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STEMI
Duc T. Nguyen, D.O.
Cape Cardiology Group
Saint Francis Medical Center
October 29, 2015
Heart Disease
Incidence in the U. S. • 785 000 Americans will have a new coronary
attack • 470 000 will have a recurrent attack
• 1 of 6 deaths is from a coronary attack
• Coronary Heart Disease is the single largest killer
Heart Disease and Stroke Statistics 2010 Update: A report from the American Heart Association
Acute Coronary Syndrome
• This is an umbrella term used to cover any group of clinical symptoms compatible with acute myocardial ischemia
• The acute imbalance between myocardial O2 demand and myocardial O2 delivery
• Ischemia presents as:
(angina, abnormal ECG and cardiac biomarkers)
The Vulnerable Plaque
Reproduced with permission from Falk E, et al. Circulation. 1998;92:657-671.
Large Lipid Core
Thin, Vulnerable, Fibrous Cap
ACS Pathophysiology Plaque Rupture, Thrombosis, and Microembolization
Quiescent plaque
Platelet-thrombin micro-emboli Plaque rupture
Process Plaque formation
Inflammation
Multiple factors
? Infection
Plaque Rupture
? Macrophages
Metalloproteinases
Thrombosis
Platelet Activation
Thrombin
Marker Cholesterol
LDL
C-Reactive Protein
Adhesion Molecules
Interleukin 6, TNFa,
sCD-40 ligand
MDA Modified LDL
D-dimer,
Complement,
Fibrinogen,
Troponin, CRP,
CD40L
Vulnerable plaque
Macrophages Foam Cells
Collagen
platelet
activation
TF Clotting
Cascade
Lipid core
Metalloproteinases
Inflammation
Courtesy of David Kandzari.
Thrombus Formation and ACS
UA NQMI STE-MI
Plaque Disruption/Fissure/Erosion
Thrombus Formation
Non-ST-Segment Elevation - Acute
Coronary Syndrome (NSTE - ACS) ST-Segment
Elevation
ACS
Old Terminology:
New Terminology:
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Acute Coronary Syndromes Hospital Discharges in the United States
1.97 million with** NSTEMI
0.46 million** with STEMI
2.43 million annual discharges*
*Estimate includes both first-listed and secondary diagnosis of ACS at discharge. **Estimates for STEMI and NSTEMI proportions of MI extrapolated from statistics in Wiviott S, et al. J Am Coll Cardiol. 2003;41(suppl 2);365A-366A. AHA Statistics Committee and Stroke Subcommittee. Circulation. 2006;113:e85-e151
Type of MI and Location of ST elevation
Type of MI EKG Leads Area of the Heart
Septal V1and V2 Septal wall
Anterior V3 and V4 Anterior wall
Lateral I, AVL, V5, V6 Lateral Wall
Inferior II, III, AVF Inferior wall
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ACC/AHA Class I Recommendations for Initial Management and
Anti-Ischemic Therapy
• Bed rest
• Continuous ECG Monitoring
• Supplemental O2 to maintain SaO2 >90%
• NTG (IV or PO as dictated clinically)
• IV Morphine prn pain, anxiety, and/or CHF
• Beta-blockers (PO and/or IV)
• ACEI for persistent hypertension in patients with LV systolic dysfunction or CHF
• IABP for hemodynamic instability
Available at: www.acc.org/clinical/guidelines/unstable/unstable.pdf.
STEMI
• Early diagnosis and rapid reperfusion therapy for ST-segment myocardial infarction (STEMI) limits infarct size and improves survival
• Current guidelines recommend reperfusion therapy within < 90 minutes of hospital arrival (door-to-balloon)
American Heart Association: Heart Disease & Stroke Statistics, 2009 update Ting HH et al: Circulation 118:2066, 2008
Facts
• Every 30 minute delay to treatment increases the risk of mortality
$ It is estimated that the combination of direct and indirect health care costs of Coronary Heart Disease will reach $503 billion by 2011
*American Heart Association. Heart Disease & Stroke Statistics- 2010 update
Why Create Better Systems of Care to Treat STEMI?
What have we learned… What we have learned…
1. Primary PCI is superior to fibrinolysis
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4
0
5
10
15
20
Death Death (shock
excl.)
Non-Fatal MI CVA Death CVA/MI
PCI Lytic
23 Randomized Trials of PCI vs Lytics:
30 day Events (n=7739)
P=0.0002P=0.0002
P=0.0003P=0.0003 P<0.0001P<0.0001
P=0.0004P=0.0004
P<0.0001P<0.0001
7
9
57
2.5
6.8
1 2
8
14
Fre
qu
en
cy (
%)
Keeley Keeley & Grines,& Grines, Lancet Lancet 2003;361:132003;361:13--2020
What we have learned…
1. Primary PCI is superior to fibrinolysis
2. Benefits of reperfusion therapy (PPCI and fibrinolysis) are time-dependent
Door-to-Balloon and Mortality NRMI 3/4, n=29,222 STEMI treated within 6 hours
7.4%
5.7%
4.2%
3.0%
0.0%
1.0%
2.0%
3.0%
4.0%
5.0%
6.0%
7.0%
8.0%
< or = 90 min 91-120 min 121-150 min > 150 min
Door-to-Balloon
In-H
os
pit
al
Mo
rta
lity
(%
)
McNamara RL, et al. JACC 2006;47:2180-2186
AHA/ACC STEMI Guidelines
Critical time-dependent period Goal: myocardial salvage
Time-independent period Goal: open IRA
Time = Myocardium Infarct Size = Outcome
B
C
A Extent of myocardial salvage
Mo
rtal
ity
red
uct
ion
D
100%
80%
60%
40%
20%
0%
0 4 8 12 16 20 24
Time from symptom onset to reperfusion therapy (hours)
60 min
240 min
30%
10%
Gersh BJ, et al., JAMA 2005; 293:979-986
What we have learned…
1. Primary PCI is superior to fibrinolysis
2. Benefits of reperfusion therapy (PPCI and fibrinolysis) are time-dependent
3. Primary PCI depends on operator and hospital experience/expertise
0
5
10
15
0 50 100 150 200
Hospitals Performing >50 PPCI/Year Associated with Lower Mortality
Annual hospital volume/year
NYS PCI Registry (n=7,321)
Risk-adjusted mortality (%)
State-wide mortality
Srinivas VS, JACC 2009;53:574-579
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Physicians Performing >10 PPCI/Year Associated with Lower Mortality
Annual physician volume/year
NYS PCI Registry (n=7,321)
Risk-adjusted mortality (%)
Physicians (no.) 52 43 33 25 21 11 22 15 7 8 8 4 2 2 0 2 4 7
0
2
4
6
0 10 20 30 36
Srinivas VS, JACC 2009;53:574-579
Case Review • Around 21:00 while watching television, developed mid-chest pressure
rated 5/10 which persisted without relief. • At 23:00, called 911
• Aspirin, nitroglycerin and heparin were administered
Coronary Angiogram
Evidence-based Strategies
1. ED physician activates the cath lab
2. One call activates the cath lab
3. Cath lab team ready in 20-30 minutes
4. Prompt data feedback
5. Senior management commitment
6. Team-based approach
Optional: Pre-hospital ECG to activate the cath lab
Target Time Metrics
Regional door-to-ECG <5 min
ECG-to-CODE STEMI activation <15 min
CODE STEMI activation-to-door2 <60 min
Door 2-to-balloon <30 min
Regional door-to-balloon <120 min total time
Measures to improve time to reperfusion
Pre-Hospital
• Early patient recognition
• Early EMS activation
• Pre hospital ECG and notification
• EMS triage to PCI centers
• Pre hospital cath lab activation
Hospital
• Rapid ECG and assessment
• Central paging system
• Early transfer of pt from the ED to cath lab
• Dedicated team to facilitate care
• Committed cath labs
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Bradley EH, et al. N Engl J Med. 2006;355(22):2308-2320
D2B Alliance: Several key strategies to reduce D2B were identified STEMI IMPOSTERS
CAUSES OF ST SEGMENT ELEVATION
• Acute myocardial infarction • Benign early repolarization • Left bundle branch block • Left ventricular hypertrophy • Ventricular aneurysm • Coronary vasospasm/printzmetal’s angina • Pericarditis • Brugada syndrome • Subarachnoid haemorrhage
STEMI IMPOSTERS
• The following are the 4 most common: • LBBB • Pericarditis • Paced rhythm • LVH
• Requires: • Recognition • Assessment of patient sign’s and symptoms • Relevant past medical history • Old ECG’s ?
LBBB
• Electrical impulses are prevented from entering the left ventricle directly through normal conduction system.
• AMI in the presence of bundle branch block carries a much worse prognosis than AMI with normal ventricular conduction
LBBB LBBB
• Usually the result of heart disease • Can be present on rare occasions in normal
hearts • Some common causes: • IHD • Cardiomyopathy & heart failure • LVH • STEMI • Hypertension
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Appropriate discordance in uncomplicated LBBB
STEMI and LBBB
PERICARDITIS
An inflammatory disease of the pericardium
Can be caused by STEMI, trauma, viral or bacterial.
Pericarditis
• Commonly mistaken for AMI as both cause chest pain and ST segment elevation.
• ST segment in pericarditis is diffuse, rather than localised
• Often present in all leads except aVR and V1
• ST segments are concave upwards rather than convex upwards
• Depression of PR segment may also be seen
• Absence of wide reciprocal changes
• Absence of Q waves
Pericarditis PACED RHYTHM
• Ventricular lead is placed in the Apex of the right ventricle
• When the lead is stimulated it produces a wave of depolarisation that spreads through the myocardium, bypassing the normal conduction system
• Right to left and apex to base
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Paced Rhythm
• Broad QRS complexes
• A left bundle branch block pattern
• Left axis deviation
• QT interval often prolonged
• T waves are broad
Paced Rhythm
LEFT VENTRICULAR HYPERTROPHY
• Compare V1 & V2, determine which has the deeper S wave and measure the depth in mm (1mm = 1 small square)
• Compare V5 & V6, determine which has the taller R wave and measure the height (mm)
• Add together the depth and height (mm). If the sum equals 35 or more, then suspect LVH
LEFT VENTRICULAR HYPERTROPHY
LEFT VENTRICULAR HYPERTROPHY
• The presence of LVH can cause difficulty in patients complaining of ischemic type chest pain
• Can be difficult to diagnose confidently acute ischemia on the basis of ST segment changes in the left precordial leads
• Old ECG’s are important for comparison.
LEFT VENTRICULAR HYPERTROPHY
Difficult in individuals under the age of 40
•Sometimes they have high amplitude QRS complexes in the absence of LV disease
•Common cause of LVH is systemic hypertension
•Others include: -
•Aortic stenosis and co-arctation of the aorta