Case Report

Post Cardiac Injury Syndrome after Uncomplicated Coronary Angioplasty

Nisar H. Shah, MBBS, MRCPI, FCPS and Anthony Scriven, MD, FRCP
Nisar H. Shah, MBBS, MRCPI, FCPS and Anthony Scriven, MD, FRCP
Author Affiliations: From the Worcestershire Royal Hospital, Worcester, United Kingdom. The authors report no conflicts of interest regarding the content herein . Manuscript submitted July 16, 2008, provisional acceptance given September 29, 2008, and final version accepted October 2, 2008. Address for correspondence: Nisar H. Shah, MBBS, MRCPI, FCPS, 16 Colton Road Armly, Leeds West Yorkshire, United Kingdom LS12 1TU.


J INVASIVE CARDIOL 2009;21:E16-E17 Chest pain after percutaneous coronary intervention (PCI) could result from a variety of causes including coronary perforation1 and stent thrombosis. Pleuropericarditis as part of post cardiac injury syndrome has been described after both complicated2 and uncomplicated3 PCI. We report three cases of post cardiac injury syndrome following uncomplicated PCI. Case 1. A 75-year-old female was admitted with non-ST elevation myocardial infarction (NSTEMI). She was transferred to a tertiary care facility for PCI. She underwent angiography and 2 bare-metal stents (BMS) were deployed, 1 in the proximal left anterior descending artery and the other in the mid-right coronary artery. The procedure was uncomplicated, but 6 hours later, she developed dull left-sided chest pain. Her electrocardiogram (ECG) revealed no new ischemic changes and her pain settled with simple analgesics. She was discharged home pain-free the next day. Ten days later, she was readmitted with severe left-sided pleuritic chest pain. On examination she was in pain, apyrexial, free from heart failure and had no detectable pericardial rub, but had reduced air entry at the left lung base. Her ECG was unchanged. She had normal cardiac markers, raised C-reactive protein (CRP) levels and elevated D-dimer levels. Computed tomographic pulmonary angiography excluded pulmonary embolism, but showed small pericardial and left pleural effusions. Echocardiography revealed a 1 cm global pericardial effusion and a small left pleural effusion. A diagnosis of pericarditis was made and she was started on colchicine. The patient recovered quickly over the next couple of days and was discharged home. On follow up 6 weeks later, she was in remission and no longer taking colchicine. Case 2. A 52 year old female with type II diabetes mellitus was admitted to our hospital with NSTEMI. She was transferred to a tertiary care facility for PCI. Angiography showed diffuse triple- vessel coronary artery disease. A BMS was deployed in the mid-circumflex artery without complications and she was discharged home the next day. She was readmitted 4 days later to our hospital with pleuritic left-sided chest pain. On examination, she was in pain, afebrile, and hemodynamically stable. There were no audible pleural or pericardial rubs. A 12-lead ECG did not reveal new ischemic changes. Cardiac markers were normal and ESR was 32. Echocardiography revealed a pericardial effusion measuring 0.79 cm globally. She was diagnosed with pericarditis and discharged home on prednisolone. On follow up 2 weeks later, she was on a tapering dose and in remission. Case 3. A 71-year-old male underwent primary PCI to his LAD for an ST-elevation myocardial infarction. He was discharged home after an uneventful recovery. He was readmitted 5 weeks later with left-sided chest pain suggestive of pericarditis. On initial evaluation, he was in distress, but afebrile and hemodynamically stable. Cardiac auscultation and chest examination were unremarkable. The 12-lead ECG was nondiagnostic and his cardiac markers were normal. He had normal CRP and chest X-ray. Echocardiography confirmed pericardial effusion and a diagnosis of pericarditis was made. He was discharged on indomethacin and made a full recovery after 1 week of treatment. Discussion. Post cardiac injury syndrome is not uncommon after any form of cardiac insult.4 Stelzner et al5 described the clinical course of the syndrome. The onset of the syndrome occurred about 20 days after the injury. An elevated ESR and pleurisy were found in 96% and 91% of the patients, respectively, whereas 2 in 3 patients had fever. The 3 cases reported above represent spectrum of the syndrome ranging from mild to florid inflammatory reaction. There are some similarities in these cases: all 3 patients presented after an uncomplicated PCI, had some evidence of pleuropericarditis and no evidence of new ischemia. The time of onset of symptoms in our case series varied from a few hours to 5 weeks. None of our patients had a history of fever, as has been described previously. Post cardiac injury syndrome after uncomplicated PCI is rare and only 2 cases have been reported. Velander and colleagues2 described a patient who presented 1 week after having PCI with symptoms suggestive of post cardiac injury syndrome. Hearne C et al3 described a second case in which the patient presented 3 weeks after an uncomplicated PCI with febrile illness, myalgias and a large left pleural effusion. The cause of post cardiac injury syndrome still remains uncertain. Some researchers have suggested a viral6 origin, while others suggest an immunologic cause.7 Engle and colleagues6 suggested that concurrent fresh or reactivated viral illness plays a role in triggering the immunologic response that characterizes the post pericardiotomy syndrome. The 3 cases reported here are linked by recent PCI. Balloon angioplasty and stent implantation cause mechanical barotrauma. This causes fracture and compression of atheromatous plaque, commonly associated with coronary artery dissection.8 Although frank rupture of coronary arteries during PCI is rare, it is likely that some cases result in periarterial hematoma with extravasation of blood into the pericardium, a known cause of inflammation. A localized pericardial reaction could cause pain without ECG changes or a systemic response. Conventionally, non-steroidal antiinflammatory drugs (NSAIDS), corticosteroids and immunosuppressive drugs have been the mainstay of treating acute pericarditis. Recent data support use of non-steroidal antiinflammatory medications for symptomatic relief in combination with colchicine for prevention of recurrence.9,10 Steroids, high doses in particular, are associated with an increased incidence of recurrence.11 In our case series, all 3 patients received different antiinflammatory drugs with successful short-term outcomes, but it is unclear if the recent data9–11 can be extrapolated to guide therapy in other forms of pericardial injury. Based on this, we suggest that a short course of NSAIDS, combined with colchicine in a dose of 1 mg per day for up to 2 weeks, would be a reasonable first choice. Steroids should be avoided if possible for this self-limiting condition. Conclusion. A diagnosis of post cardiac injury syndrome should be considered in post-PCI patients presenting with chest pain and features of an acute inflammatory reaction without ECG or biochemical markers of myocardial ischemia. Its treatment is specific and early institution of therapy will help relieve the patient’s symptoms and shorten the hospital stay.


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