Introduction.
Ectopic atrial tachycardia can be incessant. Even if it is rather uncommon, this type of supraventricular tachycardia can cause a tachy-cardiomyopathy. In individual cases, it can be difficult to distinguish ectopic atrial tachycardia from sinus tachycardia. In this respect, the evaluation of the P wave morphology and the association between P waves and QRS complex are useful. The differential diagnosis may require additional tests, e. g. adenosine infusion. In the present case, a meticulous Holter ECG analysis was particularly useful.
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A 23 year-old female patient presented with irregular heartbeats and dyspnea since 5 years. A number of 12 lead ECGs had been recorded for this reason which were always interpreted as sinus tachycardia and the patient was not treated. A representative electrocardiogram is shown in Fig. 1.
Fig. 1: 12 lead ECG (25 mm/s) with regular tachycardia with ventricular rate of about 120 bpm. There is a 2:1 conduction with upright P waves in V1 and III.
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The patient was admitted to our clinic with symptoms of palpitation and dyspnea at rest since several days. The ECG showed an atrial tachycardia at about 200 bpm after which the adenosine test was injected (Fig. 2). A presumed atrial tachycardia was terminated after a second attempt with verapamil, the ECG showed sinus rhythm at about 100 bpm which was maintained for about 6 hours.
Heart tones-irregular and accelerated
BP: 110/70 mmHg
Auscultation: no transmitted breath until middle third scapula
SpO2: 85 % without O2
The echocardiogram showed a severely depressed left and right ventricular ejection fraction of approximately 20% with severe mitral regurgitation.
Fig. 2: ECGs on admission. Top: Single lead ECG (lead II, 25 mm/s) during monitoring showing a supraventricular tachycardia with 1:1 conduction at about 200 bpm. Middle: 12 lead ECG after adenosine test which revealed a supraventricular tachycardia with 1:1-2:1 atrioventricular (AV) conduction and a ventricular rate at 150-200 bpm. Bottom: 12 lead ECG with sinus rhythm at about 100 bpm after a second attempt of verapamil.
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Preliminary Diagnosis: Ectopic atrial tachycardia with tachycardia-induced cardiomyopathy, chronic heart failure functional class NYHA III-IV (HFrEF) with a LVEF of 20%.
Biochemical blood tests showed a TSH of 7.0 mU/L, no other significant changes.
During hospitalization, the patient received standard therapy for HFrEF, including beta blocker, aldosterone antagonist, ACE inhibitor, digoxin, and a symptomatic therapy with i.v. loop diuretic together with anticoagulation and levothyroxine. An electrophysiologic study and ablation procedure were proposed to the patient which she did not want to be performed.
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Holter ECG monitoring was performed which showed an incessant atrial tachycardia, periodically with an atrioventricular Wenckebach pattern (Fig. 3).
The P-R interval shows progressive prolongation until a ventricular pause occurs, occasionally with a 2:1 atrioventricular (AV) nodal conduction (Fig. 3.1). Such sequences indicate a Wenckebach AV nodal conduction mechanism. During the tachycardia, the QRS complexes were narrow (100-106 ms).
After several days, the patient retured to our clinic for a scheduled follow up. A 12 lead ECG (Fig 3.2) and Holter monitoring were performed, showing sinus rhythm of 50 bpm at rest. Thereafter, the treatment was continued without the use of amiodarone and ACE inhibitors and a reduced dose of beta blocker. The next ECG after 3 weeks showed an atrial tachycardia at about 100 bpm. The patient complained again about palpitations, typically associated with physical activity. Holter monitoring showed self-terminating atrial tachycardia (Fig 3.3). The decision was made to increase the beta blocker dosage and to start propafenone. During further follow-up, the LVEF increased up to 60%, the patient did no longer perceive any symptoms.
Fig. 3: Atrial tachycardia with atrioventricular Wenckebach pattern.
Fig 3.1: Wenckebach pattern with 2:1 atrioventricular nodal conduction.
Fig. 3.2: 12 lead ECG at follow-up some days later with sinus rhythm at about 50 bpm.
Fig. 3.3: Holter monitoring showed self-terminating atrial tachycardia after reduction of beta blocker and discontinuation of amiodarone.
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The further follow-up with a treatment of beta blocker and propaphenone during a period of 3 years was uneventful. On the last follow-up, the patient was asymptomatic, the LVEF remained at >60%, no significant mitral valve regurgitation was found. The 12 lead ECG showed sinus rhythm (Fig 4). The 24 hour Holter monitoring showed sinus rhythm with single atrial premature beats.
Fig. 4: 12 lead ECG during 3-year follow-up with sinus rhythm at 65 bpm.
Fig. 4.1: Heart rate graph in the first versus the last 24 hour Holter monitoring.
Fig 4.2: R-R interval graph in the first versus the last 24 hour Holter monitoring.
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At this point, the patient did no longer perceive any symptoms and the LVEF increased to 60%. The further follow-up of 3 years was uneventful.
Thus, we describe a case where an ectopic atrial tachycardia was diagnosed by a constant tachycardia rate in the 24 hour Holter monitoring with a P wave almost identical to the P wave in sinus rhythm, leading to a reversible tachy-cardiomyopathy.
Key Words: Focal atrial tachycardia, Tachycardia Induced CMP. Holter monitoring.
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