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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