Discussion and conclusions
PCIS is also known as pericarditis after pericardium injury. The incidence of PCIS in adults and children has been reported to be 10–40% after cardiac surgery [
1,
2], about 1–5% after implantation of intra-cardiac devices [
1,
3,
4], and around 0.2% after coronary intervention [
5]. Our cases were consistent with previous reports which showed that the onset of PCIS could vary from hours or days, and could occur up to 5–56 days after the procedure [
6,
7]. It is therefore crucial to recognize and diagnose PCIS while taking the patient’s medical history, and the patient should be evaluated at regular follow-up visits for 1–3 months after the procedure [
8].
Although the clinical manifestations of PCIS are non-specific, there are several common indicators that should be closely monitored. Most patients present with fever (92%), dyspnea (78%), chest pain (50%), elevation of C-reactive protein (CRP) or erythrocyte sedimentation rate (ESR) (80%) and pleural effusion (61%) [
8]. Other findings include hyponatremia, unexplained anemia, or atrial fibrillation. Although pericardial effusion is observed in almost all PCIS patients, not all patients with pericardial effusion are symptomatic or require treatment. A recent study of 968 patients showed that when echocardiography was performed 24 h after implantation of a permanent pacemaker, 98 patients had some degree of pericardial effusion, while only 19 of the patients were symptomatic and 14 required an intervention. The remaining 79 patients remain asymptomatic and did not require treatment, and most of them were free of pericardial effusion after three months [
9].
In our first patient, the cause of heart failure, pericardial effusion and pleural effusion was initially unknown, and device interrogation showed normal results. The patient had low-grade fever without leukocytosis. Blood culture and thoracocentesis were performed in order to rule out infection and the possibility of hemothorax. Although there was no progression of pericardial effusion or signs of tamponade on echocardiography, chest CT scan was performed to make sure there was no perforation of the pacing leads, or venous thrombosis by the leads. This procedure was similar to a previous study by Farbod et al
. [
8], where a diagnostic flow chart was designed to rule out infection, perforation, pulmonary embolism, and lead perforation before diagnosing PCIS caused by implantation of a cardiac device.
Our second patient showed acute pericardial effusion with unstable vital signs. However, there was no direct clinical evidence which could indicate the cause of pericardial effusion. Coronary angiography and chest CT scan were repeated immediately in order to exclude all possible causes of pericardial effusion, including coronary perforation, aortic dissection, or ventricle perforation. It has been reported that patients with stable hemodynamics who have pericardial effusion can be managed conservatively and tried in patients in whom ECG, cardiac enzyme levels, and inflammatory markers indicate typical pericarditis [
10,
11]. The following course of pericardial effusion recurrence 9 months later also supported PCIS etiology, rather than micro-perforation alone.
In our patients, hypervolemic hyponatremia was treated by diuresis, water restriction and increased salt intake. The three possible mechanisms which are thought to cause hyponatremia in PCIS include (1) increased secretion of ADH [
12,
13], (2) elevation of atrial natriuretic factor [
12], and (3) decreased effective volumes due to pericardial effusion which further decrease the glomerulus filtration rate [
14]. Despite these different mechanisms, sodium levels can be corrected by simply treating the PCIS, and relieving the pericardial effusion has been shown to be sufficient to improve sodium levels without any other therapy [
12,
14].
A number of studies have investigated risk factors for PCIS after pacemaker implantation. A study of 4280 patients who underwent pacemaker implantation reported that patients with a temporary transvenous pacemaker or steroid use within 7 days prior to implantation were more likely to have PCIS [
15]. In addition, there was a higher risk of PCIS with active fixation in the right atrium (RA) (lateral, anterolateral side, or appendage) [
9,
16]. A study of 1021 pacemaker implantations showed that there were no reports of PCIS after passive fixation or active fixation in the ventricle [
17]. Female gender and antiplatelet therapy were also considered as risk factors for PCIS after pacemaker implantation [
9]. In contrast, the risk factors of PCI-induced PCIS remain poorly understood, probably due to the low incidence rate.
The pathophysiology of PCIS remains unclear, and several studies suggested that it is an autoimmune reaction related to anti-myocardial antibodies resulting from injury to the myocardium or pericardium [
1]. The autoimmune 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. However, unlike other autoimmune diseases, circulating anti-heart antibodies are detected within 14 days of PCIS rather than at the time of diagnosis [
18], and therefore do not help in PCIS diagnosis.
Both of our patients were treated with corticosteroids instead of NSAIDs, since NSAIDS were contraindicated in both patients. However, aspirin, NSAID, steroid, and colchicine have been reported as the main treatment options in a number of current case reports describing pacemaker- or PCI-induced PCIS [
8,
19], and the dosage and duration of treatment are presented in Table
1 [
20,
21]. Corticosteroids are usually considered as second-line treatment for patients who show a poor response to NSAIDS, or when NSAID use is contraindicated due to higher adverse event rates, longer disease duration, and higher recurrence rate [
6,
20,
21]. When patients are symptom-free and exhibit normalized levels of inflammatory markers, a slow tapering-down of the steroid is recommended rather than an accelerated decrease [
21]. In our case 1, the patient was administered colchicine after he had recurrent PCIS. Some case reports described simultaneous administration of colchicine along with NSAIDs or corticosteroid from the beginning, since colchicine has proved to be useful in treating refractory or recurrent post- pericardiotomy syndrome, and in lowering the recurrence rate [
22]. However, if the patient does not respond to second-line treatment with steroid plus colchicine, then a combination of NSAIDs, steroids and colchicine should be considered as the next treatment option [
21]. There is also one recent reported PCIS case rapidly occurred after pacemaker implantation, which was solved by prednisolone and colchicine successfully [
23].
Table 1
Suggested medication and dosage for post cardiac injury syndrome
Ibuprofen | 600 mg tid | 1–2 weeks for acute case, and 2–4 weeks for recurrent cases |
Indomethacin | 25–50 mg tid |
Aspirin | 750–1000 mg tid |
Corticosteroid | 0.2–0.5 mg/kg per day | 2–4 weeks of treatment before slow tapering off |
Colchicine | BW > 70 kg: 0.5 mg bid BW < 70 kg: 0.5 mg qd | 3 months for acute PCIS, 6 months for recurrent PCIS |
PCIS can have a good prognosis, and patients with PCIS can be treated conservatively using NSAIDs, steroids, and colchicine. Diagnosis of PCIS is usually based on exclusion of other possible causes of pericarditis.
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