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Postcardiac Injury Syndrome: A Rare Complication of Elective Coronary Angioplasty

Coronary angiography images demonstrating severe ostial stenosis of the intermediate artery (A) treated successfully by coronary stenting (B). ECG demonstrating global ‘saddle shaped’ ST elevation consistent with pericarditis (C). Chest radiography showing bilateral pleural effusion (D).

Coronary angiography images demonstrating severe ostial stenosis of the intermediate artery (A) treated successfully by coronary stenting (B). ECG demonstrating global ‘saddle shaped’ ST elevation consistent with pericarditis (C). Chest radiography showing bilateral pleural effusion (D).

Postcardiac injury syndrome conventionally has been described after myocardial infarction or cardiac surgery, but it is an infrequent complication of endovascular procedures. We report an unusual case of postcardiac injury syndrome occurring immediately after elective angioplasty.

A 58-year-old man attended our hospital (Northwick Park Hospital) for elective angiography for symptoms of exertional angina. He had a medical history of asthma and seropositive rheumatoid arthritis. On angiography, there was a severe ostial stenosis in a moderate-caliber intermediate artery. The lesion was predilated, and 1 drug-eluting stent (Xience Pro 2.25 × 23 mm; Abbott Vascular, Abbott Park, Ill) was deployed without complication.

Four hours after the procedure, the patient developed pleuritic chest pain, with a low-grade fever. Initial electrocardiograms (ECGs) were unremarkable, and bedside echocardiography demonstrated a global moderate-sized pericardial effusion, with a maximum width of 1.5 cm at the right atrial free wall. There were no features of cardiac tamponade. An iatrogenic hemopericardium was suspected, and he was monitored closely, with serial echocardiograms, and given simple analgesia. The following day, ECGs performed for persistent chest pain demonstrated widespread global ST elevation. He became increasingly breathless with reduced oxygen saturations, and on chest radiography there were bilateral pleural effusions. There was no change in the size of the pericardial effusion. The inflammatory markers were significantly elevated with a C-reactive protein of 234 mg/L. A septic screen was negative. Prednisolone was administered for presumed postcardiac injury syndrome. Over the next 2 days, there was a dramatic improvement in his chest pain symptoms and ECG changes, with a reduction in C-reactive protein from 234 to 96 mg/L.

Postcardiac injury syndrome refers to pericarditis after injury to the pericardium. The 3 main causes are postmyocardial infarction, postpericardiotomy syndrome (which has been reported in 20%-30% of patients after cardiac surgery), and unrecognized breaches of the pericardium complicating percutaneous procedures. In recent years, there has been an increase in iatrogenic cases as the indications for endovascular cardiac procedures expand. The incidence of pericardial complications after percutaneous coronary interventions has been reported as less than 0.5%.

Postcardiac injury syndrome is presumed to have autoimmune pathophysiology, triggered by the damage of pericardial or pleural mesothelial cells.2 The syndrome is characterized by an acute pleuropericarditis consisting of fever, pleuritic chest pain, dyspnea, pleural or pericardial rubs, and elevated inflammatory markers. Pericardial effusion is common, and there may be pleural effusion with or without pulmonary infiltrates. There is often a latent period of days to weeks between injury and symptom onset. The treatment of postcardiac injury syndrome is with anti-inflammatory drugs and low-dose corticosteroid therapy when nonsteroidal anti-inflammatory drugs are contraindicated or not tolerated. Adjunctive use of colchicine may prevent recurrences. Overall, the prognosis is favorable, although potentially fatal cardiac tamponade has been reported occasionally, and there is an intermediate risk of pericardial constriction (2%-5%) during long-term follow-up.

Postcardiac injury syndrome is a rare complication of coronary angioplasty and may cause life-threatening complications, prolonged hospitalization, and readmissions, with a moderate risk of pericardial constriction. The noteworthy aspects of this case are the absence of a latent period between a relatively uncomplicated elective percutaneous coronary intervention and the onset of symptoms. Despite the patient being unwell with hypoxia and markedly elevated inflammatory markers, there was a dramatic response to steroid therapy. The coexistence of autoimmune disease, that is, seropositive rheumatoid arthritis, in our patient is intriguing, and our subject may have been predisposed to the development of postcardiac injury syndrome through an immunopathic process.

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-Sothinathan Gurunathan, MBBS, Guy Parsons, MBBS, Grace Young, BSc, MSc, Andrew Porter, MBBS, Ahmed Elghamaz, MBBS, Roxy Senior, MD, DM

This article originally appeared in the May 2016 issue of The American Journal of Medicine.

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