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Acute Coronary Syndrome. Dr. S.A. moezzi. 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

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acs overview
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
Scope of the Problem
  • 5 million ER visits nationwide for CP
    • 800,000 experience an MI each year
      • 213,000 die from their event
        • 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%
slide5

Overview of ACS

Acute Coronary Syndromes*

1.57 Million Hospital Admissions - ACS

UA/NSTEMI†

STEMI

1.24 millionAdmissions per year

0.33 millionAdmissions 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
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 of Stable Angina and ACS

Pathophysiology

ACS

  • Decreased O2 Supply
  • Flow- limiting stenosis
  • Anemia
  • Plaque rupture/clot
  • Increased O2 Demand

Asymptomatic

Angina

Myocardial Infarction

O2 supply/demand mismatch→Ischemia

Myocardial ischemia→necrosis

slide9
Unstable Angina

STEMI

NSTEMI

  • Non-occlusive thrombus
  • sufficient to cause
  • tissue damage & mild
  • myocardial necrosis
  • ST depression +/-
  • T wave inversion on
  • ECG
  • Elevated cardiac
  • enzymes
  • Non occlusive
  • thrombus
  • Non specific
  • ECG
  • Normal cardiac
  • enzymes
  • Complete thrombus
  • occlusion
  • ST elevations on
  • ECG or new LBBB
  • Elevated cardiac
  • enzymes
  • More severe
  • symptoms
stemi
STEMI
  • Name 3 situations in which you cannot diagnose STEMI
stemi1
STEMI
  • Name 3 situations in which you cannot diagnose STEMI
    • Left Ventricular Hypertrophy
    • Chronic or Rate Dependent LBBB
    • Paced Rhythm
diagnosis of acs
At least 2 of the following

History ( angina or angina equivalent)

Acute ischemic ECG changes

Typical rise and fall of cardiac markers

Absence of another identifiable etiology

Diagnosis of ACS
likelihood of acs by hx pe
History/Examination

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.

Suggesting AMI

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
likelihood of acs by hx pe1
Likelihood of ACS by Hx/PE
  • Clinical Examination –
    • Pleuritic Chest Pain
    • Sharp or Stabbing Pain
    • Positional Chest Pain
    • Reproducible Chest Pain

Panju AA. JAMA. 1998;280:1256.

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

risk stratification by ecg
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 ecg1
Risk Stratification by ECG
  • ECG Findings and Associated LR for AMI
    • New ST-E > 1mm LR 5.7-53.9
    • New Q waves LR 5.3-24.8
    • Any ST-E LR 11.2 (7.1-17.8)
    • New Conduction Defect LR 6.3 ( 2.5-15.7)
    • New ST-D LR 3.0-5.2
    • NORMAL ECG LR 0.1-0.4

Panju AA. JAMA. 1998;280:1256.

risk stratification by ecg2
Risk Stratification by ECG
  • 1-8% AMI have a normal ECG
  • 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 ecg3
Risk Stratification by ECG
  • 1 ECG cannot exclude AMI
    • 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.

timing of release of various biomarkers after acute myocardial infarction
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

%

%

%

%

Mortality at 42 Days

%

%

831

174

148

134

50

67

Risk Stratification by Troponin
slide25

National Academy of Clinical Biochemistry Laboratory Medicine (NACB) and the Joint ESC/ACCF/AHA/WHF Task Force for the Redefinition of Myocardial Infarction

• Cardiac troponin is the preferred marker for the diagnosis of MI and for risk stratification. CK-MB by mass assay is an acceptable alternative when troponin in not available.

• CK-MB was preferred by the NACB for the detection of reinfarctionearly after the index event

increased sensitivity and specificity of cTnshould make it the marker of choice it is unnecessary to obtain both values.

Cardiac troponins I and T are equally useful.

non acs causes of troponin elevation
Non ACS causes of Troponin Elevation
  • Trauma (including contusion; ablation; pacing; ICD firings,, endomyocardial biopsy, cardiac surgery, after-interventionalclosure 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.

unstable angina nstemi cardiac care
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

slide29
TIMI Risk Score

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

timi risk score
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 24 hours

deciding between early invasive vs a conservative strategies
Deciding between Early Invasive vs a Conservative Strategies
  • Hemodynamic instability
  • Elecrical instability
  • Refractory angina
  • PCI in past 6 months
  • CABG
  • EF <40%
specifics of early hospital care

Specifics of Early Hospital Care

Anti-Ischemic Therapy

Anti-Platelet Therapy

Anticoagulant Therapy

early hospital care anti ischemic therapy
Early Hospital CareAnti-Ischemic Therapy
  • Class I
    • 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 therapy1
Early Hospital CareAnti-Ischemic Therapy
  • Class III
    • 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
Early Hospital CareAnti-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
secondary prevention
secondary prevention

At present, the United States Food and Drug Administration recommends daily doses of 75 to 325 mg,

the 2006 American College of Cardiology /American Heart Association (ACC/AHA) guidelines on recommends daily doses of 75 to 162 mg for secondary prevention [38].

The ACCP recommends a daily dose of 75 to 100 mg

early hospital care anticoagulant therapy
Early Hospital CareAnticoagulant Therapy
  • Class I
    • Unfractionated Heparin
    • Enoxaparin
    • Bivalarudin
    • Fondaparinux
    • Relative choice depends on invasive vs conservative strategy and bleeding risk
early hospital care statin therapy
Early Hospital CareStatin Therapy
  • MIRACL TrialInclusion 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
Statin Evidence: MIRACL Study

Primary Efficacy Measure

Placebo

17.4%

15

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

Cumulative Incidence (%)

5

Relative risk = 0.84P = .048

95% CI 0.701-0.999

0

0

4

8

12

16

Time Since Randomization (weeks)

Schwartz GG, et al. JAMA. 2001;285:1711-1718.

statin evidence miracl study1

2

Placebo

1.5

Cumulative Incidence (%)

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)

Statin Evidence: MIRACL Study

Fatal and Nonfatal Stroke

Waters DD, et al. Circulation. 2002;106:1690-1695.

S24

prove it trial

0

30

3

6

9

12

15

18

21

24

27

PROVE-IT Trial

All-Cause Death or Major CV Events in All Randomized Subjects

30

Pravastatin 40mg

(26.3%)

25

20

% with Event

Atorvastatin 80mg

(22.4%)

15

10

16% RR

(P = 0.005)

5

0

Months of Follow-up

summary of prove it results
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 strategy clinical trials
Invasive vs Conservative Strategy Clinical Trials

ISAR-COOL

ICTUS (05)

RITA-3 (02)

VANQWISH (98)

VINO

MATE

TRUCS

TIMI IIIB (94)

TACTICS-TIMI 18 (01)

FRISC II (99)

Weight of

the evidence

ConservativeStrategy Favored

N=920

InvasiveStrategy Favored

N=7,018

No difference

N=2,874

secondary prevention class i indications
Secondary PreventionClass 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
slide48

New

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

UA/NSTEMI Patient Groups at Discharge

Medical Therapy without Stent

Bare Metal Stent Group

Drug Eluting Stent Group

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)

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

&

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 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)

Indication for Anticoagulation?

Yes

No

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

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
Secondary PreventionClass III
  • Hormone Replacement Therapy
  • Antioxidants (Vit C, Vit E)
  • Folic Acid
shortcomings of the cure trial
Shortcomings of the CURE Trial
  • Conducted primarily at centers without routine use of early invasive strategy
  • Only 462 (3.7%) patients enrolled from the U.S.
  • 44% had catheterization during index hospitalization
  • Adverse event reduced only in nonfatal MI set
  • Major Bleeding rate of 9.6% among patients who were administered clopidogrel within 5 days of CABG
clopidogrel bleeding risk and cabg
ClopidogrelBleeding Risk and CABG
  • “In hospitals in which patients with UA/NSTEMI undergo rapid diagnostic catheterization within 24 hours of admission, clopidogrel is not started until it is clear that CABG will not be scheduled within the next several days. However, unstable patients should receive clopidogrel or be take for immediate angiography.”
prasugrel key facts
Prasugrel-Key Facts
  • Contraindicated in pts with prior TIA/Stroke
  • Not recommended for patients >75 years
  • 5 mg maintenance dose suggested in patients <60 Kg, though this dose has not been studied
summary
Summary
  • 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
ten points to remember from the 2009 stemi guideline update

Ten Points to Remember from the2009 STEMI Guideline Update

Antman EM, Hand M,

Armstrong PW, et al.,

ten points to remember from the 2009 stemi guideline update1
Ten Points to Rememberfrom the 2009 STEMI Guideline Update
  • Patients routinely taking NSAIDs (except for aspirin), both nonselective as well as COX-2 selective agents, before STEMI should have those agents discontinued at the time of presentation with STEMI because of the increased risk of mortality, reinfarction, hypertension, heart failure, and myocardial rupture associated with their use.
ten points to remember from the 2009 stemi guideline update2
Ten Points to Rememberfrom the 2009 STEMI Guideline Update
  • Oral beta-blocker therapy should be initiated in the first 24 hours for patients who do not have any of the following:
    • Signs of heart failure
    • Evidence of a low output state
    • Increased risk for cardiogenic shock
    • Other relative contraindications to beta blockade
      • PR interval > 0.24 seconds
      • Second- or third-degree heart block
      • Active asthma or reactive airway disease
ten points to remember from the 2009 stemi guideline update3
Ten Points to Rememberfrom the 2009 STEMI Guideline Update
  • STEMI patients presenting to a hospital with PCI capability should be treated with primary PCI within 90 minutes of first medical contact as a systems goal.
  • STEMI patients presenting to a hospital without PCI capability and who cannot be transferred to a PCI center and undergo PCI within 90 minutes of first medical contact should be treated with fibrinolytic therapy within 30 minutes of hospital presentation as a systems goal unless fibrinolytic therapy is contraindicated.
ten points to remember from the 2009 stemi guideline update4
Ten Points to Rememberfrom the 2009 STEMI Guideline Update
  • A strategy of coronary angiography with intent to perform PCI (or emergency CABG) is recommended for patients who have received fibrinolytic therapy and have any of the following:
    • Cardiogenic shock in patients <75 years who are suitable candidates for revascularization,
    • Severe congestive heart failure and/or pulmonary edema (Killip class III), or
    • Hemodynamically compromising ventricular arrhythmias
ten points to remember from the 2009 stemi guideline update5
Ten Points to Rememberfrom the 2009 STEMI Guideline Update
  • Patients undergoing reperfusion with fibrinolytics should receive anticoagulant therapy for a minimum of 48 hours and preferably for the duration of the index hospitalization, up to 8 days (regimens other than unfractionated heparin [UFH] are recommended if anticoagulant therapy is given for more than 48 hours because of the risk of heparin- induced thrombocytopenia with prolonged UFH treatment).
ten points to remember from the 2009 stemi guideline update6
Ten Points to Rememberfrom the 2009 STEMI Guideline Update
  • Clopidogrel 75 mg per day orally should be added to aspirin in patients with STEMI regardless of whether they undergo reperfusion with fibrinolytic therapy or do not receive reperfusion therapy. Treatment with clopidogrel should continue for at least 14 days.
  • Every tobacco user and family members who smoke should be advised to quit at every visit.
ten points to remember from the 2007 stemi guideline update
Ten Points to Rememberfrom the 2007 STEMI Guideline Update

9. For all post-PCI STEMI stented patients without aspirin resistance, allergy, or increased risk of bleeding, aspirin at a dose of 162-325 mg daily should be given for at least 1 month after bare-metal stent (BMS) implantation, 3 months after sirolimus-eluting stent implantation, and 6 months after paclitaxel-eluting stent implantation, after which long-term aspirin use should be continued indefinitely at a dose of 75-162 mg daily.

ten points to remember from the 2007 stemi guideline update1
Ten Points to Rememberfrom the 2007 STEMI Guideline Update
  • For all post-PCI patients who receive a drug-eluting stent, clopidogrel 75 mg daily should be given for at least 12 months if patients are not at high risk of bleeding. For post-PCI patients receiving a BMS, clopidogrel should be given for a minimum of 1 month and ideally up to 12 months (unless the patient is at increased risk of bleeding; then it should be given for a minimum of 2 weeks).
beta blockers in stemi
Beta-blockers in STEMI
  • Class I - oral beta-blockers should be initiated within 24 hours* LOE B
  • Class IIa - reasonable to administer IV beta-blocker at the time of presentation who are hypertensive* LOE B
  • Class III - IV beta-blockers should not be administered to patients with any of the following* LOE A

*Contraindications include 1) signs of heart failure, 2) evidence of low output state, 3) risk for cardiogenic shock (age>70, SBP<120, sinus tach>110bpm, HR<60, increased time since onset of STEMI), 4) or other relative contraindication (PR>0.24s, heart block, active asthma)

ufh lmwh in stemi
UFH/ LMWH in STEMI
  • Class I - Patients receiving fibrinolytics should receive anticoagulant therapy for a minimum of 48 hrs, LOE C. Because of heparin induced thrombocytopenia, regimens other than UFH are recommended for patients receiving anticoagulant therapy > 48 hrs, LOE A.

DOSE:

  • UFH - 60 U/kg (max 4000 U) bolus, then 12 U/kg per hr drip
  • Enoxaparin - (Cr <2.5 men, <2.0 women)
    • For pts age <75 give 30mg IV bolus followed 15min later by 1 mg/kg subq.
    • For pts >=75, no IV bolus and reduce subq dose to 0.75 mg/kg
clopidogrel in stemi
Clopidogrel in STEMI
  • Class I - Clopidogrel 75mg/ day should be added to ASA in pts with STEMI regardless of fibrinolytic use LOE A
  • Class IIa - In patients < 75yo, it is reasonable to consider a loading dose of 300mg LOE C

- recent studies suggest a loading dose of Plavix 600mg