The stunned atrial lead: Transient malfunction of a permanent atrial pacer lead following acute myocardial infarction.

Proximal right coronary artery occlusion caused transient loss of sensing and capture of the atrial lead of a permanent dual-chamber pacemaker. Forty-five days after percutaneous revascularization, the atrial lead was discovered to be functioning normally. We hypothesize that ischemia of the right atrium caused stunning of the atrial myocardium at the pacer-lead interface, which gradually improved following percutaneous coronary intervention (PCI), leading to return of lead function over time. So far only one similar case has been described in the literature.

Malfunction of atrial lead of a permanent transvenous pacemaker following acute myocardial is rare. Here we describe this unusual case of transient atrial lead malfunction of a dual chamber trans-venous permanent pacemaker following acute inferior wall myocardial infarction.

CASE REPORT

A 78-year-old average-built man with previous history of coronary artery disease was hospitalized with chest pain of few hours duration. His vital signs and physical examination were unremarkable. Two years earlier, he had presented with syncope. Thorough investigation had revealed carotid hypersensitivity (3 second pause after right carotid massage) and mixed cardioinhibitory and vasodepressor response to upright tilt. A dual-chamber pacemaker (Guidant Discovery II DR) was implanted. The atrial lead was Guidant (4480-318341) passive-fixation bipolar electrode and the ventricular lead was Guidant (4457-39232665) passive-fixation bipolar electrode. He did well thereafter, experiencing no further syncope. Pacer checks every 6 months demonstrated normal function of both leads. Pacemaker interrogation 26 days prior to the present admission showed normal function of the atrial and ventricular leads. On the day of admission, the electrocardiogram demonstrated sinus rhythm, ST-segment elevation in the inferior leads, ST-segment depression in lead V2, normal AV conduction, and no PR-segment depression. Pacer stimuli occurred at 65 bpm, uninhibited by the prevailing sinus rhythm [Figure 1].

Figure 1

Admission ECG. The tracing demonstrates sinus rhythm at 68 bpm, normal conduction, inferior current of injury and ST-Segment depression in leads I, AVL, and V2. Atrial pacer stimuli occur at 65 pulse per minute, uninhibited by the prevailing sinus rhythm, indicating lead sensing failure. Atrial pacing at maximum output (7.5 V, 1.9 ms) demonstrated no atrial capture (data not shown).

Emergent cardiac catheterization demonstrated total occlusion of the proximal right coronary artery. Angioplasty was performed at the take-off on an atrial branch. Normal flow was restored and a stent was placed. A distal lesion was opened by balloon angioplasty [Figure 2a and 2b]. After catheterization, interrogation of the pacer demonstrated no measurable P-wave: at sensitivity of 0.15 mV the atrial lead detected only a far-field QRS. It failed to capture the atrium at the highest programmable output (7.0 V at 1.9 ms). The ventricular lead functioned normally. The basic metabolic panel and electrolytes were normal. Chest radiograph demonstrated stable atrial lead position with no visible discontinuities. The device was programmed to the rate-adaptive, ventricular inhibited (VVIR) mode. Two days later, the patient was clinically stable and ready for discharge. Pacer interrogation was unchanged; the atrial lead function had not improved. Forty-five days later, he returned to the Pacer Clinic complaining of effort intolerance and fatigue. Interrogation revealed normal atrial sensing (P-wave = 3.0 mV) and capture (threshold = 0.8 V at 0.4 ms). The pacer was reprogrammed to the dual-chamber mode. Within 48 hours, his symptoms improved. Follow-up pacer interrogations 2 months and 8 months later demonstrated stable function of the atrial lead [Table 1].

Figure 2

Right coronary angiogram in the LAO cranial projection before (a) and after (b) angioplasty of the proximal occlusion. The atrial (A) and ventricular (B) leads are seen. TIMI grade 0 fl ow before angioplasty was restored to TIMI grade 3. A large right atrial branch (black arrow) is seen originating at the point of the vessel occlusion.

Table 1

Summary of atrial and ventricular lead testing before and after the day of acute inferior wall myocardial infarction (29th June, 2004)

DISCUSSION

This case demonstrates transient malfunction of a permanent passive-fixation atrial pacer lead at the time of acute myocardial infarction. The infarction was due to total occlusion of the proximal right coronary artery at the take-off of the atrial branch. Since malfunction of the lead preceded angioplasty, the stent placement in the right coronary artery cannot be implicated in the lead malfunction. We conclude that transient ischemia of the right atrial myocardium at the pacer-lead interface caused transient loss of sensing and pacing functions. This persisted for at least 48 hours but resolved within 2 months. The most plausible hypothesis to explain these observations is stunning of the atrial myocardium due to atrial ischemia. Neither PR-segment depression nor atrial fibrillation – two clinical phenomena that often indicate atrial infarction – were observed in this case.[1] Chiliang et al. have reported one similar case. In that study, the atrial lead malfunction was found to have normalized 40 days after stent implantation of right coronary artery.[2]

CONCLUSION

This case demonstrates that transient malfunction of a permanent atrial pacer lead may result from occlusion of the right coronary artery proximal to the atrial branch. In the absence of other electrocardiographic features of atrial infarction, transient malfunction of an atrial pacing lead should be included as a criterion for atrial infarction in patients with pacemakers. In this clinical setting, a new atrial lead should not be urgently implanted; the patient should be followed with the expectation that lead function may normalize over time. The precise time course of such recovery is not fully known. Thus, should other physicians encounter similar patients, it would be informative to follow patients at close intervals to determine how quickly the function may normalize.