Any depth in atrial infarction, associated with abnormal P wave morphology | Less than 1 mm, means early atrial repolarization | Often present (wherefore invariably combined with PR elevation in aVR +/− V1), indicating subepicardial atrial lesion, at least 1 mm depth, mostly in DII, aVF, V4–V6 | ||
As time goes by, QRS abates quickly in direct leads and elevates in reciprocal leads, while pathologic Q waves (or QS complexes) emerge in direct leads | High within precordial leads and left unchanged in the long run | Similar to that one before the pericarditis onset | ||
High ratio in at least one lead, STE sometimes having the “tombstoning” pattern = as the ST segment elevates, it hides beneath its shadow the decreasing R wave, while becoming rectilineal or convex upwards by engulfing the T wave | Small in any lead | Small = normal | ||
CLUSTERED in at least two adjoining leads from the same group forecasting the occluded coronary artery; DIFFUSE, for example in case of a long (wrapping) LAD, supplying the apical LV inferior wall |
CLUSTERED: a)lateral leads (type 1), b)lateral and inferior leads (type 2); DIFFUSE: lateral, inferior and V1–V3 leads (type 3) |
DIFFUSE (except aVR and V1, +/− DIII), hardly ever seen in aVL | ||
Concave upwards at first, fast increasing while becoming either upsloping or convex upwards, shortly thereafter | Concave upwards (with three subtypes: dominant ascending, symmetric and dominant descending), and J point clearly outlined / notched / beclouded | Concave upwards and dominant ascending, merged smoothly with the ascending limb of the T wave | ||
V2–V3: more than 2.5 mm in men under 40 years, more than 2 mm in men older than 40 and more than 1.5 mm in women, regardless of age; Any other standard lead, except V2–V3: more than 1 mm for any gender, any age; V7–V9: more than 0.5 mm; V3R–V4R: more than 0.5 mm (in men under 30 years, greater than 1 mm); |
ST amplitude between 1 and 3 mm within at least two adjoining leads, outside V1, V2 and V3 (so as to avoid confusion with Brugada syndrome); | At most 5 mm, highest in DII, V5, V6 (DII > DIII) | ||
ST/T amplitudes ratio at least 0.25 | Small ST/T amplitudes ratio în V6 | ST / T ratio at least 0.25 in V4–V6 | ||
Fast increase; Swift decrease toward baseline if timely coronary reperfusion, gradual decrease if late or no coronary reperfusion, or unchanged if dyskinesis / aneurysm of the infarcted wall (long lasting = “frozen” ST elevation, followed by small negative / small positive T wave) |
Dependent on autonomic tone: increased during heightened vagal tone and decreased during sympathetic stimulation | Vanishes once inflammation goes away | ||
Available in diametrically opposite leads; Absent in case of a)distal occlusion of a long LAD and in b)ventricular aneurysm; |
present in aVR in 50% of cases | Usually revealed in aVR +/− V1, sometimes as well in DIII, aVL | ||
Normal polarity and getting taller at first, inverted and going deeper thereafter. Inversion begins when STE is still in place. | Usually of normal polarity. Seldom its terminal side becomes negative and small throughout V3–V5 (+/−V1–V2), driven by changes in autonomic tone |
Usually normal polarity and amplitude during STE; Seldom terminal part small amplitude inversion during STE, but inversion AFTER ST falls to baseline is the rule |
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Wide base, symmetric limbs | Narrow base | |||
Sometimes prolonged | Normal QTc | Normal QTc |