Some basics, some reviews, some new. Review of litterature backing up what we do All based on Sept 2000 AHA-ACC recommendations on UA and NTSEMI with addition of last year trials and practical points.
Backbone of my lecture www.acc.org
Various progression of acute coronary syndrome
25% progress to Q-wave MI ie transmural infarction
Combination of 5 components leading to myocardial ischemia Mechanical + dynamic obstruction, inflammation, acute thrombosis and incr demand Most common UA: atherosclerosis and unstable plaque (60 + 30%) Printzmetal angina: atheroscledoris and vasospasm (30 + 60%)
Clinical markers fro high-intermediate-low risk for UA patient Dated 1994 No clinical correlation Still in 2000 guideline Age&gt;70 Biphasic + troponin level High risk = real positivity
Biphasic T waves in leads V2 and V3 or symmetric, often deeply inverted T waves in leads V2 and V3.
Troponin essay are antibody against specific part of the troponin molecule
Relationship of troponin to mortality. Same for troponin T ?high trop normal CKs Ck still gold standard for early reinfarction Use trop I at the RVH and trop T at the MGH
Normal, abnormal, high (0.01-0.099-0.1)
Lancet editorial of this week says the same thing…
Clear difference between true Mi and only UA but since clinically a continuum + potential difficulty at “educating” the MDs.
41 yo woman, 3 days post liposuction
You diagnosed it, ltes treat it Management of UA/NSTEMI Let’s walk through it… Nothing new Oxygen: only if sign of cyanosis or O2 sat below 90%
Diltiazem if B-blocker contraindicated + no depressed LV function ACEi if -hypertensive despite nitrate/b-blocker in the face of CHF –depressed systolic function -diabetes All level B or C evidence. CCB after maxed out on nitrates and b-Blockers IABp for sevre ongoing or recurrent ischemia despite maximal medical management. Long acting Nondihydropyridne instead of b-BLOCKERS Dihydropyridine : Nefidipine, amlodipine.
No evidence to back inclusion of high risk features.
4 modes of action B-blocker to prevent incr HR thereby incr MVO2 Use unless contraindication (viagra) Ceiling of 200u/min (300-400 X 3-4 weeks have not incr methg) ISSIS-4 Gissi-3 failed to show improved survival.
No RCT Endothelin-1 causes platelets activation EP-1 which degrades endothelin 1 concentration (2.5 – 1.7 products) (2.5), (0.8 –1.3 by-products) (0.9) 68 QwMI and 29 volunteers
No study to back iv vs po form
No good trial, just expert opinion
Great drug! But…
Adalat and norvasc Short acting adalat only when appropriatly B-blocked Danish study group on verapamil in Myocardial infarction Holland interuniversity nifedipine/metoprolol trial Good if already on B-blocker
Plavix and ticlid
Needs ISIS-2 study; 1988 ASA or streptokinase or both or neither
Primary outcome:MI, stroke, death Second number: Primary outcome + refractory ischemia After 3000 pts, switch from (no ST change or + hx of CAD) to (+ st changes or + markers) Not in McGill due to Gp2b3a + angio available… answer from all the cardiologists I asked to
Theroux used fixed dose heparin, ASA did not had anything more except risk of bleeding 460 pts
F2 (thrombin is most important) but f10 also is necessary Prediction is what is important
Pentasaccharide binds to antithrombin, needs &gt;18 saccharides to inactivate thrombin
Dalteparin (Fragmin): nonsignifcant incr end point at day 6 but subgroup analysis showed decr mortality at 6 days (6% vs 2.5%) and 40 days (14.2 vs 7.4%) in trop positive patients. Essence: enoxaparin (lovenox): 16.6% vs 19.8% at 14 days but non-weight adjusted UFH only 46% properly anticoagulated at 24hr. TIMI 11B: iv bolus LMWH + sc, MI-death at 8 days non-significant (6.9 to 5.7%) ST changes or + markers after first 700 pts (hx of CAD and CP was initially included. Composite end-point (14.5 to 12.5%) in 3910 pts
Resume of antithrombotics trials: can notice decreasing effects of added therapy on overall risk ratio. ASA vs placebo Addition of heparin Addition og GPIIb/IIIa
Conflicting results between Gusto2b and Timi9b
Prevents progression of white clot to red clots by preventing platelets aggregation through fibrinogen to form thrombus
Composite end points
Very good numbers for PCI and hard to dispute but irrelevant to ER Focus is on prism-plus and pursuit Overall 2% absolute decrease death or MI
3200 pts On average, PTT was around 80
Subgroup analysis showing good for + markers Same for trop T Independent of revascularization procedures (PCI or CABG) Heparin with + trop do worst (on right)
1900 pts Composite end-point:MI, death, refractory ischemia Non-weight based heparin NNT: 20 to 25
22 end-points: 3 strong &lt;0.01, 8 weaker 0.01 to 0.05
Major bleed: 5 gr of Hgb Cath rate: North America 79% Western Europe 58% Eastern Europe 20%
GP2b/3a if no cath lab???
Not proof that everything is time dependent as in thrombolysis
Risk factors for CAD: HTN, diabetes, current smoker, family hx of CAD, hypercholesterolemia Coronary stenosis: still valid model if do not know the answer Severe anginal symptoms: 2 or more episodes within 24 hrs CKMD or troponin
People (some cardiologist) want o use GP 2b/3a inh when score is 5 or above
Subgroup analysis of UFH vs LMW heparin; different slope
Level 5 since database group was comparing UFH to LMW heparin…
Personnalize TIMI risk program Do it slowly
From international group ECG changes or hx of CAD (no markers) Fairly good but not perfect: B-blocker 40% miss, 15% decr mortality = 6% gain Nitrates is highlighted because if CP + heparin + nitro = GP2b/3a inh
TACTICS: 97% cath vs 51% cath = 520 extra pts got cath CEP: death, MI, readmission for ACS within 6 months
11% at 6 months
1 nothing 2 stented 3 stent or CABG 4 CABG
Just to let you know
Is it really justify???
? Definition of UA vs NSTEMI
Cocaine coronary blood flow: from 140 to 120 (down to 100 with propranolol)
NSTEMI AND ANTITHOMBOTICS 1
Dr. Gilbert Boucher
R4 Emergency Medicine
• Review definitions of Non-ST-elevation
Myocardial infraction and related items.
• Prognostic factors.
• Current therapies.
• Special cases.
October 4 , 2001
Practice Guidelines: Atherosclerotic Cardiovascular Disease
September 1 , 2001
Practice Guidelines: Atrial Fibrillation
April 27 , 2001
Practice Guidelines: Percutaneous Coronary Intervention
April 27 , 2001
Expert Consensus Document: Catheterization Laboratory Standard
April 3 , 2001
Consensus Conference Report: Care of the Patient with Adult Congenital Heart Disease
April 2 , 2001
Expert Consensus Document: Standards for Acquisition, Measurement and Reporting of Intravascular Ultrasound
March 1, 2001
Teaching Slides: ACC/AHA Guidelines for the Management of Unstable Angina and Non-ST-Segment Elevation
January 1, 2001
Consensus Conference Report: Mechanical Cardiac Support 2000: Current Applications and Future Trial Design
November 1, 2000
Clinical Competence Statement: Invasive Electrophysiology Studies, Catheter Ablation, and Cardioversion
October 1, 2000
Clinical Competence Statement: Stress Testing
September 1, 2000
Practice Guidelines: Management of Patients with Unstable Angina and Non-ST-Segment Elevation Myocardial
September 1, 2000
Consensus Conference Report: Myocardial Infarction Redefined—A Consensus Document of the Joint European
Society of Cardiology/American College of Cardiology Committee for the Redefinition of Myocardial Infarction
July 1, 2000
Expert Consensus Document: Electron-Beam Computed Tomography for the Diagnosis and Prognosis of Coronary
June 1, 2000
Training Statement: Adult Cardiovascular Medicine (COCATS) Revised 6/00 Task Force #5: Training in Nuclear
ACUTE CORONARY SYNDROMEACUTE CORONARY SYNDROME
No ST ElevationNo ST Elevation ST ElevationST ElevationST ElevationST Elevation
Unstable Angina NQMI QwMI
acute, evolving, recent
Typical rise and gradual fall (troponin) or more
rapid rise and fall (CK-MB) of biochemical
markers of myocardial necrosis with at least
one of the following:
– a) ischemic symptoms;
– b) development of pathologic Q waves on the ECG;
– c) ECG changes indicative of ischemia (ST segment
elevation or depression); or
– d) coronary artery intervention (e.g., coronary angio-
• NSTEMI is an acute process of myocardial
ischemia with sufficient severity and
duration to result in myocardial necrosis.
• The initial ECG in patients with NSTEMI
does not show ST-segment elevation.
• NSTEMI is distinguished from UA by the
detection of cardiac markers indicative of
myocardial necrosis in NSTEMI and the
absence of abnormal elevation of such
biomarkers in patients with UA.
Definition: NSTEMIDefinition: NSTEMI
Definition: unstable angina
• Unstable angina—an acute process of
myocardial ischemia that is not of
sufficient severity and duration to result in
– Do not release biomarkers indicative of
myocardial necrosis into the blood.
Rest Angina* Angina occurring at rest and prolonged,
usually > 20 minutes
New-onset Angina New-onset angina of at least CCS Class III
Increasing Angina Previously diagnosed angina that has
become distinctly more frequent, longer in
duration, or lower in threshold (i.e.,
increased by > 1 CCS)class to at
least CCS Class III severity.
* Pts with NSTEMI usually present with angina at rest.
Circulation 80:410; 1989
The simplified criteria for Wellens' syndrome are as follows:
Prior history of chest pain
Little or no cardiac enzyme elevation
No pathologic precordial Q waves
Little or no ST-segment elevation
No loss of precordial R waves
Biphasic T waves in leads V2
or symmetric, often
deeply inverted T waves in leads V2
Wellens' criteria are quite specific for left anterior descending
artery disease. All of the patients (n=180) in his 1988 study had
more than 50% narrowing of the left anterior descending artery
(mean=85% narrowing) with complete or near-complete
occlusion in 59%.
• I vs T…
– Troponin I does not accumulate in renal failure
– Different assays of same troponin have different
values due to different isotopes of antibodies
• Very sensitive
– Estimate that 30% of patients with U/A are now
diagnosed with NSTEMI due to elevated troponins
• High correlation with death, being primary
cardiac or not…
• Clin Chem 2000 46: 650-657.
– 46 pts with septic shock
– 36-50% had + trops
– 12 pts nonsurvivors: negative autopsy for necrosis
– Associated with severe LV dysfunction.
• Clin Chem 2001 47: 412-417
– 244 pts, chronic hemodialysis, troponin T
– Higher trops or increasing trops associated with
• 6%, 43%, and 59% total death.
• in 0%, 14%, and 24% cardiac death
• Clin Chem 1999:National Academy of Clinical Biochemistry
Standards of Laboratory Practice: Recommendations for the Use of
Cardiac Markers in Coronary Artery Diseases
• Troponin I can be falsely elevated due to fibrin
clot, heterophilic antibodies.
• Use of 2 cut-offs point would require too much
– AHA needs to better define NSTEMI due to important
implication of being diagnosed with MI.
Figure 1. Plot of the appearance of cardiac markers in blood vs
time after onset of symptoms.
Peak A, early release of myoglobin or CK-MB isoforms after
AMI; peak B, cardiac troponin after AMI; peak C, CK-MB after
AMI; peak D, cardiac troponin after unstable angina. Data are
plotted on a relative scale, where 1.0 is set at the AMI cutoff
• Delta values at 2 hours could proved to be very
– 2 hour delta CK-MB 88% sens vs delta trop I 61%
• Specificity of 96%
• ?early marker for more aggressive treatment
Am J Emerg Med - 2000 Jan
• CRP: JACC 1998 Jun out of TIMI-11a
– Neg trop but pos CRP = 5.8% death
– Neg trop and neg CRP = 0.36% death
– Pos trop and CRP = 9.1% death
• Class I:
– Aspirin, Nitrate, B-blockers, morphine, O2 (prn).
– Nondihydropyridine (cardizem/verapamil).
– ACEi for specifics.
• Class 2a:
– ACEi for all.
– Long-acting CCB for recurrent ischemia.
– IABP if all fails.
• Class 2b:
– Extended form of Nondihydropyridine.
– Short acting dihydropyridine in the presence of B-
– Resp distress
– High risk features
• Consume resources
• Evidence is lacking.
Nitrates: Decr MVO2, incr coronaries
– Dilate venous bed: decr preload and ventricular wall
– Smaller dilatation of arterial system: decr afterload
and ventricular wall tension.
• Need B-blocker
– Dilatation of atherosclerotic coronaries
– Decreased platelets adhesiveness.
– ischemia despite nitro X 3 and iv B-blockade
– high-risk patients (non-hypotensive).
• Prethrombolytics: 35% mortality reduction.
• Potent anxiolytic and analgesic action
• Potentially beneficial
– Venous dilatation
– Decr HR
– Decr sBP (Decr MVO2)
– Activates neutral endopeptidases
• Ann Emerg Med. May 2001;37:445-449.
• Nausea and vomiting in 20%
• Meperidine if allergic
• Decr sBP
• Decr SA node rate, contractility, AV node
• Incr diastole filling time.
• iv form for high-risk pts/on going pain.
• Oral for intermediate/low risks patients.
• No preferred agents except better if B-blocker
without ISA (metoprolol, atenolol, propramolol,
• Contraindications (consensus):
degre AV block >24 msec
degre AV block without pacemaker
– Severe LV dysfunction with CHF
• Caution with:
– Bradycardia <50
– Hypotension <90
• Goal is bpm of 50-60 unless side-effects
• 13% reduction of progression of UA to
• Extrapolate data from use in AMI, recent
MI, stable angina, heart failure.
Calcium channel blockers
• Dihydropyridines: nifedipine and amlodipine
– peripheral vasodilatation
• Verapamil: DAVIT study (3200 pts)
– Only favorable trend
• Nifedipine: HINT study (500 pts)
– Incr MI by 16%, decr by 20% if with metoprolol
– But… metoprolol alone decr by 24%!!!
• Diltiazem showed trends of improved outcome
– CKMB level, reinfarction rate
– Same mortality
• … except in LV dysfunction ACS
Calcium channel blockers
– Good symptom reliever
– Trend of improved outcome with non-
• To use if unable to use B-blockers
• Aspirin ASAP!
– Thienopyridine (clopidogrel or ticlopidine) if
hypersensitivity of major GI intolerance
• Cyclooxygenase-1 inhibitor
– Prevents thromboxane A2 formation
• Dosing: 160 mg or 325 mg
– Based on ISIS-2 which definetly established
• Can use pr route.
• Clopidogrel acts faster than ticlopidine.
• Ticlodipine: Gi se, neutropenia, TTP
• Clopidogrel: minimal rash and diarrhea
– 11 TTP within 14 days (3 millions pts)
• CURE study: NEJM Aug 2001
– 12000 pts, plavix 300mg po
– 9.3 vs 11.4, 16.5 vs 18.8
– ST changes or + markers
– No GP2b3a inh or angio
Safety if angio or used with
• Lancet August 2001: PCI-CURE study
• 2600 pts.
• Plavix 300mg loading
• No increased bleeding problem whether
plavix +/- GPIIb/IIIa inh were used.
• Better outcome before an after PCI.
Other po agents
• Oral GP IIB/IIIA inhibitor:
– 4 studies: 1 PCI, 3 NSTEMI
• 2 increased mortality
• None presently recommended
• Activates antithrombin III
– Inactives thrombin (f2), f9a and f10a
• Molecular weight: 5 000 to 30 000 D
• Binds to various proteins, cells , endothelium
– Weight adjusted dosage
• Incr need in DM and smoking, lower with age
• Theroux et al. N Engl J Med 1988;319:1105–
– MI rate of 12% down to 0.8% in UA
• Molecular weight of 4200 to 6000 D
• Factor Xa to thrombin inhibition ratio of
1.9 to 3.8
• Only 25-50% have >18 saccharides
– both f2 and 10 inhibition
– Rest inhibits only factor Xa
• Can only reverse about 60% of anticoagulation
• Increase rate of minor bleeding (9.1% vs 2.5%)
• Cannot monitor ACT during PCI, needs to stop
12 hours pre CABG.
• Not for renal failure patients (GFR<30cc/min)
• Decreased incidence of HIT.
• >100kg: ?maximum of dosing vs study dosing
– Enoxaparin 100mg sc bid vs weight all the way as in
But going to cath lab…
• Start UFH without bolus 6 hours after last
• If go to cath lab, consider pt fully
anticoagulated when giving heparin
boluses – unable to monitor.
• If on UFH, wait 1 hour then give LMW
• Direct thrombin inhibtor.
• For patients with HIT or history of.
• Binds directly to catalytic site of thrombin
without going through antithrombin III
• TIMI 7: better than ASA alone in UA…
• Mild improvement compared to UFH but
increase in bleeding, no benefit in STEMI.
• Meta-analysis shows OR of 0.90
Platelet GP IIb/IIIa Receptor Antagonists
• Activation of platelets leads to
configurational change increasing affinity
for fibrin and other ligands
• Necessary final step to platelets
• Needs 80% blockade to achieve potent
GP IIb/IIIa Receptor Antagonists.
• Abciximab (reopro): non-specific binding
– Unclear significance
• Eptifibatide (integrilin), tirofiban (aggrastat):
very specific binding achieve >80% within 5
• Different antagonists can bind at different sites
and can paradoxically activates the GPIIb/IIIa
– ?what is happening with the oral form.
GP IIb/IIIa Receptor Antagonists
• 4 main studies
• 2 positives
• High-risk features
• 11.7% vs 8.7%,
• 15.7% vs 14.2%
• PRISM:Platelet Receptor Inhibition in Ischemic
– heparin (non-weight based) vs tiroban X 48hrs
ECG changes or enzymes or very strong hx of
Composite end-point better at 48hr but only
trend at 30 days.
MI/death: non-significant at 48 hrs but + at 30
days (3.6 vs 2.3%).
PRISM: Lancet 1999
Figure 1: Adjusted hazard ratios (95%
CI) for treatment with tirofiban by
troponin I quartiles
Figure 2: Event-rate curves
infarction) for 30-day follow-
up for patients with + troponin
• Prism-plus: Platelet Receptor Inhibition in
Ischemic Syndrome Management in Patients
Limited by Unstable Signs and Symptoms
• THE study
• ST changes or + enzymes
• Tiroban alone dropped due to too much
– 4.6% vs 1.1 and 1.5%??? (remember PRISM study)
• At 7 days, composite end-point: 17.9% vs
• 22% CEP reduction at 30 days (absolute 3.8%)
• PURSUIT: Eptifibatide
– Platelet Glycoprotein IIb/IIIa in Unstable
Angina:Receptor Suppression Using Integrilin
– 11 000 pts
– + ECG changes or enzymes rise
• Death or MI at 30 days: 15.7% vs 14.2%
– 9.1% vs 7.6% at 4 days
– 11.6% vs 10.1% at 7 days
– Major bleed increased by 1.5%
• Cath rate overall: 60%
• GUSTO IV:Lancet June 2001
• Abciximab: 7800 pts without PCI
• Same mortality at 30 days: 8-9%
– Despite all sorts of subgroup analysis…
Cardiogenic shock… BAD!!!
• Circulation 1999: GUSTO IIb
• 200 pts with NSTEMI and shock
– Incidence of 2.5%
• 73% mortality
• But median time to shock 76 hrs…
– 9.6 hrs in STEMI
• Journal of Emergency Medicine
– “The effect of early ED treatment with
GPIIb/IIIa inhibitors has never been formally
studied until now”.
– EARLY trial will compare early ED, vs late
CCU vs catheterization laboratory
• JAMA, August 16, 2000
• Databases of ESSENCE and TIMI11B
• 12 variables, 7 significants
– Age > 65yo
– 3 risk factors for CAD
– Prior coronary stenosis of > 50%
– St deviation
– Severe angina symptoms
– ASA use within 7 days
– Elevated serum cardiac markers
Figure 1. TIMI Risk Score
Rates of all-cause mortality, myocardial infarction, and severe recurrent ischemia prompting urgent
revascularization through 14 days after randomization were calculated for various patient subgroups based on
the number of risk factors present in the test cohort (the unfractionated heparin group in the Thrombolysis in
Myocardial Infarction [TIMI] 11B trial; n = 1957) (see Table 1). Event rates increased significantly as the TIMI risk
score increased (P<.001 by
•GP IIb/IIIa inh for score 5 or above???
Figure 2. Validation of TIMI Risk Score and Assessment of Treatment Effect According to Score
Rates of all-cause mortality, myocardial infarction, and severe recurrent ischemia prompting urgent revascularization through 14 days
after randomization were calculated for the enoxaparin and unfractionated heparin groups in the Thrombolysis in Myocardial Infarction
(TIMI) 11B trial and the Efficacy and Safety of Subcutaneous Enoxaparin in Unstable Angina and Non-Q-Wave MI trial (ESSENCE),
based on the TIMI risk score. The pattern of increasing event rates with increasing TIMI risk score was confirmed in all 3 validation
cohorts (P<.001 by
for trend). C statistics were 0.65 for the unfractionated heparin group and 0.61 for the enoxaparin group in TIMI
11B; and 0.65 for the unfractionated heparin group and 0.59 for the enoxaparin group in ESSENCE. The rate of increase in events as
more risk factors were present was significantly lower in the enoxaparin group in both studies (for TIMI 11B, P = .01; for ESSENCE, P = .
03). Positive values for absolute risk difference (ARD) and number needed to treat to prevent 1 event (NNT) indicate calculations favoring
enoxaparin, while negative values indicate calculations favoring unfractionated heparin.
As Dr. Lang would said…
• Auto-validation on its own cohort
• Specific (but large) group
• That would make it a level…4 if we want to use
it as a Clinical decision rule to know whether or
not to use GP IIb/IIIa inhibitors.
TIMI Risk Calculator For
In the blue column, please enter the patient's
age, and then answer each clinical question
with a Y (for yes) or an N (for no). The patient's
risk appears at the bottom of the blue column.
TIMI Risk Score for UA/NSTEMI Entry Score
History of Hypertension (Y or N) 0
History of Diabetes (Y or N) 0
Current Smoker (Y or N) 0
Hypercholesterolemia (Y or N) 0
Family history of Coronary Artery Disease (Y or N) 0
Prior angiographic stenosis >50% (Y or N) 0
Severe anginal symptoms (>= 2 episodes rest pain in past 24 hrs) (Y or N) 0
Use of aspirin within the last 7 days (Y or N) 0
Elevated cardiac markers (either CKMB or cardiac troponin) (Y or N) 0
ST deviation (horizontal ST depression or transient ST elevation >= 1 mm) (Y or N) 0
Total Risk Score (0-7) 1
Risk of Death/MI/Urgent Revascularization by 14 Days (%) 4.70%
• Tiroban: 950$/3 days
• Abciximab: 2000$/treatment
– But how come we are almost never using
streptokinase anymore… are we
Plavix vs GP IIb/IIIa?
18.8% vs 16.5%
17.9 vs 12.9%
JUST a thought …
But back to standard of care…
The classics: How do we do?
• In-hospital drugs treatment (%), 1998
USA Canada World
Intravenous heparin 79 88 73
Aspirin 91 92 92
B-blockers 57 73 63
Calcium antagonists 59 53 53
Intravenous nitrates 68 40 51
Angio: stat or later
• TACTICS: N Engl J Med 2001; 344:1879-1887, Jun
2220 patients, within 48 hours vs selectively
all got ASA, heparin, GPIIb/IIIa inh
15.9% vs 19.4% at 6 months
6% more CABG, 520 extra caths/1100 pts
MI: 4.8% vs 6.9%
• Pre GPIIb/IIIa inhibitors: TIMI3b (1995)
• Early 18.1% vs 16.2% late
• Decr length of stay
• VANQWISH Investigators: 920 pts
• Early 7.8% vs 3.3% late at hospital discharge
More does not equal better
• Lancet 1998; 352: 507–14
• 8 000 pts, various countries (Brazil, USA,
Canada, Australia, Hungary, Poland)
– 59% vs 21% angio rate
– Same overall MI/death rate: 4.7% at 7 days
• Late angio: decreased rate of overall
cardiovascular event (including stroke) despite
higher recurrent angina
What do we find anyway on
• Typically shows the following profile:
– 1) no severe epicardial stenosis in 10% to
– 2) 1-vessel stenosis in 30% to 35%
– 3) multivessel stenosis in 40% to 50%
– 4) significant (.50%) left main stenosis in 4%
Next: early statin???!!!…
• Myocardial Ischemia Reduction with Aggressive
Cholesterol Lowering (MIRACL)
• JAMA April 2001
• 2000 pts
• Atorvastatin 80mg/d between 24 and 96hrs of
• 17.4% vs 14.8% at 4 months, mostly recurrent
symptomatic ischemia requiring rehospitalization.
Noninvasive stress testing in low-
risk patients who have been free of
ischemia at rest or with low-level
activity and of CHF for a minimum
of 12 to 24 h. (Level of Evidence:
• Stress test only if free of:
– ST-segment abnormalities
– bundle-branch block
– LV hypertrophy
– Intraventricular conduction defect
– Paced rhythm
– Digoxin effect.
Otherwise need imaging: echo or
• Women: more atypical symptoms
– ?better outcome in UA then men
• Elderly: More disease
• Diabetics: Increased risk for any ACS
• Post-CABG: low threshold angio
• All same protocols and numbers…
• Coronary vasospasms
– Worsen by minimal atherosclerosis
– Reversed by CCB
– ST-changes in 38% of pts in detox centers
• Detoxify by cholinesterase in liver and plasma
– Less available in infants or elderly
• Increased platelets sensibility
• Decrease antithrombin III and protein C
Cocaine users as per AHA
• NTG and CCB for ST changes
• Angio if persistent ST elevation or if
– Thrombolysis if not available
• B-blockers if sBp > 150 or HR > 100
– Labetolol preferred
B-blockers for cocaine
Annals of Internal Medicine. Jun 1990
• In cath lab
• Cocaine followed by propranolol
• No change in Hr or BP but:
– 50% incr in coronary resistance with 20% decr in flow
No mention of benzos???????
• Troponemia is a bad sign.
• Lots of studies/numbers out there
• Stratification is probably the way to go to
target selected population but can we
rely on present evidences…