Israel Medical Association Journal

Background: The appearance of pericarditis following insertion of a permanent pacemaker is not widely acknowledged in the literature.

Objectives: To describe our experience with pericarditis following 395 permanent pacemaker implantations over 2 years.

Methods: We retrospectively reviewed the medical records of 395 consecutive patients in whom new pacing systems or pacemaker leads had been implanted over a 2 year period. We searched the records for pericarditis that developed within 1 month after pacemaker implantation according to the ICD-9 code. The incidence, clinical picture, response to treatment and relationship to lead design and location were studied.

Results: Eight cases (2%) of pericarditis following implantation were detected. Clinical manifestations in all patients were similar to those of post-pericardiotomy syndrome and included chest pain (n=7), friction rub (n=1), fever (n=2), fatigue (n=2), pleural effusion (n=2), new atrial fibrillation (n=2), elevated erythrocyte sedimentation rate (n=4) and echcardiographic evidence of pericardial effusion (n=8). All affected patients had undergone active fixation (screw-in) lead implantation in the atrial position. The incidence of pericarditis with screw-in atrial leads was 3% compared to 0% in other cases (P < 0.05).

Conclusions: Pericarditis is not uncommon following pacemaker implantation with active fixation atrial leads. Special attention should be paid to identifying pericardial complications following pacemaker implantation, especially when anticoagulant therapy is resumed or initiated. The use of passive fixation leads is likely to reduce the incidence of pericarditis but this issue should be further investigated.

Background: Myocardial infarction-associated pericarditis is a common cause of chest pain following MI[1], its frequency depending on how it is defined.

Objectives: To investigate the incidence of acute pericarditis and pericardial effusion in the acute phase of ST-elevation MI treated with thrombolytic therapy.

Methods: The study group comprised 159 consecutive patients fulfilling the criteria for acute MI who were admitted to our department during 18 months. Infarct-associated pericarditis was defined as the finding of a pericardial friction rub, a typical pleuropericardial pain, or both. All patients underwent physical examination of the cardiovascular system four times daily for 7 days, as well as daily electrocardiogram and echo Doppler examinations.

Results: Fourteen patients (8.8%) developed a friction rub and 11 patients (6.9%) had a mild pericardial effusion. Six patients (4.0%) had both a friction rub and pericardial effusion. Two patients had a friction rub for more than 7 days. Pleuropericardial chest pain was present in 31 patients (19.5%) but only 7 of them had a friction rub.  The in-hospital mortality rate was 1.3% and no mortality was observed in the acute pericarditis group.

Conclusion: The incidence of signs associated with acute pericarditis was lower in MI patients treated with thrombolysis, compared with historical controls, when a friction rub and/or pericardial effusion was present. There was no significant reduction in the incidence of pleuropericardial chest pain.