The Dressler Syndrome After Pulmonary Embolism

2 Linhart JW, Hildner FJ, Barold SS, Lister JW, Samet P. Left heart hemodynamics during angina pectoris induced by atrial pacing. Circulation 1969:40:483-492. 3. Hqlfant RH, Forrester JS, Hampton JR, Haft JI, Kemp HG, Gorlin R. Coronary heart disease. Differential hemodynamic, metabolic, and electrocardiographic effects in subjects with and without angina pectoris during atrial pacing. Circulation 1970:42:601-610. 4. Hcllcr GV, Arocsty JM, McKay

RG, Parker JA, Silverman KJ, Come PC, Grossman W. The pacing stress test: A reexamination of the relation between coronmy artery disease and pacing induced electrocardiographic changes. Am J Candid 1984;54:50–55. 5. Heller GV, Aromty JM, Parker JA, McKay RG, Silverman KJ, Al. AV, Come PC, Kolodny GM, Grossman W. The pacing stiess test: thallium-201 myocardial imaging after atrial pacing. JAm COUCardiol 1984;3:1197–12M. 6. Parker JO, Chiong MA, West RO, Case RB. Sequential alterations in myocardial lactate metabolism, S-T segments, and and left venrrictdar function during angina induced by atrial pacing, Circulation 1969;40:113–131. 7. .%flis SP, Scqueira JM, Akazuler HM. Commuy sinus Iysophmphatidylcholine accumulationdoring mpid ithid pacing, Am J CarcJioI19’Xf;Wi:695-698. 8. Schwartz L, Sole MJ, Vaughn-Neil EF, Hussain NM. Catecholamines in coronwy sinus and peripheral plasma during pacing-induced angina in msm. Circulation 1979;59:37-43. 9. Cohen JL, Ottenweller JE, George AK, Duvvri S. Comparison of dobutamine

and exercise echocardiography for detecting coronary artery disease, Am J Car. diol 1993;72:1226–1231. 10. .%ndler H, Dodge HT. The use of single plane angiograms for the calculation of left ventricular volume in min. Am Heart J 1968;75:325–334. 11. Sheehan FH, Bolson EL, Dudge HT, Mathey DG, Schofer J, Woo HW. Advantages and applications of the centerline method forcharacterizing regional ventricular fimction. Circulation 1986;74:293–305. 12. Cannon RO. Microvascular angina: cardiovascular investigation regarding pttthophysiology and management, In: Richter JE, Cannon RO, Reitman B, eds, Unexplained chest pain. Philadelphia: WB Saunders 1991;1097– 1118. 13. Kem MJ, Flynn MS, Caracciolo EA, Bach RG, Donohue TJ, Aguirre FV. Use of tmnslesimml cmona~ flow velocity for interventirmal decisions in a patient with multiple intermediately severe coronary stenoses, Cather Cardicwasc Diagn 1993;29:148–153. 14. DiMario C, Rams R, Gil R, Serroys PW. Slope of the instantaneous hyperemic diasrolic coronary flow velocity-pressure relation. A new index for assessment of the physiological significance of coronay srenosis in humans. Circulation 1994;90:1215- 1224. 15. Kern MJ, Wolford T, Donohue TJ, Bach RG, Aguirre FV, Caracciolo EA, Flynn MS. Quantitative demonstration of dipyridamole-induced coronary steal and afrerarionby angioplasry in man: analysis by simultaneous, continuous dual Doppler spectral flow velocity, Cather CczrdiovascDia,qn 1993;29:329-34.

The Dressier Syndrome After Pulmonary Embolism Carlos Jeries-Sanchez, MD, Alicia Ramirez-Rivera, MD, and Carlos tbarra-perez, MD

epicardial injury syndromes are known to occur in relation to myocardial infarction, 1 pericardiP otomy, chest trauma, z myopericarditis,3 implantation of epicardial and transvenous pacemakers,4 percutaneous puncture of the left ventricle,5 and pulmonary embolismc-]2 (PE). The etiology is unknown and has been attributed to immune mechanisms. Symptoms occur from a few days to several months after the promoting cause. The clinical picture is characterized by pericarditis with or without pericardial effusion, pleuritis and/or pneumonitis with or without pleural effusion, cardiac arrhythmias, fever, leukocytosis, and increased red blood cell sedimentation rate; recently, noncardiogenic pulmonary edema was also described in this syndrome.l This report updates our original communication 10on the diagnosis and management of the sometimes complex clinical picture of pericarditis after PE, firmly establishing its existence, as well as our current concepts regarding its etiology. ..* During the period 1982 to 1995,402 patients with confirmed PE were admitted to our hospital. Fourteen previously healthy patients (8 women and 6 men, aged 16 to 85 years) developed pericardial injury syndromes 5 to 20 days after the onset of symptoms of PE. Table I lists data pertinent to the diagnosis of PE. The diagnosis was considered in all patients by high clinical suspicion; and was proved by ventilatory/perfusion lung scans and angiographic diagnostic findings in 11 patients. In the last From the EmergencyCare Department,Respiratory Deportment,and the Educationond Research Division, Hospital de Cardiologia, Notional Medical Center, IMSS, Mexico City, Mexico. Dr Jerles-Sanchez’s address is: Paseo de Ios Descubridores 209, Cumbres 3er Sector, CP 64190, Monterrey, Nuevo Leon, Mexico. Manuscript received December26, 1995; revised manuscriptreceivedand acceptedFebruary 23, 1996.

@1996 by Excerpta Medica, Inc. All rights reserved.

TABLE I Basis for Diagnosis

of Pulmonary

Embolism No. of Patients (n=

14)

Maiar risk factors Obesity

5

Deep venous thrombosis

5

Prolonged

4

bed rest

Lower extremity trauma

2

Puerperium

2

Maior surgery Long travel in sitting position

2 1

Clinical picture 14

Sudden dyspnea Pleuritic chest pain

9

Bloody sputum

8

Anger-like pain

4

Chest x-ray 11

Basal densities Elevated diophragm

9

Pleural effusion

7

Electrocardiograms 14

Sinus tachycardia Right ventricular

12

strain

3

Right ventricular AMI Arterial

blood gases 13

Hypoxemia

10

Hypocapnia VentilatOry/perfusion

lung scans 15

High probability Echocardiograms

15

Pulmonary arterial hypertension Pulmonary angiograms cutoffs

8/1 1

Filling defects

6/1 1

3 patients, the diagnoses were done through proved deep venous thrombosis, high probability V/Q lung scans, and suggestive echocardiographic findings of PE.13>14 In 2 patients, a relevant finding was persistent right ventricular hypokinesia. All patients received standard and full intravenous heparin for 7 days, and oral anticoagulants were added on the fifth day. 0002-9149/96/$15.00 Pll S0002-9149[96)00290-1

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The diagnosis of the complicating pericardial syndrome (Table II) was obtained on clinical, chest radiographic, electrocardiographic, hematologic, and echocardiographic grounds. On echocardiography, pericardial effusions were calculated to range from 250 to 800 ml in 10 patients. Prednisone was started immediately after diagnosis, 30 mg/day (orally) and then gradually tapered from the seventh to the 21st day. Pericardiocentesis was not required in any patient. During hospitalization, the 2 patients with right ventricular hypokinesia on echocardiography had evidence of recurrence with hemodynamic instability. An acute right ventricular myocardial infarction was suspected by ischemic retrosternal pain, right ventricular strain, and ST-segment elevation on right ventricular leads, and progressed to cardiogenic shock. One patient died despite conventional intensive medical therapy, and another had successful thrombolysis with streptokinase 1,500,000 IU in 1 hour, without complications. In a l-year follow-up, she still had right ventricular hypokinesia on echocardiography and right ventriculography, with angiographically normal coronary arteries. In the 3year follow-up, she is in functional class I and without pulmonary arterial hypertension. Noncardiogenic pulmonary edema occurred in 4 patients without risk factors, from 24 to 72 hours after onset of the pericardial syndrome. Two patients had dramatic improvement and recovery after intravenous steroid therapy. The other 2 developed acute respiratory distress syndrome and died. Acute left ventricular failure was excluded by normal left ventricular motion on echocardiography and pulmonary capillary wedge pressures. Ten patients had complete regression of pericardial, pleural, and hematologic changes, and are currently alive and well. The mortality in this series was attributed to recurrent massive PE in 2 patients and to acute respiratory distress syndrome in the other 2. ** Two new situations arose since our previous report,lo which deserve discussion. One, the occurrence of right ventricular dysfunction 13>14 in 2 patients, highly suggestive of right ventricular myocardial infarction secondary to PE, 14’15 according to clinical, electrocardiographic, hemodynamic, and echocardiographic criteria. This finding has not been related with pericardial immunologic syndrome previously.1-12In our first communication, 104 patients had electrocardiographic signs of pulmonary arterial hypertension with subendocardial ischemia and 1 even had a ‘‘myocardial infarction image.’ Regrettably, the possibility of myocardial injury was not considered at that time. A similar situation was observed in the electrocardiograms of patients in the study of Friocourt et al.9 Although myocardial injury, as such, is currently not recognized as a potential complication of PE, it certainly could occur and induce a pericardial syndrome similar to those seen after myocardial infarction secondary to ischemic heart disease or pericardial traumal; unfortunately, ●

344

THE AMERICAN JOURNAL OF CARDIOLOGY”

VOL 78

TABLE II Basis for Diagnasis

af Pericardial

Syndrame

I

No. of Patients (n = 14) Clinical picture Pericardial

friction rub

14

Fever

14

Retrosternal

pain

11

Chest x-ray Globular

silhouette

11

New pleural effusion

2

Persistent pleural effusion

1

Electrocardiograms New or increased sinus tachycardia

14

ST-T elevations

10

Echocardiograms Pericardial

effusion (from 250

Hematologic

to 800

ml)

10/1 3

changes

Anemia (fram 15 down ta 8 g] Leukocytes (from 8,000 Sedimentation

up to 25,000

14 cu/mm)

rate (up to 59 mm h Wintrobe]

14

14

however, antiheart antibody measurements are not available in our hospital. On the other hand, in patients without myocardial injury, the pathogenesis is not clear, and anatomic vicinity and hypersensitivity could be considered.c Another important point was the presence of full criteria of noncardiogenic pulmonary edema and acute respiratory distress syndrome in 4 patients, not mentioned in previously published reports.c-12 In none of these cases were we able to identify other causes of noncardiogenic pulmonary edema. The etiology of this type of pulmonary injury also could be related to immune mechanisms.l The improvement in 2 patients with the use of corticosteroids supports this possibility. As for the treatment, previous experiences with the use of anticoagulants have shown no local pericardial or pleural hemorrhagic complications.c-12In our case, streptokinase therapy did not result in pericardial bleeding. Pericarditis with or without effusion is not an unusual event after PE and infarction: 3.4870 in this series of 402 cases studied during a 13-yearperiod. Insufficientawareness of this particular type of pericarditis may lead to unnecessary diagnostic and/or therapeutic procedures that may have harmfulpotentials.The presenceof this type of pericarditisdoes not appear to preclude the use of corticosteroids, anticoagulants, or thrombolytics. In patientswith PE and severe pulmonaryarterialhypertensionwith or without hemodynamicinstability, a pericardial syndrome of unknown etiology could occur in relation to right ventricular myocardialinjury. Chest physiciansand internistsalike should recognize not only this type of Dressier’s syndrome in its typical form, but also the various complicatingevents described in this large series.

1. Kassanoff AH, Mortirossian MG. Postpericardiotomy and postmyncardial infarction syndrome presenting as a noncdiac pulmonary edema. Chest 1991:1410-1414.

AUGUST

1, 1996

2. Tabatznick B, Issac JP. Postpericardiotomy syndrome following traumatic hemopefictudium. Am J Cai-diol 1961;7:83-96. 3. Landy SJ, McGavin CR. Dressier’s syndrome after meningococcaf myopericarditis. Respir Med 1990;84:415–416. 4. HaJ&-Kham A. The pustcdiac injury symfmmes.Clin Caniiol 1992;15:67-72. 5. Peters RH, Whalen RE, Orgain ES, McIntosch HD. Postpericardiotomy syndrome as a complication of percutaneous left ventricular puncture. AmJ Cardiol 1966;17:86-90. 6. SklaroffHJ.Postpulmonaryinfarctionsyndrome.Am He.rt J 1979;98:772-776. 7. Sklamff HJ. Post-pufmonaryinfraction syndrome.Prirmry Cardiri 1982;8:123. 8. Sklaroff HJ. Postpulmonary infarction syndrome. M Sinai J Med 1983; 50:343–347. 9. Friocom’t P, Benit CH, Batisse JP, Prolong PH, Dufout CH, Ulmam A, Lamotte M, Picard R. P&icardite at embolie pulmonaire. Un diagnostic differential difficile, une association d~routante. Arch Mal Coeur 1984;77:689-693. 10. Jerjes-Samchez C, Ibarra-Perez C, Ramirez-Rivera A, Padua GA, Gonzalez CVM. Dressier-like syndrome after pulmonary embolism and infarction. Chest 1987:92:115-117.

1I. Sansores RHM, Ramirez-Venegas A, Gaxiola MG, Morales JG, Carrillo GR, Selman ML. Post-pulmonary infarction syndrome. A cause of persistent pleural and pericardial effusion, Rev Irtst Nat Enf Resp Mex 1993;6:209-212. 12. Garty I, Mader R, Schonfeld S. Post pulmonary embolism pericarditis. A rare entity diagnosed by combinated lung scanning arrd chest radiograph study, Clin Mecl Med 1994;19:519–521. 13. Goldhaber SZ, Haire WD, Feldstein MI, Miller M, Toltiz R, Smith JL, Taveira da Silva AM, Come PC, Lee RT, Parker JA, Mogtader A, McDonough TJ, Braunwald E. Alteplase versus heparin in acute pulmonaxy embolism: randomized trial assessing right-ventricular function and pulmonary perfusion, Lancet 1993;341:507–511. 14. Jerjes-Sanchez C, Ramirez-Rivera A, Garcia MA, Arriaga-Nava R, Valencia S, Rosado-Buzzo A, Pierzo JA, Rosas E. Streptokinase and heparin versus hepuin alone in massive pulmonary embolism: A randomized controlled trial, J Thromb Thrombolysis 1995:2:67–69, 15. Adams NJE III, Siegel NA, Goldstein UA, Jaeffe AS. Elevation of CK-MB following pulmonary embolism. A manifestation of occult right ventricuhw infarction. Chest 1992:101:1203–1206.

Ablation Therapy of Type 1Atrial Flutter May Eradicate Paroxysmal Atriai Fibrillation Demosthenes Katritsis, MD, PhD, Efstathios Iliodromitis, MD, Nikolaos Fragakis, MD, Stamatis Adamopoulos, MD, and Dimitrios Kremastinos, MD

lthough approximately 8% to 30% of patients cardiogram at rest, chest x-ray, and normal echocarundergoing successful ablation of atrial flutter diogram and exercise tests. All patients had normal A may develop atial fibrillationafter the procedure,1-6 thyroid function. the response of patients presenting with both arrhythmias, and in particular with flutter/fibrillation, has not been studied in detail. In addition, late atrial fibrillation after catheter ablation of atrial flutter has been reported to occur more often in patients who had structural heart disease and, in particular, inducible atrial fibrillation after the ablation procedure than in those with a clinical history of atrial fibrillation before ablation.3 We hythat clinical atrial fibrillation pothesized complicating episodes of atrial flutter in patients without structural heart disease can also be eradicated after ablation of the flutter circuit. . . .

The study group comprised 6 consecutive patients who presented with episodes of both regular and irregular arrhythmias suggesting supraventricular tachycardia and paroxysmal atrial fibrillation. Ambulatory electrocardiographic monitoring revealed that atrial fibrillation was preceded by a narrow QRS complex tachycardia with characteristics of typical atrial flutter. Patients, 5 men and 1 woman aged 51 t 12 years, had had disabling palpitations refractory to antiarrhythmic drugs. One patient had primary hypertension and mild aortic sclerosis; his coronary arteriograms and echocardiography were normal, apart from mild left ventricular hypertrophy. The other patients had a normal physical examination, electroFrom the Departmentof Cardiology, Onassis Cardiac Surgery Center, Athens, Greece. Dr. Katritsis’s address is: Onassis Cardiac Surgery Center, 356 Sygnon Avenue, Athens 17674, Greece, Manuscript received October 4, 1995; revised manuscript received and acceptedFebruary 23, 1996.

01996

by Excerpta Medico, Inc.

All rights reserved.

During electrophysiology study, type I atrial flutter was inducible in all patients, but it was noted to degenerate spontaneously into flutter/fibrillation, with recording of flutter waves from the right atrium and typical fibrillation from the left atrium (Figure 1). The cycle length of the right atrial flutter during the episode of flutter/fibrillation was almost similar to the cycle length during typical flutter (Table I). Two of the patients had spontaneous episodes of atrial fibrillation, which was either intermittent with reemergence of typical flutter or spontaneously converted to sinus rhythm. Two patients underwent ablation during atrial flutter and the other 4 during sinus rhythm. The anatomic approach was adopted, i.e., radiofrequency energy was applied in order to create linear lesions between the ostium of the coronary sinus and the septal insertion of the tricuspid valve, the ostium of the coronary sinus and the inferior vena cava, and the septal insertion of the tricuspid valve and the inferior vena cava. The number of radiofrequency current discharges ranged from 12 to 22 (median 14). The mean procedure time was 86 ~ 23 minutes and mean fluoroscope time was 16 t 6 minutes. Reinducibility of atrial flutter was assessed 30 minutes after the procedure by programmed atrial stimulation and incremental atrial pacing, which was performed by increasing the pacing rate until a paced length of 180 to 170 ms was reached or 2:1 atrial capture was noted. Forty-eight-hour ambulatory electrocardiographic monitoring was performed immediately after and at 1-, 3-, and 6-month intervals after ablation. In 5 patients, 30 minutes after the last energy discharge, no tachycardia could be induced. In the remainder, atrial incremental pacing resulted in atrial fibrillation, which was spontaneously ter0002-9149/96/$15.00 Pll S0002-9149(96)00291-3

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