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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
Outline
Class/Evidence
General Therapy
Beta-blockers
Reperfusion
Facilitated PCI
Complications
Class IIa
Class IIb
Class III
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:
Level B:
Level C:
STEMI
1.24 million
.33 million
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
Beta-Blockers
TREATMENT:
EXCLUSION:
Effects of Metoprolol
COMMIT (N = 45,852)
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)
**
Beta-Blockers
Recommendations - Class IIa
(B)
Beta-Blockers
Recommendations - Class III
(A)
IV beta blockers SHOULD NOT be administered
*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
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
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)
Efficacy (through 30 d)
Fibrinolysis: probably superior
to placebo.*
Safety
risk of serious
bleeds
Trend toward
risk of serious
bleeds
risk of serious
bleeds
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
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
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
Case Presentation
51 y.o. man with increasing shortness
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,
Ventricular Arrhythmias
PVCs
Extremely common, along with
NOTE: Pre-lytic
study
Nordrehaug JE, van der Lippe G: Hypokalemia and ventricular fibrillation in acute myocardial
infarction. Br Heart J 50:525, 1983.
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
Post-MI VSD
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
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
Free Wall
Rupture
~10% of patients who die in
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
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?