Myocardial Infarction: Difference between revisions

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==Myocardial Ischemia==
{{authors|
 
|mainauthor= [[user:Vdbilt|I.A.C. van der Bilt, MD]]
Ischemia occurs when part of the heartmuscle, the myocardium, is deprived form oxygen and nutrients.  
|moderator= [[user:Vdbilt|I.A.C. van der Bilt, MD]]
|supervisor=  
}}
{{clr}}
{{box|
Ischemia occurs when part of the heart muscle, the myocardium, is deprived of oxygen and nutrients.  
Common causes of ischemia are:
Common causes of ischemia are:
* Narrowing or obstruction of a coronary artery.
* Narrowing or obstruction of a coronary artery.
* A fast rhythm disturbance, causing a disbalance in supply and demand of energy.  
* A rapid arrhythmia, causing an imbalance in supply and demand for energy.  


A short period of ischemia causes ''reversibele'' effects: The heartcells will be able to recover. When the ep[isode of ischemia lasts for a longer period of time, heartmuscle cells will die. This is called a '''heart attack''' or '''myocardial infarction'''. That is why it is critical to recognize ischemia on the ECG in an early stage.  
A short period of ischemia causes ''reversible'' effects: The heart cells will be able to recover. When the episode of ischemia lasts for a longer period of time, heart muscle cells die. This is called a '''heart attack''' or '''myocardial infarction'''. That is why it is critical to recognize ischemia on the ECG in an early stage.  


Severe ischemia will reuslts in ECG changes within minutes. While the ischemia lasts, several ECG changes will occur and disappear again. Therefore, it may be difficult to estimate the duration of the ischemia on the ECG, which is crucial for adequate treatment.  
Severe ischemia results in ECG changes within minutes. While the ischemia lasts, several ECG changes will occur and disappear again. Therefore, it may be difficult to estimate the duration of the ischemia on the ECG, which is crucial for adequate treatment.  


'''Signs and symptoms of myocardial ischemia:'''
'''Signs and symptoms of myocardial ischemia:'''
Line 16: Line 21:
* Nausea
* Nausea
* Shock (manifesting as paleness, low blood pressure, fast weak pulse) shock  
* Shock (manifesting as paleness, low blood pressure, fast weak pulse) shock  
* Rhythm dysturbances (in particular increasing prevalnce of ventricular ectopia, ventricular tachycardia, AV block)
* Rhythm disturbances (in particular, increasing prevalence of ventricular ectopia, ventricular tachycardia, AV block)
 
}}
===Risk assessment of ischemia===
{{clr}}
The narrowing of the coronary artery leading to a myocardial infarction, usually develops over several years. An increased risk of myocardial infarction can be estimated using [http://www.escardio.org/initiatives/prevention/prevention-tools/SCORE-Risk-Charts.htm SCORE system] which is developed by the European Society of cardiology (ESC). As shown in the figue, the most important risk factors for myocardial infarction are:
===Risk assessment of Cardiovascular disease===
*Male sexe
Narrowing of the coronary artery, leading to a myocardial infarction, usually develops over several years. An increased risk of cardiovascular disease, which may lead to a myocardial infarction or cerebrovascular accident, can be estimated using [http://www.escardio.org/communities/EACPR/toolbox/health-professionals/Pages/SCORE-Risk-Charts.aspx SCORE system] which is developed by the European Society of cardiology (ESC).  
As shown in the figure, the most important risk factors for myocardial infarction are:
*Male sex
*Smoking
*Smoking
*Hypertension
*Hypertension
Line 26: Line 33:
*Hypercholesterolemia
*Hypercholesterolemia


An exercise test such as a bicycle or treadmilltest, may be usefull in detecting myocardial ischemia after exercise.<cite>accexercise</cite> In such a test, a continuous ECG registration is performed during exercise. The ST-segment, blood pressure asnd clinical status of the patient (i.e. chest complaints) are monitorered during and after the test.
===Risk assessment of ischemia===
An [[Exercise Testing|exercise test]] such as a bicycle or treadmill test, may be useful in detecting myocardial ischemia after exercise.<cite>accexercise</cite> In such a test, continuous ECG monitoring is performed during exercise. The ST-segment, blood pressure and clinical status of the patient (i.e. chest complaints) are monitored during and after the test.


An excersize test is positive for myocardial ischemia when the following criteria are met:  
An [[Exercise Testing|exercise test]] is positive for myocardial ischemia when the following criteria are met:  
* Horizontal or downsloping ST-depression of > 1mm, 60 or 80ms after the J-point
* Horizontal or downsloping ST-depression of >1mm, 60 or 80ms after the J-point
* ST elevation of > 1.0 mm
* ST elevation of > 1.0 mm
{{clr}}
{{clr}}


==Diagnosis of myocardial infarction==
==Diagnosis of myocardial infarction==
The diagnosis of acute myocardial infarction is not only based on the ECG. A myocardial is defined as:<cite>Alpert</cite>
[[Image:Stelevatie_en.png|thumb|300px|ST elevation is measured at the junctional or J-point]]
 
The diagnosis of acute myocardial infarction is not only based on the ECG. A myocardial infarction is defined as:<cite>Alpert</cite>


* Heartenzymes ([[w:Creatine_kinase|CKMB]] or [[w:Troponin|Troponin T]]) are elevated in the blood AND  
* Elevated blood levels of cardiac enzymes ([[w:Creatine_kinase|CKMB]] or [[w:Troponin|Troponin T]]) AND  
* One of the following criteria are met:
* One of the following criteria are met:
** The patient has typical complaints
** The patient has typical complaints,
** The ECG shows ST elevation or depression
** The ECG shows ST elevation or depression.
** [[pathological Q waves]] develop on the ECG
** [[Pathologic_Q_Waves|pathological Q waves]] develop on the ECG
** A coronary intervention had been performed (such as stent placement)
** A coronary intervention had been performed (such as stent placement)


So detection of elevated serum heartenzymes is more important than ECG changes. However, the heartenzymes can only be detected in the serum 5-7 hours after the onset of the myocardial infarction. So especially in the first few hours after the myocardial infarction the ECG can be very usefull.
So detection of elevated serum cardiac enzymes is more important than ECG changes. However, the cardiac enzymes can only be detected in the serum 5-7 hours after the onset of the myocardial infarction. So, especially in the first few hours after the myocardial infarction, the ECG can be crucial.


==Development of the ECG during persistent ischemia==
ECG Manifestations of Acute Myocardial Ischaemia (in Absence of LVH and [[MI Diagnosis in LBBB|LBBB]])are <cite>Thygesen</cite>:
[[Image:AMI_evolutie.png|thumb| The evolution of an infarct on the ECG. ST elevation, Q wave formation, T wave inversion, normalisation with a persistent Q wave]]
[[Image:PathoQ.png|thumb| A [[pathological Q wave|pathological Q wave]]]]
The cardiomyocytes in the ''subendocardial'' layers are especcially vulnerable for a decreased perfusion. Subendocardial ischemia manifests as ST depression and is usually reversible. In a myocardial infarction ''transmural ischemia'' develops.


In the first hours and days after the onset of a myocardial infarction, several changes can be observed on the ECG. First, '''large peaked T waves''' (or ''hyperacute'' T waves), then '''ST elevation''', then'''negative T waves''' and finally '''[[pathological Q waves]]''' develop.
;ST elevation
:New ST elevation at the J-point in two contiguous leads with the cut-off points: ≥0.2 mV in men or ≥ 0.15 mV in women in leads V2–V3 and/or ≥ 0.1 mV in other leads.
;ST depression and T-wave changes.
:New horizontal or down-sloping ST depression >0.05 mV in two contiguous leads; and/or T inversion ≥0.1 mVin two contiguous leads with prominent R-wave or R/S ratio ≥ 1


{| class="wikitable"
A study using MRI to diagnose myocardial infarction has shown that more emphasis on ST segment depression could greatly improve the yield of the ECG in the diagnosis of myocardial infarction (sensitivity increase from 50% to 84%).<cite>martin</cite>
|-
|+'''Evolution of the ECG during a myocardial infarct'''
|-
!
!see figure
!change
|-
!minutes
| not in figure
b
| hyperacute T waves (peaked T waves)
ST-elevation
|-
!hours
| c
d
| ST-elevation, with terminal negative T wave
negative T wave (these can last for months)
|-
!days
| e
| [[pathological Q waves]]
|-
|}


Myocardial infarction diagnosis in left or right bundle branch block can be difficult, but it is explained in these seperate chapters:
*[[MI Diagnosis in LBBB|MI diagnosis in left bundle branch block or paced rhytm]]
*[[MI Diagnosis in RBBB]]
{{clr}}
{{clr}}


==The location of the infarct==
==The location of the infarct==
[[Image:coronary_anatomy.png|thumb| An overview of the coronary arteries. LM = 'Left Main' = mainstem; LAD = 'Left Anterior Descending' artery; RCX = Ramus Circumflexus; RCA = 'Right Coronary Artery'.]]
<div style="float:right;margin-left:10px">
[[Image:lead_overview.png|thumb|Overview of the seperate ECG leads. The lead with ST elevation 'highlights' the infarct. An infarction of the inferior wall will result in ST elevation in leads II, III and AVF. A lateral wall infarct results in ST elevation in leads I and AVL. An Anterior wall infarct results in ST-elevation in the precordial leads.]]
<gallery perRow="2">
[[Image:stroomgebieden.png|thumb| The Left Anterior Descending (LAD) coronary artery is the most important coronary artery. On this mercatorprojection of the heart, the darkblue area is supplied by blood by the LAD.]]
Image:coronary_anatomy.png| An overview of the coronary arteries. LM = 'Left Main' = mainstem; LAD = 'Left Anterior Descending' artery; RCX = Ramus Circumflexus; RCA = 'Right Coronary Artery'.
Image:lead_overview.png|Overview of the separate ECG leads. The lead with ST segment elevation 'highlights' the infarct. An infarction of the inferior wall will result in ST segment elevation in leads II, III and AVF. A lateral wall infarct results in ST segment elevation in leads I and AVL. An Anterior wall infarct results in ST segment elevation in the precordial leads.
Image:MI_colours_en.png|The coloured figure shows contiguous leads in matching colors
Image:MIregions.jpg|The ST segment elevation points at the infarct location. Inferior MI=ST segment elevation in red regions (lead II,III and AVF). Lateral MI = ST elevation in blue leads (lead I, AVL, V5-V6). Anterio MI: ST segment elevation in yellow region (V1-V4). Left main stenosis: ST elevation in gray area (AVR)  
Image:conduction_blood_supply.png|The coronary blockade can cause conduction block, on AV nodal, His or bundle branch level.
</gallery>
</div>
The heartmuscle itself is very limited in its capacity to extract oxygen in the blood that is being pumped. Only the inner layers (the endocardium) profit from this oxygenrich blood. The outer layers of the heart (the epicardium) are dependent on the coronary arteries for the supply of oxygen and nutrients. With aid of an ECG, the occluded coronary can be identified. This is valuable information for the clinician, because treatment and complications of for instance an '''anterior wall infarction''' is different than those of an '''inferior wall infarction'''. The anterior wall performs the main pump function, and decay of the function of this wall will lead to decrease of bloodpressure, increase of heartrate, shock and on a longer term: heart failure. An inferior wall infarction is often accompanied with a decrease in heartrate because of involvement of the sinusnode. Longterm  effects of an inferior wall infarction are usually less severe than those of an anterior wall infarction.
The heartmuscle itself is very limited in its capacity to extract oxygen in the blood that is being pumped. Only the inner layers (the endocardium) profit from this oxygenrich blood. The outer layers of the heart (the epicardium) are dependent on the coronary arteries for the supply of oxygen and nutrients. With aid of an ECG, the occluded coronary can be identified. This is valuable information for the clinician, because treatment and complications of for instance an '''anterior wall infarction''' is different than those of an '''inferior wall infarction'''. The anterior wall performs the main pump function, and decay of the function of this wall will lead to decrease of bloodpressure, increase of heartrate, shock and on a longer term: heart failure. An inferior wall infarction is often accompanied with a decrease in heartrate because of involvement of the sinusnode. Longterm  effects of an inferior wall infarction are usually less severe than those of an anterior wall infarction.


The heart is supplied of oxygen and nutrients by the right and left coronary arteries.The left coronray artery(the '''Mainstem''' or LM, left main) divides itself in the '''left anterior descending''' artery (LAD) and the '''ramus circumflexus''' (RCX). The '''right coronary artery''' (RCA) connects to the ramus descendens posterior (RDP). With 20% of the normal population the RDP is supplied by the RCX. This called '''left dominance'''.
The heart is supplied of oxygen and nutrients by the right and left coronary arteries. The left coronary artery (the '''Left Main''' or LM) divides itself in the '''left anterior descending''' artery (LAD) and the '''ramus circumflexus''' (RCX). The '''right coronary artery''' (RCA) connects to the '''ramus descendens posterior '''(RDP). With 20% of the normal population the RDP is supplied by the RCX. This called '''left dominance'''.


Below you can find several different types of myocardial infarcation.
Below you can find several different types of myocardial infarcation. Click on the specific infarct location to see examples.




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!localisation
!localisation
!ST elevation
!ST elevation
!Reciproke ST depression
!Reciprocal ST depression
!coronary artery
!coronary artery
|-
|-
| [[#Anterior Wall|anterior wall]] (anterior)
| [[Anterior MI]]  
| V1-V6
| V1-V6
| None
| None
| LAD
| LAD
|-
|-
| [[#Septal|septal]]
| [[Septal MI]]
| V1-V4, disappearance of septum Q in leads V5,V6
| V1-V4, disappearance of septum Q in leads V5,V6
| none
| none
| LAD
| LAD-septal branches
|-
|-
| [[#Lateral|lateral]]
| [[Lateral MI]]
| I, aVL, V5, V6
| I, aVL, V5, V6
| II,III, aVF
| II,III, aVF
| RCX or MO
| LCX or MO
|-
|-
| [[#inferior|inferior]] (inferior)
| [[Inferior MI]]
| II, III, aVF
| II, III, aVF
| I, aVL
| I, aVL
| RCA (80%) or RCX (20%)
| RCA (80%) or RCX (20%)
|-
|-
| [[#posterior|posterior]] (posterior)
| [[Posterior MI]]
| V7, V8, V9
| V7, V8, V9
| high R in V1-V3 with ST depression V1-V3 > 2mm (mirror view)
| high R in V1-V3 with ST depression V1-V3 > 2mm (mirror view)
| RCX
| RCX
|-
|-
| right ventricle
| [[Right Ventricle MI]]
| V1, V4R
| V1, V4R
| I, aVL
| I, aVL
| RCA
|-
| [[Atrial MI]]
| PTa in I,V5,V6
| PTa in I,II, or III
| RCA
| RCA
|-
|-
|}
|}
{{clr}}


The localisation of the occlusion can be adequately visualized using a coronary angiogram (CAG). On the CAG report,  the place of the occlusion is often graded with a number (for example LAD(7)) using the classification of the American Heart Association.<cite>AHACAG</cite>
The localisation of the occlusion can be adequately visualized using a coronary angiogram (CAG). On the CAG report,  the place of the occlusion is often graded with a number (for example LAD(7)) using the classification of the American Heart Association.<cite>AHACAG</cite>
===Anterior wall===
ECG-characteristics:<cite>Wung</cite>
ST-elevation in leads V1-V6, I and aVL. Maximum elevation in V3, maximal depression in III
later: pathological Q-wave in the precordial leads V2 to V4-V5.
[[Image:AMI_anterior.png|thumb| A typical example of an acute anterior wall infarction. ST elevation in leads I, AVL and V2-V5. Reciprocal depressions in the inferior leads (II,III,AVF)]]
[[Image:heart_with_AL_infarct.png|thumb|Anterolateral infarct caused by occlusion of the LAD.]]
[[Image:ECG_VWI_2wk.jpg|thumb| A 2 weeks old anterior infarction with Q waves in V2-V4 and persisting ST elevation, possibly as a sign of formation of an aneurysm]]
Encomprises the anterior part of the heart and a part of the ventricular septum. Is supplied by blood by the LAD.
{{clr}}
{{clr}}


===Septal===
==Development of the ECG during persistent ischemia==
QS in V1 and V2. Later the septum-Q in V5 and V6 disappears.
[[Image:AMI_evolutie.png|thumb| The evolution of an infarct on the ECG. ST elevation, Q wave formation, T wave inversion, normalisation with a persistent Q wave]]
Encomprises the ventricular septum which is supplied of blood by the septal branches of the LAD.
[[Image:PathoQ.png|thumb| A [[Pathologic_Q_Waves|pathological Q wave]]]]
[[File:DVA1995.jpg|thumb|Wellens syndrome: symmetrical negative T wave in pre-cordial leads without R loss of R waves can regularly be observed in early anterior ischemia. Many patients with Wellens syndrome / sign turn out to have a critical proximal LAD stenosis<cite>WellensSign</cite>.]]
[[Image:anteriorMInegativeT.png|thumb| Typical negative T waves post anterior myocardial infarction. This patient also shows QTc prolongation. Whether this has an effect on prognosis is debated.<cite>Novotny</cite><cite>Jensen</cite><cite>Chevalier</cite>]]
The cardiomyocytes in the ''subendocardial'' layers are especcially vulnerable for a decreased perfusion. Subendocardial ischemia manifests as ST depression and is usually reversible. In a myocardial infarction ''transmural ischemia'' develops.  


===Lateral===
In the first hours and days after the onset of a myocardial infarction, several changes can be observed on the ECG. First, '''large peaked T waves''' (or ''hyperacute'' T waves), then '''ST elevation''', then '''negative T waves''' and finally '''[[Pathologic_Q_Waves|pathologic Q waves]]''' develop.
ST elevation in I, aVL, V5 and V6
Encomprises the lateral side of the left ventricle. This is supplied with blood by the RCX or the MO. The MO, the '''marginalis obtusis''' is a sidebranch between the LAD and the RCX. In case of a lateral infarct, the maximal ST elevation is in lead V7 and the maximal depression in V2. <cite>Wung</cite>


===Antero-lateral===
'''Wellens syndrome''' or sign (see image) can be an early ECG warning sign of critical anterior ischemia before the development of overt mocardial infarction.


[[Image:AMI_Anterolateral.png|thumb]]
{| class="wikitable"
 
|-
ST-elevation in the precordial leads V2-V6
|+'''Evolution of the ECG during a myocardial infarct'''
 
|-
Later, negative T waves and Q-waves have developed in I, aVL, V5 en V6.
!Time from onset of symptoms
{{clr}}
!ECG
 
!Changes in the heart
===Inferior wall===
|-
ST elevation in II, III and aVF
!minutes
This part of the heart muscle lies on the diaphragm and is supplied of blood bij the right coronary artery (RCA) in 8% of patients. In the remaing 20% the inferior wall is supplied by the ramus circumflexus(RCX).
| hyperacute T waves (tall T waves), ST-elevation
[[Image:AMI_inferior.jpg|thumb| An example of an inferior waal infarction.]]
| reversible ischemic damage
An occlusion of the RCA can be distinguished of a RCX occulsuion on the ECG: in a RCA occlusion, there is ST depression in I and AvL and the ST-elevation is higher in III than in II. If the elevation is higher in II, suspect a RCX occlusion.
|-
{{clr}}
!hours
 
| ST-elevation, with terminal negative T waves, negative T waves (these can last for days to months)
===Posterior wall===
| onset of myocardial necrosis [[Image:Heart_ant_wall_infarction.jpg|left|150px|Thumb|An acute anterior myocardial infarction typically shows ST elevation on the ECG]]
High R-waves with ST-depression in V1-V3.
|-
[[Image:Heart_with_P_infarct.png|thumb|Posteriorinfarction caused by occlusion of the RCA]]
!days
The posterior wall is usually supplied of blood by the RCA. Because no leads "look" at the posterior wall in the normal ECG, no leads show ST-elevation in case of a posterior wall infarction. The ST depressions in V1-V3 that can be observed in case of a posterior wall infarction are in fact mirrored ST elevations and the high R-waves are the Q-waves of the infarct. To be able to confirm a posterior-infarct, leads V7, V8 and V9 may be helpfull. These leads are horizontally placed from V6 to the back and do show the ST elevations of the posterior wall.
| [[Pathologic Q Waves]]
{{clr}}
| scar formation [[Image:Heart_ant_wall_scar_sa.jpg|left|150px|Thumb|A transmural anterior myocardial infarction with scar formation and [[Pathologic Q Waves]]]]
 
|-
===Right ventricle===
|}
ST-elevation >1 mm in lead V4 right
ST elevation in lead V1
 
Can be seen after a proximal occlusion of the RCA.
 
'''V4 right''' is located at the same place as lead V4, but is placed on the right side of the patient. This means it is placed under the right nipple instead of the left. This increases the sensitivity of detecting right ventricle infarcts.
 
===Atrial infarct===
In approximately 10% of the infractpatients, atrial infarct is suspected. An atrial infarct can manifest itself in atrial rhytmdisturbances: atrial fibrillation / atrial rhythm. Because the atria are hemodynamically of minor importance, the consequences of an atrial infarct are limited (and therfore often missed!).
 
On the ECG, an atrial infarct manifests by rhythmchanges and/or chnage of the P-Ta segment (sometimes calledPTA (''P'' - ''a''triale ''T'') segment or PR or PQ or PTp (''P'' - ''T'' wave of ''P'' wave) segment)<cite>Abildskov</cite>. This is the part between the P wave and the Q. The ST segment indicates an infarct in the ventricle, the P-Ta segment indicates an infarct in the atria.
 
Diagnostic criteria for an atrial infarct <cite>Liu</cite>:
* P-Ta elevation >0.5mm in V5 and V6 with reciprocal depression in V1 and V2
* P-Ta elevation >0.5mm in I and depression in II and III
* >1.5mm P-Ta depression in precordial leads
* >1.2mm P-Ta depression in I,II or III in combination with atrial arrhytmias
 
Seceral diagnostic criteria are in use, and this is just an example of one. An important differential diagnosis of PTa segment elevation or depression is pericarditis.
 
==Infarct diagnosis in LBBB==
Bij een LBTB is de infarctdiagnostiek heel moeilijk, omdat de ST segmenten altijd afwijkend zijn bij een LBTB. Een nieuw ontstaan linker bundeltakblok is een sterk argument dat het er sprake is van een myocardinfarct, maar vaak is er geen oud ECG voorhanden. De criteria (van Sgarbossa <cite>LBTB</cite>) die wel gebruikt kunnen worden bij een LBTB ECG zijn:
*ST elevatie > 1mm in afleidingen met een positief QRS complex (concordante ST deviatie) (score 5)
*ST depressie > 1 mm in V1-V3 (discordante ST deviatie) (score 3)
*ST elevatie > 5 mm in afleidingen met een negatief QRS complex (discordante ST deviatie) (score 2)
 
Bij een score-som van 3 hebben deze criteria een specificiteit van 90%.
{{clr}}
{{clr}}


==Subendendocardial Ischemia==
[[File:Subendocardial_ischemia2.jpg|thumb|An example of subendocardial ischemia with diffuse ST depression]]
Subendocardial ischemia is ischemia that is not transmural. It is mostly caused by demand ischemia where energy supply to cardiomyocytes is insufficient for the work force, e.g. during extreme hypertension, aortic valve stenosis, extreme left ventricular hypertension, anemia, atrial fibrillation with rapid ventricular response.
On the ECG often diffuse ST depression is present. Cardiac enzymes (CK-MB, Troponine) may or may not be elevated depending on the severity.
{{box|
==References==
==References==
<biblio>
<biblio>
#Wung pmid=16777513
#Wung pmid=16777513
#Liu pmid=13762787
#martin pmid=17825710
#Abildskov pmid=13649561
#Alpert pmid=10987628
#Alpert pmid=10987628
#accexercise pmid=12356646  
#accexercise pmid=12356646  
Line 215: Line 183:
#LBTB pmid=11265742
#LBTB pmid=11265742
#AHACAG pmid=1116248
#AHACAG pmid=1116248
#Novotny pmid=18019666
#Chevalier pmid=12716101
#Jensen pmid=15851335
#Thygesen pmid=17951284
#Wong pmid=15992631
#WellensSign pmid=6121481
</biblio>
</biblio>
}}
{{box|
==External Links==
A good introduction to [[http://www.askdrwiki.com/mediawiki/index.php?title=Coronary_Angiography coronary angiography]]
}}
[[Category:ECG Textbook]]

Latest revision as of 21:53, 28 October 2012

Author(s) I.A.C. van der Bilt, MD
Moderator I.A.C. van der Bilt, MD
Supervisor
some notes about authorship


Ischemia occurs when part of the heart muscle, the myocardium, is deprived of oxygen and nutrients. Common causes of ischemia are:

  • Narrowing or obstruction of a coronary artery.
  • A rapid arrhythmia, causing an imbalance in supply and demand for energy.

A short period of ischemia causes reversible effects: The heart cells will be able to recover. When the episode of ischemia lasts for a longer period of time, heart muscle cells die. This is called a heart attack or myocardial infarction. That is why it is critical to recognize ischemia on the ECG in an early stage.

Severe ischemia results in ECG changes within minutes. While the ischemia lasts, several ECG changes will occur and disappear again. Therefore, it may be difficult to estimate the duration of the ischemia on the ECG, which is crucial for adequate treatment.

Signs and symptoms of myocardial ischemia:

  • Crushing pain on the chest (angina pectoris), behind the sternum, often radiating to the lower jaw or the left arm
  • Fear of dying
  • Nausea
  • Shock (manifesting as paleness, low blood pressure, fast weak pulse) shock
  • Rhythm disturbances (in particular, increasing prevalence of ventricular ectopia, ventricular tachycardia, AV block)


Risk assessment of Cardiovascular disease

Narrowing of the coronary artery, leading to a myocardial infarction, usually develops over several years. An increased risk of cardiovascular disease, which may lead to a myocardial infarction or cerebrovascular accident, can be estimated using SCORE system which is developed by the European Society of cardiology (ESC). As shown in the figure, the most important risk factors for myocardial infarction are:

  • Male sex
  • Smoking
  • Hypertension
  • Diabetes Mellitus
  • Hypercholesterolemia

Risk assessment of ischemia

An exercise test such as a bicycle or treadmill test, may be useful in detecting myocardial ischemia after exercise.[1] In such a test, continuous ECG monitoring is performed during exercise. The ST-segment, blood pressure and clinical status of the patient (i.e. chest complaints) are monitored during and after the test.

An exercise test is positive for myocardial ischemia when the following criteria are met:

  • Horizontal or downsloping ST-depression of >1mm, 60 or 80ms after the J-point
  • ST elevation of > 1.0 mm


Diagnosis of myocardial infarction

ST elevation is measured at the junctional or J-point

The diagnosis of acute myocardial infarction is not only based on the ECG. A myocardial infarction is defined as:[2]

  • Elevated blood levels of cardiac enzymes (CKMB or Troponin T) AND
  • One of the following criteria are met:
    • The patient has typical complaints,
    • The ECG shows ST elevation or depression.
    • pathological Q waves develop on the ECG
    • A coronary intervention had been performed (such as stent placement)

So detection of elevated serum cardiac enzymes is more important than ECG changes. However, the cardiac enzymes can only be detected in the serum 5-7 hours after the onset of the myocardial infarction. So, especially in the first few hours after the myocardial infarction, the ECG can be crucial.

ECG Manifestations of Acute Myocardial Ischaemia (in Absence of LVH and LBBB)are [3]:

ST elevation
New ST elevation at the J-point in two contiguous leads with the cut-off points: ≥0.2 mV in men or ≥ 0.15 mV in women in leads V2–V3 and/or ≥ 0.1 mV in other leads.
ST depression and T-wave changes.
New horizontal or down-sloping ST depression >0.05 mV in two contiguous leads; and/or T inversion ≥0.1 mVin two contiguous leads with prominent R-wave or R/S ratio ≥ 1

A study using MRI to diagnose myocardial infarction has shown that more emphasis on ST segment depression could greatly improve the yield of the ECG in the diagnosis of myocardial infarction (sensitivity increase from 50% to 84%).[4]

Myocardial infarction diagnosis in left or right bundle branch block can be difficult, but it is explained in these seperate chapters:


The location of the infarct

The heartmuscle itself is very limited in its capacity to extract oxygen in the blood that is being pumped. Only the inner layers (the endocardium) profit from this oxygenrich blood. The outer layers of the heart (the epicardium) are dependent on the coronary arteries for the supply of oxygen and nutrients. With aid of an ECG, the occluded coronary can be identified. This is valuable information for the clinician, because treatment and complications of for instance an anterior wall infarction is different than those of an inferior wall infarction. The anterior wall performs the main pump function, and decay of the function of this wall will lead to decrease of bloodpressure, increase of heartrate, shock and on a longer term: heart failure. An inferior wall infarction is often accompanied with a decrease in heartrate because of involvement of the sinusnode. Longterm effects of an inferior wall infarction are usually less severe than those of an anterior wall infarction.

The heart is supplied of oxygen and nutrients by the right and left coronary arteries. The left coronary artery (the Left Main or LM) divides itself in the left anterior descending artery (LAD) and the ramus circumflexus (RCX). The right coronary artery (RCA) connects to the ramus descendens posterior (RDP). With 20% of the normal population the RDP is supplied by the RCX. This called left dominance.

Below you can find several different types of myocardial infarcation. Click on the specific infarct location to see examples.


Help with the localisation of a myocardial infarct
localisation ST elevation Reciprocal ST depression coronary artery
Anterior MI V1-V6 None LAD
Septal MI V1-V4, disappearance of septum Q in leads V5,V6 none LAD-septal branches
Lateral MI I, aVL, V5, V6 II,III, aVF LCX or MO
Inferior MI II, III, aVF I, aVL RCA (80%) or RCX (20%)
Posterior MI V7, V8, V9 high R in V1-V3 with ST depression V1-V3 > 2mm (mirror view) RCX
Right Ventricle MI V1, V4R I, aVL RCA
Atrial MI PTa in I,V5,V6 PTa in I,II, or III RCA

The localisation of the occlusion can be adequately visualized using a coronary angiogram (CAG). On the CAG report, the place of the occlusion is often graded with a number (for example LAD(7)) using the classification of the American Heart Association.[5]

Development of the ECG during persistent ischemia

The evolution of an infarct on the ECG. ST elevation, Q wave formation, T wave inversion, normalisation with a persistent Q wave
Wellens syndrome: symmetrical negative T wave in pre-cordial leads without R loss of R waves can regularly be observed in early anterior ischemia. Many patients with Wellens syndrome / sign turn out to have a critical proximal LAD stenosis[6].
Typical negative T waves post anterior myocardial infarction. This patient also shows QTc prolongation. Whether this has an effect on prognosis is debated.[7][8][9]

The cardiomyocytes in the subendocardial layers are especcially vulnerable for a decreased perfusion. Subendocardial ischemia manifests as ST depression and is usually reversible. In a myocardial infarction transmural ischemia develops.

In the first hours and days after the onset of a myocardial infarction, several changes can be observed on the ECG. First, large peaked T waves (or hyperacute T waves), then ST elevation, then negative T waves and finally pathologic Q waves develop.

Wellens syndrome or sign (see image) can be an early ECG warning sign of critical anterior ischemia before the development of overt mocardial infarction.

Evolution of the ECG during a myocardial infarct
Time from onset of symptoms ECG Changes in the heart
minutes hyperacute T waves (tall T waves), ST-elevation reversible ischemic damage
hours ST-elevation, with terminal negative T waves, negative T waves (these can last for days to months) onset of myocardial necrosis
An acute anterior myocardial infarction typically shows ST elevation on the ECG
days Pathologic Q Waves scar formation
A transmural anterior myocardial infarction with scar formation and Pathologic Q Waves


Subendendocardial Ischemia

An example of subendocardial ischemia with diffuse ST depression

Subendocardial ischemia is ischemia that is not transmural. It is mostly caused by demand ischemia where energy supply to cardiomyocytes is insufficient for the work force, e.g. during extreme hypertension, aortic valve stenosis, extreme left ventricular hypertension, anemia, atrial fibrillation with rapid ventricular response. On the ECG often diffuse ST depression is present. Cardiac enzymes (CK-MB, Troponine) may or may not be elevated depending on the severity.

References

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All Medline abstracts: PubMed | HubMed


External Links

A good introduction to [coronary angiography]