Dressler’s Syndrome: A Rare Complication

Hayder Kubba, MBChB, FRCS(UK), DFFP, DPD

CardioCase presentation

Greg’s

Greg, 46, arrives at the ED at the end of the His current daily medications include: day with his wife, who was very concerned • ramipril 5 mg, about his increasing chest pain that has • bisoprolol 5 mg, been present for the last three days. • warfarin 8 mg, • clopidogrel 75 mg, History • acetylsalicylic acid 81 mg and He had a fairly extensive infarction two • atorvastatin 80 mg. months ago and was treated with © tion angioplasty with stent. Examihnatiton ribu iGregg is very anxious, witihsa tradial paulds,e of yr D wnlo Greg used to smoke 40 to 50 cigaretteps a 100 bpm thait ais rlegularnanddobilaterally equal. o rc s ca se day before he had the infarctionCand His BPeis 110/u80sermmHg anndalhius chest is m ised erso unfortunately has been unable to compleotelmy clear,thorthough heforispsomewhat restricted r C d. Au opy give this habit up. o ibite whengletakic ng a deep breath. le proh sin Sa use rint a or ised nd p He hast afstrongthfamiorly historeywof acoronary He has a normal double rhythm with a arotery diseasnaeuas both hisy, vfaither and elderly scratchy, grating, high-pitched friction rub at N U ispla brother had MIsdin their early forties. For that the left lower sternal border. reason, the local cardiologist discharged him on warfarin for three months and Greg has Though his chest wall is not tender, he has asked his physician to monitor his minimal epigastric tenderness. The rest of international normalized ratio (INR) and his examination is normal. dosing. His physician admitted him to hospital for The pain was gradual in onset and was further investigations. initially reterosternal, but became pleuritic in nature afterwards. It is worse when lying down, associated with: • increased shortness of breath, • malaise and • of 37.5 C to 38 C. For more on Greg, see page 21.

Perspectives in / April 2007 19 CardioCase discussion

ressler’s syndrome is also known as post- raised erythrocyte sedimentation rate (ESR) DMI syndrome and can occurr from two to five • Serology may show autoantibodies days, or as long as three months post-MI. Other vir- • Chest x-ray may reveal: tually identical syndromes may follow open-heart - pleural effusion (83%), surgery (postpericardiotomy or postcardiotomy - parenchymal opacities (74%), syndromes), or penetrating or blunt trauma. - enlarged cardiac silhouette from The incidence of Dressler’s syndrome is (40%) about 4% following transmural infarction and • ECG may show ST elevation in most leads probably higher in open heart surgery. without reciprocal ST depression The mechanism responsible for this syn- • Echocardiogram shows pericardial effusion drome has not been identified, but there is a likelihood that Dressler’s syndrome is the result of a hypersensitivity reaction in which antigen originates from injured myocardial tissue and/or he incidence of . T Dressler’s syndrome Presentation is about 4% following transmural infarction and The presentation of Dressler’s syndrome can be as follows: probably higher in open • Pain, often pleuritic and worse lying down heart surgery. • Malaise • Fever • Dyspnea • Rarely, it may cause or acute pneumonitis

Investigations

The following investigations may be useful when diagnosing Dressler’s syndrome: • Leucocytosis, sometimes with eosinophilia,

About the author... Dr. Kubba graduated from the University of Baghdad where he initially trained as a Trauma Surgeon. He moved to Britain, where he recieved his FRCS and worked as an ER Physician before specializing in Family Medicine. He is currently a FP, Missisauga, Ontario. Figure 1. Chest x-ray.

20 Perspectives in Cardiology / April 2007 More on Greg...

Further investigations A chest CT scan (Figure 2) was done to exclude • A complete blood count revealed an Hb of the tiny possibility of pulmonary embolism. 102 g/L with a normal hematocrit and mean Greg’s CT scan revealed a small pericardial corpuscular volume effusion with bilateral small pleural effusions. • A white blood cell count was elevated to The pulmonary arteries did not show evidence of 15.9 L, with a neutrophil count of 12.1 L, under filling, filling defects or cut-off of vessels. associated with a platelet count of 683 L • Erythrocyte sedimentation rate was elevated Management at 58 mm for the first hour and C-reactive You discussed Greg’s case and whether to refer protein rate of 175 mg/L was recorded him for echocardiogram on an urgent basis • INR was within the target therapeutic range with the cardiologist in the main city. The of 2.5 suggested to treat him with nonsteroidal • Renal, liver and thyroid function tests were all anti-inflammatory agents as a case of normal, apart from a positive D-dimer test. Dressler’s syndrome and to arrange the • Chest x-ray (Figure 1) revealed that the heart echocardiogram if things were not improving. was enlarged in transverse diameter. Pulmonary vasculature was within normal After Greg was started on 375 mg of naproxen limits, with no evidence of cardiac b.i.d., the pain completely disappeared after two decompensation or active pulmonary disease. days. A stress test was arranged for him before • ECG showed the previous anterior infarct he was discharged home, that came back with incomplete right negative.

Figure 2. Chest CT Scan before and after treatment.

Management 80 mg q.d. of prednisone) effectively suppresses the clinical manifestations of the acute illness. PCard There is no specific therapy, but bed rest and, if necessary, anti-inflammatory treatment with acetyl- Resources salicylic acid up to 900 mg q.i.d., may be given. If 1. Zipes DP, Libby P, Braunwald E, et al: Heart disease. 6th edition. WB Saunders Co. 2001. this is ineffective, one of the non-steroidal anti- 2. Paelinck B, Dendale PA: Images in clinical medicine: Cardiac tamponade inflammatory agents, such as indomethacin (25 mg in Dressler’s syndrome. N Engl J Med 2003; 348(23):e8. 3. Hope RA, Longmore M, Wilkinson I, et al: Oxford Handbook of Clinical to 75 mg q.i.d.) or glucocorticoid (e.g., 20 mg to Medicine. Fifth edition. Oxford University Press Inc, New York, 2001.

Perspectives in Cardiology / April 2007 21