Myocardial Infarction: Difference between revisions

From ECGpedia
Jump to navigation Jump to search
No edit summary
 
(100 intermediate revisions by 16 users not shown)
Line 1: Line 1:
{{ActiveDiscuss}}
<div style="float:left">__TOC__</div>
==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, sverela ECG changes will occur and disappear again. Therefore, it can be difficut 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 ventricluar 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 crietria are met:
* One of the following criteria are met:
** The patient has typical complaints
** The patient has typical complaints,
** The ECG shows toont ST elevation or depression
** The ECG shows ST elevation or depression.
** [[pathologische Q golven]] 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'.
The heartmuscle itself can 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 pf oxygen and nutrients. Met behulp van het ECG is te zien welk kransslagvat is afgesloten. Dit is van belang omdat de gevolgen van bijvoorbeeld een voorwandinfarct en een onderwandinfarct verschillen: de '''voorwand''' levert de belangrijkste bijdrage aan de pompfunctie en uitval zal dus lijden tot een bloeddrukdaling en hartslagversnelling en op de lange termijn tot hartfalen. Een '''onderwandinfarct''' gaat vaak gepaard met een polsvertraging doordat de sinusknooparterie te weinig doorbloed wordt, op de lange termijn is het effect op de conditie minder  groot omdat de bijdrage van de onderwand aan de pompfunctie minder is.
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
Het hart wordt door de rechter en linker coronair vaten voorzien van zuurstof en nutrienten. Het linker coronairvat (de '''hoofdstam''' of LM, left main) splits zich in de '''left anterior descending''' artery (LAD) en de '''ramus circumflexus''' (RCX). De '''rechter coronair arterie''' (RCA) voedt de ramus descendens posterior (RDP). Bij 20% van de bevolking wordt de ramus descendens posterior door de arteria circumflexa wordt gevoed. Dit noemt men een links dominant hart.
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.


Hieronder volgt een opsomming van de verschillende infarctvarianten. Veel voorkomend zijn het '''voorwandinfarct''' (LAD), het '''onderwandinfarct''' (meestal RCA) en het '''infero-postero-lateraalinfarct''' (vaak RCX).
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.




Line 98: Line 92:
!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 en aVL. Maximale elevatie in V3, maximale depressie in III
later: pathologische Q in de precordiale afleidingen V2 t/m V4-V5
[[Image:AMI_anterior.png|thumb| Een voorbeeld van een acuut voorwandinfarct. ST elevatie in I, AVL en V2-V5. Reciproke depressies in de onderwandsafleidingen (II,III,AVF)]]
[[Image:heart_with_AL_infarct.png|thumb|Anterolateraal infarct door occlusie van de LAD.]]
[[Image:ECG_VWI_2wk.jpg|thumb| Een 2 weken oud voorwandinfarct met beginnende Q's in V2-V4 en persisterende ST elevatie, mogelijk als teken van aneurysma-vorming]]
Omvat het voorste (anterior) deel van het hart en een deel van het kamerseptum. Wordt door de LAD van bloed voorzien.
{{clr}}
{{clr}}


===Septal===
==Development of the ECG during persistent ischemia==
QS in V1 en V2. Later verdwijnt de septum-Q in V5 en V6
[[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]]
Omvat het kamerseptum. Deze wordt door de septale takken van de LAD van bloed voorzien.
[[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 elevatie in I, aVL, V5 en V6
Omvat de laterale zijde van de linkerkamer (linker zijkant van het hart). Deze wordt door de RCX of de MO van bloed voorzien. De MO, de marginalis obtusis is een zijtak die tussen de LAD en de RCX loopt. Bij een lateraal infarct bevindt de maximale ST elevatie zich in V7 en de maximale depressie zich 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-elevatie in de precordiale afleidingen V2-V6
|+'''Evolution of the ECG during a myocardial infarct'''
 
|-
Later negatieve T golven en Q's in I, aVL, V5 en V6.
!Time from onset of symptoms
{{clr}}
!ECG
 
!Changes in the heart
===Inferior wall===
|-
ST elevatie in II, III en aVF
!minutes
Dit deel (inferior) rust op het diafragma en wordt bij 80% van de patienten door rechter coronair-arterie (RCA) van bloed voorzien, bij de overige 20% komt het bloed uit de circumflex (RCX).
| hyperacute T waves (tall T waves), ST-elevation
[[Image:AMI_inferior.jpg|thumb| Een voorbeeld van een onderwandinfarct.]]
| reversible ischemic damage
Een RCA afsluiting kan zich onderscheiden van een RCX afsluiting op het ECG: bij een RCA afsluiting is er vaak depressie in I en aVL en is de ST elevatie in III groter dan in II.
|-
{{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]]
Hoge R-toppen met ST-depressie in V1-V3.
|-
[[Image:Heart_with_P_infarct.png|thumb|Posteriorinfarct caused by occlusion of the RCA]]
!days
De achterwand (posterior) wordt meestal door de RCA van bloed voorzien. Omdat er normaal gesproken geen ECG-afleidingen naar de achterwand kijken, zijn er normaal ook geen afleidingen waar de ST elevatie te zien is die hier bij hoort. De ST depressies in V1-V3 zijn dus eigenlijk gespiegelde ST elevaties en de hoge R-toppen weerspiegelen de Q-golven van het infarct. Om toch zeker te zijn dat het om een posterior-infarct gaat wordt er wel eens doorgepoold met V7, V8 en V9. Deze afleidingen worden dan horizontaal vanaf V6 doorgepoold naar de rug en tonen vaak wel de ST elevatie bij een posterior-infarct.
| [[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 loacted 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 infracts.
 
===Atrial infarct===
In ongeveer 10% van de infarctpatiënten zijn er aanwijzingen voor een atriaal infarct. Een atriaal infarct kan zich uiten in atriale ritmestoornissen: boezemfibrilleren / boezemritme. Omdat de atria hemodynamisch van ondergeschikt belangrijk zijn, zijn de consequenties van een atriaal infarct meestal beperkt (en daardoor wordt het ook meestal over het hoofd gezien).
 
Op het ECG uit een atriaal infarct zich dus door een ritmeverandering en / of verandering van het P-Ta segment (soms PTA (''P'' - ''a''triale ''T'') segment genoemd of PR of PQ of PTp (''P'' - ''T'' top van ''P'' golf) segment)<cite>Abildskov</cite>. Dit is het stukje tussen de p-top en de q (NB in angelsaksische literatuur wordt dus PR segment gezegd, maar dit reikt tot aan de Q en niet tot aan de R). Zoals het ST segment een infarct aangeeft in de ventrikel, geeft het P-Ta segment een infarct aan van de boezems.
 
Diagnostische criteria voor een atriaal infarct <cite>Liu</cite>:
* P-Ta elevatie >0.5mm in V5 en V6 met reciproke depressie in V1 en V2
* P-Ta elevatie >0.5mm in I en depressie in II en III
* >1.5mm P-Ta depressie in precordiale afleidingen
* >1.2mm P-Ta depressie in I,II of III in combinatie met atriale aritmiën
 
Er zijn meerdere diagnostische criteria in omloop en dit is een voorbeeld. Een belangrijke differentiaal diagnose van PTa segment elevatie of depressie 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 216: 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

  • An overview of the coronary arteries. LM = 'Left Main' = mainstem; LAD = 'Left Anterior Descending' artery; RCX = Ramus Circumflexus; RCA = 'Right Coronary Artery'.

    An overview of the coronary arteries. LM = 'Left Main' = mainstem; LAD = 'Left Anterior Descending' artery; RCX = Ramus Circumflexus; RCA = 'Right Coronary Artery'.

  • 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.

    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.

  • The coloured figure shows contiguous leads in matching colors

    The coloured figure shows contiguous leads in matching colors

  • 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)

    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)

  • The coronary blockade can cause conduction block, on AV nodal, His or bundle branch level.

    The coronary blockade can cause conduction block, on AV nodal, His or bundle branch level.

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
A pathological 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

  1. Gibbons RJ, Balady GJ, Bricker JT, Chaitman BR, Fletcher GF, Froelicher VF, Mark DB, McCallister BD, Mooss AN, O'Reilly MG, Winters WL Jr, Gibbons RJ, Antman EM, Alpert JS, Faxon DP, Fuster V, Gregoratos G, Hiratzka LF, Jacobs AK, Russell RO, Smith SC Jr, and American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Update the 1997 Exercise Testing Guidelines). ACC/AHA 2002 guideline update for exercise testing: summary article: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Update the 1997 Exercise Testing Guidelines). Circulation. 2002 Oct 1;106(14):1883-92. DOI:10.1161/01.cir.0000034670.06526.15 | PubMed ID:12356646 | HubMed [accexercise]
  2. Alpert JS, Thygesen K, Antman E, and Bassand JP. Myocardial infarction redefined--a consensus document of The Joint European Society of Cardiology/American College of Cardiology Committee for the redefinition of myocardial infarction. J Am Coll Cardiol. 2000 Sep;36(3):959-69. DOI:10.1016/s0735-1097(00)00804-4 | PubMed ID:10987628 | HubMed [Alpert]
  3. Thygesen K, Alpert JS, White HD, Joint ESC/ACCF/AHA/WHF Task Force for the Redefinition of Myocardial Infarction, Jaffe AS, Apple FS, Galvani M, Katus HA, Newby LK, Ravkilde J, Chaitman B, Clemmensen PM, Dellborg M, Hod H, Porela P, Underwood R, Bax JJ, Beller GA, Bonow R, Van der Wall EE, Bassand JP, Wijns W, Ferguson TB, Steg PG, Uretsky BF, Williams DO, Armstrong PW, Antman EM, Fox KA, Hamm CW, Ohman EM, Simoons ML, Poole-Wilson PA, Gurfinkel EP, Lopez-Sendon JL, Pais P, Mendis S, Zhu JR, Wallentin LC, Fernández-Avilés F, Fox KM, Parkhomenko AN, Priori SG, Tendera M, Voipio-Pulkki LM, Vahanian A, Camm AJ, De Caterina R, Dean V, Dickstein K, Filippatos G, Funck-Brentano C, Hellemans I, Kristensen SD, McGregor K, Sechtem U, Silber S, Tendera M, Widimsky P, Zamorano JL, Morais J, Brener S, Harrington R, Morrow D, Lim M, Martinez-Rios MA, Steinhubl S, Levine GN, Gibler WB, Goff D, Tubaro M, Dudek D, and Al-Attar N. Universal definition of myocardial infarction. Circulation. 2007 Nov 27;116(22):2634-53. DOI:10.1161/CIRCULATIONAHA.107.187397 | PubMed ID:17951284 | HubMed [Thygesen]
  4. Martin TN, Groenning BA, Murray HM, Steedman T, Foster JE, Elliot AT, Dargie HJ, Selvester RH, Pahlm O, and Wagner GS. ST-segment deviation analysis of the admission 12-lead electrocardiogram as an aid to early diagnosis of acute myocardial infarction with a cardiac magnetic resonance imaging gold standard. J Am Coll Cardiol. 2007 Sep 11;50(11):1021-8. DOI:10.1016/j.jacc.2007.04.090 | PubMed ID:17825710 | HubMed [martin]
  5. Austen WG, Edwards JE, Frye RL, Gensini GG, Gott VL, Griffith LS, McGoon DC, Murphy ML, and Roe BB. A reporting system on patients evaluated for coronary artery disease. Report of the Ad Hoc Committee for Grading of Coronary Artery Disease, Council on Cardiovascular Surgery, American Heart Association. Circulation. 1975 Apr;51(4 Suppl):5-40. DOI:10.1161/01.cir.51.4.5 | PubMed ID:1116248 | HubMed [AHACAG]
  6. de Zwaan C, Bär FW, and Wellens HJ. Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction. Am Heart J. 1982 Apr;103(4 Pt 2):730-6. DOI:10.1016/0002-8703(82)90480-x | PubMed ID:6121481 | HubMed [WellensSign]
  7. Novotný T, Sisáková M, Floriánová A, Toman O, Dohnalová I, Poloczek M, Kala P, Kyselová I, Dostálová L, Vít P, and Spinar J. [QT dynamicity in risk stratification in patients after myocardial infarction]. Vnitr Lek. 2007 Sep;53(9):964-7. PubMed ID:18019666 | HubMed [Novotny]
  8. Jensen BT, Abildstrom SZ, Larroude CE, Agner E, Torp-Pedersen C, Nyvad O, Ottesen M, Wachtell K, and Kanters JK. QT dynamics in risk stratification after myocardial infarction. Heart Rhythm. 2005 Apr;2(4):357-64. DOI:10.1016/j.hrthm.2004.12.028 | PubMed ID:15851335 | HubMed [Jensen]
  9. Chevalier P, Burri H, Adeleine P, Kirkorian G, Lopez M, Leizorovicz A, André-Fouët X, Chapon P, Rubel P, Touboul P, and Groupe d'Etude du Pronostic de l'Infarctus du Myocarde. QT dynamicity and sudden death after myocardial infarction: results of a long-term follow-up study. J Cardiovasc Electrophysiol. 2003 Mar;14(3):227-33. DOI:10.1046/j.1540-8167.2003.02431.x | PubMed ID:12716101 | HubMed [Chevalier]
  10. Wung SF and Kahn DY. A quantitative evaluation of ST-segment changes on the 18-lead electrocardiogram during acute coronary occlusions. J Electrocardiol. 2006 Jul;39(3):275-81. DOI:10.1016/j.jelectrocard.2005.10.007 | PubMed ID:16777513 | HubMed [Wung]
  11. Menown IB, Mackenzie G, and Adgey AA. Optimizing the initial 12-lead electrocardiographic diagnosis of acute myocardial infarction. Eur Heart J. 2000 Feb;21(4):275-83. DOI:10.1053/euhj.1999.1748 | PubMed ID:10653675 | HubMed [Menown]
  12. Sgarbossa EB. Value of the ECG in suspected acute myocardial infarction with left bundle branch block. J Electrocardiol. 2000;33 Suppl:87-92. DOI:10.1054/jelc.2000.20324 | PubMed ID:11265742 | HubMed [LBTB]
  13. Wong CK, French JK, Aylward PE, Stewart RA, Gao W, Armstrong PW, Van De Werf FJ, Simes RJ, Raffel OC, Granger CB, Califf RM, White HD, and HERO-2 Trial Investigators. Patients with prolonged ischemic chest pain and presumed-new left bundle branch block have heterogeneous outcomes depending on the presence of ST-segment changes. J Am Coll Cardiol. 2005 Jul 5;46(1):29-38. DOI:10.1016/j.jacc.2005.02.084 | PubMed ID:15992631 | HubMed [Wong]
All Medline abstracts: PubMed | HubMed


External Links

A good introduction to [coronary angiography]

Retrieved from "https://en.ecgpedia.org/index.php?title=Myocardial_Infarction&oldid=16521"