Patient: 79-year-old man with treated arterial hypertension; consultation for palpitations occurring since a few days;
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Left atrial enlargement and atrial fibrillation
ECG 4A: Characteristic pattern of atrial fibrillation; rapid, disorganized atrial activity with baseline tremor; broad, irregular QRS complexes with typical complete right bundle branch block pattern (QRS > 120 ms, rsR’ pattern in V1 with major delay of the intrinsicoid deflection, wide S wave in V6 and lead I);
ECG 4B: ECG recorded after performing a programmed electric shock; left atrial enlargement with prolonged P wave (> 120 ms), bifid in leads I, II and aVL; right bundle branch block identical to that for tachycardia;
Comments: We have previously seen that initiation of an atrial fibrillation requires a trigger (usually an early atrial extrasystole from the pulmonary veins). This tracing also shows that the risk is increased in patients with favorable substrate. The P wave pattern in sinus rhythm in this patient is evocative of an abnormal and disrupted atrial activation with a typical «left atrial enlargement» pattern. The electrocardiogram does not allow differentiating between an enlargement of the atrium, a conduction disturbance within the atrium or a dilatation of the atrium. Indeed, if the atrial mass is dilated, the P wave widens due to the increased duration of the depolarization in relation to the resulting greater distance travelled by the activation wave. The term electrocardiographic atrial enlargement can therefore correspond to either a true atrial wall thickening, a dilatation of the cavity, a marked intra-atrial conduction disorder or a combination of these different elements.
In the electrocardiographic “left atrial enlargement”, the left atrial component of the P wave is increased both in terms of voltage and duration. The prolongation of the activation of the left atrium leads to an extension of the duration of the P wave beyond the pathological threshold of 110 ms.
The predominance of the left atrial vectors tends to move the activation vector to the left and backward. The electrical axis of the P wave in the frontal plane can be deviated to the left between 0 and 30° with a large and tall P wave in lead I and of lower voltage or biphasic in leads II and III. In these same leads, the P wave is often of abnormal morphology, notched, bifid or slurred. Indeed, P wave morphology is modified by an individualization of the late left atrial component resulting in a double-peaked, bifid pattern, the second being slightly higher than the first, which can be visualized in leads I and aVL, less often in lead II.
In the horizontal plane, the vectors of the P wave are typically directed to the left and backward. The P wave in V1 can be of prominent size with a biphasic aspect. The surface area of the negative terminal component exceeds that of the positive initial component. Frequently, a bifid P wave is found in precordial leads from V3 to V6.
The main causes of left atrial enlargement are mitral stenosis, mitral insufficiency and diseases with increased left ventricular pressure (aortic stenosis, aortic insufficiency, arterial hypertension, etc.).
Take-home message: The sinus ECG in patients with episodes of atrial arrhythmia can reveal different elements: 1) premature atrial extrasystoles (P-on-T phenomenon) as a trigger for arrhythmia induction, 2) a left atrial “enlargement” indicative of a favorable atrial substrate, 3) a QRS pattern suggestive of the presence of heart disease (infarction sequela, left ventricular hypertrophy, etc.).
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What abnormality(ies) is(are) found on this tracing?
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