Acute

Acute Coronary
Coronary Syndromes
Syndromes #1
#1

Management of Acute STEMI

 Prevalence of total coronary occlusion during the early
hours of transmural myocardial infarction
MA DeWood, J Spores, R Notske, LT Mouser, R
1980 Burroughs, MS Golden, and HT Lang
To define the prevalence of total coronary occlusion in the
hours after transmural myocardial infarction, we used
coronary arteriography to study the degree of coronary
obstruction in 322 patients admitted within 24 hours of
infarction. Total coronary occlusion was observed in
110 of 126 patients (87 per cent) who presented within
4 hoursthis proportion decreased significantly, to 37
of 57 (65 per cent), when patients were studied 12 to 24
hours after the onset of symptoms. Among 59 patients
with angiographic features of coronary thrombosis, the
thrombus was retrieved by Fogarty catheter in 52 (88
per cent) Thus, total coronary occlusion is frequent
during the early hours of transmural infarction and
decreases in frequency during the initial 24 hours,
suggesting that coronary spasm or thrombus formation
with subsequent recanalization or both may be
important in the evolution of infarction.
 Historical Perspective:
Acute Coronary Syndromes
1980: Paradigm shift Angioscopy provides
proof that ACS results from sudden thrombotic
events, not gradual plaque accumulation -
1.5 million per year

750,000 admissions

750,000 admissions

Cairns et al, Can J Cardiol 1996; 12:1279

Spectrum of Acute Coronary Syndromes

ACUTE CORONARY SYNDROME

No ST Elevation ST Elevation

NSTEMI

Unstable Angina NQMI Q wave

Myocardial Infarction
 Myocardial Infarction
Overview

Estimated 200-300,000 sudden (out-of-hospital)

deaths per year in U.S.
Approximately 1 million hospitalizations for MI per
year in U.S.
Absolute number of MI events and fatality rates
declining
Remains principal cause of death in Western
world
Management of Acute STEMI
Diagnosis
Risk Stratification
Acute Therapy
Reperfusion
Adjunctive
Complications
Pre-Discharge
Management
 Acute Myocardial Infarction:
Definition
A rise and fall ( above normal) of cardiac-specific enzymes
( CPK-MB or troponin) and either one of the following:

Prolonged ischemic pain

Pathologic Q-waves on ECG
Ischemic ST segment abnormalities on
ECG
 Time Course of Enzyme Markers
Myoglobin CK-MB Troponin I MB Isoforms Troponin T
1000
Relative Marker Increase

100

10
Upper Reference Interval
1

0
0 12 24 36 48 60 72
Hours After Chest Pain Onset
Antman EM. In: Braunwald E, ed. Heart Disease: A Textbook in Cardiovascular Medicine, 5th ed. Philadelphia, Pa: WB
Saunders; 1997.
 Cardiac Biomarkers in STEMI

100
Multiples of the URL

50
Cardiac troponin-no reperfusion
20 Cardiac troponin-reperfusion
10 CKMB-no reperfusion
CKMB-reperfusion
5

2
Upper reference limit
1

0 1 2 3 4 5 6 7 8
URL = 99th %tile of
Days After Onset of STEMI Reference Control Group

Alpert et al. J Am Coll Cardiol 2000;36:959.

Wu et al. Clin Chem 1999;45:1104.
Management of Acute STEMI
Diagnosis
Risk Stratification
Acute Therapy
Reperfusion
Adjunctive
Complications
Pre-Discharge
Management
 Acute MI
Impact of Ejection Fraction on Mortality
5500%
%
Mortality (2-Year)
4400%
%

3300%
%

2200%
%

1100%
%

00
2200 3300 4
400 5500 6600 7
700
E je c tio n F ra c tio n (% )
Gottlieb et al. Am J Cardiol 1992;69:977-984
 Long Term Survival After Myocardial
Infarction: Importance of Patent Infarct
Related Artery

SAVE study Lamas et al Circ 1995;92:1101

Predictors of In-hospital Mortality in STEMI

(n = 84,663)
Odds Ratio
Prior CHF +
Diabetes +
Female +
Prior stroke +
Anterior MI +
Killip 3 +
Age 65-75
+
Age > 75
Killip 4
ll
0 1 2 3 4 5 16 17 18 19 20
Barron, Circ 97:1150, 98
 Acute MI - Risk Stratification
Hemodynamic Subgroups - Killip Class

GISSI-1 (%)
Killip Definition Incidence Control Lytic
Class Mortality
Mortality
I No CHF 71 7.3 5.9
II S3 gallop or 23 19.9 16.1
basilar rales
III Pulmonary edema 4 39.0 33.0
(rales >1/2 up)
IV Cardiogenic shock 2 70.1 69.9
 TIMI RISK SCORE for STEMI

HISTORICAL POINTS RISK 30-DAY MORTALITY

Age 75 3 SCORE IN InTIME II(%)*
65-74 2 0 0.8
DM or HTN or angina 1 1 1.6
EXAM
2 2.2
3 4.4
SBP < 100 mmHg 3
4 7.3
HR >100 bpm 2 5 12
Killip II-IV 2 6 16
Weight < 67 kg (150 lb) 1 7 23
8 27
PRESENTATION >8 36
Anterior STE or LBBB 1
Time to Rx > 4 hrs 1
*Entry criteria: CP > 30 min, ST , sx onset < 6hrs,
RISK SCORE = Total points (0 -14) fibrinolytic-eligible

Morrow et al. Circulation 2000;

For more info go to www.timi.org 102:2031-7
Management of Acute STEMI
Diagnosis
Risk Stratification
Acute Therapy
Reperfusion
Adjunctive
Complications
Pre-Discharge
Management
 Myocardial Reperfusion
The Original Paradigm

Re -establish
Re-establish
Limit Infarct
Infarct Vessel Mortality
Size
Patency
 Historical Perspective: Thrombolytic
Therapy
1980s: Paradigm Shift leads
to Novel Therapeutic
Approaches
Major Breakthrough
c/w Placebo, thrombolytics
for STEMI resulted in:
Greater IRA patency
Improved Function
Improved blood flow
Decreased Ischemia
Lower Mortality

ISIS-2 Lancet 2(349) 1988

 Acute MI

TIMI Perfusion Grades

Grade
0 No flow
1 Minimal flow or
incomplete filling of vessel
2 Delayed but complete filling of vessel
3 Normal flow
 Long Term Survival After Myocardial Infarction:
Benefits from Thrombolysis is Observed in
Patients with TIMI 3, not TIMI 2 Flow

Lenderink et al Circulation 92: 1110-1116

 Myocardial Reperfusion
The New Paradigm

Re -establish
Re-establish Limit Infarct
Infarct Vessel Size Mortality
Patency and and Restore
Restore Flow Microvascualar Flow
Thrombolysis in Acute MI: Limitations

No diagnostic confirmation (15% non-occluded)

0.5-2.0% life threatening bleeds
Coronary anatomy not defined
Hemodynamic data not available
Uncertainty of Reperfusion ( ? 60% )
TIMI 3 flow restored in only 50% of patients
Reocclusion occurs in 15%
No Benefit in Cardiogenic Shock
 Thrombolysis in Acute STEMI
Relative Contraindications
Uncontrolled HTN (BP > 180/110) on presentation
History prior CVA beyond 1 yr
Anticoagulant Rx with INR > 2-3; bleeding
diathesis
Recent trauma (within 2-4 wks)
Noncompressible vascular punctures
Recent internal bleeding (within 2-4 wks)
Pregnancy
Active peptic ulcer
Prior exposure (5 day - 2 yr) for SK or APSAC
Thrombolysis in Acute STEMI
Absolute Contraindications

Previous hemorrhagic stroke

CVA within previous yr

Intracranial neoplasia or AVM

Active internal bleeding (not

menses)

Suspected aortic dissection

Reperfusion Strategies in STEMI
Reperfusion
Reperfusion

11oo PCI
PCI Thrombolysis
Thrombolysis Facilitated
Facilitated

Salvage/Rescue
Salvage/Rescue
 Initial Randomized Trials: PAMI

Reinfarction Free Survival 395 patients

randomized to tPA v.
100 PTCA
In fa rc t F re e S u rv iv a l %

98 10% emergent
96 CABG
94 63% tPA with
92
tPA unplanned cath
90
PTCA
88
86
84
82
80

0 30 60 90 120 150 180

Days
Grines NEJM 1993;328
Primary Angioplasty versus Thrombolysis
23 Randomized Trial (N=7739)
PCI (n=3872) Thrombolysis (n=3867)
25

20
* P=0.004
% 15
OR= 0.73
10 * *
* * * *
5

0
Death MI Ischemia Stroke Death MI
Short Term Long Term

Keeley Lancet 361:13 03

 Relationship of TIMI-3 Flow on 30-
Day Mortality After MI

10
Hospital Mortality, %

8 SK-GUSTO
Accel tPA-GUSTO

6 tPA&SK-GUSTO PTCA-GUSTO IIB

4 PTCA-PAR
PTCA-PAMI-2
2 PTCA-PAMI-1

0
10 30 50 70 90
% Patients with TIMI 3 Flow
 Primary Angioplasty: Limitations

Most Hospitals do not have Catheterization

Labs

Most Catheterization Labs are diagnostic,

without 24 hr capabilities

Most Catheterization Labs not

organized/efficient enough to open infarct
vessels in < 90 minutes
 Primary Angioplasty: Issues to
Address
Debate over PCI vs. Thrombolysis of historical interest only
Changes in Risk Stratification Strategies
How to improve access to PCI?
Importance of Timing
Cardiogenic Shock
Non-Cath Lab Hospitals: Transfer, Lyse or Both?
What is optimal pretreatment for PCI?
Facilitated Angioplasty Glycoprotein inhibitors/low-dose
Thrombolytics
What adjunctive therapy can enhance myocardial salvage?
Stents v. PTCA
Glycoprotein Inhibitors (Reopro)
Distal Protection/Thrombectomy devices
Novel adjunctive therapies
 Primary PCI for Acute MI:
Modern Approach stents +GP inhibitors
2x2 Design
PTCA v. Stent,
GP inhib v. placebo

Profound Early
benefit of Reopro

Profound Early
and Late benefit of
Stenting

Stone et al, NEJM 2002 346:957-966

ADMIRAL Trial -Montalescot et al. ,

NEJM 2001 344 1895 ,

 Evolution of PCI for STEMI
AngioJet
l A SA
id og r e
Clop
Platelet

GP IIb/IIIa inhibitor Embolization

Protection Device

Thrombus
Balloon Antiplatelet Stent DES Removal and
Rx Distal
Embolization
Protection
Antman. Circulation 2001;103:2310.
Devices
Effect of Time to Treatment on
Reperfusion Rates
Why do we have Door-Balloon Time
Standards?

NRMI-2 database
>27,000 patients

JAMA. 2000;283:2941-2947.
Ischemic Time and Mortality in 1o PCI
12
12
10 Mortality is increased by
10
mortality%%

7.5% for each 30 min delay

yearmortality

88

66
44
11year

N=1791
22

00
60
60 120
120 180
180 240
240 300
300 360
360
Ischemic
IschemicTime
Time

De Luca Circ 109:1223 04

 Primary PTCA Protocol:
Logistics and Goals to Limit
Door to Balloon Time
Early recognition of acute MI: ST elevation, new pain
Activate Catheterization Laboratory
Initiate treatment:
Chewable ASA (325 mg)
Heparin Bolus
IV Beta Blocker if appropriate (Metoprolol 5mg I.v.)
Limited exam and labs (no CXR)
Goals:
In catheterization laboratory: 40-60 minutes
Open artery: 60-90 minutes
 Primary PCI or Fibrinolysis?
PCI preferred if Fibrinolysis preferred if
Door to balloon< 90 min Prolonged transport
Cardiogenic shock Door-balloon > 90 min
Bleeding risk Sx <3 hrs
CHF
Age> 75
Sx > 3 hrs
New Paradigms for Risk Stratification
after STEMI: PAMI 2
Rationale:
Low Risk patients may have limited mortality benefit with
PTCA c/w lysis, but significant economic, qol benefit
Cath Data may be helpful in triage/risk stratification

Acute MI <12 hours (n=400)

Primary PTCA

High Risk Low Risk

Age <70
EF >45
1or2 VD
ICU Successful PCI No ICU
>5 day admit No VT 3 day admit
Pre DC ETT No ETT
Thrombolysis or Transfer for Primary
PCI : DANAMI 2

Danish study, 5 PCI centers, 22 referring centers

62% of Danish population
Mean transfer 35 miles
1100 patients randomized at referral centers, 800 at invasive
centers
Halted early by DSMB (1129 and 443 patients enrolled)
Referral arm: randomized within 12 hours, and 3 additional
hours allowed for transport (96% within 2hrs)
 DANAMI 2: Primary Endpoint at 30 days
(Death, Reinfarction, CVA)

Benefit of PCI is the same for patients transferred as it is for those

treated at cath-lab hospitals
 PRAGUE 2: Primary PCI after
Transfer vs. SK
850 patients, <12 hours,
Time to treat: 245 v. 277 min (Transfer -> 48 minutes)
Primary Endpoint at 30 days (Death)
 Rescue Angioplasty after Failed
Fibrinolytic Therapy in Large STEMI
(9 studies, n = 1,456)
PTCA No PTCA

14

12

10

8
%
6

0
Death Reinfarction Severe CHF
One year
Ellis, AHJ 139:1046; 00
Management of Acute STEMI
Diagnosis
Risk Stratification
Acute Therapy
Reperfusion
Adjunctive
Complications
Pre-Discharge
Management
What Adjunctive Therapy should
be given?
Antithrombotic
Aspirin
Heparin
IIb/IIIa antagonists
Improve healing/ischemia
Beta Blockers
ACE Inhibitors
Calcium Channel Blockers
Nitrates
 Antiplatelet Trialists Collaboration
STROKE/MI/VASCULAR DEATH

Totals Antiplatelet therapy vs. control

Trials analyzed Events People Odds ratio & CL Redn SD
3 Primary 1176 27210 12% 6
20 Cerebral 1916 9530 24% 5
11 Post MI 2270 15529 24% 4
11 Acute MI 2783 18126 28% 4
12 Angina 398 3450 39% 9
20 CABG/PTCA 215 3057 33% 13
28 PVD 444 3884 25% 104
51 Anti-DVT 67 4771 2% 19
30 Other 283 3948 44% 10
189 Trials 9789 90297 25% 2

0.0 0.5 1.0 1.5 2.0

Br Med J 1994 Treatment effect 2p < 0.00001
 Efficacy of Aspirin Doses on Vascular
Events in High Risk Patients
Aspirin Dose # Trials OR* (%) Odds Ratio
5001500 mg 34 19
160325 mg 19 26
75150 mg 12 32
<75 mg 3 13
Any aspirin 65 23
0 0.5 1.0 1.5 2.0
Antiplatelet Better Antiplatelet Worse

*Odds reduction.
Treatment effect P < 0.0001.
Adapted with permission from the BMJ Publishing Group. Antithrombotic Trialists Collaboration. BMJ.
2002;324:71
 Acute STEMI
Heparin
Intravenous heparin recommended with t-PA
(intial bolus 5000 U, infusion 1000 U/hr, adjust
for weight < 50 kg)
Favor enoxaparin except in elderly
No clear data for benefit with streptokinase
and increased bleeding
Discontinue after 24 hrs, except for:
atrial fibrillation
recurrent ischemia
anteroapical MI for CVA prophylaxis
 Enox vs UFH with Fibrinolysis
Meta-analysis
ASSENT-3, HART-II, ENTIRE (n=4717)
(805 pts underwent urgent angio 1st day)
Odds ratio (95% CI)
Endpoint
.88
Death
.74
Death/MI
.80
Death/MI/RI
1.34 1.95
Major bleeding

0.50 0.75 1.0 1.25 1.50

Enox better Enox worse
 What is optimal pretreatment for PCI?
Facilitated Angioplasty Glycoprotein
inhibitors/low-dose Thrombolytics
Hypothesis: antecedent pharmacologic therapy will partially
recanalize IRA before PCI improving clinical outcomes
Trial (n) comparison 10 endpt Result Comment
BRAVE AMI<12 hr; Infarct size Negative Higher TIMI flow
(253) Reopro v rtPA/Reo in combo
Immediate PCI
GRACIA-2 AMI<12 hr; Infarct size Negative Better ST resolution
(212) PCI v. TNK +PCI ST resolution with
Combo (61v 43%)
ON-TIME AMI <6 hr Initial TIMI 3 Negative Better early TIMI 2
(487) Tirofiban early (ambu) v flow flow
late (cath lab)
TIGER-PA AMI <12 hr TIMI grade Positive No clinical data
(100) Tirofiban early (ER) v flow, cTFC,
late (cath lab) TMPG
 Beta Blockers in Acute STEMI
Recommendations

IV to oral beta blocker therapy in patients

without contraindications in first 24 hours

Avoid early therapy in patients with

bradycardia, hypotension, inferior MI, CHF,
impaired LV function, AV block, asthma

Continue treatment for at least 2-3 years

 TIMI 2
Immediate vs Deferred Metoprolol
% of Patients % of Patients
30 2
Immediate
1.5
20 Delayed 21 1.4
p<0.01
1
15
p<0.03
10
p<0.02 0.5
2
4 0.28
0 0
Reinfarction Recurrent Ischemia IC Hemorrhage
48% of patients eligible for randomization to beta blocker
10% discontinued due to hypotension or bradycardia
TIMI Study Group. N Engl J Med 1989;320:618.
 ACE Inhibitors in Acute STEMI
Pooled Analysis of Randomized Trials
Study Agent N Mortality Odds Ratio & 95%
CI
ISIS-4 Captopril 58,050

During
MI GISSI-3 Lisinopril 19,394
CONSEN II Enalaprilat6,090

SAVE Captopril 2,231

Post
AIRE Ramipril 2,006
MI
TRACE 1,749
Trandolapril

0 1 2
Rx Better Control Better
Hennekens et al. NEJM 1996;335:1660.
 Adjunctive Therapy for Acute STEMI
Calcium Channel Antagonists
Agent N Odds Ratio & 95% CI Ca+2Ant Control

Nifedipine 1358 15.0% 13.0%

Verapamil 1775 10.8% 13.3%

Diltiazem 2466 13.5% 13.5%

Verapamil/ 4241 12.4% 13.4%

Diltiazem

Pooled 5599 13.0% 13.3%

0 1 2
Less Mortality More Mortality
Held et al, in Topol: Text Int Cardiol 2nd Ed 1993, p.52.
 Adjunctive Therapy in STEMI
Antithrombotic Recommendations
Aspirin All pts ( clopidogrel)
Heparin UFH or Enox
IIb/IIIa antagonists All PCI
Improve healing/ischemia
Beta Blockers IV < 24hrs
ACE Inhibitors Ant MI,CHF
Calcium Channel Blockers Only if ischemia
Nitrates Ischemia,CHF,HTN
 In-Hospital STEMI Pathways
Door Pt
Ptwith
withChest
ChestPain<
Pain<12
12hrs
hrs Therapy
<10 min
Data ASA, O2
<10 min Obtain
ObtainECG,
ECG,ST
STelevation?
elevation? MSO4, BB
Decision Heparin,NTG
<10 min Contraindications
Contraindicationsfor
forLytic?
Lytic?
No Yes

Door
Doorto
toBalloon>
Balloon>90
90min?
min?
Goals Yes No
D-N <30
D-B <90 Thrombolysis
Thrombolysis 11ooPCI
PCI IIb/IIIa if PCI
Management of Acute STEMI
Diagnosis
Risk Stratification
Acute Therapy
Reperfusion
Adjunctive
Complications
Pre-Discharge
Management
 Complications of Acute STEMI

Extension / Ischemia Arrhythmia

Pericarditis

Expansion / Aneurysm Acute MI RV Infarct

Mechanical Heart Failure Mural Thrombus

Acute MI - Mechanical Complications
Free Wall Rupture

Less frequent (1-3.4%), but earlier, with

thrombolysis

Uncontained sudden EMD or asystole

Pseudoaneurysm transient
hypotension, EMD, bradycardia, emesis,
restlessness

Echocardiogram usually diagnostic

Surgical repair - may require

pericardiocentesis for uncontained
rupture
Acute MI - Mechanical Complications
Interventricular Septal Rupture
Incidence 1-3% of transmural MIs
Acute shock, PE, right heart
failure, new loud pan-systolic
murmur (thrill in 50%)
Diagnose with echocardiogram
or O2 saturation step-up
Medical stabilization and IABP for
CHF, shock
Early surgical repair; mortality
complex ruptures involving RV
(~70%), lowest for apical ruptures
(~30%)
Acute MI - Mechanical Complications
Acute Mitral Regurgitation
Transient MR common in early MI
(20-40%)
Associated with age, prior MI,
CHF, female gender
Persistent MR, associated with
increased long-term mortality
May be due to papillary muscle, or
chordal rupture or dilation of
ventricle
Most common with inferior MI - MI
often small
 Acute Mitral Regurgitation
Diagnosis and Management

harsh, short systolic murmur - may be muffled

sudden CHF +/- hypotension or shock 2-7 days post MI
echocardiography (surface or TEE) usually diagnostic -
LV function often normal or hyperkinetic
stabilize medically, IABP, then surgical repair
surgical mortality high if shock is present

role of surgery in MR not due to rupture less clear

 Diagnosis?

V4R

Modified from Wellens. N Engl J Med

1999;340:381.
 Right Ventricular Infarction
Often found with IMI, related to Proximal
RCA occlusion
Clinical findings:
Shock with clear lungs, elevated JVP
Kussmaul 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:
V4R Maintain RV preload
Lower RV afterload (PA---PCW)
Modified from Wellens. N Engl J Med Inotropic support
1999;340:381. Reperfusion
 Acute MI - RV Infarction
Management
Irreversible infarction is unusual - transient
ischemic dysfunction with recovery common
Marked by sensitivity to preload reduction (nitrates,
diuretics, morphine), bradycardia, AV block
Fluid infusion for hypotension and low CO
PCWP elevation may occur due to septal shift
Heart block common
Dobutamine if fluids RA and PCWP without
improved BP and CI
 AMI complicated by Cardiogenic Shock
No study with thrombolytics has shown effect on patients with cardiogenic shock
 Early Invasive Strategy for Cardiogenic Shock
~ SHOCK Trial ~Mortality: Age < 75 Years
p<0.01
80 p>0.01
70 65%
60 57%
Mortality (%)

50 45%
41% Early revascularization
40
Intensive medical therapy
30
20 Treatment x Age group
10 Interaction p-values:
30-day: 0.012
0 6-month: 0.003
30-Day 6-Month
(n=246) (n=244)
Hockman NEJM
 PCI for Cardiogenic Shock

I IIa IIb III Primary PCI is recommended for patients less than
75 years with ST elevation or LBBB or who develop
shock within 36 hours of MI and are suitable for
revascularization that can be performed within 18
hours of shock.

I IIa IIb III

Primary PCI is reasonable for selected patients
75 years or older with ST elevation or LBBB or
who develop shock within 36 hours of MI and
are suitable for revascularization that can be
performed within 18 hours of shock.
 Acute MI - Arrhythmias
Prophylactic Lidocaine
Prophylactic use for suppression of VT or VF
controversial

Overview of randomized trials:

33% reduction in primary ventricular arrhythmias
trend toward 38% increased mortality (asystole)

Potential benefit in reperfusion era - GUSTO I (but not a

randomized comparison)

Should likely avoid unless VT / VF or non-sustained VT

occurs
 Acute MI - Arrhythmias
Atrial Fibrillation

Incidence reduced with thrombolysis (<5%)

Associated with large MI (especially if sustained)

Prognostic of adverse events over following year

Rate control with digoxin, or (without CHF) beta

blockers, verapamil, or diltiazem

Consider IV amiodarone

Electrical cardioversion for hemodynamic compromise

or ischemia
 Acute MI - Arrhythmias
Ventricular Tachycardia or Fibrillation

Prognosis of VT or VF in first 48 hours not associated

with increased in-hospital or long term mortality
VT or VF after first 48 hours associated with poorer
long-term prognosis
Acute management - K+ replacement, antiarrhythmic
therapy (lidocaine, procainamide, or amiodarone) if
stable, electrical shock if unstable
Long term management - pharmacologic therapy
limited benefit, ICD is beneficial if LVdysfx remains, or
VT/VF after 48 hrs
 Acute MI - Arrhythmias
Indications for Temporary Pacing
asystole
complete (third-degree) AV block
second-degree Mobitz II AV block
second-degree Mobitz I AV block with hypotension
new bifascicular block, esp with first-degree AV
block (Anterior MI especially)
symptomatic bradycardia, unresponsive to
atropine
Transcutaneous standby pacing for new LBBB,
sick sinus syndrome with sinus pauses
 Acute MI - Arrhythmias
Indications for Permanent Pacing

persistent complete (third-degree) AV block

persistent sinus node dysfunction -
symptomatic bradycardia
intermittent second-degree Mobitz II or third-
degree AV block
second-degree Mobitz II or third-degree AV
block with new bundle branch block
Management of Acute STEMI
Diagnosis
Risk Stratification
Acute Therapy
Reperfusion
Adjunctive
Complications
Pre-Discharge
Management
 Acute MI Management
Pharmacologic Therapy on Hospital Discharge

Aspirin indefinitely (clopidogrel for aspirin

allergy or intolerance)
Beta blockers for at least 2-3 years
ACE inhibitors for CHF, LVEF<40%, or large
infarction (even with preserved LVEF)
Lipid lowering agents
Coumadin for mural thrombus, extensive
anterior infarct, DVT, atrial fibrillation
 PCI for Cardiogenic Shock
Cardiogenic Shock

Early Shock, Diagnosed on Delayed Onset Shock

Hospital Presentation Echocardiogram to Rule Out
Mechanical Defects
Fibrinolytic therapy if all of the
following are present:
Arrange rapid transfer to invasive
1. Greater than 90 minutes to PCI IABP procedure-capable center
2. Less than 3 hours post STEMI
onset
3. No contraindications
Cardiac Catheterization and Coronary
Arrange prompt transfer to
invasive procedure-capable center
Angiography

1-2 vessel CAD Moderate 3-vessel CAD Severe 3-vessel CAD Left main CAD

PCI IRA PCI IRA Immediate CABG

Cannot be
Staged Multivessel Staged CABG performed
PCI
 SHOCK Trial
Hochman et al, NEJM Volume 341:625-634 August 26, 1999