ST Segment Elevation

Lucaci, Laurențiu

doi:10.2478/rjc-2022-0014

Figures & Tables

ST segment deviations in direct and indirect leads.

The layout of the ST elevations (RED) and of the reciprocal ST depressions (GREEN) due to single vessel occlusions of the left anterior descending artery (LAD), right coronary artery (RCA) and left circumflex artery (LCX), respectively. NDDO = non-dominant artery with distal occlusion, NDPO = non-dominant artery with proximal occlusion, DDO = dominant artery with distal occlusion, DPO = dominant artery with proximal occlusion. For each one of the following cases RCA-DPO and LCX-DPO, the versions where the result of subtraction of the ST elevations conveyed by diametrically opposite territories is NOT zero (diametrically opposite ST elevations do not nullify each other) are displayed (the last two charts from the last column).

Electrocardiographic locating algorithm of expected acute single coronary occlusion, based upon the highest ST segment elevation found in precordial leads. LAD = left anterior descending artery, OCC = occlusion, D1 = first diagonal artery, S1 = first septal artery, “<” = proximal to, “>” = distal to. (data according to references 3, 15, 17, 36–42)

Acute occlusion of a)PROXIMAL LAD b)before and c)after drug-eluting stent primary angioplasty, as seen in RAO view (dr. Alexandru Burlacu). Acute occlusion of d)DISTAL LONG LAD e)before and f)g)after drug-eluting stent primary angioplasty, as seen in RAO view (dr. Marius Adoamnei). RAO = right anterior oblique.

Electrocardiographic locating algorithm of expected acute coronary single occlusion, based upon the highest ST segment elevation found in the inferior leads. RCA = right coronary artery, LCX = left circumflex artery. (data according to references 3, 15, 17, 36–42).

Acute occlusions of a)PROXIMAL RCA b)before and c)after drug-eluting stent primary angioplasty, as seen in LAO view (dr. Dan Năstasă) and d)DISTAL RCA e)before and f)after drug-eluting stent primary angioplasty, as seen in LAO view (dr. Nicușor Lovin). LAO = left anterior oblique.

Acute occlusion of a a)PROXIMAL left circumflex artery b)before and c)after the drug-eluting stent primary angioplasty, as seen in RAO view (dr. Dan Năstasă).

Left ventricular wall segments blood supply versions (data according to references 42, 43).

Acute occlusion of the first diagonal artery.

a)”tombstoning” and b)”shark fin” configurations of the ischaemic ST segment elevation.

ST-elevation acute myocardial infarction inferred from fulfilling modified Sgarbossa criteria 1 and 3 in a patient with left bundle branch block and anterior chest pain.

Left main coronary trunk severe stenosis.

Wellens syndrome a)b)electrocardiographic features and c)angiogram in a patient with proximal LAD severe stenosis, c)dilated later on and secured by drug-eluting stent deployment. (dr. Dan Năstasă).

a)de Winter ST-T pattern b)before and c)d)after the drug-eluting stent angioplasty (dr. Dan Năstasă) of a proximal left anterior descending artery occlusion.

Electrocardiographic image of a left ventricular anterior wall aneurysm.

Electrocardiographic course of a patient with Takotsubo cardiomyopathy.

Acute myocarditis featuring a)ST-elevation within the inferior leads in a young patient with chest pain and myocardial injury enzymes variation, against the background of normal CT angiographic appearance of subepicardial coronary arteries and b)c)MRI markings of myocardial oedema (dr. Anatolie Cazacu) with d)ST segment fallen to baseline three weeks later.

Acute pulmonary embolism, displaying ST segment elevation within the precordial leads.

The type 1 diagnostic electrocardiographic pattern of Brugada syndrome a)enhanced by 39°C fever, as well as b)diminished after fever remission under paracetamol, reinforced thereafter by a flecainide challenge test (by kind permission of dr. Mircea Balasanian, from his personal collection).

Electrocardiographic pattern of early repolarization, showing J wave across lateral leads.

Electrocardiogram in hyperkalaemia, revealing ST segment elevation in lead V1, following a wide and rightward shifted QRS complex, related to a rhythm presumably idioventricular in origin, alongwith high and sharply pointed T wave in V4–V6. The amplitudes alike of the S and T waves promote the automatic erroneous heart rate double counting (an event not specific to, but nevertheless possible in hyperkalaemia).

ST elevation within the right precordial leads and wide QRS complex in sinus rhythm, alternating with episodes of accelerated idioventricular rhythm, against the background of a deliberate intoxication with flecainide.

Pseudo ST elevation in the inferior leads, created by the F wave of the atrial flutter.

The manifold of causes of pseudo-STEMI_

Types of single cause ST segment elevation_

Comparison between ST elevation in myocardial ischaemia, early repolarization and acute pericarditis_

		TRANSMURAL MYOCARDIAL ISCHAEMIA (STEMI, VASOSPASTIC ANGINA, TAKOTSUBO CARDIOMYOPATHY, LEFT VENTRICULAR ANEURYSM)	EARLY REPOLARIZATION (ER)	ACUTE PERICARDITIS
PR SEGMENT DEPRESSION		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
QRS COMPLEX		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
ST SEGMENT ELEVATION (STE)	ST/QRS AMPLITUDES RATIO	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
	USEFUL ECG LEADS	1) CLUSTERED in at least two adjoining leads from the same group forecasting the occluded coronary artery; 2) DIFFUSE, for example in case of a long (wrapping) LAD, supplying the apical LV inferior wall	1) CLUSTERED: a)lateral leads (type 1), b)lateral and inferior leads (type 2); 2) DIFFUSE: lateral, inferior and V1–V3 leads (type 3)	DIFFUSE (except aVR and V1, +/− DIII), hardly ever seen in aVL
	SHAPE	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
	ST AMPLITUDE AT J POINT	1) 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; 2) Any other standard lead, except V2–V3: more than 1 mm for any gender, any age; 3) V7–V9: more than 0.5 mm; 4) 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 RATIO	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
	TIME DEPENDENCY	1) Fast increase; 2) 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
RECIPROCAL ST DEPRESSION		1) Available in diametrically opposite leads; 2) 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
T WAVE	POLARITY AND AMPLITUDE	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	1) Usually normal polarity and amplitude during STE; 2) Seldom terminal part small amplitude inversion during STE, but inversion AFTER ST falls to baseline is the rule
T WAVE	MORPHOLOGY	Wide base, symmetric limbs	Narrow base
QT INTERVAL		Sometimes prolonged	Normal QTc	Normal QTc

ST Segment Elevation

Figures & Tables

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The manifold of causes of pseudo-STEMI_

Types of single cause ST segment elevation_

Comparison between ST elevation in myocardial ischaemia, early repolarization and acute pericarditis_

Scenario of ST segment elevation and troponin variation over time_

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