Acute Coronary Syndrome.pdf

Acute Coronary Syndrome dr. Muhammad Ridwan, MAppSc, SpJP (K) Bagian Kardiologi dan Kedokteran Vaskular FK Unsyiah Bagian Fisiologi FK Unsyiah 2015

Goals and Objectives   

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Discuss the definition & pathophysiology of ACS Recognize the clinical features of low, intermediate and high risk ACS Be able to identify and treat patients appropriate for a conservative or invasive strategy Discuss new and controversial pharmacological treatments

INTRODUCTION 

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Coronary Artery Disease – leading cause of morbidity & mortality in industrialised nations. Although decrease in cardiovascular mortality  still major cause of morbidity & burden of disease. South African perspective of cardiovascular disease: “A World in One Country” - Yusuf et al Epidemiological transitions of cardiovascular disease.

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HIGH RISK POPULATION FOR CAD/ACS: INDIAN/WHITE/COLOURED

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INCREASING rate in Black population – lifestyle/socioeconomic changes, urbanisation

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GF Jooste stats: 23.8% of admissions to resus. unit for chest pain/acs related (stats 1Jan 2009 – 28 Feb 2009) 150/628 entries.

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In US – 2004 – 1.56 million admissions for ACS – 669 000 for unstable angina, 896 000 for MI Higher prevelance for NSTEMI.

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DEFINITIONS 

CAD is a continuum of disease….

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Angina -> unstable angina -> AMI -> sudden cardiac death

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Acute coronary syndrome encompasses unstable angina, NSTEMI, STEMI

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Stable angina – transient episodic chest pain d/t myocardial ischaemia, reproducible, frequency constant over time.usually relieved with rest/NTG.

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Classification of angina – Canadian Cardiovascular Society classification.

Canadian Cardiovascular Association Classification of Angina CLASS 1

NO PAIN WITH ORDINARY PHYSICAL ACTIVITY

CLASS 2

SLIGHT LIMITATION OF PHYSICAL ACTIVITY – PAIN OCCURS WITH WALKING, CLIMBING STAIRS,STRESS

CLASS 3

SEVERE LIMITATION OF DAILY ACTIVITY – PAIN OCCURS ON MINIMAL EXERTION

CLASS 4

UNABLE TO CONDUCT ANY ACTIVITY WITHOUT PAIN, PAIN AT REST

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UNSTABLE ANGINA – Pain occurring at rest – duration > 20min, within one week of first visit New onset angina – ~ Class 2 severity, onset with last 2 months Worsening of chest pain – increase by at least 1 class, increases in frequency, duration Angina becoming resistance to drugs that previously gave good control.

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NB! ECG – normal, ST depression(>0.5mm), T wave changes

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ACUTE MYOCARDIAL INFARCTION – ECC/ACC DEFN –rise and fall in cardiac enzymes with one or more of the following: Ischaemic type chest pain/symptoms ECG changes – ST changes, pathological Q waves Coronary artery intervention data Pathological findings of an acute MI NSTEMI = UNSTABLE ANGINA SYMPTOMS/FINDINGS + POSITIVE CARDIAC ENZYMES STEMI = ST ELEVATION ON ECG + SYMPTOMS

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WHY IS IT IMPORTANT TO RECOGNISE PATIENTS WITH UNSTABLE ANGINA??

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5 -17% suffer an MI within a week after admission. 3 -15% die within a year.

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ACS PATHOPHYSIOLOGY 

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Distruption of coronary artery plaque -> platelet activation/aggregation /activation of coagulation cascade -> endothelial vasoconstriction >intraluminal thrombus/embolisation -> obstruction -> ACS Severity of coronary vessel obstruction & extent of myocardium involved determines characteristics of clinical presentation

APPROACH       

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Identifying those with chest pain suggestive of IHD/ACS. Thorough history required: Character of pain Onset and duration Location and radiation Aggravating and relieving factors Autonomic symptoms TYPICAL VS ATYPICAL HISTORY Failure to recognise symptoms other than chest pain -> approx 2 hr delay in seeking medical attention

CHARACTERISTICS OF TYPICAL ANGINAL CHEST PAIN (ADAPTED FROM ROSEN’S, EMERGENCY MEDICINE) CHARACTERISTIC

SUGGESTIVE OF ANGINA

LESS SUGGESTIVE OF ANGINA

TYPE OF PAIN

DULL PRESSURE/CRUSHING PAIN

SHARP/STABBING

DURATION

2-5 MIN, <20 MIN

SECONDSTO HOURS/CONTINUOUS

ONSET

GRADUAL

RAPID

LOCATION/CHEST WALL TENDERNESS

SUBSTERNAL, NOT TENDER TO PALP.

LATERAL CHEST WALL/TENDER TO PALP.

REPRODUCIBALITY

WITH EXERTION/ACTIVITY

WITH BREATHING/MOVING

AUTONOMIC SYMPTOMS

PRESENT USUALLY

ABSENT

ATYPICAL PAIN

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RISK FACTORS FOR DEVELOPING ATYPICAL PAIN: Diabetes, females, non white patients, elderly, dementia, no prior history of MI ATYPICAL SYMPTOMS: GIT symptoms Syncope SOB Pleuritic/positional pain Chest wall tenderness No chest pain/symptoms NRMI 2 STUDY – MI without chest pain -> increased risk of death (23% vs 9%) More complications – hypotension,heart failure, stroke Delayed ED presentation, delayed intervention

RISK STRATIFICATION IN ACS

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Reasons : Provides prognostic information

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Determines treatment and level of intervention -> low risk patients –early discharge, high risk -> admission to high care

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Helps decongest the ED and make available medical resources to more needy patients

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Risk stratification should be ongoing – at admission, 6-8 hrs, 24hrs, discharge

TOOLS USED IN RISK STRATIFICATION 

HISTORY

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ECG

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BIOCHEMICAL MARKERS

ECG 

First point of entry into ACS algorithm

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Abnormal or normal

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Neither 100% sensitive or 100% specific for AMI

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Single ECG for AMI – sensitivity of 60%, specificity 90%

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Represents single point in time –needs to be read in context

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Normal ECG does not exclude ACS – 1-6% proven to have AMI, 4% unstable angina

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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)

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ECG adjuncts – leads V7 –V9, RV 4 (Class 2a B)

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Continuous 12 lead ECG monitoring reasonable alternative to serial ECGs (Class 2a B)

BIOCHEMICAL MARKERS      

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IDEAL MARKER: High concentration in myocardium Myocardium specific Released early in injury Proportionate to injury Non expensive testing Troponins CKMB Myoglobin Other markers

TROPONINS T/I

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Troponin T vs I – both equivalent in diagnostic and prognostic abilities ( except in renal failure – Trop T less sensitive)

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Elevation ~ 2hrs to 12hrs

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~30 – 40% of ACS patients without ST elevation – had normal CKMB but elevated troponins on presentation

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Meta-analysis (Heindereich et al) – odds of death increased 3 to 8 fold with positive troponin

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Mortality at 42 days in troponin positive patients

MYOGLOBIN 

Rapid release within 2 hours

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Not cardiac specific

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Rule out for NSTEMI rather than rule in.

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

MARKER CHANGE SCORES 

2 hour delta CKMB mass

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Aim – to exclude MI within 6hrs of symptom onset

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

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

OTHER MARKERS 

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INDICATORS OF INFLAMMATION OR ACTIVATION OF COAGULATION CASCADE: Myeloperoxidase, soluble CD40 ligand, IL6, hsCRP, d dimer, prothrombin fragment 1 & 2

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Elevated before onset of irreversible injury

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Lack specificity

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Complex lab assays

ISCHAEMIA MODIFIED ALBUMIN     

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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

RISK STRATIFICATION MODELS

TIMI RISK SCORE –increase in mortality with increasing score ~40% all cause mortality at 14 days for patients requiring urgent revascularisation

WHICH MODEL IS MOST APPROPRIATE??

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2007 ACS/AHA GUIDELINES: Risk stratification models useful in decision making with regard to treatment options ( Class 2a B) TIMI vs GRACE vs PURSUIT

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PURSUIT & GRACE risk scores allow better discrimination of in hospital and 1 year mortality in patients compared to TIMI. (Andrew et al, Risk scores for risk stratification in ACS …)

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What’s appropriate in our setting???

MANAGEMENT ALGORITHM

Gold Standard for Treatment of ACS

ACC/AHA 2007 Guidelines for the Management of Patients With Unstable Angina/Non–ST-Elevation Myocardial Infarction

http://circ.ahajournals.org/cgi/content/full/102/10/1193

Algorithm for evaluation and management of patients suspected of having ACS. Anderson JL, et al. J Am Coll Cardiol 2007;50:e1–e157, Figure 2.

ACS Overview      

Overview of ACS Assessment of “Likelihood of ACS” Early Risk Stratification Invasive vs Conservative Strategy Pharmacotherapy Long-term Therapy/Secondary Prevention

Scope of the Problem 

5 million ER visits nationwide for CP 

800,000 experience an MI each year 

213,000 die from their event 

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½ of those die before reaching the ER

Pre-CCU, mortality for MI was >30% 

Fell to 15% with CCU 

With current interventions, in hospital mortality of STEMI is 6-7%

Overview of ACS Acute Coronary Syndromes* 1.57 Million Hospital Admissions - ACS UA/NSTEMI†

STEMI

1.24 million

0.33 million

Admissions per year

Admissions per year

*Primary and secondary diagnoses. †About 0.57 million NSTEMI and 0.67 million UA. Heart Disease and Stroke Statistics – 2007 Update. Circulation 2007; 115:69–171.

Acute Coronary Syndrome (ACS) 

Definition: The spectrum of acute ischemia related syndromes ranging from UA to MI with or without ST elevation that are secondary to acute plaque rupture or plaque erosion. [----UA---------NSTEMI----------STEMI----]

Pathophysiology of Stable Angina and ACS Pathophysiology

ACS

•Anemia •Plaque rupture/clot

Increased O2 Demand O2 supply/demand mismatch→Ischemia Myocardial ischemia→necrosis

Angina

•Flow- limiting stenosis

Asymptomatic

Decreased O2 Supply

Pathophysiology of ACS Evolution of Coronary Thrombosis

Unstable Angina Non occlusive thrombus Non specific ECG Normal cardiac enzymes

NSTEMI Non-occlusive thrombus sufficient to cause tissue damage & mild myocardial necrosis

STEMI Complete thrombus occlusion ST elevations on ECG or new LBBB

ST depression +/T wave inversion on ECG

Elevated cardiac enzymes

Elevated cardiac enzymes

More severe symptoms

STEMI 

Name 3 situations in which you cannot diagnose STEMI

STEMI 

Name 3 situations in which you cannot diagnose STEMI Left Ventricular Hypertrophy  Chronic or Rate Dependent LBBB  Paced Rhythm 

Cardiac Catheterization 

Name the only 3 situations that demand emergent cardiac catheterization.

Cardiac Catheterization 

Name the only 3 situations that demand emergent cardiac catheterization. STEMI or new LBBB  ACS with hemodynamic or electrical instability despite optimal medical management  Uncontrolled CP despite optimal medical management 

Diagnosis of ACS 

At least 2 of the following 

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History ( angina or angina equivalent) Acute ischemic ECG changes Typical rise and fall of cardiac markers Absence of another identifiable etiology

Initial Evaluation and management of Non ST-elevation ACS Initial Evaluation and Management •History and Physical •ECG •Cardiac Biomarkers

Establish the Likelihood that Clinical Presentation Represents an ACS Secondary to CAD

Risk Stratify for Short-term Adverse Outcomes

Likelihood of ACS by Hx/PE 

History/Examination  

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Suggesting AMI

Pain in Chest or Left Arm CP Radiation  Right Shoulder  Left Arm  Both Left & Right Arm Diaphoresis 3rd Heart Sound SBP < 80 mm Hg Pulmonary Crackles

Panju AA. JAMA. 1998;280:1256.

LR 2.7 LR 2.9 (1.4-6.0) LR 2.3 (1.7-3.1) LR 7.1 (3.6-14.2) LR 2.0 (1.9-2.2) LR 3.2 (1.6-6.5) LR 3.1 (1.8-5.2) LR 2.1 (1.4-3.1)

Likelihood of ACS by Hx/PE 

Clinical Examination –  Pleuritic Chest Pain  Sharp or Stabbing Pain  Positional Chest Pain  Reproducible Chest Pain

Against AMI LR 0.2 (0.2-0.3) LR 0.3 (0.2-0.5) LR 0.3 (0.2-0.4) LR 0.2-0.4

Panju AA. JAMA. 1998;280:1256.

Risk Stratification by ECG     

Simple, quick, noninvasive tool Universally available, cheap Correlates with risk and prognosis Guides treatment decisions Can identify alternative causes

Risk Stratification by ECG 

ECG Findings and Associated LR for AMI

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New ST-E > 1mm New Q waves Any ST-E New Conduction Defect New ST-D

LR 5.7-53.9 LR 5.3-24.8 LR 11.2 (7.1-17.8) LR 6.3 ( 2.5-15.7) LR 3.0-5.2

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NORMAL ECG

LR 0.1-0.4

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Panju AA. JAMA. 1998;280:1256.

Risk Stratification by ECG CAVEATS 

1-8% AMI have a normal ECG

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Only Approx 50% of AMI patients have diagnostic changes on their initial ECG Peter J. Zimetbaum, M.D., N Engl J Med 2003;348:933-40.

Risk Stratification by ECG CAVEATS cont.  1 ECG cannot exclude AMI 

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Brief sample of a dynamic process

Small regions of ischemia or infarction may be missed Peter J. Zimetbaum, M.D., N Engl J Med 2003;348:933-40.

How Sensitive is the ECG Alone?

How Predictive is NTG response?

Timing of Release of Various Biomarkers After Acute Myocardial Infarction

Shapiro BP, Jaffe AS. Cardiac biomarkers. In: Murphy JG, Lloyd MA, editors. Mayo Clinic Cardiology: Concise Textbook. 3rd ed. Rochester, MN: Mayo Clinic Scientific Press and New York: Informa Healthcare USA, 2007:773–80. Anderson JL, et al. J Am Coll Cardiol 2007;50:e1–e157, Figure 5.

Risk Stratification by Troponin 7.5 %

Mortality at 42 Days

8 7

6.0 %

6 5 4 3 2 1 0

1.0 % 831

3.4 %

3.7 %

148

134

1.7 % 174

50

0 to <0.4 0.4 to <1.0 1.0 to <2.0 2.0 to <5.0 5.0 to <9.0 Cardiac troponin I (ng/ml)

67  9.0

Non ACS causes of Troponin Elevation 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21.

Trauma (including contusion; ablation; pacing; ICD firings,, endomyocardial biopsy, cardiac surgery, after-interventional closure of ASDs) Congestive heart failure (acute and chronic) Aortic valve disease and HOCM with significant LVH Hypertension Hypotension, often with arrhythmias Noncardiac surgery Renal failure Critically ill patients, especially with diabetes, respiratory failure Drug toxicity (eg, adriamycin, 5 FU, herceptin, snake venoms) Hypothyroidism Coronary vasospasm, including apical ballooning syndrome Inflammatory diseases (eg, myocarditis, Kawasaki disease, smallpox vaccination, Post-PCI Pulmonary embolism, severe pulmonary hypertension Sepsis Burns, especially if TBSA greater than 30% Infiltrative diseases: amyloidosis, hemachromatosis, sarcoidosis, and scleroderma Acute neurologic disease, including CVA, subarchnoid bleeds Rhabdomyolysis with cardiac injury Transplant vasculopathy Vital exhaustion

Modified from Apple FS, et al Heart J. 2002;144:981-986.

Combined Sensitivities for ACS

Early Invasive

Conservative

Unstable angina/NSTEMI cardiac care 

Evaluate for conservative vs. invasive strategy based upon:  Likelihood

of actual ACS  Risk stratification by TIMI risk score  ACS risk categories per AHA guidelines Low

High Intermediate

TIMI Risk Score Predicts risk of death, new/recurrent MI, need for urgent revascularization within 14 days

TIMI Risk Score T: Troponin elevation (or CK-MB elevation) H: History or CAD (>50% Stenosis) R: Risk Factors: > 3 (HTN, Hyperlipidemia, Family Hx, DM II, Active Smoker) E: EKG changes: ST elevation or depression 0.5 mm concordant leads A2:Aspirin use within the past 7 days; Age over 65 T: Two or more episodes of CP within 2 hours

Deciding between Early Invasive vs a Conservative Strategies Definitive/Possible ACS Initiate ASA, BB, Nitrates, Anticoagulants, Telemetry

Early Invasive Strategy • TIMI Risk Score >3 • New ST segment deviation • Positive biomarkers

•Hemodynamic instability •Elecrical instability •Refractory angina •PCI in past 6 months •CABG •EF <40%

Coronary angiography (24-48 hours)

Conservative Strategy •TIMI Risk Score <3 (Esp. Women) •No ST segment deviation •Negative Biomarkers

Recurrent Signs/Symptoms Heart failure Arrhythmias

Remains Stable ↓ Assess EF and/or Stress Testing ↓ EF<40% OR Positive stress Go to Angiography

Specifics of Early Hospital Care Anti-Ischemic

Therapy Anti-Platelet Therapy Anticoagulant Therapy

Early Hospital Care Anti-Ischemic Therapy 

Class I      

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Bed/Chair rest and Telemetry Oxygen (maintain saturation >90%) Nitrates (SLx3 Oral/topical. IV for ongoing iscemia, heart failure, hypertension) Oral B-blockers in First 24-hours if no contraindications. (IV B-blockers class IIa indication) Non-dihydropyridine Ca-channel blockers for those with contraindication fo B-blockers ACE inhibitors in first 24-hours for heart failure or EF<40% (Class IIa for all other pts) (ARBs for those intolerant) Statins

Early Hospital Care Anti-Ischemic Therapy 

Class III     

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Nitrates if BP<90 mmHg or RV infarction Nitrates within 24-hrs of Sildenafil or 48 hrs of Tadalafil Immediate release dihydropyradine Ca-blockers in the absence of B-Blocker therapy IV ACE-inhibitors IV B-blockers in patients with acute HF, Low output state or cardiogenic shock, PR interval >0.24 sec, 2nd or 3rd degree heart block, active asthma, or reactive airway disease NSAIDS and Cox-2 inhibitors

Early Hospital Care Anti-Platelet Therapy 

Class I Aspirin (162-325 mg), non enteric coated  Clopidogrel for those with Aspirin allergy/intolerance (300-600 mg load and 75 mg/d)  GI prophylaxis if a Hx of GI bleed  GP IIb/IIIa inhibitors should be evaluated based on whether an invasive or conservative strategy is used  GP IIb/IIIa inhibitors recommended for all diabetics and all patient in early invasive arm 

Early Hospital Care Anticoagulant Therapy 

Class I Unfractionated Heparin  Enoxaparin  Bivalarudin  Fondaparinux 

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Relative choice depends on invasive vs conservative strategy and bleeding risk

Early Hospital Care Statin Therapy 

MIRACL Trial Inclusion Criteria 3086 patients with Non ST ACS  Total cholesterol <270 mg/dl  No planned PCI  Randomized to Atorvastatin vs Placebo  Drug started at 24-96 hours 

Statin Evidence: MIRACL Study Primary Efficacy Measure

Placebo Cumulative Incidence (%)

15

17.4% 14.8%

Atorvastatin 10 Time to first occurrence of: • Death (any cause) • Nonfatal MI • Resuscitated cardiac arrest • Worsening angina with new objective evidence and urgent rehospitalization

5

Relative risk = 0.84 P = .048 95% CI 0.701-0.999

0 0

4

8

12

Time Since Randomization (weeks) Schwartz GG, et al. JAMA. 2001;285:1711-1718.

16

Statin Evidence: MIRACL Study Fatal and Nonfatal Stroke

Cumulative Incidence (%)

2

Placebo

1.5

1

Atorvastatin

0.5

Relative risk = 0.49 P = .04 95% CI 0.24-0.98

0 0

4

8

12

16

Time Since Randomization (weeks) Waters DD, et al. Circulation. 2002;106:1690-1695.

S24

PROVE-IT Trial All-Cause Death or Major CV Events in All Randomized Subjects 30

Pravastatin 40mg (26.3%)

25 20

% with 15 Event

Atorvastatin 80mg (22.4%)

10 16% RR (P = 0.005)

5 0 0

3

6

9

12

15

18

21

Months of Follow-up

24

27

30

Summary of PROVE-IT Results In

patients recently hospitalized within 10 days for an acute coronary syndrome:  “Intensive” high-dose LDL-C lowering (median LDL-C 62 mg/dL) compared to “moderate” standard-dose lipid-lowering therapy (median LDL-C 95 mg/dL) reduced the risk of all cause mortality or major cardiac events by 16% (p=0.005)  Benefits emerged within 30 days post ACS with continued benefit observed throughout the 2.5 years of follow-up  Benefits were consistent across all cardiovascular endpoints, except stroke, and most clinical subgroups

Invasive vs Conservative Strategies

Invasive vs Conservative Strategy Clinical Trials ISARCOOL VANQWISH (98)

ICTUS (05)

RITA-3 (02)

MATE

VINO

TIMI IIIB (94)

TRUCS TACTICSTIMI 18 (01)

Weight of the evidence

Conservative Strategy Favored N=920

No difference N=2,874

FRISC II (99) Invasive Strategy Favored N=7,018

How Early is Early?

Secondary Prevention Class I Indications Aspirin  Beta-blockers: (all pts, slow titration with moderate to severe failure  ACE-Inhibitors: CHF, EF<40%, HTN, DM (All pts-Class IIa) ARB when intolerant to ACE. (Class IIa as alternative to ACEI) Aldosterone blockade: An ACEI, CHF with either EF<40% or DM and if CrCl>30 ml/min and K<5.0 mEq/L  Statins  Standard Risk Factor Management 

Long-Term Antithrombotic Therapy at Hospital Discharge after UA/NSTEMI New

UA/NSTEMI Patient Groups at Discharge

Medical Therapy without Stent

ASA 75 to 162 mg/d indefinitely (Class I, LOE: A)

Bare Metal Stent Group

Drug Eluting Stent Group

ASA 162 to 325 mg/d for at least 1 month, then 75 to 162 mg/d indefinitely (Class I, LOE: A)

&

& Clopidogrel 75 mg/d for at least 1 month and up to 1 year (Class I, LOE:B)

Clopidogrel 75 mg/d at least 1 month (Class I, LOE: A) and up to 1 year (Class I, LOE: B)

ASA 162 to 325 mg/d for at least 3 to 6 months, then 75 to 162 mg/d indefinitely (Class I, LOE: A) & Clopidogrel 75 mg/d for at least 1 year (Class I, LOE: B)

Indication for Anticoagulation? Yes

Add: Warfarin (INR 2.0 to 2.5) (Class IIb, LOE: B)

No

Continue with dual antiplatelet therapy as above

Anderson JL, et al. J Am Coll Cardiol 2007;50:e1–e157, Figure 11. INR = international normalized ratio; LOE = level of evidence.

Secondary Prevention Class III   

Hormone Replacement Therapy Antioxidants (Vit C, Vit E) Folic Acid

Summary 

ACS includes UA, NSTEMI, and STEMI

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Management guideline focus Immediate assessment/intervention (MONA+BAH)  Risk stratification (UA/NSTEMI vs. STEMI)  RAPID reperfusion for STEMI (PCI vs. 

Thrombolytics)

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Conservative vs Invasive therapy for UA/NSTEMI

Aggressive attention to secondary prevention initiatives for ACS patients 

Beta blocker, ASA, ACE-I, Statin

Questions?