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Myocardial Infarction: Difference between revisions
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===Risk assessment of Cardiovascular disease=== | ===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 [http://www.escardio.org/ | 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: | As shown in the figure, the most important risk factors for myocardial infarction are: | ||
*Male sex | *Male sex | ||
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** 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 | 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 [[MI Diagnosis in LBBB|LBBB]])are <cite>Thygesen</cite>: | ECG Manifestations of Acute Myocardial Ischaemia (in Absence of LVH and [[MI Diagnosis in LBBB|LBBB]])are <cite>Thygesen</cite>: | ||
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Myocardial infarction diagnosis in left or right bundle branch block can be difficult, but it is explained in these seperate chapters: | 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 LBBB|MI diagnosis in left bundle branch block or paced rhytm]] | ||
*[[MI Diagnosis in RBBB]] | *[[MI Diagnosis in RBBB]] | ||
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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 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'''. | 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. | 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 | ||
! | !Reciprocal ST depression | ||
!coronary artery | !coronary artery | ||
|- | |- | ||
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| 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 MI]] | | [[Lateral MI]] | ||
| I, aVL, V5, V6 | | I, aVL, V5, V6 | ||
| II,III, aVF | | II,III, aVF | ||
| | | LCX or MO | ||
|- | |- | ||
| [[Inferior MI]] | | [[Inferior MI]] | ||
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[[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: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 [[Pathologic_Q_Waves|pathological Q wave]]]] | [[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>]] | [[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. | 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|pathologic Q waves]]''' develop. | 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. | ||
'''Wellens syndrome''' or sign (see image) can be an early ECG warning sign of critical anterior ischemia before the development of overt mocardial infarction. | |||
{| class="wikitable" | {| class="wikitable" | ||
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==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| | {{box| | ||
==References== | ==References== | ||
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#Thygesen pmid=17951284 | #Thygesen pmid=17951284 | ||
#Wong pmid=15992631 | #Wong pmid=15992631 | ||
#WellensSign pmid=6121481 | |||
</biblio> | </biblio> | ||
}} | }} | ||