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ACLS 2009Acute Coronary Syndromes
M. LaCombeMDFMR
June 3, 2009
Our first case:
Chief Complaint: 30 minutes of squeezing substernal chest pain
History of Present Illness: A 60-year-old hypertensive diabetic male presents to the emergency room (ER) with 30 minutes of
squeezing substernal chest pain, relieved by sublingual nitroglycerin and nasal oxygen.
Risk factors: positive for hypertension and diabetes mellitus
Physical Findings:
Age: 60Gender: MaleWeight: 60 kg
Blood Pressure: 130/76 mm HgPulse: 86 bpm
Head and Neck: Normal jugular venous pressureChest and Lungs: clear
Cardiac Exam: Regular rhythm, no murmurs, gallopsExtremities: 2+ symmetric
EKG:
Labs:
troponin is 4.2
(what other labs are absolutely essential in this case?)
Stool for occult blood
renal function studies
How will you treat this patient?
Times to remember
• 10 minutes time for ED eval• 30 minutes door to needle• 90 minutes door to balloon• 3 hours (symptom onset) Fibrinolytic vs.
PCI therapy• 12 hours (symptom onset) Time limit for
revascularization therapies as supported by data
Initial Therapy/Recognition
• Starts in transport to ED– O2– Aspirin– Nitro– Morphine– Beta Blockers?
–12 lead EKG
Therapy and recognition in ED
• 12 lead EKG Will be used to stratify patients into treatment groups
• O2, ASA, Nitro, Morphine MONA• Physical exam• Cardiac biomarkers troponins
• 10 minute time frame
Treatment Groups Stratification
• ST-elevation MI (STEMI) ST-segment elevation or presumed new LBBB in 2 or more contiguous precordial or limb leads
• UA/non-ST-elevation MI (NSTEMI) ischemic ST-segment depression or dynamic T wave inversion with pain. Transient ST-segment elevation.
• Normal or nondiagnostic changes with pain
Copyright ©2005 American Heart Association
Circulation 2005;112:IV-89-IV-110
Acute Coronary Syndromes Algorithm
Medications to Consider for a NONSTEMI:
• Nitroglycerine • Beta blockers• Clopidogrel• Heparin• Glycoprotein IIb/IIIA inhibitors
Should be managed with invasive strategy if:
• New ST-segment depression and positive troponins
• Persistent or recurrent symptoms
• Hemodynamic instability or VT
• Depressed LV function (ejection fraction <40%)
• ECG or functional study that suggests multivessel CAD
Definite ACSDefinite ACSDefinite ACSDefinite ACSPossible ACSPossible ACS
(–) ECG;(–) ECG;Normal biomarkersNormal biomarkers
(–) ECG;(–) ECG;Normal biomarkersNormal biomarkers
Observe; repeat ECG,Observe; repeat ECG, markers at 4-8 hmarkers at 4-8 h
Observe; repeat ECG,Observe; repeat ECG, markers at 4-8 hmarkers at 4-8 h
No recurrent pain;No recurrent pain;(–) follow-up studies(–) follow-up studiesNo recurrent pain;No recurrent pain;
(–) follow-up studies(–) follow-up studiesRecurrent pain;Recurrent pain;
(+) follow-up studies(+) follow-up studiesRecurrent pain;Recurrent pain;
(+) follow-up studies(+) follow-up studies
Stress test; Stress test; LV LVfunction if ischemiafunction if ischemia
Stress test; Stress test; LV LVfunction if ischemiafunction if ischemia
(–) test: outpatient follow-up(–) test: outpatient follow-up(–) test: outpatient follow-up(–) test: outpatient follow-up
(+) test(+) test(+) test(+) test
Use 2007 NSTE ACS Use 2007 NSTE ACS GuidelinesGuidelines
Use 2007 NSTE ACS Use 2007 NSTE ACS GuidelinesGuidelines
ST ST
Use 2004Use 2004Updated MIUpdated MI GuidelinesGuidelines
Use 2004Use 2004Updated MIUpdated MI GuidelinesGuidelines
No ST No ST
ST-T ST-T ’s, ’s, def. pain,def. pain,markersmarkers
ST-T ST-T ’s, ’s, def. pain,def. pain,markersmarkers
ACS Risk GuidedACS Risk GuidedAlgorithmAlgorithm
Symptoms Suggestive of ACSSymptoms Suggestive of ACSSymptoms Suggestive of ACSSymptoms Suggestive of ACS
Class I Benefit >>> Risk
Procedure/ Treatment SHOULD be performed/ administered
Class IIa Benefit >> RiskAdditional studies with focused objectives needed
IT IS REASONABLE to perform procedure/administer treatment
Class IIb Benefit ≥ RiskAdditional studies with broad objectives needed; Additional registry data would be helpful
Procedure/Treatment MAY BE CONSIDERED
Class III Risk ≥ BenefitNo additional studies needed
Procedure/Treatment should NOT be performed/administered SINCE IT IS NOT HELPFUL AND MAY BE HARMFUL
shouldis recommendedis indicatedis useful/effective/
beneficial
is reasonablecan be useful/effective/
beneficialis probably recommended
or indicated
may/might be consideredmay/might be reasonableusefulness/effectiveness is
unknown /unclear/uncertain or not well established
is not recommendedis not indicatedshould notis not
useful/effective/beneficialmay be harmful
Applying Classification of Recommendations
17
Class I Benefit >>> Risk
Procedure/ Treatment SHOULD be performed/ administered
Class IIa Benefit >> RiskAdditional studies with focused objectives needed
IT IS REASONABLE to perform procedure/administer treatment
Class IIb Benefit ≥ RiskAdditional studies with broad objectives needed; Additional registry data would be helpful
Procedure/Treatment MAY BE CONSIDERED
Class III Risk ≥ BenefitNo additional studies needed
Procedure/Treatment should NOT be performed/administered SINCE IT IS NOT HELPFUL AND MAY BE HARMFUL
Applying Classification of Recommendations and Level of Evidence
Level A: Recommendation based on evidence from multiple randomized trials or meta-analyses Multiple (3-5) population risk strata evaluated; General consistency of direction and magnitude of effect
Level B: Recommendation based on evidence from a single randomized trial or non-randomized studies Limited (2-3) population risk strata evaluated
Level C: Recommendation based on expert opinion, case studies, or standard-of-care Very limited (1-2) population risk strata evaluated
ST-segment Elevation
Acute Evaluation of ACS
Chest pain or Short of Breath
NSTEMI
ST-segment Depression
– + +
Presentation
ECG
Diagnosis
Normal
Markers
STEMI
–+
Rule-Out
Adapted from: Anderson JL. J Am Coll Cardiol 2007;50:e1-157
Initial Evaluation - Risk Stratification
12-lead ECG within 10 min for all patients with chest pain or symptoms suggestive of ACSEarly risk stratification by symptoms, physical findings, ECG, cardiac markersCardiac markers, Troponins and CK-MB, for initial assessment Use of risk stratification models (TIMI, PURSUIT, GRACE) can be useful to assist in decision making for treatment options
12-lead ECG within 10 min for all patients with chest pain or symptoms suggestive of ACSEarly risk stratification by symptoms, physical findings, ECG, cardiac markersCardiac markers, Troponins and CK-MB, for initial assessment Use of risk stratification models (TIMI, PURSUIT, GRACE) can be useful to assist in decision making for treatment options
IIII IIaIIaIIaIIa IIbIIbIIbIIb IIIIIIIIIIII
JACC 2007.JACC 2007.
20
Anti-Ischemic Therapy
It is reasonable to administer intravenous beta blockers at the time of presentation for hypertension to UA/NSTEMI patients who do not have 1 or more of the following: 1) signs of HF, 2) evidence of a low-output state, 3) increased risk* for cardiogenic shock, or 4) other relative contraindications to beta blockade (PR interval greater than 0.24 s, second or third degree heart block, active asthma, or reactive airway disease).
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
*Risk factors for cardiogenic shock (the greater the number of risk factors present, the higher the risk of developing cardiogenic shock): age greater than 70 years, systolic blood pressure less than 120 mmHg, sinus tachycardia greater than 110 or heart rate less than 60, increased time since onset of symptoms of UA/NSTEMI. Chen ZM, et al. Lancet 2005;366:1622–32.
I → IIa
21
Anti-Ischemic Therapy
It may be harmful to administer intravenous beta blockers to UA/NSTEMI patients who have contraindications to beta blockade, signs of HF or low-output state, or other risk factors* for cardiogenic shock.
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
*Risk factors for cardiogenic shock (the greater the number of risk factors present, the higher the risk of developing cardiogenic shock): age greater than 70 years, systolic blood pressure less than 120 mmHg, sinus tachycardia greater than 110 or heart rate less than 60, increased time since onset of symptoms of UA/NSTEMI. Chen ZM, et al. Lancet 2005;366:1622–32.
New
22
Anti-Ischemic Therapy
Oral beta-blocker therapy should be initiated within the first 24 h for patients who do not have 1 or more of the following: 1) signs of HF, 2) evidence of a low-output state, 3) increased risk* for cardiogenic shock, or 4) other relative contraindications to beta blockade (PR interval greater than 0.24 s, second or third degree heart block, active asthma, or reactive airway disease).
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
*Risk factors for cardiogenic shock (the greater the number of risk factors present, the higher the risk of developing cardiogenic shock): age greater than 70 years, systolic blood pressure less than 120 mmHg, sinus tachycardia greater than 110 or heart rate less than 60, increased time since onset of symptoms of UA/NSTEMI. Chen ZM, et al. Lancet 2005;366:1622–32.
Major Change
Alert:
Avoid beta blockers in ACS if there is impending cardiogenic shock!
Cardiogenic Shock: Current Concepts and Improving Outcomes Reynolds HR, Hochman JSCirculation. 2008;117:686-697
Cardiogenic Shock: Basics and Clinical ConsiderationsGowda RM, Fox JT, Khan IA Int J Cardiol. 2008;123:221-228
Cardiogenic shock (CS) is defined as a state of tissue hypoperfusion resulting from cardiac failure. Hypoperfusion may manifest as systemic hypotension, peripheral vasoconstriction and diminished pulses, decreased urine output,
decreased mental status, or significantly reduced cardiac indices (cardiac index) despite correction of preload.
CS occurs in 5% to 10% of patients hospitalized with MI (ST-segment elevated MI) and is a common cause of death in this group.
An unknown additional number of prehospital patients die from CS, making the exact incidence uncertain.
Risk factors for development of post-MI CS include older age, anterior location of MI, hypertension, diabetes, multivessel occlusions, left bundle
branch block, and prior history of cardiac disease or heart failure.Tachycardia and/or hypotension at admission predict CS in patients with
MI.
25
Anti-Ischemic Therapy
Because of the increased risks of mortality, reinfarction, hypertension, HF, and myocardial rupture associated with their use, nonsteroidal anti-inflammatory drugs (NSAIDs), except for ASA, whether nonselective or cyclooxygenase (COX)-2–selective agents, should be discontinued at the time a patient presents with UA/NSTEMI.
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
The selective COX-2 inhibitors and other nonselective NSAIDs have been associated with increased cardiovascular risk. An AHA scientific statement on the use of NSAIDs concluded that the risk of cardiovascular events is proportional to COX-2 selectivity and the underlying risk to the patient (Antman EM, et al. Use of nonsteroidal antiinflammatory drugs. An update for clinicians. A scientific statement from the American Heart Association. Circulation 2007;115:1634–42. Further discussion can be found in Anderson JL, et al. J Am Coll Cardiol 2007;50:e1–e157 and in the Secondary Prevention Section of this slide set.
New
26
Antiplatelet Therapy
Aspirin should be administered to UA/NSTEMI patients as soon as possible after hospital presentation and continued indefinitely in patients not known to be intolerant of that medication.
Clopidogrel (loading dose [LD] followed by daily maintenance dose)* should be administered to UA/NSTEMI patients who are unable to take ASA because of hypersensitivity or major gastrointestinal intolerance.
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
*Some uncertainty exists about optimum dosing of clopidogrel. Randomized trials establishing its efficacy and providing data on bleeding risks used a loading dose of 300 mg orally followed by a daily oral maintenance dose of 75 mg. Higher oral loading doses such as 600 or 900 mg of clopidogrel more rapidly inhibit platelet aggregation and achieve a higher absolute level of inhibition of platelet aggregation, but the additive clinical efficacy and the safety of higher oral loading doses have not been rigorously established.
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
LD added
27
Select Management Strategy:
Initial Invasive Versus Initial Conservative Strategy
Major ChangesNew Trial Data
28
Selection of Initial Treatment Strategy: Initial Invasive Versus Conservative Strategy
Invasive Recurrent angina/ischemia at rest with low-level activities despite intensive medical therapy
Elevated cardiac biomarkers (TnT or TnI)
New/presumably new ST-segment depression
Signs/symptoms of heart failure or new/worsening mitral regurgitation
High-risk findings from noninvasive testing
Hemodynamic instability
Sustained ventricular tachycardia
PCI within 6 months
Prior CABG
High risk score (e.g., TIMI, GRACE)
Reduced left ventricular function (LVEF < 40%)
Conservative
Low risk score (e.g., TIMI, GRACE)
Patient/physician presence in the absence of high-risk features
29
Risk Scores
TIMI GRACE
Histo
ry
AgeHypertensionDiabetesSmoking↑ CholesterolFamily historyHistory of CAD
Age
Pre
sen
tatio
n
Severe anginaAspirin within 7 daysElevated markersST-segment deviation
Heart rateSystolic BPElevated creatinineHeart failureCardiac arrestElevated markersST-segment deviation
Antman EM, et al. JAMA 2000;284:835–42. Eagle KA, et al. JAMA 2004;291:2727–33. GRACE = Global Registry of Acute Coronary Events; TIMI = Thrombolysis in Myocardial Infarction.
30
Algorithm for Patients with UA/NSTEMI Managed by an Initial Invasive Strategy
Proceed to Diagnostic Angiography
ASA (Class I, LOE: A)Clopidogrel if ASA intolerant (Class I,
LOE: A)
Diagnosis of UA/NSTEMI is Likely or Definite
Invasive StrategyInit ACT (Class I, LOE: A)
Acceptable options: enoxaparin or UFH (Class I, LOE: A) bivalirudin or fondaparinux (Class I, LOE: B)
Select Management StrategyProceed with an
Initial Conservative
Strategy
Anderson JL, et al. J Am Coll Cardiol. 2007;50:e1-e157, Figure 7. ACT = anticoagulation therapy; LOE = level of evidence.
Prior to AngiographyInit at least one (Class I, LOE: A) or
both (Class IIa, LOE: B) of the following:
ClopidogrelIV GP IIb/IIIa inhibitor
Factors favoring admin of both clopidogrel and GP IIb/IIIa inhibitor include:
Delay to AngiographyHigh Risk Features
Early recurrent ischemic discomfort
31
Initial Invasive Strategy: Antiplatelet Therapy
For UA/NSTEMI patients in whom an initial invasive strategy is selected, antiplatelet therapy in addition to ASA should be initiated before diagnostic angiography (upstream) with either clopidogrel (loading dose followed by daily maintenance dose)* or an IV GP IIb/IIIa inhibitor.
Abciximab as the choice for upstream GP IIb/IIIa therapy is indicated only if there is no appreciable delay to angiography and PCI is likely to be performed; otherwise, IV eptifibatide or tirofiban is the preferred choice of GP IIb/IIIa inhibitor.†
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
*Some uncertainty exists about optimum dosing of clopidogrel. Randomized trials establishing its efficacy and providing data on bleeding risks used a loading dose of 300 mg orally followed by a daily oral maintenance dose of 75 mg. Higher oral loading doses such as 600 or 900 mg of clopidogrel more rapidly inhibit platelet aggregation and achieve a higher absolute level of inhibition of platelet aggregation, but the additive clinical efficacy and the safety of higher oral loading doses have not been rigorously established; †Factors favoring administration of both clopidogrel and a GP IIb/IIIa inhibitor include: delay to angiography, high-risk features, and early ischemic discomfort.
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
32
Clopidogrel in Unstable angina to preventRecurrent ischemic Events (CURE)
•12,562 patients within 24 h UA/NSTEMI
•Placebo vs clopidogrel (LD 300 mg → 75 mg qd)
•Other meds: ASA
•↓ CV death, MI, or stroke, rate of recurrent ischemia & revasc with clopidogrel
•↑ Major (non–life-threatening) bleeding with clopidogrel
•No routine inv strategy, 23% revasc during initial admission
•Although well tolerated, < 10% GP IIb/IIIa + ASA + clopidogrel + heparin use in study patients
Yusuf S, et al. N Engl J Med 2001;345:494–502.
33
Platelet glycoprotein IIb/IIIa in Unstable angina: Receptor Suppression Using InTegrilin (PURSUIT)
•10,948 patients within 24 h UA/NSTEMI
•Low-dose eptifibatide (n=1,487) vs high-dose eptifibatide (n=4,722) vs placebo (n=4,739)
•Other meds: ASA, heparin
•↓ Death/MI @ 96 hours, 7 d, 30 d with eptifibatide
― 1.5% ARR 4–30 d
― ↑ major bleeding
― no diff stroke
•↑ Event rate in 11% of patients not treated with concomitant heparin
The PURSUIT Trial Investigators. N Engl J Med 1998;339:436–43. Boersma E, et al. Circulation 2000;101:2557–67. ARR= absolute risk reduction.
34
Platelet Receptor Inhibition in Ischemic Syndrome Management
in Patients Limited by Unstable Signs and Symptoms (PRISM-PLUS)
•1,915 patients within 12 h UA/NSTEMI
•Tirofiban alone, UFH alone, or both for 48–108 h.
•Tirofiban-alone arm discontinued d/t ↑ mortality rate.
•↓ Death, MI, or refractory ischemia at 7 d, 30 d & 6 mo by tirofiban + heparin
•High rate of angio could have contributed to important ↓ in event rates
•Recommend: Tirofiban + heparin for medical rx or during PCI
PRISM-PLUS Study Investigators. N Engl J Med 1998;338:1488–97.
30-Day Death or Nonfatal MIRisk Ratio and 95% CI
Placebo BetterGP IIb/IIIa Inhibitor Better
Trial
Pooled 11.5%
PlaceboGP IIb/IIIa Inhibitor
10.7%29,855
n
0.92 (0.86, 0.995)P=.037
PRISM-PLUS 11.9% 10.2%1,915
PURSUIT 15.7% 14.2%9,461
PARAGON A 11.7% 11.3%2,282
7.1%PRISM 5.8%3,232
0.5 1.0 1.5
PARAGON B 11.4% 10.5%5,165
GUSTO-IV ACS
8.0% 8.7%7,800
GP IIb/IIIa Inhibition for Non–ST-Elevation ACS
Boersma E, et al. Lancet. 2002;359:189-198.
CI = confidence interval.
Benefits of GP IIb/IIIa by Troponin Status in Clinical Trials
Newby KL, et al. Circulation. 2001;103:2891-2896.
TnT-NegativeTnT-Positive
PARAGON-B
PRISM
CAPTURE
Combined
0.125 1 20.5 0.125 1 20.5GP IIb/IIIa
BetterGP IIb/IIIa
WorseGP IIb/IIIa
BetterGP IIb/IIIa
Worse
ISAR-REACT 2: Cumulative Incidence of Death, MI, or Urgent TVR in Subsets
With and Without Elevated Troponin levels (>0.03 µg/L)
ISAR-REACT 2 = Intracoronary Stenting and Antithrombotic Regimen: Rapid Early Action for Coronary Treatment 2.
Adapted with permission from Kastrati A, et al. JAMA. 2006;295:1531-1538.
20
15
10
5
0
0 5 10 15 20 25 30Days After Randomization
Cum
ulati
ve R
ate
ofPr
imar
y En
d Po
int,
%
Placebo Group (n=1010)Abciximab Group (n=1012)
Troponin >0.03 µg/LLog-Rank P=.02
Troponin <0.03 µg/LLog-Rank P=.98
The Bottom Line for IV GP IIb IIIa Inhibitors
• Consider starting upfront (ED) when patients at highest risk undergoing early invasive
• Consider in lab if PCI and not started upfront • Clopidogrel complementary, not competitor• Dose appropriately for renal function
39
Initial Invasive Strategy:Anticoagulant TherapyAnticoagulant therapy should be added to antiplatelet therapy in UA/NSTEMI patients as soon as possible after presentation.
•For patients in whom an invasive strategy is selected, regimens with established efficacy at a Level of Evidence: A include enoxaparin and unfractionated heparin (UFH), and those with established efficacy at a Level of Evidence: B include bivalirudin and fondaparinux.
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
New Drugs
40
Initial Conservative Strategy
Major Changes•New Drugs•Longer Duration of Rx•Revised Algorithm
41
Init clopidogrel (Class I, LOE: A) Consider adding IV eptifibatide or tirofiban (Class
IIb, LOE: B)
Conservative StrategyInit anticoagulant therapy (Class I, LOE: A):
Acceptable options: enoxaparin or UFH (Class I, LOE: A) or fondaparinux (Class I, LOE: B), but
enoxaparin or fondaparinux are preferable (Class IIa, LOE: B)
Select Management Strategy
ASA (Class I, LOE: A)Clopidogrel if ASA intolerant (Class I, LOE: A)
Diagnosis of UA/NSTEMI is Likely or Definite
Algorithm for Patients with UA/NSTEMI Managed by an Initial Conservative Strategy
Proceed with Invasive Strategy
(Continued)Anderson JL, et al. J Am Coll Cardiol. 2007;50:e1-e157, Figure 8. ACT = anticoagulation therapy; LOE = level of evidence.
42
Any subsequent events necessitating angiography?
EF greater than 40%
Evaluate LVEF
Low Risk
Cont ASA (Class I, LOE A) Cont clopidogrel (Class I, LOE A) and ideally up to 1 yr (Class I, LOE B)
DC IV GP IIb/IIIa if started previously (Class I, LOE A) DC ACT (Class I, LOE A)
(Class I, LOE: B)
Proceed to Dx Angiography
Yes
EF 40% or less Stress Test
(Class I, LOE: A)
No
Not Low Risk
(Class IIa, LOE: B)
Algorithm for Patients with UA/NSTEMI Managed by an Initial Conservative Strategy
(Continued)
Anderson JL, et al. J Am Coll Cardiol. 2007;50:e1-e157, Figure 8. ACT = anticoagulation therapy; LOE = level of evidence.
(Class I, LOE: A)
(Class IIa, LOE: B)
(Class I,
LOE: B)
(Class I, LOE: A)
43
Initial Conservative Strategy:Antiplatelet Therapy
For UA/NSTEMI patients in whom an initial conservative (i.e., noninvasive) strategy is selected, clopidogrel (loading dose followed by daily maintenance dose)* should be added to ASA and anticoagulant therapy as soon as possible after admission and administered for at least 1 month (Level of Evidence: A) and ideally up to 1 year. (Level of Evidence: B)
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
*Some uncertainty exists about optimum dosing of clopidogrel. Randomized trials establishing its efficacy and providing data on bleeding risks used a loading dose of 300 mg orally followed by a daily oral maintenance dose of 75 mg. Higher oral loading doses such as 600 or 900 mg of clopidogrel more rapidly inhibit platelet aggregation and achieve a higher absolute level of inhibition of platelet aggregation, but the additive clinical efficacy and the safety of higher oral loading doses have not been rigorously established.
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
44
Initial Conservative Strategy:Antiplatelet Therapy
For UA/NSTEMI patients in whom an initial conservative (i.e., noninvasive) strategy is selected, it may be reasonable to add eptifibatide or tirofiban to anticoagulant and oral antiplatelet therapy.
Abciximab should not be administered to patients in whom PCI is not planned.
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
45
Initial Conservative Strategy:Anticoagulant TherapyAnticoagulant therapy should be added to antiplatelet therapy in UA/NSTEMI patients as soon as possible after presentation.
•For patients in whom a conservative strategy is selected, regimens using either enoxaparin* or UFH (Level of Evidence: A) or fondaparinux (Level of Evidence: B) have established efficacy.
•In patients in whom a conservative strategy is selected and who have an increased risk of bleeding, fondaparinux is preferable.
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
*Limited data are available for the use of other low-molecular-weight heparins (LMWHs), e.g., dalteparin.
New Drugs
46
Initial Conservative Strategy:Anticoagulant TherapyFor UA/NSTEMI patients in whom an initial conservative strategy is selected, enoxaparin* or fondaparinux is preferable to UFH as anticoagulant therapy, unless CABG is planned within 24 h.
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
*Limited data are available for the use of other low-molecular-weight heparins (LMWHs), e.g., dalteparin.
47
Initial Conservative Strategy:Additional Management Considerations
b. If, after stress testing, the patient is classified as being at low risk, the instructions noted below should be followed in preparation for discharge:
1. Continue ASA indefinitely. (Level of Evidence: A)
2. Continue clopidogrel for at least 1 month (Level of Evidence: A) and ideally up to 1 year. (Level of Evidence: B)
3. Discontinue IV GP IIb/IIIa inhibitor if started previously. (Level of Evidence: A)
4. Continue UFH for 48 h or administer enoxaparin or fondaparinux for the
duration of hospitalization, up to 8 d, and then discontinue anticoagulant therapy. (Level of Evidence: A)
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
48
Long-Term Antithrombotic Therapy at Hospital Discharge after UA/NSTEMI
Medical Therapy
without Stent
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)
Add: Warfarin (INR 2.0 to 2.5) (Class IIb, LOE: B)
Continue with dual antiplatelet therapy as
above
Yes
No
Indication for Anticoagulation?
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 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)
Anderson JL, et al. J Am Coll Cardiol 2007;50:e1–e157, Figure 11. INR = international normalized ratio; LOE = level of evidence.
UA/NSTEMI Patient Groups at Discharge
New
49
Beta Blockers
Beta blockers are indicated for all patients recovering from UA/NSTEMI unless contraindicated. (For those at low risk, see Class IIa on the next slide). Treatment should begin within a few days of the event, if not initiated acutely, and should be continued indefinitely.
Patients recovering from UA/NSTEMI with moderate or severe LV failure should receive beta-blocker therapy with a gradual titration scheme.
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII New
50
Inhibition of the Renin-Angiotensin-Aldosterone SystemACE inhibitors are reasonable for patients recovering from UA/NSTEMI in the absence of LV dysfunction, hypertension, or diabetes mellitus unless contraindicated.
ACE inhibitors are reasonable for patientswith HF and LVEF > 0.40.
In UA/NSTEMI patients who do not tolerate ACE inhibitors, an ARB can be useful as an alternative to ACE inhibitors in long-term management provided there are either clinical or radiological signs of HF and LVEF < 40%.
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
New
New
51
Lipid Management
Lipid management should include assessment of a fasting lipid profile for all patients, within 24 h of hospitalization.
Hydroxymethyl glutaryl-coenzyme A reductase inhibitors (statins), in the absence of contraindications, regardless of baseline LDL-C and diet modification, should be given to post-UA/NSTEMI patients, including postrevascularization patients.
For hospitalized patients, lipid-lowering medications should be initiated before discharge.
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
Major Changes
52
Heart Protection Study (HPS)
•20,536 patients with CHD•Simvastatin (40 mg qd) vs placebo
•↓ Total mortality by simvastatin
― ↓ Total CHD, total stroke, revascularization
― ↑ Benefit over time, irrespective of initial cholesterol level and in broad spectrum of patients (e.g., women, elderly & patients with diabetes)
•Recommend: Statin in all patients at discharge regardless of baseline LDL-C (Class I, LOE: A)
Heart Protection Collaborative Group. Lancet 2002;360:7–22.LOE = level of evidence.
53
Lipid Management
For UA/NSTEMI patients with elevated LDL-C (≥ 100 mg per dL), cholesterol-lowering therapy should be initiated or intensified to achieve an LDL-C < 100 mg per dL.Further titration to less than 70 mg per dL is reasonable. (Class IIa, Level of Evidence: A)
Therapeutic options to reduce non–HDL-C* are recommended, including more intense LDL-C–lowering therapy.
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
*Non-HDL-C = total cholesterol minus HDL-C
New Lower LDL-C Goal
54
PRavastatinOr atorVastatin Evaluation and Infection Therapy–
Thrombolysis In Myocardial Infarction 22 (PROVE-IT TIMI 22)
•4,162 patients within 10 d of ACS
•40 mg pravastatin vs 80 mg atorvastatin daily
•↓ All-cause death, MI, UA requiring hosp, revasc & stroke @ 2 y by atorvastatin
― Median LDL-C ↓ (62 vs 95 mg/dL)
Cannon CP, et al. N Engl J Med 2004;350:1495–504.
55
Lipid Management
Further reduction of LDL-C to < 70 mg per dL is reasonable.
If baseline LDL cholesterol is 70 to 100 mg per dL, it is reasonable to treat LDL-C to < 70 mg per dL.
Further reduction of non-HDL-C* to < 100 mg per dL is reasonable; if TG are 200 to 499 mg per dL, non- HDL-C target is < 130 mg per dL. Therapeutic options to reduce non-HDL-C* (after LDL-C lowering) include niacin† or fibrate‡ therapy.
*Non-HDL-C = total cholesterol minus HDL-C.†The combination of high-dose statin plus fibrate can increase risk for severe myopathy. Statin doses should be kept relatively low with this combination. Dietary supplement niacin must not be used as a substitute for prescription niacin. ‡Patients with very high triglycerides should not consume alcohol. The use of bile acid sequestrants is relatively contraindicated when triglycerides are greater than 200 mg per dL.
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
Next Case:
Chief Complaint: Subxiphoid burning sensation and dyspnea
History of Present Illness: A 48-year-old female who smokes two packs per day presents with 1 hour of a
subxiphoid burning sensation with dyspnea and diaphoresis, which are ongoing. She denies any prior
cardiovascular or gastrointestinal history.
Risk factor: positive family history of premature coronary artery disease
Age: 48Gender: Female
Blood Pressure: 170/95 mm HgPulse: 96 bpm
Head and Neck: Jugular venous pressure, 10Chest and Lungs: Clear
Cardiac Exam: Regular rhythm, normal S1/S2; S4 present
Extremities: 2+ pulses, no edema
Her EKG:
Copyright ©2005 American Heart Association Circulation 2005;112:IV-89-IV-110
Acute Coronary Syndromes Algorithm
Initial Therapy/Recognition
• Starts in transport to ED– O2– Aspirin– Nitro– Morphine– Beta Blockers?
–12 lead EKG
Therapy and recognition in ED
• 12 lead EKG Will be used to stratify patients into treatment groups
• O2, ASA, Nitro, Morphine MONA• Physical exam• Cardiac biomarkers troponins
• 10 minute time frame
Treatment Groups Stratification
• ST-elevation MI (STEMI) ST-segment elevation or presumed new LBBB in 2 or more contiguous precordial or limb leads
• UA/non-ST-elevation MI (NSTEMI) ischemic ST-segment depression or dynamic T wave inversion with pain. Transient ST-segment elevation.
• Normal or nondiagnostic changes with pain
ED Evaluation of ED Evaluation of Patients With STEMIPatients With STEMI
1. Airway, Breathing, Circulation (ABC)
2. Vital signs, general observation
3. Presence or absence of jugular venous distension
4. Pulmonary auscultation for rales
5. Cardiac auscultation for murmurs and gallops
6. Presence or absence of stroke
7. Presence or absence of pulses
8. Presence or absence of systemic hypoperfusion (cool, clammy, pale, ashen)
Brief Physical Examination in the ED
ED Evaluation of ED Evaluation of Patients With STEMIPatients With STEMI
Aortic dissection
Pulmonary embolus
Perforating ulcer
Tension pneumothorax
Boerhaave syndrome
(esophageal rupture with
mediastinitis)
Differential Diagnosis of STEMI: Life-Threatening
ED Evaluation of ED Evaluation of Patients With STEMIPatients With STEMI
PericarditisAtypical anginaEarly repolarizationWolff-Parkinson-White
syndromeDeeply inverted T-waves
suggestive of a central nervous system lesion or apical hypertrophic cardiomyopathy
LV hypertrophy with strain
Brugada syndrome
Myocarditis
Hyperkalemia
Bundle-branch blocks
Vasospastic angina
Hypertrophic cardiomyopathy
Differential Diagnosis of STEMI: Other Cardiovascular and Nonischemic
Gastroesophageal reflux (GERD) and spasm
Chest-wall pain
Pleurisy
Peptic ulcer disease
Panic attack
Cervical disc or neuropathic pain
Biliary or pancreatic pain
Somatization and psychogenic pain disorder
ED Evaluation of ED Evaluation of Patients With STEMIPatients With STEMI
Differential Diagnosis of STEMI: Other Noncardiac
ElectrocardiogramElectrocardiogram
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.
In patients with inferior STEMI, ECG leads should
also be obtained to screen for right ventricular
infarction.
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
Right Ventricular InfarctionRight Ventricular Infarction
Clinical findings:Shock with clear lungs, elevated JVPKussmaul sign
Hemodynamics: Increased RA pressure (y descent)Square root sign in RV tracing
ECG:ST elevation in R sided leads
Echo:Depressed RV function
Rx:Maintain RV preloadLower RV afterload (PA---PCW)Inotropic supportReperfusion
V4R
Modified from Wellens. N Engl J Med 1999;340:381.
Cardiac-specific troponins should be used as the
optimum biomarkers for the evaluation of patients
with STEMI who have coexistent skeletal muscle
injury.
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.
Biomarkers of Cardiac DamageBiomarkers of Cardiac Damage
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
00 11 22 33 44 55 66 7788
Cardiac troponin-no Cardiac troponin-no reperfusion reperfusion
Days After Onset of STEMIDays After Onset of STEMI
Mu
ltip
les
of
the
UR
LM
ult
iple
s o
f th
e U
RL
Upper reference limitUpper reference limit11
22
55
1010
2020
5050
URL = 99th %tile of URL = 99th %tile of Reference Control GroupReference Control Group
100100
Cardiac troponin-Cardiac troponin-reperfusion reperfusion
CKMB-no reperfusion CKMB-no reperfusion
CKMB-CKMB-reperfusion reperfusion
Cardiac Biomarkers in STEMICardiac Biomarkers in STEMI
Alpert et al. J Am Coll Cardiol 2000;36:959.Wu et al. Clin Chem 1999;45:1104.
STEMIST-segment elevation or
presumed new LBBB in 2 or more contiguous precordial
or limb leads
STEMI• Immediate reperfusion therapy
indicated
–Fibrinolytics –PCI
Medications for STEMI
• Clopidogrel• Beta blockers• Heparin• fibrinolytics
FibrinolysisFibrinolysis
In the absence of contraindications, fibrinolytic therapy should be administered to STEMI patients with symptom onset within the prior 12 hours.
In the absence of contraindications, fibrinolytic therapy should be administered to STEMI patients with symptom onset within the prior 12 hours and new or presumably new left bundle branch block (LBBB).
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
FibrinolysisFibrinolysis
In the absence of contraindications, it is reasonable to administer fibrinolytic therapy to STEMI patients with symptom onset within the prior 12 hours and 12-lead ECG findings consistent with a true posterior MI.
In the absence of contraindications, it is reasonable to administer fibrinolytic therapy to patients with symptoms of STEMI beginning in the prior 12 to 24 hours who have continuing ischemic symptoms and ST elevation > 0.1 mV in ≥ 2 contiguous precordial leads or ≥ 2 adjacent limb leads.
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
FibrinolysisFibrinolysis
Fibrinolytic therapy should not be administered to
asymptomatic patients whose initial symptoms of
STEMI began more than 24 hours earlier.
Fibrinolytic therapy should not be administered to
patients whose 12-lead ECG shows only ST-
segment depression, except if a true posterior MI
is suspected.
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
Assessment of ReperfusionAssessment of Reperfusion
It is reasonable to monitor the pattern of ST elevation, cardiac rhythm and clinical symptoms over the 60 to 180minutes after initiation of fibrinolytic therapy.
Noninvasive findings suggestive of reperfusion include:
Relief of symptoms
Maintenance and restoration of hemodynamic and/or electrical instability
Reduction of ≥ 50% of the initial ST-segment elevation pattern on follow-up ECG 60 to 90 minutes after initiation of therapy.
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
Ancillary Therapy to ReperfusionAncillary Therapy to Reperfusion
Unfractionated heparin (UFH) should be given intravenously in:
Patients undergoing PCI or surgical revascularization
After alteplase, reteplase, tenecteplase
After streptokinase, anistreplase, urokinase in patients at high risk for systemic emboli.
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
ThienopyridinesThienopyridines
In patients taking clopidogrel in whom CABG is
planned, the drug should be withheld for at
least 5 days, and preferably for 7 days, unless
the urgency for revascularization outweighs the
risk of excessive bleeding.
NOTE: Surgeons at MMC will take a patient to
the OR for bypass even if given a loading dose
of Plavix that day. This represents a change.
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
ACE/ARB: Within 24 HoursACE/ARB: Within 24 Hours
An ACE inhibitor should be administered orallywithin the first 24 hours of STEMI to the followingpatients without hypotension or known class ofcontraindications:
• Anterior infarction Pulmonary congestion
LVEF < 0.40
An ARB should be given to ACE-intolerant patients with either clinical or radiological signs of HF or LVEF < 0.40.
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
All-Cause Mortality
Years
Pro
bab
ilit
y o
f Even
t
0
0.05
0.1
0.15
0.2
0.25
0.3
0 1 2 3
0.35
0.4
4
ACE-I
Placebo
ACE-I 2995 2250 1617 892 223
Placebo 2971 2184 1521 853 138
Flather MD, et al. Lancet. 2000;355:1575–1581
OR: 0.74 (0.66–0.83)OR: 0.74 (0.66–0.83)
ACE-I: 702/2995 (23.4%)ACE-I: 702/2995 (23.4%)
Placebo: 866/2971 (29.1%)Placebo: 866/2971 (29.1%)
TRACEEchocardiographicEF 35%
AIREClinical and/or radiographic signs of HF
SAVERadionuclideEF 40%
Last Case:
A 58 y.o. man presents to the ER with a complaint of chest pain.
His EKG and initial troponin are both normal.
How will you proceed?
First, characterize the chest pain
• Where is its location?• What provokes it?• What relieves it?
Typical or classical angina:
• Is located in the center of the chest and may have textbook radiation to the arm, neck, or jaw
• Is provoked by exercise or emotion• Is relieved by rest or nitroglycerine
To establish the likelihood of your patient having an acute coronary syndrome, first determine whether:
• All three characteristics are present, and therefore the patient has typical angina
• Two of three are present, i.e. this is atypical angina
• One or none are present, i.e. this is non-anginal chest pain
Then, use the medical literature:
Diamond and Forrester: New England Journal of Medicine 1979; 300 (24): 1350 300 (24): 1350- -1358
Diamond and Forrester: New England Journal of Medicine 1979; 300 (24): 1350 300 (24): 1350- -1358
And to these probabilities, add some history:
• Family history of premature coronary disease?• Lipid profile known?• History of HTN?• Of diabetes?• Smoking?
Now, you need to use Bayes’ Theorem… that is of course unless you are like me and want a
short-cut.
Here’s a short cut:
It’s called the Fagan nomogram:
…together with your pretest probability you have estimated for
your patient.
And the likelihood ratios…for mibis, the +LR is about 2.4 and
the –LR is about .2
But look at the nomogram again! Are you convinced that stress testing is most helpful for the patient with intermediate pretest probability?
Remember, central to the ACS algorithm is the 12-lead EKG.
Which of these are acute MI’s?
And which of these is V. Tach?
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