Coronary sinus rhythm is an ectopic atrial rhythm supposedly originating from a pacemaker at the mouth of the coronary sinus; recognized in the electrocardiogram by P-waves that are inverted in leads II, III, and VF with a normal or prolonged P-R interval. In myocardial infarction, this presentation can reveal a wandering atrial pacemaker. We present a case of a wandering atrial pacemak- er with inferior wall MI complicated by complete atrio-ventricular block.
Coronary sinus rhythm is an ectopic atrial rhythm supposedly originating from a pacemaker at the mouth of the coronary sinus; recognized in the electrocardiogram by P-waves that are inverted in leads II, III, and VF with a normal or prolonged P-R interval. In myocardial infarction this presentation can reveal a wandering atrial pacemaker.
We present a case of wandering atrial pacemaker with inferior wall MI complicated by complete atrio-ventricular block.
A 86-year-old woman was admitted to emergency department of a comminatory hospital due to persisting angina for an hour and syncope. Pain was 4/10 on scale His She had no previous medical history, a non-smoker. Electrocardiogram (ECG) showed ST segment elevation in leads II, III and VF and reciprocal ST segment depression in leads V1–V6. She was treated before the arrival of our pre hospital team with dual oral anti platelets such us aspirin 250 mg and clopidogrel 300 mg, intra venous loading doses of unfractionated heparin 50 mg and atropine (0,5 mg) for brady ar- rhythmia.
On physical examination by our prehospital physician the cardiac sounds and breathing were normal on auscultation. The patient was dizzy and somnolent. Her pulse was irregular at 50 bpm, her blood pressure was 50/30 mm Hg. The ECG showed ST elevation in leads II, III, Vf, V3, V4, V3R and V4R. an inverted P wave was noted in inferior leads consistent with coronary sinus rhythm complicated by a complete atrio-ventricular dissociation (Figure 1). She was medicated by Dobutamine at 10 γ/Kg/min with Nor- epinephrine at 0,5 mg/h. the patient was transferred to Cath lab for primary Per cutaneous Coronary Intervention (PCI).
On the way, the ECG has changed and demonstrate Second Degree Heart Block (Mobitz type 2), ST segment elevation in leads II, III, Vf, V1, V3, V4 and V6 with low atrial rhythm (Figure 2).
On admission she was conscious, heart rhythm was irregular at 65 bpm, and blood pressure 80/50 mmhg. Serum troponin 0.30 ng/mL (normal range (NR) 0–0.14 ng/mL). His electrocardiogram showed sinus tachycardia with decrease in ST segment elevation (Figure 3).
After an initial evaluation, coronary angiography (CAG) was immediately performed and revealed total occlusion with a thrombus in the proximal segment of the right coronary artery (RCA) with a TIMI 0 flow. A Laying bare stent of (3 * 15mm) was placed with good result. During the course several ventricular Fibrillation occurred treated by electrical shock.
After coronary angioplasty the ECG showed new-onset atrial fibrillation (AF) (Figure 4). The transthoracic echocardiography performed too days later revealed hypokinesia of the inferior wall with a good left ventricular ejection.
3. Discussion
A wandering pacemaker is a sign of cardiac irritability in the atrial. This dysrhythmia may occur in normal hearts as a result of fluctua- tions in vagal tone. Schamroth and Goldberg [2] attempted to clar- ify the definition of wandering pacemaker in 1972. they explained the mechanism of the wandering pacemaker as an escape rhythm overloaded with extreme bradycardia. They postulated that the si- nus bradycardia was considered to be the main cause of the escape beat which occur in the first place, and it is a benign physiological condition. New theory concerning the wandering pacemaker have been described following the more in-depth studies of the anatomy and physiology of the sinoatrial node [2]. A recent review of physi- ology suggests too theories for P-wave changes morphology in the wandering stimulator. The variation of the initial stimulation sig- nal in the sinoatrial node causes the change of the morphology of the p wave. The theory holds that too or more physiological pacing sites (leading and subsidiary) within the structure alternate the role of primary pacer during episodes of WAP. Following the change of the site of first stimulator, the wave of the action potential changes and consequently the axis of the P wave.
The other modern theory that could account for P-wave mor- phology changes is that the action potential comes from a very extended area: The sinoatrial node is actually a more extensive tadpole-shaped structure that includes a para nodal area and artic- ulations into the atrial muscle structure. The potential action can come from a different location but the pacemaker site is stable, which explains the change of the P-wave axis in a single lead.
It has also been shown that a wandering atrial pacemaker is a po- tential long-term complication of high-dose sympathomimetics at toddler, [5].
In other study, the others described the possibility of atrial infarction when considering inferior, and/or posterior infarctions with atrial arrhythmias, hypotension and a cardiac output status. Atrial infarction is frequently accompanied by a variety of complications include arrhythmia, rupture, loss of atrial ‘kick’ and thromboem- bolic phenomena. Wandering atrial pacemaker is not quite com- mon in the setting of atrial infarctions [1]. In our case the WAP was associated with MI and cardiac outputs status. It’s unfortunately possible to miss an association with atrial infarction which has been a relatively understudied entity.
4. Conclusion
This case is presented to highlight the possibility of WAP and hypotension and a cardiac output status with inferior myocardial infarction. PAW occurs on the occasion of a change of balance be- tween sympathetic and parasympathetic tone this during this con- sequent rhythm as Benin can indicate a different speech. This may be a most enriching contribution when future studies are needed to determine if WAP in MI was B flat or a benign heart rate note.
Reference
Heart Lung. 1972; 1 (4): 519-522.
Atrial Tachycardia Advanced Critical Care. 2015; 26 (1): 73-76