ECG in myocardial infarction and ischemia
Acute myocardial infarction (AMI)
O Generally, the term Jnfarction" can be used for any local acute ischemia with necrosis, irrespectively of affected organ
O However, myocardial and cerebral infarction most usually lead to death or invalidity
O Myocardial infarction is the most common life threatening complication of coronary atherosclerosis
O In most cases, its cause is a rupture of unstable atherosclerotic plaque with subsequent thrombosis
O Rare causes: thrombembolism, coronary artery dissection, acute overload of ischemized myocardium
O The ischemia leads to decrease of ATP and subsequent overload of cardiomyocyte by Ca2+, local lactacidosis, permanent depolarization
O Cell death: myocardial necrosis, apoptosis in prolonged ischemia, autophagy is rather protective
O Compared to AMI, causes of cerebral stroke are much more heterogenous,
atherosclerosis is often not required (thrombosis, thrombembolism, hemorrhage...)
AMIs and strokes during the day
O Higher incidence of cerebral and myocardial infarctions in the morning is caused with higher activity of sympathetic nervous system and higher blood pressure in morning hours
O An important exception are the patients with sleep apnea syndrome
Changes of ST segment during myocardial infarction
Changes of ST segment 2
O ST elevations or depressions during AMI are caused mainly by a shift of isoelectric line, not ST segment
O During diastole, an ischemic focus generates electric currents
O Depending on its prevailing direction, we can observe elevations (transmural AMI) or depressions (non-transmural AMI) of ST segment - in fact, there is a shift of isoelectric line in opposite direction
O The differences in the plateau phase and repolarization lead into different shape of ST segment
1
mm
Upsloping, horizontal and downsloping ST
segment depressions
O Subendocardial ischemia -horizontal or downsloping depressions of ST segment
O Downsloping depressions occur also e.g. in bundle branch blocks (phase of plateau is different for each part of the ventricle) or digoxin intoxication
O On the other hand, mild (0.1-0.2 mV) upsloping ST depressions occur frequently in healthy heart during exercise
ST elevations
A - concave (often in the hypertrophy of LV) B - straight   acute transmural myocardial C - convex infarctj0n
ECG changes during Q-MI
O A. initial physiological state O B. superacute phase
O Tall positive T waves (minutes)
O C. acute phase
O ST elevation = Pardee's waves (tens of minutes to hours) - STEMI
O D. subacute phase
O Normalization of ST segment
O E. Q-wave devolopment (hours to days], event. T -inversion (persists weeks)
O F. ECG after Q-MI O persistence of Q
Pathologic Q
• During several hours after transmural Ml, pathologic Q develops
• Pathologic Q corresponds to depolarization of opposing cardiac wall, observed through electrically dead tissue - a scar
• Its depth is > % R (or R is not present at all - QS wave) and its duration is at least 40 ms)
• It usually persists lifelong (except certain cases of stunned myocardium)
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Clinical case
O 59 years old man with acute chest pain, because of ST elevations, coronary arteriography was performed within 1 hour after onset
O LAD occlusion was detected and recanalization was performed
O The finding at coronary arteriography well corresponds with the diagnosis of anterior wall STEMI, based on ECG findings