Transcript Document 7220702

Acute Coronary
Syndromes
Adam Oster, R4.
Dr. Gill Curry, FRCP
Core Rounds.
July 8, 2004.
Topics
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Master of the ECG
Evidence for various therapeutic
interventions
NSTEMI Risk Stratification
Thrombolysis
AMI in LBBB
Pre-hospital lytics
Cardiogenic shock
ACS Rounds
55M with atypical chest pain for 60mins
Hyperacute T waves
Hyperacute T waves
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Early sign of infarct
Normal T <7mm
Hyperacute >8mm
Ischemic are more
symmetric
–
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Upgoing side still
slopes up gradually
Other Causes;
–
–
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Hyperkalemia (steep
and sharp)
LVH
LBBB
Master of the ECG
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Progression of changes…
STE
Evolving STEMI
Evolving STEMI
Post-STEMI 3 weeks
Case
Case
Case
Role of the 15 lead
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Inferior MI
– RV infarct occurs in 25% of inferior MIs
– Different therapeutic and resuscitation
needs
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Posterior MI
– Dorsal region of LV
– Usually LCX or RCA-posterior descending
branch
Limitations of the ECG
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Specificity approx 50% for ischemia
– The normal or non-diagnostic ECG
Special ECGs
LM Disease
Wellens’ Syndrome
Wellens’ Syndrome:
T Wave Inversion
Pope et al. Missed Diagnoses of Acute Cardiac
Ischemia in the Emergency Department. New
England Journal of Medicine vol. 342, no. 16,
2000.
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10 689 patients
Data collected for 30d (hospitalised
patients) or at 24 to 72hrs for nonhospitalised patients
Outcomes assigned by physicians at
study sites using pre-defined criteria
Pope et al. Missed Diagnoses of Acute Cardiac
Ischemia in the Emergency Department. New
England Journal of Medicine vol. 342, no. 16,
2000.
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Final Diagnosis
– 1866 (17%) ACI
– 894 (8.5%) AMI
– 972 (9%) unstable angina
– 21% non-ischemic cardiac problem
– 55% non-cardiac
Pope et al. Missed Diagnoses of Acute Cardiac
Ischemia in the Emergency Department. New
England Journal of Medicine vol. 342, no. 16,
2000.
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22 missed unstable angina (2.26%)
– MC diagnosis;
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stable angina, atypical chest pain
Pope et al. Missed Diagnoses of Acute Cardiac
Ischemia in the Emergency Department. New
England Journal of Medicine vol. 342, no. 16,
2000.
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19 missed AMIs (2.1% of 894)
– MC diagnosis;
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non-cardiac chest pain, pulmonary conditions
and stable angina
Pope et al. Missed Diagnoses of Acute Cardiac
Ischemia in the Emergency Department. New
England Journal of Medicine vol. 342, no. 16,
2000.
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Factors associated with non-hospitalisation
for patients with missed ACI
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female
<55
non-white
chief complaint of SOB
normal ECG
30d adjusted risk of mortality 1.7 times
higher if not hospitalised (95% CI 0.7 to
5.2)
AMI Mortality
3 Cases of Chest Pain;
1.
50M with 1hr of RSCP. No known CAD.
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2.
65F with 120mins RSCP. No known CAD.
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3.
No DM/HTN/FHx. Smoker.
ECG normal. 10hr TnT neg
T2DM/HTN/recent non-smoker.
ECG non-specific. 10hr TnT neg.
74M with 3hrs RSCP
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prior 4xCABG, daily ASA.
ECG nil acute, TnT positive
ACS Risk Stratification
Thrombolysis in Myocardial
Infarction (TIMI):
Risk Stratification
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Antman et al. JAMA. 2000. Vol. 284, No.7.
– TIMI RS based on data from TIMI 11b (N=3910)
and ESSENCE (N=3171)
– Test cohort (TIMI UFH)
– Validation cohort (TIMI and ESSENCE enoxaparin
groups and ESSENCE UFH)
– TIMI RS derived in test cohort
TIMI Risk Stratification
Antman et al. JAMA. 2000. Vol. 284, No.7.
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Endpoints
– all-cause death, new or recurrent MI or UR at
14d post-randomisation
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Eligibility (1 of following)
– admitted patients who presented within 24hrs
with symptoms of unstable angina/NSTEMI
– transient STE or STD or 0.05mV (TIMI) or
0.01mV (ESSENCE)
– known CAD*
– increased Troponin
TIMI Risk Stratification
Antman et al. JAMA. 2000. Vol. 284, No.7
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All patients received ASA
randomised to enoxaparin or UFH
Derivation cohort;
– tested 12 candidate variables
age
at least 3 CAD risk factors
significant coronary stenosis
prior MI
prior CABG
prior PTCA
ST deviation
>2 anginal events in 24hrs
use of ASA in last 7d
elevated cardiac markers
prior history of CHF
TIMI Risk Stratification
Antman et al. JAMA. 2000. Vol. 284, No.7
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Derivation cohort
– 7 variables remained statistically significant after
multivariate analysis
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Age >65
at least 3 CAD RF
STD
severe anginal symptoms
prior stenosis >50%
use of ASA over previous 7d
elevated serum cardiac markers
TIMI Risk Stratification
Antman et al. JAMA. 2000. Vol. 284, No.7
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Small numbers of
patients in extreme risk
scores required
combining
criteria of known
stenosis >50%,
insensitive to missing
data and remained a
significant predictor
TIMI Risk Stratification
Antman et al. JAMA. 2000. Vol. 284, No.7
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Validation Phase
– different rate of increase
for rate of composite
endpoint in UFH vs
enoxaparin
– merged the databases
– TIMI RS and treatment
were both significant
predictors of risk of the
composite endpoint
TIMI Risk Stratification
Antman et al. JAMA. 2000. Vol. 284, No.7
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Predicting the
individual components
of the composite
endpoint
all statistically sig.
TIMI Risk Stratification
Antman et al. JAMA. 2000. Vol. 284, No.7
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Caveats and Critique
– tested on admitted patients with unstable
angina/NSTEMI
– Validation Phase not prospective
– cohort who qualified for enrolment in a phase III study;
?generalisabilty to all-comers with chest pain
– enrolment criteria for TIMI 11b changed during the trial
– duration of treatment different between UFH (3-8d) and
enoxaparin (8d or hospital discharge)
– elevated CKMB was both a predictor of an endpoint as well
as part of the definition of an endpoint
– CKMB was the marker in TIMI but now use Troponin
without study to prove similarly predictive
TIMI Risk Stratification
Antman et al. JAMA. 2000. Vol. 284, No.7
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Support
– consider using on chest pain patients to be
admitted
– simple to use and to communicate to consultants
– cannot use to determine who is at low risk
– cannot use to determine who is safe for
discharge
How Predictive are
Routine Historic
Features?
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Goodacre et al. How Useful are Clinical Features
in the Diagnosis of Acute, Undifferentiated Chest
Pain? Academic Emergency Medicine, vol. 9, no. 3,
2002.
– Prospectively evaluated 893 CPOU (normal ECG, no CHF or
arrhythmia)
– ST seg monitoring, troponin T >6hrs, +/-EST or thallium
– F/U at 3d and 6mo, 12mo
– Endpoints: AMI at presentation and ACS (AMI at any time,
pos. EST cardiac death, arrhythmia, revascularisation
procedure)
– Assessed predictive power of routine historic features
Goodacre et al. How Useful are Clinical Features
in the Diagnosis of Acute, Undifferentiated
Chest Pain? Academic Emergency Medicine, vol.
9, no. 3, 2002.
Features Predictive of AMI:
Feature
Radiation to Shoulder
Radiation to Both Arms
Burning/Indigestion
Nausea/Vomiting
Exertional Pain
Tender Chest Wall
OR
5.7
4.9
3.4
1.3
3.3
0.2
CI
1.5-21.4
1.3-19.4
0.4-31.0
0.5-3.3
1.3-8.4
0.05-0.97
p
sig
sig
NS
NS
sig
sig
Goodacre et al. How Useful are Clinical Features
in the Diagnosis of Acute, Undifferentiated
Chest Pain? Academic Emergency Medicine, vol.
9, no. 3, 2002.
Features Predictive of ACS:
Feature
Radiation to shoulder
Radiation to left arm
Radiation to both arms
Exertional pain
Pleuritic pain
Tender chest wall
OR
5.2
2.1
4.8
2.4
0.6
0.6
CI
2.0-13.4
1.0-4.4
1.8-13.2
1.3-4.5
0.2-1.7
0.3-1.2
p
sig
sig
sig
sig
NS
NS
Once Risk Stratified…
What to give?
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ASA
Heparin/LMWH
hirudin
Bblocker
CCB
Nitro
Morphine
O2
Lytic
Clopidegril (plavix)
G2b3a
Bed Rest
NSTEMI
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Acute rupture of plaque
Fibrin and platelets
Incomplete occlusion of CA
?chlamydial
Inflammatory reaction
Shear forces
Pharmacology...
Better Living Through
Chemistry
O2
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Makes intuitive sense since imbalance
between O2 demand of myocardium and
supply
Hypoxemia in AMI most likely caused by
V/Q mismatch from LV dysfunction
Evidence to support routine use is weak
Reduces amount of STE in precordial leads
with anterior MI
– Madias, et al. Circulation 1976.
Anti-Platelet Therapy
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ASA
Clopidegril
2b3a
ASA
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ISIS-2
– Randomised AMI to “normal therapy” or
ASA or streptokinase
– Reduction in mortality with ASA or strepto
– ASA RRR 23%
– NNT 20 to save 1 life in STEMI
– Benefit and risk profile better than
thrombolytic since you can give ASA to
virtually all with ACS
ASA
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NSTEMI
– RRR 50%
– ARR 3%
– NNT death/MI 30
ASA
ASA:
– 160-325mg to chew ASAP
– All trials have shown mortality benefit
that extends to 2 years
– Contraindications:
Allergy??
 Active bleeding (GI, retinal)
 Hemophilia

Putting it all together…
Anti-platelet therapy
Clopidogrel
– CAPRIE (1996), RCT ASA vs Plavix
(N=19,185)
3 year ischemic stroke, MI or death ARR =
0.5% (NNT = 200)
 Plavix equal to ASA but increased side effects
(diarrhea, rash, GI bleed)
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Anti-platelet therapy
Clopidogrel:
– CURE trial (2001) RCT Plavix + ASA vs ASA
UA/NSTEMI within 24 hr
 Death, MI, or stroke 3 and 12 month ARR
= 2.2% (NNT = 45)
 Excess in major bleed of 1% (NNH = 100)
 Risk of bleed with CABG increased in 1st 5 days
 Recommended in UA/NSTEMI when
noninvasive course is anticipated
 BOTTOM LINE: appears to work but not
for us to start in the ED
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Anti-platelet therapy
GPIIbIIIa Receptor Antagonists:
– Inhibits the cross-linking of platelets by
fibrinogen
GPIIbIIIa RA
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EPIC (abcixamab) NEJM 1994
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PRCT, N=2,099 pts
High risk pts going for PCI (AMI, USA)
Reopro(bolus, bolus +infusion) vs placebo
Placebo vs bolus similar
F/U 30 days
Bolus/infusion: lower rate triple end-point
(Death, MI or urgent revascularization) 8.3% vs
12.8% (ARR 4.5%, RRR 35%)
– 2 fold increase in major bleeds: 14% vs 6.6 (ARI
7.4%, RRI 112%!!!
GPIIbIIIa RA
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CAPTURE (abcixamab) Lancet 1997
– PRCT, N=1050 pts (stopped early)
– Pts with refractory USA, after cath and before
plasty
– Reopro vs placebo , 18-24hrs before plasty, and
1 hr after
– F/U 30 days then 6 months
– Composite endpoint at 30 days(Death, MI,
urgent intervention ): 2.6% vs 5.5% (ARR 2.9%,
RRR 53%)
– At 6 months: no difference! (decreased early
events only)
– Major bleeding: 3.8% vs 1.9% (ARI 1.9%, RRI
GPIIbIIIa RA
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CAPTURE (substudy)
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Predictive value of TnT
Increased TnT(>0.1 ng/ml): 30.9%
F/U 6 months: Death or MI
TnT +ve
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Reopro 9.5% vs placebo 23.9% (ARR 14.4%, RRR
60%
– TnT –ve
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Reopro 7.5% vs 9.4% (not significant)
– Conclusion: TnT +ve identifies a high risk
population that seems to benefit from GIIb-IIa
GPIIbIIIa RA
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PRISM-PLUS (tirofiban) NEJM 1998
– PRCT, N=1,570 pts
– Non-ST segment elevation ACS and likely to go
to catheterization
– Heparin vs tirofiban vs combination
– Tirofiban alone arm stopped (increased mortality
at 7 days)
– F/U 7 and 30 days and 6 months
– Composite endpoint (Death, MI or recurrent
ischemia): 7 days: 12.9 vs 17.9% (p=0.004), 30
days: not significant, 6 months: 27.7 vs 32.2%
(p=0.02)
GPIIbIIIa RA
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PURSUIT (eptifibatide)
– PRCT, N=10,948 pts
– Eligible if ECG changes : transient ST elevation,
ST depression, T wave inversion, or positive
CKMB
– Eptifibitide vs placebo
– F/U 30 days and 6 months
– Double endpoint (Death or MI): 30 days: 14.2 vs
15.7% (ARR 1.5%, RRR 10%), 6 months: 12.1
vs 13.6% (ARR 1.5%, RRR 11%)
– Medical Management: US benefit, Europe and
Latin America no benefit
– Didn’t work in females!!!!!
GPIIbIIIa RA
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GUSTO IV
– PRCT, N=7800 pts
– ECG changes, +ve troponin level
– Early revascularization strongly
discouraged
– Abcixamab vs placebo (24-48 hr infusion)
– No difference in MI or Death
GPIIbIIIa RA
BOTTOM LINE:
– They are definitely indicated as an adjunct
to PCI
– Role in UA/NSTEMI is questionable, there
appears to be a small reduction in death or
MI in high risk groups (ongoing or
recurrent pain, dynamic ST changes)
– Not enough evidence for us to start in the
ED
Heparins
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Does heparin add anything in addition
to ASA?
Ollier, et al. Meta-analysis. JAMA 1996
– small 33% RRR in MI
– NNT 40-80
– Barely statistically significant
– All high risk patients
Anti-thrombotic therapy
Unfractionated Heparin:
 Theroux et al (1993) RCT ASA+hep vs
ASA
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Decreased rates of MI (fatal and nonfatal)
3% (NNT = 33)
RISC (1990) ASA vs UFH vs UFH +ASA
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ASA + UFH had lowest events in 1st 5 days
Anti-thrombotic therapy
LMWH:
 ESSENCE (1997) RCT enoxaparin vs UFH
– No difference in mortality
– Composite endpoint of death, MI or recurrent
angina, ARR = 3.2% (NNT=33)
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TIMI 11B (1999) RCT enoxaparin vs UFH
– Composite endpoint death, MI, urgent need for
PTCA, ARR = 2.1% (NNT = 50)
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2 trials (1 dalteparin, 1 nadroparin) had
neutral or unfavorable trends
Heparin
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Use in moderate to high risk patients
NNH 40
– Significant bleed
– thrombocytopenia
B-Blockade
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Shown to decrease all cause mortality
by 2.6% if started within 5-21days of
infarct (NNT = 38)
 early treatment:
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Metoprolol 15 mg vs placebo f/u at 3 month,
36% RRR of death
TIMI IIB showed lower reinfarction or
recurrent CP
 If HR > 70 and BP can tolerate give
Metoprolol 5-15 mg iv
Nitro
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Intuitively should help
– Combat vasospasm
– Dilate coronary arteries improving
perfursion
– Reduce pre-load reducing myocardial O2
consumption
– Afterload reduction
Nitro
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No mortality benefit clearly established
Shown to decrease post infarct angina
– Give sl to patients with ischemic sounding
CP unless SBP < 90, HR < 50,
tachycardia, or suspected RV infarct
Case
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64F no known CAD
– 2 hrs atypical chest pain after mowing
lawn.
No cardiac RF
 ECG normal
 c/o 6/10 pain
 3/10 post 3 sprays nitro
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Response to nitro
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Annals of Internal Medicine 2003, Dec
16; 139:979-86.
– Enrolled 459 patients prospectively admitted
with chest pain. Observational study.
– Use a combined Gold Standard for active CAD
and no active CAD
– Defined response to nitro as >50% decline in
pain at 5mins post-dose
– All pts followed for 4 months after index visit
Annals of Internal Medicine
2003, Dec 16; 139:979-86.
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Active CAD
– 35% responsive (49/141)
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No active CAD
– 41% responsive (113/275)
Annals of Internal Medicine
2003, Dec 16; 139:979-86.
Annals of Internal Medicine
2003, Dec 16; 139:979-86.
Annals of Internal Medicine
2003, Dec 16; 139:979-86.
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Limitations
– Self-reported pain (reporting bias)
– Unvalidated pain-scale (reliability)
– Non-blinded physicians (work-up bias)
– 43 pts with chest pain of unclear origin
Management of AMI
Thrombolytics:
 Goal “door-to-needle” time of 30
minutes
 FTT Trial (N=58,000)
– No survival benefit after 12 hours
– ARR 2%, NNT 40-50
Management of AMI
Fibrinolytics started
First hour
Second hour
Third hour
3-6 hour
6-12 hour
12-24 hour
Additional lives saved
per 1000 pts
treated
65
37
29
26
18
9
To Lyse? Or not to…
Lysis?
Lysis?
Lysis?
Lytic Criteria
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Canadian Consensus Conference on Coronary
Thrombolysis: 1994 Recommendations.
– Indications:
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>30mins chest pain and
At least 1mm STE in at least 2 limb leads or
At least 2mm in at least 2 adjacent precordial leads or
Complete BBB
Within 12 hrs of symptoms
Target time <1hr from patient arrival
Benefit extends to those 75 and older
Canadian Consensus Conference on Coronary
Thrombolysis: 1994 Recommendations
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Contraindications
– Absolute
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Pericarditis
Dissection
Active bleeding
– Relative
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Any time cerebral bleed, malignancy/AVM
<6mo GI/GU bleed
Severe uncontrolled hypertension
Management AMI - PTCA
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Meta-analysis Weaver et al
– 10 RCT, N = 2606
– ARR 30 day mortality PTCA vs lytic =
2.1%, NNT = 50
– ARR 30 day mortality or reinfarction =
4.7% NNT = 21
Management AMI - PTCA
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Primary angioplasty vs (any agent)
thrombolysis
– Reduction in 30d mortality (7% v 9%)
– non-fatal reinfarction (3% v 7%)
– stroke (1% v 2%)
– and a combination of these three end
points (8% v 14%)
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(P < 0.001 for all comparisons).
Management of AMI PTCA
Interventions vs 30d
Mortality
Local Initiatives
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STEMI
ASCENT-IV
Local Practice
ASCENT - IV
55M with RSCP for 4hrs
at PLC
– STE anteriorly
– Delay to PCI of
approx 90mins
– ??…
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ASCENT IV
Division of Research
Dept. of Emergency Medicine
Room C231, 1403 - 29 Street N.W.
Calgary, AB., T2N 2T9
Telephone: (403) 944-8797
Fax:
(403) 944-1341
ASCENT IV
Study Design
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A randomized open –label cardiology/emergency
collaborative project evaluating the efficacy and safety of
full dose TNK together with heparin prior to PCI as
compared to standard primary PCI in pts. with acute MI.
Patients will be considered for this study only if there is a
delay from ED presentation to the PCI lab between 1-3
hours.
Cardiology Interventionalists when contacted by the
emergency physician will prompt staff to consider the
patient for the Ascent IV trial based on their
calculation/interpretation of the time to PCI.
When prompted to consider patient for Ascent IV trial ED
physicians will complete inclusion/exclusion criteria
checklist and consent willing candidates to participate in
the study
Contact Cardiology study nurse: Carrie Ellis Pager #
2781 with questions or concerns.
Inclusion/Exclusion
Criteria
Inclusion
 Patients with acute MI presenting within 6 hours of
symptom onset
 Delay in transportation to the PCI lab of between 1-3
hours
 Must meet all other inclusion/exclusion criteria in the
screening checklist
Start Date
March 15, 2004
Enrolment packages
and drug kits
Enrolment packages consisting of ;
 Consent
 inclusion/exclusion criteria form
 enrolment flow sheet
Drug kits
Investigators
Contact Info
All located in labeled Ascent IV box on shelf above
respiratory desk in major area
Dr. M. Traboulsi , Dr. Christine Hall
Cardiology Study Nurse: Carrie Ellis Pager # 2781
ER research coordinator: Rod Iwanow Ph# 944-8797,
Pager# 2331
email: [email protected]
50F with chest pain and this
ECG…
50F with chest pain and this ECG…
AMI in LBBB
Sgarbossa EB et al, NEJM
1996;334:481-7
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Derived rule from GUSTO-1 subgroup
with;
– Enzyme proven AMI
– LBBB on initial ECG
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Compared to databank of LBBB with
cath-proven CAD but without chest
pain during ECG
ECGs analyzed by 4 blinded readers
Sgarbossa EB et al, NEJM
1996;334:481-7
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Univariate analysis;
– 1mm or more elevation concordant with
QRS
Sens 73% (64-80), specificity 92% (86-96)
 LR 9.54 (3.1-17.3)
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– 5mm or more STD discordant with QRS
Sensitivity 31% (23-39) specificity 92% (8596)
 LR 3.63 (2.0-6.8)

Sgarbossa EB et al, NEJM
1996;334:481-7
Sgarbossa EB et al, N Engl J
Med 1996;334:481-7

For a specificity of 90%, need a
score of 3 or more.
Sgarbossa EB et al, NEJM
1996;334:481-7

Validation Sample (in cohort of 45 pts)
– Score =/>3
Sens 36% (compared to 73% in derivation
cohort)
 Spec 96%
 LR 9.0
 PPV 88%
 NPV 61%

Since Sgarbossa
Kontos et al. Annals of Emergency Medicine Vol 37,
no.5, 2001.
– Prospective evaluation of all chest pain patients (n=7725)
– 2.4% LBBB (n=182)
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AMI in 13% of these (n=24)
– Sgarbossa performance
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Concordant STE 1mm [sens 8%, spec 100% (98-100)]
– PPV 100 (33-100), NPV 88 (82-92)
STD 1mm in V1-3 [sens 17%, spec 100% (98-100]
– PPV 100 (50-100), NPV 89 (83-93)
STE discordant 5mm [sens 21, spec 93 (88-96)]
– PPV 31 (14-56), NPV 89 (83-96)
Sgarbossa and Kontos
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Comments and Take Home
– Low prevalence of AMI in pts with LBBB
– ECG criteria occur infrequently and have low PPV

Only 11/24 of AMI with LBBB met 1 of the 3 criteria
– Highest specificity criteria was >1mm
concordant STE
– Very few (approx 3%) meet any of the criteria
– Cannot use as rule-out test
Case
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67F with 3hrs RSCP
– ECG is non-specific
– TnT neg
Troponin T
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Test
Characteristics
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Troponin: increase levels?
– Ischemia/ infarction
– Cardiomyopathy
– Electrical injury
– Pericarditis
– Myocarditis
– Cardiac contusion
– Hypertensive
emergencies
– End- stage renal failure
– Pulmonary embolus
Troponin T
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Time to detection
– 2-6hrs
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Peaks
– 10hrs to 24hrs
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Time to normalisation
– 10-15days
Troponin
100
90
80
70
60
50
40
30
20
10
0
0.1
0.2
0
2hr
4hr
6hr
8hr
10hr
12hr
Troponin T
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Troponin should NOT determine disposition
General Numbers to remember
– 6 -----------------> 60% sensitive
– 8 -----------------> 80% sensitive
– 10 -----------------> 90% sensitive
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Patients with TnT + and CKMB – have worse
prognosis (increased death and CV events
at 30 days)
Case

55M with ESRD
– HD 3/week
– No previous IHD
– Cath 4 years ago demonstrated nonocclusive disease
– 6hrs atypical chest pain
– TnT .15
TnT in RF
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
Tricky
Some research in the area
Starting points
– Cardiovascular death makes up 50% of death in
ESRD
– Prevalence of CAD is approx 75%
– Higher risk of silent ischemia and atypical
presentations
– ECG may also be difficult to interpret d/t LVH
TnT in RF

Hypotheses on why elevated
– Uremic cardiomyopathy
– Clinically silent micro-infarctions
– LVH
– Unlikely d/t decreased renal clearance
Similar molecular wt as albumin
 Post-Tx still have elevated TnT

TnT in RF

Elevation: What does it mean?
– No true GS of IHD in ESRD
Lower sens/spec of stress testing
 Less prevalence of cath in this population
 Have to rely on outcomes

TnT in RF:
Elevation: What does it
mean? No suspicion of ACS.
– Significant difference in 1 yr cardiovascular
mortality >0.1
Nephrol Dial Transplant 1999;14:1961–7
– 102 patients with ESRD without any clinical
evidence of acute ischemic heart disease
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Troponin T > 0.1 ng/ml was strongly associated with
all cause mortality
TnT 0.05 ng/ml was associated with fatal
cardiovascular events.
– This association was independent of baseline presence
of heart disease.

All patients with non-detectable TnT were alive at
follow up.
Circulation 2000; 102:1964–9
TnT in RF:
Elevation: What does it
mean? No suspicion of ACS.
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
244 patients on chronic hemodialysis for up
to 34 months.
Troponin T significantly associated with
death from all causes
– strongest association for TnT values above 0.1
– A trend of increasing TnT measurements during
longitudinal follow up was also predictive of
progression of cardiac disease and all-cause
mortality
TnT in RF:
Elevation: What does it
mean? Suspicion of ACS.

7,033 patients from the GUSTO-IV
– prognostic value of cardiac TnT was not
diminished in patients presenting with
renal insufficiency and suspected ACS
– Patients with positive TnT and renal
insufficiency had the highest overall risk
of cardiac death or acute MI
N Engl J Med 2002;346:2047-52.
TnT in RF:
Elevation: What does it
mean? Suspicion of ACS.
TnT in RF:
Elevation: What does it
mean? Suspicion of ACS.
TnT in RF:
Elevation: What does it
mean? Suspicion of ACS.
Case

60M with chest pain for 12hrs
– STE anteriorly
– BP 80/50, HR= 120
– Sats 90% NRB
Cardiogenic shock
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Complicates 7-10% of AMI
70-80% mortality
Diagnosis:
– SBP< 90mmHg
– Evidence of end organ hypoperfusion
(cool extremities, oliguria, altered
mentation)
Management –
cardiogenic shock

Oxygenation and ventilation

Improve systolic function
– Catecholamines (dopamine, dobutamine
if BP tolerates)
– IABP

revascularization
Cardiogenic shock – PTCA vs
lytic
SHOCK (1999)
 RCT PTCA vs lytic, N= 302
 2.7% cross over to PTCA group within
54 hrs
 9.8% ARR at 30 day mortality (not
stat sig)
 13% ARR at 6 month mortality (NNT
= 8)
Pre-hospital Lytics

45M with 45mins severe RSCP
– Medics patch in that this guy has
widespread anterior STE and they want
to give lytic
– Transport time 30-45mins
– What do you say?
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<6hrs chest pain
N=840 to PCI or
pre-hospital lytic
Pre-specified subgroups
– <2hrs, >2hrs