A Simple Case of Atrial Fibrillation?

Case presentation

A 70-year-old female patient with a history of controlled arterial hypertension presented to her cardiologist for palpitations, chest pain and dyspnoea of progressive onset over the last few days. She had suffered intermittent palpitations for the past 4 weeks, some episodes lasting for several hours. Her cardiologist diagnosed atrial fibrillation (AF) with global left ventricular (LV) dysfunction, and prescribed oral anticoagulation and metoprolol.

However, symptoms increased despite drug treatment, prompting an emergency room admission. At presentation she was tachycardic at 170 bpm, without signs of peripheral hypoperfusion; her blood pressure was normal. Lung auscultation revealed mid-lung crackles. The rest of the physical examination was unremarkable.

The initial ECG is shown in Figure 1a; it is similar to the ECG performed by her physician 24 hours earlier.

Question

Do you agree with the diagnosis of AF?

Commentary

The ECG (Figure 1a) shows an irregular wide-complex tachy cardia with a QRS duration of 140 ms and an atypical right bundle-banch block (RBBB) morphology with a qRR’ in V1, rS in V6, right axis deviation and qR in lead aVR [2]. Furthermore, there are visible sinus P waves (positive in leads I and II, negative in aVR) with atrioventricular dissociation (Figure 1b).

Note the presence of captured beats (when an atrial impulse depolarises the ventricles through the normal conduction system, producing a narrow native QRS complex) and fusion beats [when a sinus impulse partially depolarises the ventricle and fuses with a ventricular tachycardia (VT) QRS complex producing a mixed and relatively narrow QRS] (Figure 1b). These features are diagnostic of VT with a RBBB pattern [1,2].

The laboratory workup was unremarkable. A transthoracic echocardiogram showed a severely globally depressed ejection fraction of 25%. A coronary angiogram was normal.

The irregularity of the arrhythmia cycle length speaks against a reentry mechanism but supports an automatic focus as the origin of the VT. In the absence of underlying disease incessant idiopathic left VT was suspected.

ECG morphology was atypical for a fascicular or an outflow tract VT and compatible with an anterolateral papillary muscle origin; however, papillary muscle arrhythmias are rarely expressed as incessant VT, but more often as ventricular premature beats [3,4,5]. The LV was endocardially mapped and successful ablation was performed in the antero-apical wall of the LV where early polyphasic potentials were recorded. Cardiac function improved progressively after the ablation and normalised within 3 months after the procedure. The ECG in sinus rhythm showed no major abnormality (Figure 2). During follow-up, a cardiac magnetic resonance imagining scan with intravenous gadolinium contrast was normal, allowing us to exclude myocardial scar and giving extra weight to the diagnosis of idio pathic VT.

The patient was uneventfully discharged following arrhythmia ablation. During 6 months of follow-up, Holter recordings confirmed the absence of significant ventricular arrhythmia recurrence.

This case reminds us of the importance of the 12-lead ECG in daily practice; misdiagnosis of arrhythmia can lead to unnecessary prescription of potentially dangerous medication.

Disclosure statement

No financial support and no other potential conflict of interest relevant to this article was reported.