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Catalin Pestrea1, Alexandra Gherghina1, Diana-Georgiana Miron1, Florin Ortan2

1 Intensive Cardiac Care Unit, Emergency County Clinical Hospital, Brasov, Romania
2 Interventional Cardiology Unit, Emergency County Clinical Hospital, Brasov, Romania

Abstract:    Post-pacemaker insertion pericarditis is a rare form of post cardiac injury syndrome.

We present a 78-year-old woman, who received a VVIR pacemaker for sick sinus syndrome with the lead placed on the septal side of the right ventricular outfl ow tract. Eleven days later she presented with persistent fever and severe dyspnea. The echocardiography revealed a large circumferential pericardial effusion with signs of cardiac tamponade. Percutaneous pericardial drainage using the apical approach was performed and about 1000 ml of serofibrinous fluid were drained. The laboratory analyses showed highly elevated inflammatory markers with negative blood and pericardial fluid cultures. The patient was started on ibuprofen and colchicine with a favourable course and normalization of infl ammatory markers.

Keywords: inflammatory pericarditis, tamponade, cardiac pacing, pericardiocentesis.

INTRODUCTION
Post-pacemaker insertion pericarditis is a rare form of post cardiac injury syndrome (PCIS) and represents a potential complication of permanent cardiac pacing with various clinical courses from a benign self-limiting condition to life-threatening cardiac tamponade.

CASE REPORT
A 78-year-old woman was admitted in our hospital for dizziness and fatigue. Her ECG showed atrial fi-brillation with rapid ventricular rate which converted spontaneously to a period of sinoatrial block with low junctional escape rhythm (Figure 1).
The laboratory analyses were unremarkable and her echocardiography showed a normal left ventricular function and mild mitral regurgitation.
The case was interpreted as a sick sinus node di-sease with a bradytachy syndrome and a VVIR pacemaker with the lead placed on the septal side of the right ventricular outflow tract (RVOT) was implanted without any complications and the patient was dis-charged the next day.
Eight days later the patient experienced fever (38.7°C) and on the eleventh day postdischarge she presented to the emergency unit for severe dyspnea and fatigue.
The ECG showed atrial fibrillation with a ventri-cular rate of 140 bpm. Device interrogation showed normal impedance, sensing and pacing parameters. Blood tests showed markedly elevated inflammatory markers (white blood count – 15.690/mm3, C-reactive protein – 235mg/l, erythrocyte sedimentation rate – 72 mm/h). The chest X-ray showed an enlarged cardiac silhouette with a normal lung image and no apparent dislodgement of the lead (Figure 2).
The echocardiography revealed a large circumfe-rential pericardial effusion with collapse of the right cavities. A CT scan was performed which confirmed the septal placement of the lead without any signs of perforation and identified the pericardial fluid as ha-ving a low density, much lower than blood (Figure 3).
In this situation a pericardiocentesis was performed using the apical approach, which revealed a serofibri-nous pericardial fluid. A 8F drainage tube was placed in the pericardial cavity and a total of 1000 ml of fluid was drained with significant symptomatic relief.
The laboratory analyses of the fluid showed exsu-date characteristics and both cultures from the blood and pericardial fl uid were negative.
The patient was started on ibuprofen (600 mg three times daily for two weeks, then 400 mg three times daily for another two weeks) and colchicine (0.5 mg once daily for three months) with a favourable course and normalization of inflammatory markers. The pericardial drainage tube was removed after four days and she was discharged after seven days from the day of admittance.
The one month and three month echocardiographic follow-up showed no recurrence of pericarditis (Figure 4).

Figure 1. Presenting ECG rhythm: (A) Atrial fibrillation with rapid ventri-cular rate spontaneously converted to (B) Sinoatrial block with low junc-tional escape rhythm.

Figure 2. Chest X-ray image showing an enlarged cardiac silhouette with a normal lung image and no apparent dislodgement of the lead.

Figure 3. Chest CT image showing a circumferential large pericardial ef-fusion and the ventricular lead placed on the septal side of the right ven-tricular outflow tract.

Figure 4. Echocardiography image showing no pericardial effusion recurrence after three months.

DISCUSSION
Acute pericardial effusion developing shortly after pa-cemaker implantation is due either to cardiac perfora-tion with hemopericardium1 or to an acute inflamma-tory pericarditis in the context of a post cardiac injury syndrome2,3, the latter being reported with an inci-dence of 1 to 2%.
PCIS is a well described clinical entity for decades and usually follows heart surgery or trauma4. Nevert-heless, any kind of myocardial injury, including percu-taneous cardiac interventions as ablation procedures, coronary angioplasties or heart device implantations could cause PCIS.
The presumed mechanisms of PCIS after pacema-ker implantation are an autoimmune inflammatory process triggered by myocardial injury after an active lead fixation and mediated by antimyocardial antibodies, or a minimally protruding exposed helix which directly irritates the pericardium, either mechanically or through minor bleeding, causing inflammation and fluid secretion5.
The differential diagnosis between cardiac perfo-ration and PCIS could be difficult to make6. Howe-ver, there are signs and symptoms which could point towards an infl ammatory process:

• Fever >38°C; 2) pericardial or pleural friction rub; 3) no proof of cardiac perforation on imaging stu-dies; 4) elevated inflammatory markers; 5) a yellow serofibrinous pericardial fl uid; 6) development betwe-en 7 days and 4 weeks after the procedure; 7) acute response to anti-inflammatory drugs (NSAIDs, colchi-cine, cortisone).

The case we described fulfilled almost all of the above criteria.
The vast majority of PCIS cases following pacema-ker implantation were reported in patients with atrial active fixation leads7, with very few cases after passive fixation leads and ventricular only pacing8,9.
Although myocardial injury occurs irrespective of ventricular pacing site, as a particularity, we didn`t find any other mention of RVOT placed leads causing PCIS.
PCIS is considered usually a benign condition, but occasionally could lead to cardiac tamponade as it was in our case10.
Fortunately, pericardial drainage and anti-inflammatory medication resolves this problem in almost all cases.
CONCLUSION
Cardiac pacing could be a cause of post cardiac injury syndrome and implanters should take this diagnosis in consideration whenever symptoms of inflammatory pericarditis occur in the fi rst month after the procedure.

Conflict of interest: none declared.
References
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