ST Elevation Myocardial
Infarction (STEMI)
William J. Mosley II, MD
Cardiovascular Disease Fellow
(Updated from John Rapp with 2007
guidelines)
ACS-STEMI
No ST elevation
Stable
angina
Unstable
angina
NSTEMI
ST elevation
STEMI
ACUTE CORONARY SYNDROMES
Outline
Class/Evidence
General Therapy
Beta-blockers
Reperfusion
Facilitated PCI
Complications
Applying Classification of Recommendations
and Level of Evidence
Class I
Class IIa
Class IIb
Class III
Benefit >>> Risk
Benefit >> Risk
Additional studies with
focused objectives
needed
Benefit Risk
Additional studies with
broad objectives
needed; Additional
registry data would be
helpful
Risk Benefit
No additional studies
needed
Procedure/
Treatment SHOULD
be performed/
administered
IT IS REASONABLE to
perform
procedure/administer
treatment
Procedure/Treatment
MAY BE CONSIDERED
Procedure/Treatment
should NOT be
performed/administered
SINCE IT IS NOT
HELPFUL AND MAY
BE HARMFUL
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
Hospitalizations in the U.S. Due to Acute
Coronary Syndromes (ACS)
Acute Coronary
Syndromes*
1.57 Million Hospital Admissions - ACS
UA/NSTEMI
STEMI
1.24 million
.33 million
Admissions per year
Admissions per year
Heart Disease and Stroke Statistics 2007 Update. Circulation 2007;
115:69-171. *Primary and secondary diagnoses. About 0.57 million
NSTEMI and 0.67 million UA.
General Therapy
General Therapy
MONA
Morphine (q
( 5-15 min CLASS I)
Oxygen (pulse
ox>90% CLASS I)
(
Nitroglycerin (0.4
mg SL NTG x 3 for
(
ischemic pain CLASS I)
Aspirin
Aspirin
Aspirin should be chewed by patients who have not
taken aspirin before presentation with STEMI. The
initial dose should be 162 mg (Level of Evidence: A) to
325 mg (Level of Evidence: C). Class I
In a dose of 162 mg or more, aspirin produces a rapid
clinical antithrombotic effect caused by immediate and
near-total inhibition of thromboxane A2 production.
(ISIS-2-->ASA led to 23% reduction in mortality):
1. Antithrombotic Trialists Collaboration. Collaborative meta-analysis of randomised trials of
antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk
patients. BMJ. 2002; 324: 7186.
2. ISIS-2 (Second International Study of Infarct Survival) Collaborative Group. Randomised trial
of intravenous streptokinase, oral aspirin, both, or neither among 17187 cases of suspected
acute myocardial infarction. Lancet 1988;ii:349-60.
Beta-Blockers
COMMIT: Study design
INCLUSION:
>45,000 patients with suspected acute
MI (ST change or LBBB) within 24 h of
symptom onset
TREATMENT:
Metoprolol 15 mg iv over 15 mins, then
200 mg oral daily vs matching placebo
EXCLUSION:
Shock, systolic BP <100 mmHg, heart
rate <50/min or II/III AV block
1 OUTCOMES: Death & death, re-MI or VF/arrest up to
4 weeks in hospital (or prior discharge)
Mean treatment and follow-up: 16 days
Effects of Metoprolol
COMMIT (N = 45,852)
Totality of Evidence (N = 52,411)
Death
13%
P=0.0006
30% relative
increase in
*cardiogenic
shock
ReMI
22%
P=0.0002
VF
15%
P=0.002
*Risk factors for cardiogenic shock :heart failure, age > 70 , systolic blood
pressure < 120, sinus tachycardia > 110 or heart rate < 60, increased time
since onset of STEMI symptoms
Lancet. 2005;366:1622.
Beta-Blockers
Recommendations - Class Ia
(B)
ORAL beta-blocker therapy SHOULD BE initiated
in the first 24 hours for patients who DO NOT
have any of the following:
1) signs of heart failure,
2) evidence of a low output state,
3) increased risk for cardiogenic shock, or
4) relative contraindications to beta blockade
1AVB > 0.24 sec,
2nd- or 3rd-degree heart block
reactive airway disease
**
There is no study evaluating oral beta blockers
*Risk factors
for cardiogenic shock :heart failure, age > 70 , systolic blood pressure < 120,
alone
sinus tachycardia > 110 or heart rate < 60, increased time since onset of STEMI symptoms
Beta-Blockers
Recommendations - Class IIa
(B)
It is reasonable to administer an IV BETA
BLOCKER at the time of presentation to STEMI
patients who are HYPERTENSIVE and who do
not have any of the following:
1) signs of heart failure,
2) evidence of a low output state,
3) increased risk for cardiogenic shock, or
4) relative contraindications to beta blockade
1AVB > 0.24 sec,
2nd- or 3rd-degree heart block
reactive
*Risk factors for cardiogenic
shock :heart
failure, age
> 70 , systolic blood pressure < 120, sinus
airway
disease
tachycardia > 110 or heart rate < 60, increased time since onset of STEMI symptoms
Beta-Blockers
Recommendations - Class III
(A)
IV beta blockers SHOULD NOT be administered
to STEMI patients who have any of the following:
1) signs of heart failure
2) evidence of a low output state
3) increased risk* for cardiogenic shock
4) relative contraindications to beta blockade
1AVB > 0.24 sec,
2nd- or 3rd-degree heart block
reactive airway disease
*Risk factors for cardiogenic shock :heart failure, age > 70 , systolic blood
pressure < 120, sinus tachycardia > 110 or heart rate < 60, increased time
since onset of STEMI symptoms
Reperfusion
Time is Muscle
Reperfusion
STEMI patients presenting to a hospital with PCI
capability should be treated with primary PCI
within 90 min of first medical contact as a
systems goal. Class Ia
STEMI patients presenting to a hospital without
PCI capability, and who cannot be transferred to a
PCI center and undergo PCI within 90 min of first
medical contact, should be treated with fibrinolytic
therapy within 30 min of hospital presentation as
a systems goal, unless fibrinolytic therapy is
contraindicated. Class Ib
PCI vs Fibrinolysis for STEMI:
Short-Term Clinical Outcomes
Frequency (%)
PCI
N=7739
Fibrinolysis
P<.0001
P<.0001
P=.0002
P=.0003
P<.0001
P=.032
P=.0004
Death
Death,
no shock
data
ReMI
Rec.
Total
Ischemia Stroke
P<.0001
Hem.
Stroke
Major
Bleed
Death
MI
CVA
Keeley E, et al. Lancet . 2003;361:13-20.
Brief Review of Thrombolytic
Trials
GISSI-1: Streptokinase 18% reduction in mortality at 21 d
GUSTO-1: tPA. 15% reduction in 30-day mortality compared
to Streptokinase
GUSTO-3: Reteplase had no benefit over tPA but is easier to
use (double bolus)
ASSENT: TNKase is similar to tPA but with less non-cerebral
bleeding and better mortality with symptoms>4 hrs: Single
bolus, fibrin selective, resistance to PAI-1
*Overall risk of ICH is 0.7%; Strokes occurred in 1.4%
Anticoagulants
Patients undergoing reperfusion with
fibrinolytics should receive anticoagulant
therapy for a minimum of 48 hours
(unfractionated heparin) or up to 8 days
Anticoagulant regimens with established
efficacy include:
UFH (LOE: C)
Enoxaparin (LOE:A)
Fondaparinux (LOE:B)
Summary of Observations from Trials of Anticoagulants for STEMI
Anticoagul
ant
Reviparin
Efficacy (through 30 d)
Fibrinolysis: probably superior
to placebo.*
Safety
risk of serious
bleeds
No data on reviparin alone
during PCI. Additional
anticoagulant with anti-IIa
activity, such as UFH or
bivalirudin, recommended.
Trend toward
risk of serious
bleeds
risk of catheter thrombosis
when fondaparinux used
alone. Additional
anticoagulant with anti-IIa
activity, such as UFH or
bivalirudin, recommended.
risk of serious
bleeds
Enoxaparin can be used to
support PCI after fibrinolysis.
No additional anticoagulant
needed.
No reperfusion: probably superior to
placebo.*
Fondaparinux
Fibrinolysis: appears superior to
control rx (placebo/UFH). Relative
benefit vs placebo and UFH
separately cannot be reliably
determined from available data.*
Use During PCI
Primary PCI: when used alone, no
advantage over UFH and trend
toward worse outcome.
No reperfusion: appears superior to
control therapy (placebo/UFH).
Relative benefit versus placebo and
UFH separately cannot be reliably
determined from available data.*
Enoxaparin
Fibrinolysis: appears superior to UFH
Antman EM, et al. J Am Coll Cardiol 2008. Published ahead of print on December 10, 2007. Available at
http://content.onlinejacc.org/cgi/content/full/j.jacc.2007.10.001. Table 10.
Facilitated PCI
Meta-analysis: Facilitated PCI vs
Primary PCI
Mortality
Lytic alone
Reinfarction
1.43
(1.01-2.02)
1.81
(1.19-2.77)
1.03
(0.49-2.17)
1.40
(0.49-3.98)
Major Bleeding
N=2953
IIb/IIIa
alone
N=1148
Lytic
+IIb/IIIa
N=399
All
(N=4500)
3.07
(0.18-52.0)
1.38
(1.01-1.87)
0.1
Fac. PCI
Better
Keeley E, et al. Lancet 2006;367:579.
1.03
(0.15-7.13)
1.71
(1.16 - 2.51)
1
10 0.1
PPCI
Better
Fac. PCI
Better
1.51
(1.10 - 2.08 )
1
10
PPCI
Better
0.1
Fac. PCI
Better
10
PPCI
Better
Rescue PCI
If evidence of
cardiogenic shock,
severe heart failure
hemodynamically compromising
ventricular arrhythmias.
If fibriolysis has failed
Evaluate 90 minutes for a <50% ST
resolution in lead with greatest elevation
Summary of Acute STEMI
Treatment
Stabilize, MONA/BB
ASA if MI is even considered.
The artery is CLOSED; time is muscle
PCI is preferred method of reperfusion
Cath lab (regardless of method of reperfusion)
if
Hemodynamic or electrical instability
Failed Fibrinolysis
Case Presentation
51 y.o. man with increasing shortness
of breath and chest pain x 60min
Came to ED because she can no longer
walk up a flight of stairs or lay down
flat.
No N/V/Diaphoresis. No LH or
dizziness
No known history of cardiac or
pulmonary disease.
Physical Exam
Vital Signs: HR 120; BP 90/60; RR 28.
General: Alert and oriented x 3. Mild
respiratory distress.
HEENT: NC, no trauma.
Neck: Supple, no lymphadenopathy.
Heart: Regular S1 and S2. 2/6 early SEM along L
sternal border (no significant radiation). No
carotid bruits. ? JVD.
Lungs: Tachypnic. Rales 1/3 up the back
bilaterally. Otherwise clear.
Abdomen: Obese. Benign
Extremities: Warm. No C/C. Trace edema.
EKG
Chest X-Ray
Treatment
MONA - Morphine, Oxygen, Aspirin
No nitrates because hypotensive
No beta-blocker b/c in heart failure
Primary PCI LAD occlusion
Complications of Myocardial
Infarction
Arrhythmias
Ventricular Septal Perforation
Ischemic Mitral Regurgitation,
Papillary Muscle Rupture
Ventricular Free Wall Rupture
Systemic Embolism
Ventricular Aneurysm
Pericarditis
Cardiogenic Shock (another lecture)
Ventricular Arrhythmias
60-110 BPM; Up to 20% STEMI patients have this
Usually a result of reperfusion; no specific therapy
needed if HD stable. Otherwise, atropine or even atrial
pacing may increase sinus rate to overdrive pace the
AIVR
PVCs
Extremely common, along with
short runs of NSVT
Amiodarone wont increase
mortality, other antiarrhythmics
(other than B-blockers) do.
B-blockers, electrolytes
Best if no antiarrhythmics are
used
Not So Benign Rhythm
Ischemic VT is often polymorphic; HR>100-110 BPM
Higher risk with more LV damage and in first 2 days after MI
Treat: DCCV, cath lab (if needed), electrolyte correction,
amiodarone, lidocaine, B-Blockers
If That Didnt Make You
Nervous
Primary VF: Sudden event with no warning--10% STEMI patients
before lytics. MUCH MUCH less now
Secondary VF: Occurring in setting HF or shock
Late VF: >48 hrs after MI-->Increased risk with IVCD, anterior wall
MI, persistent SVT early in course, and RV infarction requiring
pacing
***Have to worry about structural complication (free wall
rupture)/ischemia
Treat: Non-synced DCCV, electrolyte correction
Why get worked up about
electrolytes?
NOTE: Pre-lytic
study
Nordrehaug JE, van der Lippe G: Hypokalemia and ventricular fibrillation in acute myocardial
infarction. Br Heart J 50:525, 1983.
Sinus Bradycardia/Junctional Escape
Rhythm
4-5% of STEMI patients have a
bradyarrhythmia
Sinus node ischemia--Blood supply to SA
node is: 65% RCA, 25% LCX, 10% dual
supply.
Most commonly seen in Inferior/posterior
MIs.
Often induced by vagal reaction that may
be protective
Atrioventricular Block
First-Degree: Usually the RCA and does not require
treatment. Hold the B-blocker for PR>240 ms
Second-Degree: Usually RCA disease and does not require
treatment unless HR less than 50 and arrhythmia or
symptoms. Otherwise, atropine or pace
Third-Degree: Can be from any location of infarct. Can be
preceded by Mobitz II Block
Pace for symptoms and for hemodynamic support. Usually
not needed in inferior MIs as block is transient (pace for
HR<40-50)
Post-MI VSD
~2% of acute MIs prior to reperfusion era
~0.2% in GUSTO-I streptokinase trial
Without reperfusion, usually occurs within first week
Day 1--Large intramural hematomas that dissect
Day 3-5--Coagulation necrosis
24 hr or less if receive lysis--Lytics reduce infarct
size but may promote hemorrhagic dissection of
myocardium
Symptoms, Exam, and Diagnosis
Chest pain, dyspnea
PE: Harsh, holosystolic murmur
along sternal border radiating
to base/apex/R parasternum;
thrill in 1/2 patients; S3; Loud
P2; TR.
Compared to acute MR, murmur
is loud. Up to 20% of patients
may have MR as well though
CCU Management
IABP
Ventilation
Diuresis/HF Management
Inotropes (can increase shunt)
Nitroprusside if tolerated (can cause
hypotension)
Mortality with conservative management is
HIGH (24%, 46%, 67-82% at 24 hrs, 1 wk, and 2
months, respectively)
Ultimately, mechanical closure needed (surgery
vs. percutaneous)-TIMING is questionable but
clinical status should not preclude this
Acute Mitral Regurgitation
Caused by papillary muscle ischemia or rupture
(less likely). Rupture is usually partial since
total is essentially incompatible with life
Usually in setting of inferior MI involving the
posteromedial papillary muscle (single PDA
blood supply as opposed to anterolateral)
Rupture usually occurs 3-5 days post-MI and in
1% of MIs and requires emergent operative
repair (50% mortality in 24 hrs)
Accounts for 7% of cardiogenic shock and 5% of
mortality associated with acute MI
Area of infarction does NOT have to be large
Symptoms, Exam, Diagnosis
Symptoms: Those of
heart failure
PE: May or may not
hear loud systolic
murmur (need a
gradient)
CCU Management
Mechanical ventilation if needed
IABP--especially for hypotension
PCI if papillary m. ischemia (not rupture)
Afterload reduction (nitroprusside if
possible) to MAP of 70-80 mm Hg
Since mortality is 90% with medical
therapy alone, surgery is the major
therapy of choice
Perioperative mortality 20-25%
Overall surgical mortality is even higher
Free Wall
Rupture
~10% of patients who die in
hospital from STEMI
Most commonly between 1 and 4
days (up to 3 weeks)
Caused by tear or dissecting
hematoma
More common with fibrinolysis
compared to PCI
More common in patients without
previous infarction
Symptoms, Exam, Diagnosis
Acute symptoms include sudden chest pain
(esp with cough, strain) and sudden death
Subacute symptoms: Pericarditis-like
symptoms (chest pain, nausea, vomiting)
Exam (think HF and tamponade): JVD,
pulsus, diminished heart sounds, rub,
possibly a new murmur
Treatment
Pericardiocentesis if time
Surgical repair is the only treatment
Mortality is reasonable if
patient gets to the OR
in time
90% mortality without
surgery
Summary of Acute STEMI
Complications
Much more rare in the reperfusion era
Look for them especially in delayed presentation
Arrhythmias are most common
complication and may require emergent
treatment
VSDs, papillary muscle rupture, and free
wall ruptures carry a VERY high mortality
and require emergent surgical consultation
Support mechanically until patient receives
operation
Other References
1. Crawford PA, ed. The Washington Manual
Subspecialty Consult Series: Cardiology
Subspecialty Consult. Philadelphia:
Lippincott Williams and Wilkins, 2004.
2. Griffin BP, Topol EJ, eds. Manual of
Cardiovascular Medicine, 2nd ed.
Philadelphia: Lippincott Williams and
Wilkins, 2004
3. Zipes, Libby, Bonow, Braunwald, eds.
Braunwalds Heart Disease: A Textbook of
Cardiovascular Medicine, 7th ed.
Philadelphia: Elsevier Saunders, 2005
Questions?
