ECG in myocardial infarction and ischemia
Acute myocardial infarction (AMI)
 Generally, the term „infarction“ can be used for any local acute ischemia with
necrosis, irrespectively of affected organ
 However, myocardial and cerebral infarction most usually lead to death or invalidity
 Myocardial infarction is the most common life threatening complication of coronary
atherosclerosis
 In most cases, its cause is a rupture of unstable atherosclerotic plaque with
subsequent thrombosis
 Rare causes: thrombembolism, coronary artery dissection, acute overload of
ischemized myocardium
 The ischemia leads to decrease of ATP and subsequent overload of cardiomyocyte
by Ca2+, local lactacidosis, permanent depolarization
 Cell death: myocardial necrosis, apoptosis in prolonged ischemia, autophagy is
rather protective
 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
 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
 An important exception are the patients with sleep apnea
syndrome
Changes of ST segment during
myocardial infarction
Changes of ST segment 2
 ST elevations or depressions
during AMI are caused mainly by a
shift of isoelectric line, not ST
segment
 During diastole, an ischemic focus
generates electric currents
 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
 The differences in the plateau
phase and repolarization lead into
different shape of ST segment
Upsloping, horizontal and downsloping ST
segment depressions
 Subendocardial ischemia horizontal
or downsloping
depressions of ST segment
 Downsloping depressions
occur also e.g. in bundle
branch blocks (phase of
plateau is different for each
part of the ventricle) or digoxin
intoxication
 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
C – convex
acute transmural myocardial
infarction
J-point
ECG changes during Q-MI
 A. initial physiological state
 B. superacute phase
 Tall positive T waves
(minutes)
 C. acute phase
 ST elevation = Pardee‘s
waves (tens of minutes to
hours) - STEMI
 D. subacute phase
 Normalization of ST segment
 E. Q-wave devolopment
(hours to days), event. T –
inversion (persists weeks)
 F. ECG after Q-MI
 persistence of Q
Pathologic Q
• During several hours after transmural MI, pathologic Q develops
• Pathologic Q corresponds to depolarization of opposing cardiac wall,
observed through electrically dead tissue – a scar
• Its depth is > ¼ 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)
Clinical case
 59 years old man with acute chest pain, because of ST
elevations, coronary arteriography was performed within
1 hour after onset
 LAD occlusion was detected and recanalization was
performed
 The finding at coronary arteriography well corresponds
with the diagnosis of anterior wall STEMI, based on ECG
findings