Rodney Dangerfield makes an encore performance!
Episode 154

August 11, 2014


aVR - the forgotten 12th lead
ST-segment elevation (STE) in aVR with other ischemic findings is BAD!
(i.e. LMCA occlusion, proximal LAD occlusion, or triple vessel disease)
 
In the setting of ACS, STE in aVR…
  • + STE in aVL = LMCA occlusion
  • + STE in V1 = LMCA or proximal LAD occlusion
  • STE in aVR > STE V1 = LMCA occlusion
  • STE in aVR> 1.0mm should make you worry!

Some literature indicates…

  • 70% mortality without immediate PCI
  • Medical therapy including lytics does not improve mortality
  • LMCA occlusion may require CABG, so avoid drugs like clopidogrel
  • Emergent PCI may decrease mortality to 40%
  • Time delay to PCI is the only predictor of survival
  • Immediate transfer for PCI if necessary!

This is not yet in the ACC/AHA guidelines for emergent cath lab activation!

Rokos IC, French WJ, Mattu A, et al. Appropriate cardiac cath lab activation: optimizing the electrocardiogram interpretation and clinical decision making for acute ST-elevation myocardial infarction. Am Heart J. 2010 Dec; 160(6):995-1003. PMID: 21146650
Rodney Dangerfield makes an encore performance!
Episode 154

August 11, 2014


aVR - the forgotten 12th lead
ST-segment elevation (STE) in aVR with other ischemic findings is BAD!
(i.e. LMCA occlusion, proximal LAD occlusion, or triple vessel disease)
 
In the setting of ACS, STE in aVR…
  • + STE in aVL = LMCA occlusion
  • + STE in V1 = LMCA or proximal LAD occlusion
  • STE in aVR > STE V1 = LMCA occlusion
  • STE in aVR> 1.0mm should make you worry!

Some literature indicates…

  • 70% mortality without immediate PCI
  • Medical therapy including lytics does not improve mortality
  • LMCA occlusion may require CABG, so avoid drugs like clopidogrel
  • Emergent PCI may decrease mortality to 40%
  • Time delay to PCI is the only predictor of survival
  • Immediate transfer for PCI if necessary!

This is not yet in the ACC/AHA guidelines for emergent cath lab activation!

Remember: STE of aVR in very tachycardic rhythms (i.e. SVT), or in the setting of severe hypertension & LVH/RVH may be a normal variant and may have no clinical significance. Hence, the rule does not apply to asymptomatic patients without ST changes indicative of ischemia!


Want more practice/references? Check out these previous episodes & learn to respect aVR:


Reference:
Rokos IC, French WJ, Mattu A, et al. Appropriate cardiac cath lab activation: optimizing the electrocardiogram interpretation and clinical decision making for acute ST-elevation myocardial infarction. Am Heart J. 2010 Dec; 160(6):995-1003. PMID: 21146650
Brugada Part II: 2014 revelations
Episode 153

August 4, 2014


If you interpret ECG’s in patients with syncope…
You have to know how to diagnose Brugada syndrome!
  • Consider Brugada syndrome in patients presenting after syncope
  • Diagnosis of the syndrome requires ECG findings + clinical findings
  • Coved STE is most concerning
  • Discussion/referral to electrophysiologist can be life saving

In case you missed it, start by watching last weeks episode: Brugada Part I

Brugada ECG Abnormalities in V1-V2
  • RBBB or incomplete RBBB pattern
  • ST-segment elevation - 2 types
    • ​​"Coved-type" (most common & concerning)
    • "Saddle-type" (lower mortality)
  • ​Moving leads (V1-V2) one interspace higher may increase the abnormality

Diagnosis of the syndrome requires 2 parts:
  1. Typical ECG abnormality (especially coved type) +
  2. Clinical characteristics, one of the following:
  • ​History of VT/VF
  • FHx of sudden cardiac death
  • FHx of coved-type ECG
  • Agonal respirations during sleep
  • Inducibility of VT/VF during EP study

For the fellow ECG Nerds:

  • First onset of symptoms (VT,VF, syncope, sudden death) ~ 40 years old
    • ​41 +/- 15 years on average of VF episodes
    • Arrhythmias reported from 2-84 years
    • Is reported cause of SIDS & sudden cardiac death in young children
    • ​​Arrhythmic events tend to occur at rest or sleep
    • Vagal tone and fever thought to increase VF episodes
  • Mortality ~10%/yr without internal cardioverter-defibrillator (ICD)
    • Mortality & VF episode rates are highest in Type I (coved) pattern
    • Also associated with supraventricular arrhythmias (A.fib & SVT)
    • Antidysrhythmics have no effect on prognosis
    • Best treatment is ICD placement

References:

Martini B, Nava A, Thiene G, et al. Ventricular fibrillation without apparent heart disease:description of six cases. Am Heart J. 1989;6:1203-9. PMID: 2589161

Hoogendijk MG, Opthof T, Postema PG, et al. The Brugada ECG Pattern: A Marker of Channelopathy, Structural Heart Disease or Neither? Towards a Unifying Mechanism of the Brugada Syndrome. Circ Arrhythm Electrophysiol. 2010;3:283–290. PMID: 20551422

Mizusawa Y, Wilde AA. Brugada syndrome. Circ Arrhythm Electrophysiol. 2012;3:606-16. PMID: 22715240

Brugada Part II: 2014 revelations
Episode 153

August 4, 2014


If you interpret ECG’s in patients with syncope…
You have to know how to diagnose Brugada syndrome!
  • Consider Brugada syndrome in patients presenting after syncope
  • Diagnosis of the syndrome requires ECG findings + clinical findings
  • Coved STE is most concerning
  • Discussion/referral to electrophysiologist can be life saving

In case you missed it, start by watching last weeks episode: Brugada Part I

Brugada ECG Abnormalities in V1-V2
  • RBBB or incomplete RBBB pattern
  • ST-segment elevation - 2 types
    • ​​"Coved-type" (most common & concerning)
    • "Saddle-type" (lower mortality)
  • ​Moving leads (V1-V2) one interspace higher may increase the abnormality

Diagnosis of the syndrome requires 2 parts:
  1. Typical ECG abnormality (especially coved type) +
  2. Clinical characteristics, one of the following:
  • ​History of VT/VF
  • FHx of sudden cardiac death
  • FHx of coved-type ECG
  • Agonal respirations during sleep
  • Inducibility of VT/VF during EP study

For the fellow ECG Nerds:

  • First onset of symptoms (VT,VF, syncope, sudden death) ~ 40 years old
    • ​41 +/- 15 years on average of VF episodes
    • Arrhythmias reported from 2-84 years
    • Is reported cause of SIDS & sudden cardiac death in young children
    • ​​Arrhythmic events tend to occur at rest or sleep
    • Vagal tone and fever thought to increase VF episodes
  • Mortality ~10%/yr without internal cardioverter-defibrillator (ICD)
    • Mortality & VF episode rates are highest in Type I (coved) pattern
    • Also associated with supraventricular arrhythmias (A.fib & SVT)
    • Antidysrhythmics have no effect on prognosis
    • Best treatment is ICD placement

References:

Martini B, Nava A, Thiene G, et al. Ventricular fibrillation without apparent heart disease:description of six cases. Am Heart J. 1989;6:1203-9. PMID: 2589161

Hoogendijk MG, Opthof T, Postema PG, et al. The Brugada ECG Pattern: A Marker of Channelopathy, Structural Heart Disease or Neither? Towards a Unifying Mechanism of the Brugada Syndrome. Circ Arrhythm Electrophysiol. 2010;3:283–290. PMID: 20551422

Mizusawa Y, Wilde AA. Brugada syndrome. Circ Arrhythm Electrophysiol. 2012;3:606-16. PMID: 22715240

A near-disaster in the stress test lab
Episode 152

July 28, 2014


Brugada Syndrome

  • A hereditary sodium channelopathy associated with sudden cardiac death (SCD) in patients with structurally normal hearts
  • More common cause of SCD than previously recognized
  • Most common in young males
  • First onset of symptoms (syncope, sudden death) ~ 40 years old
  • Mortality about 10% per year if not treated with internal cardioverter-defibrillator (ICD)
  • Syndrome characterized by
    • ​ECG abnormalities in leads V1-V2
    • Polymorphic or monomorphic VT
    • Structurally normal heart
    • Familial occurence in about half of patients
  • ​Discuss/refer to electrophysiologist
ECG Findings in V1-V2​
  • RBBB or incomplete RBBB pattern
  • ST-segment elevation - 2 types
    • ​​"Coved-type" (most common & concerning)
    • "Saddle-type"

A near-disaster in the stress test lab
Episode 152

July 28, 2014


Brugada Syndrome

  • A hereditary sodium channelopathy associated with sudden cardiac death (SCD) in patients with structurally normal hearts
  • More common cause of SCD than previously recognized
  • Most common in young males
  • First onset of symptoms (syncope, sudden death) ~ 40 years old
  • Mortality about 10% per year if not treated with internal cardioverter-defibrillator (ICD)
  • Syndrome characterized by
    • ​ECG abnormalities in leads V1-V2
    • Polymorphic or monomorphic VT
    • Structurally normal heart
    • Familial occurence in about half of patients
  • ​Discuss/refer to electrophysiologist
ECG Findings in V1-V2​
  • RBBB or incomplete RBBB pattern
  • ST-segment elevation - 2 types
    • ​​"Coved-type" (most common & concerning)
    • "Saddle-type"

Should you workup trauma with an ECG??
Episode 151

July 21, 2014


Upcoming ECG CME:
Emergency Cardiology in Las Vegas 
Oct 2-5, 2014

Quick Estimation of QT interval

T-waves should typically end before the midpoint of the R-R interval. Beware of a prolonged QT-interval when the T-wave ends after the midpoint of the R-R interval (half way between the R-waves).

Differential for Prolonged QTc

  • Hypokalemia
  • Hypomagnesemia
  • Hypocalemia
  • Hypothermia
  • Acute coronary syndromes / ischemia
  • Increased intracranial pressures
  • Medications (many)
  • Congenital

Prolonged QTc

  • Check lytes & medications
  • Beware of torsades 
    • Can present as seizures
    • ​Treat with Mg2+, shock, overdrive pacing

Check out more cases on prolonged-QT intervals & hypokalemia:
Should you workup trauma with an ECG??
Episode 151

July 21, 2014


Upcoming ECG CME:
Emergency Cardiology in Las Vegas 
Oct 2-5, 2014

Quick Estimation of QT interval

T-waves should typically end before the midpoint of the R-R interval. Beware of a prolonged QT-interval when the T-wave ends after the midpoint of the R-R interval (half way between the R-waves).

Differential for Prolonged QTc

  • Hypokalemia
  • Hypomagnesemia
  • Hypocalemia
  • Hypothermia
  • Acute coronary syndromes / ischemia
  • Increased intracranial pressures
  • Medications (many)
  • Congenital

Prolonged QTc

  • Check lytes & medications
  • Beware of torsades 
    • Can present as seizures
    • ​Treat with Mg2+, shock, overdrive pacing

Check out more cases on prolonged-QT intervals & hypokalemia:
See how cereal saves lives!
Episode 150

July 14, 2014


Some patients with STEMI will have non-diagnostic INITIAL ECGs. 
 
Have a low threshold to get serial ECGs!
 
Repeat the ECG with persistent or changing pain. 
 

Here are links to more cases where serial ECGs made a difference:


Reference:

Riley RF, Newby LK, Don CW, et al. Diagnostic time course, treatment, and in-hospital outcomes for patients with ST-segment elevation myocardial infarction presenting with nondiagnostic initial electrocardiogram: A report from the American Heart Association Mission: Lifeline program. Am Heart J. 2013;165(1):50–56. PMID: 23237133

See how cereal saves lives!
Episode 150

July 14, 2014


Some patients with STEMI will have non-diagnostic INITIAL ECGs. 
 
Have a low threshold to get serial ECGs!
 
Repeat the ECG with persistent or changing pain. 
 

Here are links to more cases where serial ECGs made a difference:


Reference:

Riley RF, Newby LK, Don CW, et al. Diagnostic time course, treatment, and in-hospital outcomes for patients with ST-segment elevation myocardial infarction presenting with nondiagnostic initial electrocardiogram: A report from the American Heart Association Mission: Lifeline program. Am Heart J. 2013;165(1):50–56. PMID: 23237133

Posterior STEMI or anterior ischemia?
Episode 149

July 7, 2014


Upcoming Conference:

October 15-17, 2014
Baltimore, MD

Differential for ST-Depression in Anteroseptal Leads
  1. Posterior STEMI
  2. Anteroseptal ischemia
  3. Miscellaneous
    • RBBB, Hypokalemia, etc.

Posterior Myocardial Infarction

  • Usually associated with Inferior MI due to RCA or circumflex occlusion
  • 4% of STEMI’s are isolated PMI’s with increased M&M compared to Isolated inferior MI’s
  • Mirror image of septal MI in leads V1-V2
    • Large R-waves instead of Q’s
    • ST-segment depression (STD)  instead of ST-elevation (STE)
    • Upright T-waves instead of T-wave inversions

ECG Changes in Leads V1-V2 (-V3)

Septal STEMI
ST-segment
Elevation
Inverted
T-waves
Q-waves
develop over hours
Posterior STEMI
(Mirror image)
ST-segment
Depression 
Upright
T-waves
Tall R’s
develop over hours

In doubt? Get posterior leads when there’s ST-depression in septal leads! 

Posterior STEMI or anterior ischemia?
Episode 149

July 7, 2014


Upcoming Conference:

October 15-17, 2014
Baltimore, MD

Differential for ST-Depression in Anteroseptal Leads
  1. Posterior STEMI
  2. Anteroseptal ischemia
  3. Miscellaneous
    • RBBB, Hypokalemia, etc.

Posterior Myocardial Infarction

  • Usually associated with Inferior MI due to RCA or circumflex occlusion
  • 4% of STEMI’s are isolated PMI’s with increased M&M compared to Isolated inferior MI’s
  • Mirror image of septal MI in leads V1-V2
    • Large R-waves instead of Q’s
    • ST-segment depression (STD)  instead of ST-elevation (STE)
    • Upright T-waves instead of T-wave inversions

ECG Changes in Leads V1-V2 (-V3)

Septal STEMI
ST-segment
Elevation
Inverted
T-waves
Q-waves
develop over hours
Posterior STEMI
(Mirror image)
ST-segment
Depression 
Upright
T-waves
Tall R’s
develop over hours

In doubt? Get posterior leads when there’s ST-depression in septal leads! 

How to evaluate fast and wide
Episode 148

June 30, 2014


Upcoming ECG CME:
 
"Cruisin’ with Cardiograms"
Sept 14-21, 2014
 
Emergency Cardiology in Las Vegas 
Oct 2-5, 2014

Causes of QRS prolongation

  • Ventricular ectopy

  • BBB (LBBB or RBBB) or paced rhythm

  • Tox/Metabolic (Na2+ channel blocker toxicity, acidosis, hyperkalemia)

  • Pre-excitation (WPW)

  • Nonspecific intraventricular conduction delay (eg. LVH)

Atrial Fibrillation with WPW

  • Very rapid, irregularly irregular tachycardia 

  • Rates may approach 250-300 bpm or higher

  • Changing QRS complex shape and width

  • Often misdiagnosed as SVT, VT, or A.fib with aberrancy

  • AV nodal blockade (BB’s, CCB’s, Amiodarone, etc.) can cause ventricular fibrillation and death

  • Amiodarone has AV nodal blockade properties & may have proarrhythmic effects in Afib with WPW (can accelerate ventricular rate and precipitate Vfib)


References:
 

Boriani G, Biffi M, Frabetti L, et al. Ventricular fibrillation after intravenous amiodarone in Wolff-Parkinson-White syndrome with atrial fibrillation. Am Heart J. 1996 Jun;131(6):1214-6. PMID: 8644602

Gaita F, Giustetto C, Riccardi R, et al. Wolff-Parkinson-White syndrome. Identification and management. Drugs. 1992 Feb;43(2):185-200. PMID: 1372217

Schützenberger W, Leisch F, Gmeiner R. Enhanced accessory pathway conduction following intravenous amiodarone in atrial fibrillation. A case report. Int J Cardiol. 1987 Jul;16(1):93-5. PMID: 3610399

Sheinman BD, Evans T. Acceleration of ventricular rate by fibrillation associated with the Wolff-Parkinson-White syndrome. Br Med J (Clin Res Ed). 1982 Oct 9; 285(6347), 999–1000. PMID: 6812745

Tijunelis  MA, Herbert ME. Myth: Intravenous amiodarone is safe in patients with atrial fibrillation and Wolff-Parkinson-White syndrome in the emergency department. CJEM. 2005 Jul;7(4), 262–265. PMID: 17355684

How to evaluate fast and wide
Episode 148

June 30, 2014


Upcoming ECG CME:
 
"Cruisin’ with Cardiograms"
Sept 14-21, 2014
 
Emergency Cardiology in Las Vegas 
Oct 2-5, 2014

Causes of QRS prolongation

  • Ventricular ectopy

  • BBB (LBBB or RBBB) or paced rhythm

  • Tox/Metabolic (Na2+ channel blocker toxicity, acidosis, hyperkalemia)

  • Pre-excitation (WPW)

  • Nonspecific intraventricular conduction delay (eg. LVH)

Atrial Fibrillation with WPW

  • Very rapid, irregularly irregular tachycardia 

  • Rates may approach 250-300 bpm or higher

  • Changing QRS complex shape and width

  • Often misdiagnosed as SVT, VT, or A.fib with aberrancy

  • AV nodal blockade (BB’s, CCB’s, Amiodarone, etc.) can cause ventricular fibrillation and death

  • Amiodarone has AV nodal blockade properties & may have proarrhythmic effects in Afib with WPW (can accelerate ventricular rate and precipitate Vfib)


References:
 

Boriani G, Biffi M, Frabetti L, et al. Ventricular fibrillation after intravenous amiodarone in Wolff-Parkinson-White syndrome with atrial fibrillation. Am Heart J. 1996 Jun;131(6):1214-6. PMID: 8644602

Gaita F, Giustetto C, Riccardi R, et al. Wolff-Parkinson-White syndrome. Identification and management. Drugs. 1992 Feb;43(2):185-200. PMID: 1372217

Schützenberger W, Leisch F, Gmeiner R. Enhanced accessory pathway conduction following intravenous amiodarone in atrial fibrillation. A case report. Int J Cardiol. 1987 Jul;16(1):93-5. PMID: 3610399

Sheinman BD, Evans T. Acceleration of ventricular rate by fibrillation associated with the Wolff-Parkinson-White syndrome. Br Med J (Clin Res Ed). 1982 Oct 9; 285(6347), 999–1000. PMID: 6812745

Tijunelis  MA, Herbert ME. Myth: Intravenous amiodarone is safe in patients with atrial fibrillation and Wolff-Parkinson-White syndrome in the emergency department. CJEM. 2005 Jul;7(4), 262–265. PMID: 17355684

Something you better know if your patient speaks Italian!
Episode 147

June 23, 2014


ECG Differentials for Syncope:

  • Ischemia
  • Dysrhythmias & AV-blocks
  • Intervals
    • WPW / Pre-excitation
    • Long / Short QT syndromes
  • Hypertrophic cardiomyopathy
  • Brugada syndrome
  • Arrhythmogenic RV dysplasia​ (ARVD)

ARVD - Epsilon waves

Background

  • Not common except in certain populations
    • ​General population: 1/1,000-1/10,000
    • Italy: 40/10,000
      • Most common cause of sudden death in young
  • Familial (autosomal dominant)
  • Male > Female
  • Caused by progressive replacement of RV myocardium by fibrofatty tissue that interferes with impulse conduction

Clinical 

  • Common cause of ventricular arrhythmias and sudden death in adolescents and young adults, athletes
  • Usually manifests between puberty - 60 years of age
  • Often have FHx of premature sudden death in family members < 35 years old
  • ECG findings are imperfect
  • ECHO, MRI, MDCT, and endomyocardial biopsy used for diagnosis

ECG findings

  • Leads V1-V3
    • ​Epsilon waves
    • TWI’s 
    • Slight prolongation of QRS
  • LBBB-type VT or many PVC’s

Management

  • Consult electrophysiology
  • Active ventricular dysrhythmias
    • Stable: Beta blockers, Class III antiarrhythmics
    • ICD placement in patients with cardiac arrest, syncope, VT
  • ​​Heightened concern if
    • Young, especially males
    • Family Hx of early sudden death
    • Many PVC’s
    • LBBB-type VT
    • Epsilon Waves with TWI in V1-V3

Reference:

Basso C, Corrado D, Marcus FL, et al. Arrhythmogenic right ventricular cardiomyopathy. Lancet. 2009 Aril 11;373(9671):1289-300. PMID:19362677

Something you better know if your patient speaks Italian!
Episode 147

June 23, 2014


ECG Differentials for Syncope:

  • Ischemia
  • Dysrhythmias & AV-blocks
  • Intervals
    • WPW / Pre-excitation
    • Long / Short QT syndromes
  • Hypertrophic cardiomyopathy
  • Brugada syndrome
  • Arrhythmogenic RV dysplasia​ (ARVD)

ARVD - Epsilon waves

Background

  • Not common except in certain populations
    • ​General population: 1/1,000-1/10,000
    • Italy: 40/10,000
      • Most common cause of sudden death in young
  • Familial (autosomal dominant)
  • Male > Female
  • Caused by progressive replacement of RV myocardium by fibrofatty tissue that interferes with impulse conduction

Clinical 

  • Common cause of ventricular arrhythmias and sudden death in adolescents and young adults, athletes
  • Usually manifests between puberty - 60 years of age
  • Often have FHx of premature sudden death in family members < 35 years old
  • ECG findings are imperfect
  • ECHO, MRI, MDCT, and endomyocardial biopsy used for diagnosis

ECG findings

  • Leads V1-V3
    • ​Epsilon waves
    • TWI’s 
    • Slight prolongation of QRS
  • LBBB-type VT or many PVC’s

Management

  • Consult electrophysiology
  • Active ventricular dysrhythmias
    • Stable: Beta blockers, Class III antiarrhythmics
    • ICD placement in patients with cardiac arrest, syncope, VT
  • ​​Heightened concern if
    • Young, especially males
    • Family Hx of early sudden death
    • Many PVC’s
    • LBBB-type VT
    • Epsilon Waves with TWI in V1-V3

Reference:

Basso C, Corrado D, Marcus FL, et al. Arrhythmogenic right ventricular cardiomyopathy. Lancet. 2009 Aril 11;373(9671):1289-300. PMID:19362677

15 yo girl with anxiety? Check the ECG!
Episode 146

June 16, 2014


15 yo girl with anxiety? Check the ECG!
Episode 146

June 16, 2014


ECG Differentials for syncope / palpitations:
  • Ischemia
  • Tachy / Bradycardias & AV-blocks
  • Intervals
    • WPW / Pre-excitation
    • Long / Short QT syndromes
  • Hypertrophic cardiomyopathy
  • Brugada syndrome
  • Arrhythmogenic RV dysplasia

WPW Syndrome 

Ventricular pre-excitation
  • 0.1-3% of the population
  • Classic triad
    • Shortened PR interval
    • Widened QRS interval
    • Delta wave (Not always present!)​
  • ​Predisposition to atrial tachydysrhythmias 
  • ​​WPW can be intermittent
 

Don’t hesitate to get ECGs on young patients!

Look in all 12 leads and suspect WPW if you notice a short PR-interval.


For more syncope cases, check out… #Syncope

33yo with reflux? Just slap yourself!
Episode 145

June 9, 2014


AMI in Pregnancy

     Pregnancy increases risk of AMI 3-4X
  • Slight overall risk
  • 3rd trimester to 6 weeks post-partum
  • Maternal mortality = 5-11%
  • Fetal mortality = 9%
  • ​Increased with pregnancy at older ages
  • Increased atherosclerosis and risk factors
     Most common causes
         1.  Coronary artery dissection (35-50%)
  • Usually anterior wall
  • Hormonal changes to vessel wall
  • Shear forces
  • Underlying disease (i.e. connective tissue disorders)
         2.  ​​Plaque rupture due to atherosclerosis (40%)
 
ECG changes in Pregnancy
  • Axis changes (LAD or RAD)
  • Small Q in III
  • Non-specific TWI’s
  • Increased R/S ration in V1-V2
​Treatment
  • Coordinate with OB and Cardiology
  • Usual Care (ASA probably ok)
  • PCI > Thrombolytics 
    • Concern for hemorrhage peripartum
    • Concern for coronary artery dissection
    • Thrombolytics: placental transfer is low
    • Heparin is ok
Young women do get MI’s!

33yo with reflux? Just slap yourself!
Episode 145

June 9, 2014


AMI in Pregnancy

     Pregnancy increases risk of AMI 3-4X
  • Slight overall risk
  • 3rd trimester to 6 weeks post-partum
  • Maternal mortality = 5-11%
  • Fetal mortality = 9%
  • ​Increased with pregnancy at older ages
  • Increased atherosclerosis and risk factors
     Most common causes
         1.  Coronary artery dissection (35-50%)
  • Usually anterior wall
  • Hormonal changes to vessel wall
  • Shear forces
  • Underlying disease (i.e. connective tissue disorders)
         2.  ​​Plaque rupture due to atherosclerosis (40%)
 
ECG changes in Pregnancy
  • Axis changes (LAD or RAD)
  • Small Q in III
  • Non-specific TWI’s
  • Increased R/S ration in V1-V2
​Treatment
  • Coordinate with OB and Cardiology
  • Usual Care (ASA probably ok)
  • PCI > Thrombolytics 
    • Concern for hemorrhage peripartum
    • Concern for coronary artery dissection
    • Thrombolytics: placental transfer is low
    • Heparin is ok
Young women do get MI’s!

Reference:

Sahni G. Chest Pain Syndromes in Pregnancy. Cardiology Clinics. 2012;30(3):343–367. PMID: 22813362