Br Heart J 1991;65:360-2

Early constrictive pericarditis and anaemia afterDressler's syndrome and inferior wall myocardialinfarction

Po Kee Cheung, Mary Lee Myers, J Malcolm 0 Arnold

AbstractEarly constrictive pericarditis andanaemia developed in a 52 year old manafter he had an inferior wall myocardialinfarction complicated by Dressler'ssyndrome. Total pericardiectomy at thetime of coronary artery bypass surgeryresulted in complete resolution of signsand symptoms.

Constrictive pericarditis after myocardialinfarction has been rarely reported. There arethree reports of this complication developingsix to 12 months after frank haemoperi-cardium had occurred with prophylacticanticoagulant treatment.`13 However, threerecent cases occurred in the absence of anovert haemopericardium during the initialpost-infarction period and two of thesepatients did not receive anticoagulants.45 Thethird received an eight week course ofanticoagulants for venous thrombosis but thiswas started four months after his presentationwith myocardial infarction and pericarditis.6All six patients had evidence of clinicalpericarditis during the acute myocardialinfarction and in two patients Dressler's post-myocardial infarction syndrome preceded thedevelopment of constrictive pericarditis by sixmonths and 10 months.45 Anaemia developedin only one patient and the bone marrowaspirate was consistent with the diagnosis ofanaemia of chronic disease. We describe apatient with an inferior wall myocardialinfarction who developed constrictive peri-carditis and reversible anaemia a monthafter Dressler's syndrome. Pericardiectomycorrected the constriction and the symptomsresolved.

Department ofMedicine, VictoriaHospital, University ofWestern Ontario,London, Ontario,CanadaP K CheungJ M 0 Arnold

Department ofCardiovascularSurgery, VictoriaHospital, University ofWestern Ontario,London, Ontario,CanadaM L MyersCorrespondence toDr J Malcolm 0 Arnold,Division of Cardiology,Victoria Hospital, London,Ontario, Canada N6A 4G5.

Case reportA 52 year old man was admitted because ofacute onset (five hours before) of sharp leftsided chest pain which was made worse bybreathing and lying down but was improved bysitting forward. He was a long term smoker andhad no history of angina or tuberculosis.Physical examination showed a triphasicpericardial rub and bi-basilar crackles but no

paradoxical pulse or increase in jugular venouspressure. There were significant Q waves and

flattened T waves in the inferior leads of the

electrocardiogram with T wave inversion in I,aVL, and V4-V6. There was no ST elevation to

suggest acute myocardial injury or pericarditis.Chest x ray showed mild cardiomegaly and

pulmonary congestion and a small loculatedpleural effusion. The echocardiogram showedinferoapical akinesis with hypokinesia of theseptum and inferior wall. No pericardialeffusion was detected. The clinical diagnosiswas Dressler's syndrome complicating aninferior myocardial infarction, though it wasnot possible to determine clearly the timing ofthe infarction. No serial changes in theelectrocardiogram or cardiac enzyme activitieswere seen. A viral aetiology was consideredunlikely because the patient had no precedinghistory of a recent viral illness and his total anddifferential white cell counts on admission werenormal.He was treated with indomethacin 50 mg

three times daily for three days then 25 mgthree times daily for an additional three days.His pericardial rub and crackles resolvedwithin 48 hours. Neither subcutaneous heparinnor oral warfarin were given. A treadmillexercise test (modified Bruce protocol) wascarried out five days after admission and wasabnormal with chest pain and ST segmentelevation in the inferolateral leads. Cardiaccatheterisation showed severe triple vesselcoronary artery disease. The right coronaryartery was totally occluded in its mid third aswas the left anterior descending artery beyondthe first major septal perforator. The circumflexartery seemed free of important disease butthere was a 75% proximal stenosis of theintermediate artery. The left ventriculogramshowed inferoapical akinesis and a leftventricular ejection fraction of 35%. He wasaccepted for coronary artery bypass surgeryand discharged on once daily atenolol (100 mg)and enteric coated aspirin (325 mg).He remained free of symptoms for three

weeks when he was readmitted because ofincreasing shortness of breath with anorexia,abdominal and chest discomfort, orthopnoea,and peripheral oedema. Physical examinationshowed an increased jugular venous pressureof 10 cm above the sternal angle, pulsusparadoxus (15 mm Hg difference), bi-basilarcrackles, moderate peripheral oedema, and amild degree of ascites but no pericardialfriction rub. The electrocardiogram had notchanged and there were no subsequent changesin serial activities of cardiac enzymes. Becauseof some clinical evidence suggestive of bi-ventricular failure, he was initially treated withdiuretics and intravenous dobutamine andwithin 24 hours he responded well. An echo-cardiogram obtained after the start of thistreatment showed moderate perlcardial effusionand possible early diastolic collapse of the right

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Early constrictive pericarditis and anaemia after Dressler's syndrome and inferior wall myocardial infarction

ventricle. Repeat echocardiogram five days latershowed resolution of the pericardial effusionand abnormal right ventricular motion. Hishaemoglobin had dropped from 139 g/l at thefirst admission to 1 16 g/l, without any evidenceof blood loss or haemolysis. Red cell indicesand white cell and platelet counts remainednormal.He was readmitted two weeks later because

of increasing orthopnoea with more abdominaldistension. Physical examination showed amuch increased jugular venous pressure (12 cmabove the sternal angle), no pulsus paradoxus, atender liver enlarged to 3 cm below the rightcostal margin, moderate ascites, peripheraloedema, and bi-basilar crackles. Again, theelectrocardiogram showed no new changes.The echocardiogram showed the previous seg-mental wall motion abnormalities, no pericar-dial effusion, but evidence of a paradoxicalventricular septal motion though withoutappreciable thickening of the pericardium. Hishaemoglobin concentration had dropped fur-ther to 103 g/l with normocytic normochromicindices. Reticulocyte count, serum B12, andfolate and ferritin concentrations were normal.Antinuclear factor was negative. Bone marrowbiopsy showed only non-specific reactivechanges. He was treated with diuretics andhis clinical state improved somewhat. Thedecision was made to proceed with surgery.At operation the anterior pericardium was

found to be grossly thickened and firmlyadherent to the underlying right ventricle andadjacent portion of the left ventricle as well asto the proximal segments of the aorta andpulmonary artery. There was old haemorrhagicand fibrinous exudate over the anterior aspectof the right atrioventricular groove and rightatrium. There was evidence of an earlier largeinferior infarction. There was an extensiveepicardial inflammatory reaction which made it

difficult to identify the coronary vessels. Theleft internal thoracic artery was used toconstruct a bypass to the left anterior descend-ing artery and a saphenous vein bypass graftwas placed to the intermediate artery. Totalpericardiectomy was performed and a signifi-cant improvement in right ventricular contrac-tility was noted at the end of the procedure.The right atrial pressure decreased from 25mm Hg before operation to 17 mm Hg afteroperation. By the second postoperative day, ithad fallen to 14 mm Hg. Pathological examina-tion of the excised pericardium showed chronicinflammatory infiltrate throughout its entirethickness (fig) with adherent thromboticmaterial. One month after operation, thejugular venous pressure was normal and theascites, peripheral oedema, and hepatomegalyhad resolved. A radionuclide blood pool ven-triculogram showed normal right ventricularcontractility with a right ventricular ejectionfraction of 55%. The left ventricle showedinferior segmental wall motion abnormalitiesand an ejection fraction of 45%. His haemo-globin concentration returned to normal with-out further need for transfusion after opera-tion. He remained well and symptom free eightmonths after surgery.

DiscussionThe incidence of early pericarditis duringmyocardial infarction is reported to vary from6% to 23%.7 Dressler's post-myocardialinfarction syndrome occurs in up to 4% ofpatients.8 A single episode is usually self-limited and responds well to treatment with anon-steroidal anti-inflammatory agent as in thispatient. The syndrome may recur though thelong term sequelae are not clearly defined. It canbe diffuse and may obliterate the pericardial sac,but subsequent development of constrictive

Thickened pericardiumshowing fibrin (f) andinflammation. (Originalmagnification x 25.)

- ,,bt *.|:!F

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Cheung, Myers, Arnold

pericarditis has been reported only twice andhas occurred six to 10 months after the initialmyocardial infarction.45 In this patientconstrictive pericarditis developed one monthafter Dressler's syndromne in the absence ofprior anticoagulation and in association withanaemia. Some degree of intrapericardialhaemorrhage was evident during surgery andhistological examination also showed throm-botic material adherent to the pericardium. It ispossible that severe pericarditis will causeleakage of blood into the pericardial sac thoughits contribution to the progression of constric-tive pericarditis is not known. All three caseshave occurred in men with an inferior wallmyocardial infarction. Whether this is a chanceassociation or relates to an anatomical factor,such as increased adherence of the inferiorpericardium to the diaphragm or myocardium,is not known. All showed an excellent responseto pericardiectomy.A few cases of protracted Dressler's syn-

drome have been associated with anaemia, butthe aetiology was not clear because bonemarrow studies were not performed.9 Ourpatient showed the development of earlyreversible anaemia and constrictive pericarditisin Dressler's syndrome similar to that reportedby Kanawaty et al.5 Bone marrow biopsy inboth cases showed non-specific changes. It ispossible that myocardial injury initiated animmune reaction leading to both pericarditisand anaemia. It is interesting to speculate thatthe early development of anaemia may be amarker for a more severe immune response.Recent evidence suggests that inflammatorymediators, such as interleukin 1, released insevere inflammatory conditions may decreasethe erythroblast response to erythropoietin andcause anaemia which may respond to cortico-steroids.'0 A recent retrospective analysisof a related condition, postpericardiotomy syn-

drome, concluded that steroids, non-steroidalanti-inflammatory drugs, or the combinationdid not seem to prevent the future developmentof constrictive pericarditis." A prospectivecontrolled trial in tuberculous pericarditissuggested that adjunctive treatment withprenisolone improves clinical symptoms andsurvival as well as reducing pericardiocentesisand possibly pericardiectomy.'2 Furtherstudies may be needed to resolve this issuein the subgroup of patients with Dressler'ssyndrome and anaemia.

Dr J M 0 Arnold is the recipient of a Career Health ScientistAward from the Pharmaceutical Manufacturers Association ofCanada. We thank Dr M Troster for the pathological analysisof the pericardium.

1 Laszlo MH. Constrictive pericarditis as sequel tohemopericardium: report ofa case following anticoagulanttherapy. Ann Intern Med 1957;46:403-13.

2 Beaufils PH, Bardet J, Temkine J, Masquet CH, SebastienPH, Zelasko Y. Syndrome de Dressler: pericardite con-strictive post-infarctus operee avec succes. Arch MalCoeur 1975;68:651-6.

3 Karim AH, Salomon J. Constrictive pericarditis aftermyocardial infarction: sequela of anticoagulant-inducedhemopericardium. Am J Med 1985;79:389-90.

4 Goldhaber SZ, Lorell BH, Green LH. Constrictivepericarditis, a case requiring pericardiectomy followingDressler's post myocardial infarction syndrome. J ThoracCardiovasc Surg 1981;81:793-6.

5 Kanawaty DS, Burggraf GW, Abdollah H. Constrictivepericarditis and anaemia post myocardial infarction. CanJ Cardiol 1989;5(30):147-8.

6 Ramsdale DR, Epstein EJ, Coulshed N. Constrictivepericarditis after myocardial infarction. Br Heart J 1986;56:476-8.

7 Toole JC, Silverman ME. Pericarditis of acute myocardialinfarction. Chest 1975;67:647-53.

8 Davidson C, Oliver MD, Robertson RF. Post-myocardialinfarction syndrome. BMJ 1961;ii:535-9.

9 Glasser M. Post-myocardial infarction syndrome withanaemia. Conn Med J 1970;34:413-4.

10 Schooley JC, Kullgren B, Allison AC. Inhibition byinterleukin-I of the action of erythropoietin on erythroidprecursors and its possible role in the pathogenesis ofhypoplastic anaemia. Br J Haematol 1987;67:11-5.

11 Cimino JJ, Kogan AD. Constrictive pericarditis after cardiacsurgery: report of three cases and review of the literature.Am Heart J 1989;118:1292-301.

12 Strang JIG, Kakaza HH, Gibson DG, et al. Controlled trialof complete open surgical drainage and of prednisolonetreatment of tuberculous pericardial effusion in Transkei.Lancet 1988;ii:759-64.

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myocardial infarction.after Dressler's syndrome and inferior wall Early constrictive pericarditis and anemia

P K Cheung, M L Myers and J M Arnold

doi: 10.1136/hrt.65.6.3601991 65: 360-362 Br Heart J 

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