Post cardiac injury syndrome (PCIS) is characterized by the development of pericarditis with or without pericardial effusion due to a recent cardiac injury. The pathogenesis of PCIS is unclear, it may be an autoimmune process after heart injury, with antigens derived from damaged myocardial tissue.

Causes of PCIS include myocardial infarction, pericardiotomy, blunt trauma, and minor damage to the heart, such as coronary intervention, insertion of pacemaker leads, or radiofrequency ablation [1, 2]. Post-pacemaker insertion pericarditis is a rare type of PCIS that occurs in 1% to 2% of patients after pacemaker implantation [7]. Previous reports have shown that PCIS can occur within hours or days, or as early as 5–56 days after the procedure [8]. A patient’s medical history is essential for the recognize and diagnosis of PCIS, and patients undergoing the procedure should be followed up regularly from 1 to 3 months after the procedure [9]. The patient in our case is a 94-year-old male with a history of sick sinus syndrome managed with a dual-chamber pacemaker who presented with PCIS after two months of pacemaker implantation.

The mechanism of PCIS in general and post pacemaker insertion pericarditis in particular is still not well understood. Advanced age, female gender and the use of active fixation leads, a temporary transvenous pacemaker or steroid use are independent risk factors for the development of post pacemaker insertion pericarditis [10]. A proposed theory is that injury to mesothelial pericardial cells induces an immune response, leading to immune complex deposition in the pericardium, pleura, and lungs, which causes an inflammatory response [1, 7, 11]. The auto-immune nature of PCIS is supported by clinical features such as the latent period between the insult and symptoms, elevation of inflammatory markers, good response to NSAIDs, and a tendency to recur [4]. However, unlike other autoimmune diseases, circulating anti-cardiac antibodies are not detected until 14 days after the onset of PCIS, rather than at the initial diagnosis, and thus are not helpful in the diagnosis of PCIS [12].

The clinical manifestations of PCIS are pleurisy chest pain, fever, pericardial effusion and/or pleurisy with or without pleural effusion, and elevated reactants in the acute phase. Although almost all patients with PCIS have pericardial effusion, not all patients with pericardial effusion have symptoms or require treatment [10]. Distant heart sounds can be heard on physical examination, with signs of pericardial or pleural friction and pleural effusion. Chest imaging and echocardiography confirmed the presence of pleural and/or pericardial effusion and lead location. The diagnosis of post-cardiac injury syndrome after dual pacemaker implantation can only be diagnosed when other common infectious, autoimmune, or malignant causes have been excluded. An important differential diagnosis of PCIS is overt or minor lead perforation, which is also a common complication of pacemaker implantation [13]. There is no clear standard to distinguish pacemaker lead perforated from PCIS without perforation. Capture threshold increases, R wave amplitude decreases, lead impedance increases or decreases significantly, indicating lead perforation [6]. However, normal pacemaker function does not rule out the possibility of a perforated lead. In rare cases, lead perforation may be visible on imaging [7]. The patient in our case has typical symptoms and laboratory results consistent with the characteristics of PCIS, and was stable after 3 months of treatment according to the treatment regimen of PCIS. Reexamination of the UCG showed no increase in pericardial effusion, so the diagnosis of PCIS was considered.

The treatment of PCIS consists of similar treatment to other cases of acute pericarditis. The first-line therapy includes a combination of non-steroidal anti-inflammatory drugs and colchicine [8, 9, 14, 15]. Patients who do not tolerate NSAIDs and colchicine therapy or have a resolution of symptoms may be given a course of corticosteroids, which are tapered over weeks as the symptoms resolve [1, 9, 10, 16, 17]. If the patient develops pericardial effusion leading to cardiac tamponade, treatment with a pericardial window or surgical drainage may be necessary. Our patient showed adequate improvement with colchicine treatment and pericardium puncture though we reduced his colchicine dosage because of his advanced age. PCIS may be an immune process produced after heart injury, and attention to bed rest, avoid fatigue and strengthen nutritional support after heart injury may reduce the risk of PCIS.