Download - Referat ACS Yusrina
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Acute Coronary
SyndromeREFERAT PENYAKIT DALAM
RSUD BANYUMAS
Yusrina Adani08/267821/KU/12737
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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
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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)
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▪ Typical angina—All 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 chestdiscomfort. J Am Coll Cardiol. 1983;1:574.
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CCS Classification
Classification System of Angina PectorisClass Activities Triggering Chest Pain
1 Angina only during strenuous or prolonged physical activity
2 Slight limitation, with angina only during vigorous physical activity
3 Symptoms with everyday living activities, i.e., moderate limitation
4 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 36:970–1062, 2000
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ACS
NSTEACS
UAP
NSTEMI
STEACS STEMI
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▪ 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
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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.
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Atherothrombosis reduces life expectancy
Analysis of data from the Framingham Heart StudyAMI = Acute myocardial infarction
Healthy History of CV disease
History of AMI
History of stroke
1. Peeters et al. Eur Heart J 2002; 23: 458–466
Atherothrombosis reduces life expectancy by approximately 8–12 years in patients aged over 60 years1
Average remaining life expectancy at age 60 (men)
0
2
4
6
8
10
12
14
16
18
20
Yea
rs
-9.2 years
-7.4 years
-12 years
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3. Anatomi dan Fisiologi
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Heart Region and Most Likely Associated Vessels
Anterolateral: a. circumflexa
Posterior dan
inferior: a. Coronaria
dextra
Anteroseptal: A.
Interventrikularis
anterior
Anteroapical: a. Interventrikularis anterior bag. distal
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4. Patofisiologi
Different stages of atherosclerotic plaque development
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Characteristics of the stable atherosclerotic plaque
Fibrous cap(VSMCs and matrix)
Lipid core
Adventitia
Endothelial cells
Intimal VSMCs (repair
phenotype)
Medial VSMCs(contractile phenotype)Weissberg, 1999
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Plaque disruption
17
(plaque cracking, fissuring, rupture – thrombosis start point)
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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
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Faktor Resiko
MODIFIABLE RISK FACTOR
Diabetes mellitus
Dyslipidaemia
Active and passive cigarette smoking
Hypertension
High-fat diet
Physical inactivity
Obesity/insulin resistance
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
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6. Diagnosis
Chest pain typically to angina/infarction
Acute Coronary Syndrome
Circulation 2001;104:365; Lancet 2001; 358:1533-1538; J Am Coll Cardiol. 2007
Trombosis
ECG ST Elevation
No ST Elevation
FinalDiagnosis
NQwMI Qw MI
Unstable Angina Pectoris
Myocardial Infarction
NSTEMICardiac Enzyme UAP
Non-STEACS Non-STEACS
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Diagnosis of Angina
▪ Diagnosis:
Anamnesis
Pemeriksaan fisik
EKG
Biormarker
Non-invasive Stress Test
Coronary angiography
Imaging (rarely done)
10 menit
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Anamnesis
▪ Aid in diagnosis and rule out other causes1. Onset 2. Location and radiation of pain3. Duration4. Characteristic and quality of
discomfort5. Palliative/Provocative factors6. Symptoms associated with
discomfort7. Cardiac risk factors8. Past medical history -especially
cardiac
▪ Reperfusion questions1. Timing of presentation2. ECG c/w STEMI 3. Contraindication to fibrinolysis4. Degree of STEMI risk
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Pemeriksaan Fisik
1. ABC2. Vital signs, general observation3. Presence or absence of jugular venous distension (JVD)4. Pulmonary auscultation for rales5. Cardiac auscultation for murmurs and gallops6. Presence or absence of stroke7. Presence or absence of pulses8. Presence or absence of systemic hypoperfusion (cool,
clammy, pale, ashen)
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EKG
ST Elevation atau LBBB baruSTEMI
Non-specific ECGUnstable Angina
ST Depression or dynamicT wave inversions
NSTEMI
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Normal or non-diagnostic EKG
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ST Depression or Dynamic T wave Inversions
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ST-Segment Elevation MI
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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)
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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:e1–e157, Figure 5.
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Prinsip ACS
1. If the initial ECG is not diagnostic of STEMI, serial ECGs (every 15-30 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.
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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
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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.
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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.
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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
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Differential Diagnosis of STEMI:
Other Noncardiac▪ Gastroesophageal reflux (GERD)
and spasm▪ Chest-wall pain▪ Pleurisy▪ Peptic ulcer disease▪ Panic attack
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7. Tata Laksana
TIME = MUSCLE▪ Decrease amount of myocardial necrosis▪ Preserve LV function▪ Prevent major adverse cardiac events ▪ Treat life threatening complications
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Chest discomfort suggestive of ischemia
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Chest discomfort suggestive of ischemiaEMS 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
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Chest discomfort suggestive of ischemia
Concurrent ED assessment (<10’)1. Check vital signs; evaluate oxygen
saturation2. Establish IV access3. Obtain 12 lead ECG4. Perform brief, targeted history,
physical exam5. Review fibrinolytic checklist, check
contraindications6. Obtain initial cardiac marker levels,
initial electrolyte and coagulation studies
7. Obtain portable chest x-ray (<30’ )
EMS assessment and care and hospital preparation:1. Monitor, support ABCs. Be prepared to provide CPR and
defibrillation2. Administer aspirin, & consider oxygen, NTG, and morphine if
needed3. 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
Immediate ED general treatment1. If SpO2 <94%, start oxygen at 4 lpm2. Aspirin 160-325 mg (if not given by
EMS)3. Nitroglycerin SL or spray4. Morphine IV if pain is not relieved by
NTG
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Chest discomfort suggestive of ischemia
ECG interpretation
Concurrent ED assessment (<10’)1. Check vital signs; evaluate oxygen
saturation2. Establish IV access3. Obtain 12 lead ECG4. Perform brief, targeted history,
physical exam5. Review fibrinolytic checklist, check
contraindications6. Obtain initial cardiac marker levels,
initial electrolyte and coagulation studies
7. Obtain portable chest x-ray (<30’ )
EMS assessment and care and hospital preparation:1. Monitor, support ABCs. Be prepared to provide CPR and
defibrillation2. Administer aspirin, & consider oxygen, NTG, and morphine if
needed3. 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
Immediate ED general treatment1. If SpO2 <94%, start oxygen at 4 lpm2. Aspirin 160-325 mg (if not given by
EMS)3. Nitroglycerin SL or spray4. Morphine IV if pain is not relieved by
NTG
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Chest discomfort suggestive of ischemia
ECG interpretation
Concurrent ED assessment (<10’)1. Check vital signs; evaluate oxygen
saturation2. Establish IV access3. Obtain 12 lead ECG4. Perform brief, targeted history,
physical exam5. Review fibrinolytic checklist, check
contraindications6. Obtain initial cardiac marker levels,
initial electrolyte and coagulation studies
7. Obtain portable chest x-ray (<30’ )
EMS assessment and care and hospital preparation:1. Monitor, support ABCs. Be prepared to provide CPR and
defibrillation2. Administer aspirin, & consider oxygen, NTG, and morphine if
needed3. 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
Immediate ED general treatment1. If SpO2 <94%, start oxygen at 4 lpm2. Aspirin 160-325 mg (if not given by
EMS)3. Nitroglycerin SL or spray4. Morphine IV if pain is not relieved by
NTG
ST depression or dynamic T wave inversion; strongly suspicious for
ischemiaHigh risk UA/ NSTEMI
ST elevation or new or presumably new LBBB;
strongly suspicious for injury STEMI
Normal or nondiagnostic changes in ST segment/ T
waveIntermediate/ low risk UA
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Start adjunctive treatments(Dont delay reperfusion)- B receptor blockers- Clopidogrel - Heparin (UFH/ LMWH)
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Start adjunctive treatments(Dont delay reperfusion)- B receptor blockers- Clopidogrel - Heparin (UFH/ LMWH)
Time from onset of symptoms ≤ 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)
≤ 12 hours
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Start adjunctive treatments(Dont delay reperfusion)- B receptor blockers- Clopidogrel - Heparin (UFH/ LMWH)
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 risk-stratify
Time from onset of symptoms ≤ 12
hours?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)
≤ 12 hours
≥ 12 hours
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Start adjunctive treatments-Nitroglycerin-B receptor blockers- Clopidogrel- Heparin (UFH/ LMWH)- Glycoprotein IIb/ IIIa inhibitor
Start adjunctive treatments(Dont delay reperfusion)- B receptor blockers- Clopidogrel - Heparin (UFH/ LMWH)
Time from onset of symptoms ≤ 12
hours?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)
≤ 12 hours
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Start adjunctive treatments-Nitroglycerin-B receptor blockers- Clopidogrel- Heparin (UFH/ LMWH)- Glycoprotein IIb/ IIIa inhibitor
Start adjunctive treatments(Dont delay reperfusion)- B receptor blockers- Clopidogrel - Heparin (UFH/ LMWH)
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 risk-stratify
Time from onset of symptoms ≤ 12
hours?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)
≤ 12 hours
≥ 12 hours
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Start adjunctive treatments-Nitroglycerin-B receptor blockers- Clopidogrel- Heparin (UFH/ LMWH)- Glycoprotein IIb/ IIIa inhibitor
Start adjunctive treatments(Dont delay reperfusion)- B receptor blockers- Clopidogrel - Heparin (UFH/ LMWH)
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 risk-stratify
Time from onset of symptoms ≤ 12
hours?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)
≤ 12 hours
≥ 12 hours
Develops high risk/ intermediate risk criteria OR
troponin (+)?
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Start adjunctive treatments-Nitroglycerin-B receptor blockers- Clopidogrel- Heparin (UFH/ LMWH)- Glycoprotein IIb/ IIIa inhibitor
Start adjunctive treatments(Dont delay reperfusion)- B receptor blockers- Clopidogrel - Heparin (UFH/ LMWH)
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 risk-stratify
Time from onset of symptoms ≤ 12
hours?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)
≤ 12 hours
≥ 12 hours
Develops high risk/ intermediate risk criteria OR
troponin (+)?Yes
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Start adjunctive treatments-Nitroglycerin-B receptor blockers- Clopidogrel- Heparin (UFH/ LMWH)- Glycoprotein IIb/ IIIa inhibitor
Start adjunctive treatments(Dont delay reperfusion)- B receptor blockers- Clopidogrel - Heparin (UFH/ LMWH)
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 risk-stratify
Time from onset of symptoms ≤ 12
hours?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)
≤ 12 hours
≥ 12 hours
Develops high risk/ intermediate risk criteria OR
troponin (+)?Yes
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Start adjunctive treatments-Nitroglycerin-B receptor blockers- Clopidogrel- Heparin (UFH/ LMWH)- Glycoprotein IIb/ IIIa inhibitor
Start adjunctive treatments(Dont delay reperfusion)- B receptor blockers- Clopidogrel - Heparin (UFH/ LMWH)
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 risk-stratify
Time from onset of symptoms ≤ 12
hours?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)
≤ 12 hours
≥ 12 hours
Develops high risk/ intermediate risk criteria OR
troponin (+)?
Consider admission to ED chest pain unit/ to monitored bed in EDFollow:- Serial cardiac markers (including troponin)- Repeat EKG/ continuous ST segment monitoring- Consider stress test
Develops high/ intermediate risk criteria OR troponin (+)?
If no evidence of ischemia/
infarction, can discharge with
follow up
Yes
Yes
No
No
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Absolute contraindications for Fibrinolysis
If presentation is < 3 hours, check for
5 KEPALA 1 DARAH1 DADA
1. Malignant intracranial neoplasm (primary or
metastatic)2. Ischemic stroke within 3
months EXCEPT acute ischemic stroke within 3 hours
3. Prior intracranial hemorrhage4. Structural cerebral vascular
lesion (e.g., AVM) 5. Significant closed-head or facial trauma within 3 months
Active bleeding or bleeding diathesis (excluding menses)
Suspected aortic dissection
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8. Prognosis
1. TIMI Risk Score
2. GRACE Risk Score more complex!
3. PURSUIT Risk Score
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TIMI Risk Score
TIMI Risk ScorePredicts 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)
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Killip Classification
Killip Classification and Mortality Rate of Acute MI*Class PAO2† Clinical Description Hospital Mortality
Rate1 Normal No clinical evidence of left
ventricular (LV) failure3–5%
2 Slightly reduced Mild to moderate LV failure 6–10%
3 Abnormal Severe LV failure, pulmonary edema
20–30%
4 Severely abnormal Cardiogenic shock: hypotension, tachycardia, mental obtundation, cool extremities, oliguria, hypoxia
> 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 20:457–464, 1967.
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Komplikasi
▪ Arrythmia
▪ Heart Failure
▪ Hypotension and cardiogenic shock
▪ Recurrent ischemia
▪ Pericarditis
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9. Prevensi
▪ SMOKING CESSATION
▪ DIET MODIFICATION/WEIGHT CONTROL
▪ BP CONTROL
▪ LIPID MANAGEMENT
▪ EXERCISE
▪ DIABETES MANAGEMENT
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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
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Referensi
▪ Rani A. et al., 2006, Perhimpunan Dokter Spesialis Penyakit Dalam Indonesia, halaman 63
▪ Fauci A. et al., 2005, Harrison’s 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, 2012,1387–97.
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TERIMA KASIHMOHON ASUPAN
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Tata Laksana
•Supplemental oxygen should be administered to patients with arterial oxygen desaturation (SaO2 < 90%).
•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.
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
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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.
•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)
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
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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.
•It is reasonable to administer intravenous beta-blockers promptly to STEMI patients without contraindications, especially if a tachyarrhythmia or hypertension is present.
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
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Reperfusion
Door-to- needle (or medical contact–to-needle) time for initiation of fibrinolytic therapy can be achieved within 30 minutes, Door-to-balloon (or medical contact–to- balloon) time for PCI can be kept within 90 minutes.
Fibrinolysis 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 preferred if: 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
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▪ 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)
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EKG
▪ 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
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Troponin I/ T
▪ 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
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Myoglobin & CKMB
▪ 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
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▪ 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.
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Ischemia modified albumin
▪ 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
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▪ 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
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▪ 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
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▪ 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
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Management updates
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)
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UA/ NSTEMI 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)
▪ MORPHINE downgraded from Class 1 to 2a – findings from CRUSADE Registry
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NSTEMI updates
▪ 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)
▪ 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)
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STEMI
▪ 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)
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▪ 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 -> re- evaluated 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
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▪ 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)
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Reperfusion
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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
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▪ 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)
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▪ 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)
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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)
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ANTICOAGULANTS
▪ CLASS 2a recommendation to use anticoagulants in STEMI without reperfusion.
▪ UFH (LOE B)
▪ LMWH (LOE C)
▪ Fondaparinux (LOE B)
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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)
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SECONDARY PREVENTION
▪ INCREASED FOCUS ON SECONDARY PREVENTION:
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▪ 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
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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
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A. Normal ECG
B. ‘Tall T
C. ‘Injury’, ST elevation
D. Biphasic T waves
E. Q - Biphasic T waves
F. Q - abnormal
Evolution of STEMI
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ACS risk criteria
Low Risk ACS
No intermediate or high risk factors
<10 minutes rest pain
Non-diagnositic ECG
Non-elevated cardiac markers
Age < 70 years
Intermediate Risk ACS
Moderate to high likelihood of CAD
>10 minutes rest pain, now resolved
T-wave inversion > 2mm
Slightly elevated cardiac markers
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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
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Secondary Prevention and Long Term Management
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Secondary Prevention and Long Term Management
• 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.
Smoking Goal: Complete Cessation
Goals Recommendations
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Secondary Prevention and Long Term Management
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.
Blood pressure control:Goal: < 140/90 mm Hg or <130/80 mm Hg if chronic kidney disease or diabetes
Goals Recommendations
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Secondary Prevention and Long Term Management
• 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.
Physical activity:Minimum goal:30 minutes 3 to 4 days per week;Optimal daily
Goals Recommendations
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Secondary Prevention and Long Term Management
• 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:
Lipid management:(TG less than 200 mg/dL)Primary goal:LDL-C << than 100 mg/dL
Goals Recommendations
LDL-C < 100 mg/dL (baseline or on treatment):Statins should be used to lower LDL-C.
LDL-C ≥ 100 mg/dL (baseline or ontreatment):
Intensify LDL-C–lowering therapy with drug treatment, giving preference to statins.
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Secondary Prevention and Long Term Management
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-C–lowering therapy, consider adding fibrate or niacin.
If TG is ≥ 500 mg/dL: Consider fibrate or niacin before LDL-C–lowering therapy.Consider omega-3 fatty acids as adjunct for high TG.
Lipid management:(TG 200 mg/dL or greater)Primary goal:Non–HDL-C << 130 mg/dL
Goals Recommendations
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NCEP ATP III Guidelines
Patients withDrug therapy
considered if LDL
* TLC: therapeutic lifestyle changesNational Cholesterol Education Program, Adult Treatment Panel III. JAMA 2001;285:2486–2497
Initiate TLC* if LDL
LDLtreatment
goal
0 1 risk factors ³ 160 mg/dL† ³ 190 mg/dL (160 – 189 mg/dL:
drug optional)
<160 mg/dL†
2 risk factors(10 year risk 20%)
³ 130 mg/dL† 10 year risk 10 –
20%: ³ 130 mg/dL
10-year risk <10%:³ 160 mg/dL
<130 mg/dL†
CHD and CHD risk equivalents(10 year risk >20%)
³ 100 mg/dL† <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
³ 130 mg/dL
drug optional)(100–129 mg/dL:
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Secondary Prevention and Long Term Management
Goals Recommendations
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.
Weight management:Goal:BMI 18.5 to 24.9 kg/m2
Waist circumference:Women: < 35 in.Men: < 40 in.
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REFERENCES
▪ EDITORS MARX ET AL, ROSEN’S 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
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▪ 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