oxygen desaturation (SaO2 < 90%).

I IIa IIb III

I IIa IIb III

Patients with ongoing ischemic discomfort should receive NTG (0.4 mg) SL every 5 for a total of 3 doses assess whether we need intravenous NTG.

Tata Laksana
Morphine sulfate (2 to 4 mg intravenously with increments of 2 to 8 mg intravenously repeated at 5 to 15 minute intervals) is the analgesic of choice for management of pain associated with STEMI.

I IIa IIb III

I IIa IIb III

Aspirin should be chewed by patients who have not taken aspirin before presentation with STEMI. The initial dose should be 162 mg (Level of Evidence: A) to 325 mg (Level of Evidence: C)

Tata Laksana
Oral beta-blocker therapy should be administered promptly to those patients without a contraindication, irrespective of concomitant fibrinolytic therapy or performance of primary PCI.

I IIa IIb III

I IIa IIb III

It is reasonable to administer intravenous betablockers promptly to STEMI patients without contraindications, especially if a tachyarrhythmia or hypertension is present.

Reperfusion
Door-to- needle (or medical contactto-needle) time for initiation of fibrinolytic therapy can be achieved within 30 minutes, Door-to-balloon (or medical contactto- balloon) time for PCI can be kept within 90 minutes.

Fibrinolysis preferred if:

PCI preferred if:

<3 hours from onset PCI not available/delayed door to balloon > 90min door to balloon minus door to needle > 1hr No contraindications

PCI available Door to balloon < 90min Door to balloon minus door to needle < 1hr Fibrinolysis contraindications Late Presentation > 3 hr High risk STEMI Killip 3 or higher STEMI dx in doubt

 GUIDELINES:
Initial 12 lead ECG goal door to ECG time 10min, read by experienced doctor (Class 1 B)

If ECG not diagnostic/high suspicion of ACS serial ECGs initially 15 -30 min intervals (Class 1 B) ECG adjuncts leads V7 V9, RV 4 (Class 2a B) Continuous 12 lead ECG monitoring reasonable alternative to serial ECGs (Class 2a B)

 First point of entry into ACS algorithm

Abnormal or normal

Neither 100% sensitive or 100% specific for AMI

Single ECG for AMI sensitivity of 60%, specificity 90% Represents single point in time needs to be read in context Normal ECG does not exclude ACS 1-6% proven to have AMI, 4% unstable angina

EKG

 Troponin T vs I
both equivalent in diagnostic and prognostic abilities ( except in renal failure Trop T less sensitive) Elevation ~ 2hrs to 12hrs

~30 40% of ACS patients without ST elevation had normal CKMB but elevated troponins on presentation
Meta-analysis (Heindereich et al) odds of death increased 3 to 8 fold with positive troponin

Troponin I/ T

 Rapid release within 2 hours

Not cardiac specific

Rule out for NSTEMI rather than rule in.

CKMB
Used in conjunction with troponins
Useful in diagnosing re-infarction

Myoglobin & CKMB

 2 hour delta CKMB mass

Aim to exclude MI within 6hrs of symptom onset

Determine changes in serum marker levels over certain time intervals delta values

Increasing values while still within normal range suggestive of ischaemia more rapid anti- ischaemic mxn.

 Measured with albumin cobalt binding assay

In ischaemia -> decreased binding of albumin to cobalt Increased with minutes of ischaemia elevated for 6-12hrs gone by 24hrs ~90% negative predictive value Combined with myoglobin/CKMB/troponin increases diagnostic sensitivity of ischaemia by 40% Possible role for rule criteria in low risk patients Positive IMA high risk patients more aggressive mxn Positive in hypoxic disorders poor specificity in this setting

Ischemia modified albumin

 B type Natriuretic Peptide:

released from heart muscle in response to increased ventricular wall stress. Studies BNP not a specific marker but a strong predictor of ACS especially in patients with chest pain, no ECG changes, non diagnostic troponins. Also positive in heart failure, PE, atrial arrythmias, renal failure Pregnancy Associated Plasma Protein A (PAPP-A): Released when plaque ruptures Predictor of ischaemia

 HEART FATTY ACID BINDING PROTEIN (HF ABP)

Identifies AMI <4hrs after onset Protein involved in myocardial lipid synthesis, but also expressed outside heart Therefore may be sensitive but not specific for injury Possible role in multi-marker strategy IMAGING MODALITIES Cardiac MRI Multidetector CT for coronary calcification Coronary CT angiography Undergoing clinical evaluation

 2007 ACC/AHA guidelines:

Cardiac biomarkers measured in all patients with suspicion of ACS (Class 1 B) Troponin preferred marker( Class 1 B)

If troponin negative within 6 hours of onset, repeat 8-12hours later(Class 1 B)

Remeasuring of positive biomarkers to determine infarct size/necrosis (Class 2a B) Patients presenting within 6 hours of symptom onset myoglobin in conjunction with troponin measured (Class 2b B) 2hr delta CKMB/Delta troponin considered in <6hr presentation (Class 2b B)

BNP level for global risk assessment(Class 2b B)

Class 3 AST/LDH/CK without CKMB

2007ACS/AHA GUIDELINES:
Rapid categorization of patient (Class 1 C) Possible ACS, non diagnostic ECG/biomarkers observed in facility with cardiac monitoring (Class 1 C)

Alternative to in patient treatment: for those with 12hr ECG/markers negative stress ECG in 72hrs (Class 1 C)
Giving precautionary treatment for those for OPD stress (Class 1 B)

Management updates

 GENERAL:

IV B Blockers downgraded from Class 1 to 2a recommendation. (COMMIT Trial)

Oral B Blockers in first 24hrs still Class 1 but not used in signs of heart failure, cardiogenic shock and reactive airway disease.(LOE B)

UA/ NSTEMI updates

MORPHINE downgraded from Class 1 to 2a findings from CRUSADE Registry

 ANTIPLATELET THERAPY:
CLASS 1 RECOMMENDATION Aspirin to all patients as soon as possible and continued (if no C/I) (LOE A) Initial dose 162 -325mg Maintenance 75 -162mg No added benefit from higher doses except post stenting Clopidogrel for those allergic to aspirin or major GI bleeding (LOE A)

NSTEMI updates
For initial invasive strategy aspirin + clopidogrel or IV glycoprotein 2b/3a therapy (LOE A) Abciximab if no delay in angiography/PCI, eptifibatide/tirofiban if delayed angiography(LOE B)

 PHARMACOLOGICAL UPDATE:
ANALGESIA changes from 2004 guidelines MORPHINE: still remains Class 1 C for STEMI, titrated doses

NSAIDS/COX 2 INHIBITORS: those on it should have it discontinued ( increased risk of mortality, re infarction, heart failure, myocardial rupture) Class 1 C
NSAIDS should not be administered in hospital for MI (Class 3)

STEMI

 BETA BLOCKERS
Modified recommendation Oral Beta Blockers should be initiated in first24rs, if no contra-indications (heart failure, risk of cardiogenic shock) Class 1 B Patients with early contraindications -> reevaluated later for possible use Role of IV B blockers used in hypertensive patients with STEMI Class 2a B Class 3 LOE A IV B blockers should not be administrated to patients with heart failure, risk of cardiogenic shock

 No major changes to reperfusion strategies.

Emphasis on decreasing ischaemic time.

Increase use of prehospital 12 lead ECG emphasised.

In PCI capable hospital door to PCI time 90 min (Class 1 A)

In non PCI capable hospital door to needle time 30 min or timeous transfer to PCI capable hospital. (Class 1 B)

Reperfusion

FIBRINOLYTICS

AVAILABLE FIBRINOLYTICS: STREPTOKINASE 1.5mu infusion over 30min (1hour ACLS) rtPA accelerated infusion over 1.5hrs - 15mg IV bolus, 0.75mg/kg over 30 min, 0.5mg/kg over 1hr ANISTREPLASE 30 U IV over 5 min TENECTEPLASE 30 TO 50 MG RETEPLASE 10 U IV bolus, ffd. 10U IV after 30 min

WHICH FIBRINOLYTIC TO USE??? GISSI 2 trial tPA vs Streptokinase , no difference in mortality, marginally higher stroke rate with tPA (1.3% vs 1%) GUSTO 1 trial early vessel patency post infract assoc. with better survival. Accl. tPA/heparin cf comb. Streptokinase/tPA/heprain cf strep with IV vs S/C heparin Outcome better flow rates with accl. tPA -> lower mortality rates

 ASSENT 2 TRIAL tenecteplase vs aTPA - tenecteplase was equally or minimally more effective, especially in those presenting > 4hrs after symptom onset.

Fibrinolysis combined with glycoprotein 2b/3a inhibitors no overall advantage (ASSENT 3, GUSTO 5 trials)

 RESCUE PCI:

CLASS 1 LOE B angiography with +/- PCI in patients (<75 yrs)with cardiogenic shock, severe heart failure, ventricular dysrythmias
Class 2a persistent ischaemic symptoms post fibrinolysis, haemodynamic instability, electrical instability (LOE C) New recommendation PCI for failed fibrinolytic therapy (less than 50% decrease in ST elevation in worst lead, 90min post fibrinolytic therapy, or large area of myocardium injured) LOE B Class 3 angiography performed if invasive strategy contraindicated, or patient refusal (LOE C)

ANTICOAGULANT ADJUNCTS

NEW RECOMMENDATIONS:

CLASS 1
Patients undergoing fibrinolysis should be kept on anticoagulants for atleast 48 hrs and preferably the duration of hospital stay. LOE A

Anti coagulants with proven efficacy: Unfractionated Heparin keeping aPTT 1.5 2 sec above control (LOE C) Enoxaparin (Clexane) initial dosage of 30mg IV bolus ffd by 1mg/kg 12hrly, caution in renal impairment (LOE A) Fondaparinux 2.5mg IV, ffd by 2.5mg dly S/C maintenance for duration of hospitalisation (LOE B)

ANTICOAGULANTS

CLASS 2a recommendation to use anticoagulants in STEMI without reperfusion. UFH (LOE B) LMWH (LOE C) Fondaparinux (LOE B)

THIENOPYRIDINES

CLASS I CLOPIDOGREL now recommended in all STEMI patients in addition to aspirin, whether undergoing reperfusion or not. Dosage 75mg daily(LOE A) Duration -14 days (LOE B)

CLASS 2 A In patients < 75yrs Clopidogrel 300mg loading dose recommended(LOE C)

Long term maintenance therapy should be considered, 75mg dly for 1 year (LOE C)

SECONDARY PREVENTION

INCREASED FOCUS ON SECONDARY PREVENTION:

 Despite good reperfusion strategies approx. 1/3 of patients worldwide miss out. Attributed to delayed presentation, atypical presentation, complicated disease presentation, older age

SYMPTOMS OF INFARCT BUT NO ESTABILISHED ECG CHANGES - keep in mind aortic dissection, GIT disease, other chest pathology

CONCLUSION
With increase burden of CVD, and lack of health resources risk stratification becomes important.

Emphasis should also be placed on primary &secondary prevention of ACS.

Early intervention helps prevent complications, decreases morbidity & mortality

The way forward fully equipped CHEST PAIN OBSERVATION UNIT

Evolution of STEMI
A.
B.

Normal ECG
Tall T

C. Injury, ST elevation

D. Biphasic T waves
E. F. Q - Biphasic T waves Q - abnormal

ACS risk criteria

Low Risk ACS
No intermediate or high risk factors <10 minutes rest pain

Intermediate Risk ACS

Moderate to high likelihood of CAD >10 minutes rest pain, now resolved T-wave inversion > 2mm

Non-diagnositic ECG
Non-elevated cardiac markers Age < 70 years

Slightly elevated cardiac markers

High Risk ACS

Elevated cardiac markers New or presumed new ST depression

Recurrent ischemia despite therapy

Recurrent ischemia with heart failure High risk findings on non-invasive stress test Depressed systolic left ventricular function Hemodynamic instability Sustained Ventricular tachycardia PCI with 6 months

Prior Bypass surgery

Secondary Prevention and Long Term Management

Secondary Prevention and Long Term Management

Goals Smoking Recommendations

Goal: Complete Cessation

Assess tobacco use.

Strongly encourage patient and family to stop smoking and to avoid secondhand smoke. Provide counseling, pharmacological therapy (including nicotine replacement and bupropion), and formal smoking cessation programs as appropriate.

Secondary Prevention and Long Term Management

Goals
Blood pressure control:

Recommendations
If blood pressure is 120/80 mm Hg or greater: Initiate lifestyle modification (weight control, physical activity, alcohol moderation, moderate sodium restriction, and emphasis on fruits, vegetables, and low-fat dairy products) in all patients. If blood pressure is 140/90 mm Hg or greater or 130/80 mm Hg or greater for individuals with chronic kidney disease or diabetes: Add blood pressure-reducing medications, emphasizing the use of beta-blockers and inhibitors of the renin-angiotensin-aldosterone system.

Goal: < 140/90 mm Hg or <130/80 mm Hg if chronic kidney disease or diabetes

Secondary Prevention and Long Term Management

Goals
Physical activity:

Recommendations

Minimum goal: 30 minutes 3 to 4 days per week; Optimal daily

Assess risk, preferably with exercise test, to guide prescription. Encourage minimum of 30 to 60 minutes of activity, preferably daily but at least 3 or 4 times weekly (walking, jogging, cycling, or other aerobic activity) supplemented by an increase in daily lifestyle activities (e.g., walking breaks at work, gardening, household work). Cardiac rehabilitation programs are recommended for patients with STEMI.

Secondary Prevention and Long Term Management

Goals
Lipid management: (TG less than 200 mg/dL)

Recommendations
Start dietary therapy in all patients (< 7% of total calories as saturated fat and < 200 mg/d cholesterol). Promote physical activity and weight management. Encourage increased consumption of omega-3 fatty acids. Assess fasting lipid profile in all patients, preferably within 24 hours of STEMI. Add drug therapy according to the following guide: LDL-C < 100 mg/dL (baseline or on treatment): Statins should be used to lower LDL-C.

Primary goal: LDL-C << than 100 mg/dL

LDL-C 100 mg/dL (baseline or on treatment): Intensify LDL-Clowering therapy with drug treatment, giving preference to statins.

Secondary Prevention and Long Term Management

Goals
Lipid management: (TG 200 mg/dL or greater) Primary goal: NonHDL-C << 130 mg/dL

Recommendations
If TGs are 150 mg/dL or HDL-C is < 40 mg/dL: Emphasize weight management and physical activity. Advise smoking cessation.

If TG is 200 to 499 mg/dL: After LDL-Clowering therapy, consider adding fibrate or niacin.
If TG is 500 mg/dL: Consider fibrate or niacin before LDL-Clowering therapy. Consider omega-3 fatty acids as adjunct for high TG.

NCEP ATP III Guidelines

Patients with
0 1 risk factors

Initiate TLC* if LDL 160 mg/dL

Drug therapy considered if LDL

190 mg/dL (160 189 mg/dL: drug optional) 10 year risk 10 20%: 130 mg/dL 10-year risk <10%: 160 mg/dL

LDL treatment goal <160 mg/dL

2 risk factors (10 year risk

20%)

130 mg/dL

<130 mg/dL

CHD and CHD risk equivalents (10 year risk >20%)

100 mg/dL

130 mg/dL (100129 mg/dL: drug optional)

<100 mg/dL
Optimum: < 70 mg/dl

100 mg/dL = 2.6 mmol/L; 130 mg/dL = 3.4 mmol/L; 160 mg/dL = 4.1 mmol/L

* TLC: therapeutic lifestyle changes

National Cholesterol Education Program, Adult Treatment Panel III. JAMA 2001;285:24862497

Secondary Prevention and Long Term Management

Goals Weight management: Recommendations

Goal: BMI 18.5 to 24.9 kg/m2 Waist circumference: Women: < 35 in. Men: < 40 in.

Calculate BMI and measure waist circumference as part of evaluation. Monitor response of BMI and waist circumference to therapy.

Start weight management and physical activity as appropriate. Desirable BMI range is 18.5 to 24.9 kg/m2.
If waist circumference is 35 inches in women or 40 inches in men, initiate lifestyle changes and treatment strategies for metabolic syndrome.

REFERENCES
EDITORS MARX ET AL, ROSENS EMERGENCY MEDICINE: CONCEPTS AND CLINICAL PRACTICE, 6TH EDITION

PAUL PD ET AL, KEY ARTICLES IN MANAGEMENT OF ACS & PCI -2007 UPDATE, PHARMACOTHERAPY 2007:27(12), 1722 -1750

WHITE HD, DEFINING THE LIMITS OF ACS, CARDIOLOGY AT THE LIMITS IV, EDITORS: OPIE LH, YELLON DM

YUSUF S, THE GLOBAL EPIDEMIC OF ATHEROSCLEROTIC CARDIOVASCULAR DISEASE, CARDIOLOGY AT THE LIMITS IV, EDITORS: OPIE LH, YELLON DM

FOX KA, MANAGEMENT OF ACS: AN UPDATE, HEART.2004 JUNE, 90(6):698 -706

ANDERSON ET AL, ACC/AHA 2007 GUIDELINES FOR MXN OF U/A,NSTEMI EXECUTIVE SUMMARY DOWNLOADED content.onlinejacc.org

SIX AJ ET AL, CHEST PAIN IN THE ER: VALUE OF THE HEART SCORE, NETH. HEART J. 2008 JUNE,16(6):191 -196

 ANTMAN EM ET AL, 2007 FOCUSSED UPDATE OF ACC/AHA 2004 GUIDELINES FOR MAXN OF PATIENTS WITH STEMI, DOWNLOADED http://circ.ahajournals.org

McCANN CJ ET AL, NOVEL BIOMARKERS IN EARLY DIAGNOSIS OF AMI COMPARED WITH CARDIAC TROPONIN T, EUROPEAN HEART JOURNAL 2008,29(23): 2843 -2850

KING III SB ET AL, 2007 FOCUSSED UPDATE OF ACC..FOR PCI, JOURNAL OF AMERICAN COLLEGE OF CARDIOLOGY, VOL 51, NO 2, 2008