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Post Myocardial Infarction Syndrome: An Early Complication of Acute Myocardial Infarction
Post Myocardial Infarction Syndrome: An Early Complication of Acute Myocardial Infarction* Warren A. Kossowsky, M.D. oo , Peter]. Epstein, M.D.t, and Richard S. Levine, M.D., F.C.C.P.:!:
Five patients with acute myocardial infarction developed pleuropericarditis during the first week of their illness. Angiocardiography was diagnostic for peri. cardial effusion in four patients and in the fifth patient the effusion was demonstrated by echocardiogram. Prednisone therapy resulted in dramatic relief of symptoms and signs in one patient in whom subsequent withdrawal of the drug was associated with prompt recurrence. The other four patients experienced spontaneous resolution of the pleuropericardial and pulmonary findings. The observations reported here suggest that a pericardial rub heard during the first days of acute myocardial infarction is sometimes a manifestation of the Dressler syndrome, and not always simply the reflection of transmural infarction.
The post myocardial infarction syndrome, first described by Dressler in 1956,1 is an uncommon complication of myocardial infarction 2 characterized by a latency period, fever and recurrent polyserositis. l •a Pleuropericarditis with effusion is not generally recognized as an early complication of myocardial infarction,2.4 but its occurrence one or more weeks after onset is characteristic of the Dressler syndrome. a.s This report describes five patients in whom features of the post myocardial infarction syndrome appeared within one week following an acute myocardial infarction, and indicated that pericarditis and effusion occurring early in this illness may sometimes be a manifestation of the Dressler syndrome. °From the section of Cardiology, Department of Medicine, The Brookdale Hospital Center, Brooklyn. OOPhysician-in-Charge, Coronary Care Unit, The Brookdale Hospital Center; Assistant Professor, Clinical Medicine, New York University School of Medicine. tFellow in Cardiology, The Brookdale Hospital Center. ~Physician-in-Charge, Adult Cardiac Catheterization Laborjltory, The Brookdale Hospital Center; Assistant Professor, Clinical Medicine, New York University School of Medicine.
Reprint mquests: Dr. Kossowsky, Brookdale Hosl>ital Medical Center, Brooklyn 11212
CHEST, VOL. 63, NO.1, JANUARY, 1973
CASE HEPORTS CASE
1
A 48-year-old machinist was admitted to The Bnxlkdale Hospital Center on October 26, 1970 because of chest pain. Four days earlier, while working, he complained of central chest pressure and heaviness in both arms that subsided completely after three to four minutes. On the morning of admission he experienced a similar but more intense pain that now lasted four hours and was a':sociated with diaphoresis. Physical examination revealed an acutely ill white man. The blood pressure was 135/90, pulse 56 per minute and regular, temperahlre ggoF. The neck veins were not distended. Fine moist rales were audible at the right lung hase posteriorly. An Sa gallop was heard hut no murnmrs or mhs were audible. The remainder of the examination was within normal limits. An electrocardiogram showed changes of an acute anterolateral wall myocardial infarction. The white blood cell count was 15,600 per cuhic millimeter, the creatine phosphokinase (CPK) was 75 IU and peaked to 186 IU 24 hours later. The semm glutamic oxaloacetic transaminase (SCOT) was 165 IU on the first day and 3.54 IU on the second day. Morphine sulfate was given for pain, oxygen was administer£'nt hegan to complain of a "catching" pain over the xiphoid area that was clearly aggravated hy respiration and relieved by sitting up and leaning forward. His temperature was 100°F and Ill' developed a pulsus alternans at a rate of 120 per minuh'.
35
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KOSSOWSKY, EPSTEIN, LEVINE
Bronchial breath sounds and egophony were heard over the lower third of the left chest posteriorly. A summation gallop was audible. One hour later a pericardial friction ntb wa~ heard. TI1l' e1t'ctrocardiogram revealed a sinus tachycardia at a rate of 124 per minute and an evolving anterolateral wall myocardial infarction. Neither the administration of parenteral furo~:emide nor rapid digitalization with ouabain produced a clinical response and the tachycardia and pulmonary findings remained unchanged. On the third hospital day, a diagnostic thoracentesis (yielding .50 ml of serosanguineous Huid with protein mntent of .5.1 gms percent) confirmed the chcst x-ray finding of a It'ft pleural effusion (Fig lA). In the differential diagnosis, pulmonary emboli with infarction and the post myocardial infarction syndrome were mnsidered and, on day four, angiocardiography wa~ performed. The study was compatible with the presence of significant pericardial effusion (Fig 2). An air bronchogram also demonstrated consolidation of the left lower lobe, but no filling defects were detectable in the pulmonary arteries. A working diagmd;; of the Dressler syndrome was enter10130170
FIGURE 2. Angiocardiogram revealing soft tissue density lateral to the right atrial border and consistent with the presence of a pericardial effusion. tained, but neither aspirin nor corticosteroids wa~ administered. At that time the prothrombin time was 12/19 seconds; warfarin sodium (Coumadin) was discontinued. The pericardial friction mb and pleuropericardial pain persisted for three more days until November 2, 1970 when the patient became both afebrile and pain free. A chest film showed clear lung fields and a return in heart size to normal (Fig IB). The patient's subsequent course was uneventful and he was discharged on the 23rd day on a maintenance digoxin dose of 0.375 mg daily. CASE 2 10/30170
1/1110
FIf;URE 1A (upper). P-A chest film demonstrating enlargement of the cardiac silhouette and a haze obscuring the left costophrenic angle. FIGURE IB (lower). P-A chest picture one week later showing clear lung fields and marked decrease in size of the cardiac silhouette.
A 51-year-old white man was admitted to The Brookdale Hospital Center on July 26, 1968 because of increasingly severe anterior chest pain of one day's duration. One year earlier, he had had an uncomplicated inferior wall myocardial infarction. Physical examination revealed an acutely ill middle-aged white man. The blood pressure was 122/80, pulse 92 and regular and temperature 100AoF. There was no neck vein distention. Fine moist rail'S were heard in the lung bases, but no murmurs or mbs were audible, nor was a gallop rhythm described. The electrocardiogram showed both the old inferior wall infarction and changes of an acute anterior wall infarction. Serial enzyme determinations and electrocardiograms confirmed this diagno~is. Twenty-four hours after admission, the patient was digitalized because of pump failure manifested by dyspnea, a sinus tachycardia of 126 per minute and a summation gallop. After 48 hours, a pericardial friction mb was heard; one day later he began to complain of severe anterior and left lateral chest pain clearly wor.:ened by respiration. A chest x-ray examination revealed cardiomegaly and bilateral pleural effusion ( Fig 3A). On the fourth hospital day, because of the persistence of dyspnea, tachycardia and the friction rub, a pulmonary angiogram was obtained. Patency of all pulmonary arteries was demonstrated, but an unequivocal increase in the space between the left ventricular cavity and the outer left heart border was seen. Dressler's syndrome was diagnosed and prednisone in a dose of 80 mg daily administered.
CHEST, VOL. 63, NO.1, JANUARY, 1973
37
POST MYOCARDIAL INFARCTION SYNDROME
Within 12 hours, the pain largely subsided. The patient became afebrile, (Fig 4) and his pulse fell below 100 for the first time. A chest x-ray picture obtained one week later showed clear lung fields and a striking decrease in cardiac size (Fig 3B). He remained asymptomatic until August 11, 1968 when, 12 hours after prednisone therapy was discontinued, he had a recurrence of fever and pleuropericardial pain. The reinstitution of prednisone therapy effected prompt relief and in 48 hours he was asymptomatic again. The patient was discharged on the 29th hospital day on 15 mg prednisone daily. Prednisone was subsequently discontinued, but a typical recurrence six months later again required the use of corticosteroids. CASE
FIGURE 3A (upper). P-A chest film demonstrating cardiomegaly and bilateral pleural effusions. FIGURE 3B (lower). P-A chest picture after one week of prednisone therapy.
104
A 50-year-old building inspector with no prior history of heart disease, was admitted to The Brookdale Hospital Center on November 8, 1970 because of burning retrosternal pain of three hours' duration. Physical examination revealed an acutely ill obese white man. The blood pressure was 150/90, pulse 60 per minute, temperahlre 98.6°F. The neck veins were not distended. Scattered rhonchi were audible over both lung bases. The heart was not enlarged. An S4 gallop was audible at the apex, but no murmur or rubs were heard. The rest of the examination was within normal limits. An electrocardiogram revealed changes of an acute inferolateral wall infarction. The white blood cell count was 16,630 per cubic millimeter with a predominance of neutrophils. The CPK and SCOT reached peak values 36 hours after admission of 80 and 250 IU, respectively. Anticoagulation with warfarin sodium (Coumadin) was started on admission and atropine was administered for ventricular premature contractions associated with a sinus bradycardia. Two days after admission, the patient began to complain of pleuropericardial pain; a friction rub was audible for the first time. On the third hospital day, pump failure, manifested by sinus tachycardia, alternans and gallop rhythm, was treated with parenteral ouabain. One day later, on November 12, 1970, an angiogram was obtained which was compatible with the presence of a pericardia! effusion (FigS).
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CHEST, VOL. 63, NO, 1, JANUARY, 1973
FIGURE 4. Temperature curves demonstrating the prolonged febrile course in all five patients. Institution of prednisone therapy (in case 2) is denoted by the upward arrows and its withdrawal by the downward arrow.
38
KOSSOWSKY, EPSTEIN, LEVINE An electrocardiogram showed ehanges of an extensive acute anterior wall myocardial infaretion and an old inferior wall infarction. The CPK elevated on admission, rose to 1,386 IV on the second day. Rapid digitalization was accomplished with intravenous ouabain. Three days after admission the patient complained of pleuritic pain relieved by sitting up. His temperahire was elevated to 101°F and a pericardial friction mb was heard for th,· first time. An echoeardiogram was consistent with a small amount of pericardial fluid anteriorly (Fig 6). Five days after admission physical examination suggested the presence of a left pleural effusion. This was confirmed by a ehe~t film examination. A repeat x-ray examination in four days showed it~ complete resolution. The pericardial friction mb, pain and fever persisted through the 12th hospital day when he became afebrile and pain free for the first time. The remainder of the hospital course was unventful and he was discharged on the 21st hospital day on di~oxin. 0.25 mg PO daily.
FIC:UHE .5. An~iocardiogram compatible with the presence of pericardial effusion. At that time the prothrombin time was 12/18 seconds; warfarin sodium (Coumadin) was discontinued. The friction TIl!> persisted for another 24 hours, and the pain and fever for an additional 48 hours. The remainder of the patient's hospital course was uneventful and he was discharged on the 21st hospital day on maintenanee di~oxin. A chest x-ray picture obtained at time of diseharge was within normal limits. CASE 4 A 49-year-old laborer with maturity onset diabetes and prl'vious myocardial infarction was admitted to The Brookdale Hospital Center on April 6, 1971 with a three day history of increasingly severe chest pain. Physical examination revealed a well developed, obese, Negro man in respiratory distress. Blood pressure was 160/100. Heart rate was 130 per minute. Pulsus alternans was present. Neck veins were distended at 30° and a summation gallop was audible at the cardiac apex. The liver was not palpable and the remainder of the examination was unremarkable.
. , - _......- . . - . -......- ECG
.'--.::1=-__-..... PERICARDIUM PERICARDIAL FLUID R. V. WALL R. V. CAVITY
CASE 5 A 44-year-old Puerto Riean man with mahlrity onset of diabetes and a three year history of angina peetoris was admitted to The Brookdale Hospital Center on January 6. 1970 because of severe chest pain radiatin~ down both arms of four hours' duration. Physical examination revealed a diaphoretic man with blood pressure of 140/100, temperahlre of 98.8°F and pulse rate of 90 per minute. Rail'S were present at the right lun~ base. On examination of the heart, an S4 gallop was heard. The liver was not palpable and the remainder of the examination was unremarkable. An electrocardiogram revealed an acute extensive anterior wall myocardial infarction. CPK peaked to 1,600 IV and the SCOT to 315 IV on the second hospital day. Two days after admission, parenteral digoxin was given because of the development of signs of pump failure as manifested by sinus tachycardia, pulsus aItemans and summation gallop. A pericardial friction mb was clearly audible. The tachycardia persisted for the first two weeks of the patient's illness as did the pericardial friction mb. In addition, he had a temperature ranging from l00AOF to 103.2° during the entire period. Chest x-ray pichlre on the tenth hospital day showed a fine reticular pulmonary infiltrate involving the lower two-thirds of the right chest and left base. Repeat chest x-ray examination on day 13 showed clearing of the infiltrate. A pulmonary angiogram was obtained on the 14th day of hospitalization and demonstrated a 10 mm distance between the right atrial endocardium and the outer border of the heart, consistent with a significant pericardial effusion, and no evidence of pulmonary embolism. After the 16th hospital day, the patient was afebrile and pain free and his subsequent course was uneventful. Chest film just prior to discharge revealed an enlarged heart with left ventricular prominence. He was discharged on the 25th hospital day on digoxin, 0.25 mg and tolbutamide (Orinase), 500 mg PO daily. DISCUSSION
F1GUHE 6. Echocardiogram consistent with the presence of lwrieardial fluid. .
The postmyocardial infarction syndrome is a well recognized clinical entity of unknown etiology.'-4 Although a viral etiology has recently been proposed,6 the Dressler syndrome is generally thought CHEST, VOL. 63, NO.1, JANUARY, 1973
39
POST MYOCARDIAL INFARCTION SYNDROME
of as an immune disorder resulting from a hypersensitivity reaction to injured cardiac tissue. 3.7 Lending support to the concept of an altered immunity in the pathogenesis of this disorder are the similarity between the clinical features of the postinfarction syndrome and diseases commonly thought to have an immune basis/'s the frequent presence of circulating antibodies to heart tissue,9-11 and the response to both corticosteroids3 and antimetabolites. 12 A pericardial friction rub heard during the first days of acute myocardial infarction is characteristically evanescent and is generally thought to reflect transmural infarction. 13.14 The persistence of the rub, a prolonged febrile course (Fig 4), the presence of pleuropericardial effusion, or the appearance of the rub after the first week of illness, however, suggests a complication of myocardial infarction such as a pulmonary embolus, pneumonia, congestive heart failure or the postmyocardial infarction syndrome. 2.3.14 In patients receiving anticoagulants the appearance of a pericardial effusion may suggest the additional diagnosis of a drug related hemopericardium. ls' ls Angiocardiography was diagnostic for pleuropericardial effusion in three of our patients on the fourth day and in one patient on the 14th day of illness. In the fifth patient, the diagnosis of pericardial effusion was made echocardiographically on the fourth hospital day. In none of our patients did alternate explanations such as pulmonary emboli, severe congestive heart failure, pneumonia or anticoagulant-related hemorrhagic pericarditis prove to be diagnostically tenable. Neither progressive heart failure nor pulmonary emboli could be documented in any of our patients. Although a warfarin sodium (Coumadin) related hemopericardium was a consideration in two of our patients, this diagnosis was unlikely since hemorrhagic pericarditis complicating anticoagulant therapy in acute myocardial infarction is generally a late complication of therapy.IS.IS Furthermore, the pericarditis occurred after only two days of warfarin sodium therapy when the prothrombin time was not in a therapeutic range in either patient. Pericardial effusion due solely to the myocardial infarction was an additional consideration in all of our patients but this too seemed unlikely. The case described by NichoP9 of pericardial effusion complicating acute coronary thrombosis, and cited by Friedberg20 in his textbook, is that of a patient who satisfied all clinical criteria of the Dressler syndrome. The rarity of pericardial effusion complicating myocardial infarction is perhaps underlined by CHEST, VOL. 63, NO.1, JANUARY, 1973
the experience of Mintz and Katz 21 who failed to find evidence of such effusion in 572 patients with recent myocardial infarction. The clinical features in the patients described in this report were consistent with the postmyocardial infarction syndrome except for the very early appearance of pleuropericarditis. The spontaneous resolution of the fever, pleuropericardial and pulmonary findings in four of the five patients and the dramatic response to corticosteroids in the other is characteristic of the Dressler syndrome and adds support to this diagnosis. Our experience with the five patients reported here supports the observation that the postmyocardial infarction syndrome more frequently follows extensive infarction. 12.22 The observations add to the clinical spectrum of this syndrome by suggesting that a pericardial rub heard during the first days of acute myocardial infarction is sometimes a manifestation of the Dressler syndrome. REFERENCES
2 3 4 5
6 7 8 9 10
11
12
13
14 15
16
Dressler W: A post myocardial infarction syndrome. Preliminary report of a complication resemhling idiopathic recurrent benign pericarditis. JA~fA 160: 1379, 1956 Connolly DC, Burchell HB: Pericarditis: A ten year survey. Am J CardioI7:7, 1961 Dressler W: The post myocardial infarction syndrome. A report on 45 cases. Arch Intern Med 103:28, 1959 Levin JW, Bryk D: Dressler syndrome (post myocardial infarction syndrome). Radiology 87:731,1966 Hurst JW, Logue RB: The Heart (Arteries and Veins). Sec ed. New York, McGraw-Hili Book Company, The Blakiston Division, 1970, p 1966 Burch GE, Colcolough HL: Post cardiotomy and post infarction syndromes-a theory. Am Heart J 80:290, 1970 Kaplan \fH, Frengley JD: Autoimmunity to the heart in cardiac disease. Am J CardioI24:459, 1969 Davies A~f, Gery I: Autoimmunity in heart disease. Biochem Clin 1: 19, 1963 Davies AM, Gery I: The role of autoantihodies in heart disease. Am Heart J 60:669, 1960 Van Der Geld H: Antiheart antihodies in the post-pericardiotomy and the post myocardial infarction syndromes. Lancet 2:617, 1964 Faivre G, Gilgenkrantz JM, Duheille J, et al: Immunofluorescence et syndromes postcommissurotomie ou post infarctus. Arch ~fal Coeur 60:484, 1967 Kossow~ky WA, Kim KS, Tobin MS: Antimetabolite therapy in the post myocardial infarction syndrome. Am Heart J, in press Harvey WP: Some pertinent physical findings in the clinical evaluation of acute myocardial infarction. Circulation 40: (suppl IV) 175, 1969 Evans E: Introduction to symposium on pericarditis. Am J CardioI7:1,1961 Goldstein R, Wolff L: Hemorrhagic pericarditis in acute myocardial infarction treated with bishydroxycoumarin. JAt-1A 146:616, 1951 Anderson M, Christensen N, Edwards J: Hemopericar(Hum complicating myocardial infarction in the absence of
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KOSSOWSKY, EPSTEIN, LEVINE
cardiac rupture. Arch Intern Moo 90:634, 1952 17 Aarseth 5, Lange HF: The influence of anticoagulant therapy on the occurrence of cardiac rupture and hemopericardium following heart infarction. 1. A study of 89 cases of hemopericardium. Am Heart J 56:250, 1958 18 Lange HF, Aarseth 5: The influence of anticoagulant therapy on the occurrence of cardiac and hemopericar(lium following heart infarction. II. A controlled study of a selected treated group base on 1,044 autopsies. Am
Heart J 56:257, 1958 19 Nichol ES: Large pericardial effusion complicating acute coronary thrombosis. Ann Intern Med 11:1900, 1937 20 Friedberg CK: Disease of the heart. Philadelphia and London, WB Saunders Company, 1966, p 809 21 Mintz 55, Katz LN: Recent myocardial infarction. Analysis of 572 cases. Arch Intern Med 80:205, 1947 22 Ravnskov V: Aneurysm of the heart in the post-myocardial infarction syndrome. Acta Med Scand 183:393, 1968
Editorial Expression
their five patients to rule out pulmonary embolism, it is likely that echocardiography and pulmonary scanning would establish the diagnosis in many such patients. Why these patients manifest what is frequently considered an autoimmune response to myocardial necrosis so early in the course of their infarction is not clear, particularly since two of the five patients had no prior evidence of heart disease. Herbert J. Ledne
It has not been appreciated previously that the post myocardial infarction syndrome may develop during the first week of a coronary attack and sometimes blend imperceptibly with the pericarditis of transmural infarction. Fever and a pericardia! friction rub which outlasts that of acute myocardial necrosis are helpful signs. While the authors employed angiocardiography in four of
Boston
African Safari Vacations are desirable for getting away from the tension of business and professional responsibilities or from the drab monotony of every day routine. Years ago safaris had been accessible to the financial and social elite only. Hunting expeditions of this sort cost well over $6,000 for two for a thirty-day period, in addition to expenses for air travel and other requisites. Of course, bagging the "big five" (lion, leopard, rhinoceros, elephant, buffalo) means precious trophies and gives a tremendous boost to one's ego and social prestige. A great many people, however, prefer to go on a nonshooting safari. Currently this represents a major contingent of the tourist revenue of East Africa. Sightseers and those interested in wild life in its natural surroundings are not concerned with hair-raising encounters with wild animals or with demonstration of hunting skill or courage. Rather they are craving for relief from the tedium of customary living and want to escape from the city into aimless wanderings in exotic scenery and wrap themselves in a comforting sense of isolation. They follow the urge to roam around in the shades of massive forests, treading luminous arabesques of sunrays on the carpet of heavy grass. They enjoy being lulled into a strange, thoughtless enchantment by the exuberant vegetation, prodigious Howers, the sight and songs of colorful birds. Communing with nature in this manner is an enrichment of the soul, a grandiose experience in recreation, an amalgam of relaxation, langor and what the Italian so aptly calls "dolce far niente,"
meaning sweet doing nothing. The only dissonant note I am obliged to record is the remote possibility of illness acquired on a safari. Although the vector mosquito, Anopheles is not common in Africa, malaria may be acquired occasionally. Occurrence of pneumonia, bronchitis, asthma and pleurisy with effusion (serofibrinous or hemorrhagic) have been attributed to plasmodium. Confirming previous pertinent findings of others, Godard and Hansen observed a patient with x-ray evidence of diffuse interstitial pulmonary edema. It disappeared on intensive antimalarial treatment. In their view pulmonary hypersensitivity would best account for the local changes in the pulmonary capillaries resulting in malarial pulmonary edema (Radiology 101:523, 1971). In some instances, encephalitis, involvement of the abdominal organs may develop. Cardiovascular manifestations are infrequent; they vary from angina pectoris to fatty degeneration of the myocardium. During a brief stay in Africa, infection with Entamoeba histolytica may pose a serious problem. It may compromise not only the digestive system but also the lung, pleura and pericardium, either by direct extension from the liver or by hematogenous spread. A number of potent antimalarial drugs are available. In pneumonitis and other forms of extraintestinal forms of amebiasis, the administration of chloroquine and hydroxychloroquine is recommended by Krantz et al (Pharmacologic Principles in Medical Practice, Baltimore, Williams & Wilkins, 1969). Andrew L. Banyai, M.D.
CHEST, VOL. 63, NO.1, JANUARY, 1973
Five patients with acute myocardial infarction developed pleuropericarditis during the first week of their illness. Angiocardiography was diagnostic for peri. cardial effusion in four patients and in the fifth patient the effusion was demonstrated by echocardiogram. Prednisone therapy resulted in dramatic relief of symptoms and signs in one patient in whom subsequent withdrawal of the drug was associated with prompt recurrence. The other four patients experienced spontaneous resolution of the pleuropericardial and pulmonary findings. The observations reported here suggest that a pericardial rub heard during the first days of acute myocardial infarction is sometimes a manifestation of the Dressler syndrome, and not always simply the reflection of transmural infarction.
The post myocardial infarction syndrome, first described by Dressler in 1956,1 is an uncommon complication of myocardial infarction 2 characterized by a latency period, fever and recurrent polyserositis. l •a Pleuropericarditis with effusion is not generally recognized as an early complication of myocardial infarction,2.4 but its occurrence one or more weeks after onset is characteristic of the Dressler syndrome. a.s This report describes five patients in whom features of the post myocardial infarction syndrome appeared within one week following an acute myocardial infarction, and indicated that pericarditis and effusion occurring early in this illness may sometimes be a manifestation of the Dressler syndrome. °From the section of Cardiology, Department of Medicine, The Brookdale Hospital Center, Brooklyn. OOPhysician-in-Charge, Coronary Care Unit, The Brookdale Hospital Center; Assistant Professor, Clinical Medicine, New York University School of Medicine. tFellow in Cardiology, The Brookdale Hospital Center. ~Physician-in-Charge, Adult Cardiac Catheterization Laborjltory, The Brookdale Hospital Center; Assistant Professor, Clinical Medicine, New York University School of Medicine.
Reprint mquests: Dr. Kossowsky, Brookdale Hosl>ital Medical Center, Brooklyn 11212
CHEST, VOL. 63, NO.1, JANUARY, 1973
CASE HEPORTS CASE
1
A 48-year-old machinist was admitted to The Bnxlkdale Hospital Center on October 26, 1970 because of chest pain. Four days earlier, while working, he complained of central chest pressure and heaviness in both arms that subsided completely after three to four minutes. On the morning of admission he experienced a similar but more intense pain that now lasted four hours and was a':sociated with diaphoresis. Physical examination revealed an acutely ill white man. The blood pressure was 135/90, pulse 56 per minute and regular, temperahlre ggoF. The neck veins were not distended. Fine moist rales were audible at the right lung hase posteriorly. An Sa gallop was heard hut no murnmrs or mhs were audible. The remainder of the examination was within normal limits. An electrocardiogram showed changes of an acute anterolateral wall myocardial infarction. The white blood cell count was 15,600 per cuhic millimeter, the creatine phosphokinase (CPK) was 75 IU and peaked to 186 IU 24 hours later. The semm glutamic oxaloacetic transaminase (SCOT) was 165 IU on the first day and 3.54 IU on the second day. Morphine sulfate was given for pain, oxygen was administer£'nt hegan to complain of a "catching" pain over the xiphoid area that was clearly aggravated hy respiration and relieved by sitting up and leaning forward. His temperature was 100°F and Ill' developed a pulsus alternans at a rate of 120 per minuh'.
35
36
KOSSOWSKY, EPSTEIN, LEVINE
Bronchial breath sounds and egophony were heard over the lower third of the left chest posteriorly. A summation gallop was audible. One hour later a pericardial friction ntb wa~ heard. TI1l' e1t'ctrocardiogram revealed a sinus tachycardia at a rate of 124 per minute and an evolving anterolateral wall myocardial infarction. Neither the administration of parenteral furo~:emide nor rapid digitalization with ouabain produced a clinical response and the tachycardia and pulmonary findings remained unchanged. On the third hospital day, a diagnostic thoracentesis (yielding .50 ml of serosanguineous Huid with protein mntent of .5.1 gms percent) confirmed the chcst x-ray finding of a It'ft pleural effusion (Fig lA). In the differential diagnosis, pulmonary emboli with infarction and the post myocardial infarction syndrome were mnsidered and, on day four, angiocardiography wa~ performed. The study was compatible with the presence of significant pericardial effusion (Fig 2). An air bronchogram also demonstrated consolidation of the left lower lobe, but no filling defects were detectable in the pulmonary arteries. A working diagmd;; of the Dressler syndrome was enter10130170
FIGURE 2. Angiocardiogram revealing soft tissue density lateral to the right atrial border and consistent with the presence of a pericardial effusion. tained, but neither aspirin nor corticosteroids wa~ administered. At that time the prothrombin time was 12/19 seconds; warfarin sodium (Coumadin) was discontinued. The pericardial friction mb and pleuropericardial pain persisted for three more days until November 2, 1970 when the patient became both afebrile and pain free. A chest film showed clear lung fields and a return in heart size to normal (Fig IB). The patient's subsequent course was uneventful and he was discharged on the 23rd day on a maintenance digoxin dose of 0.375 mg daily. CASE 2 10/30170
1/1110
FIf;URE 1A (upper). P-A chest film demonstrating enlargement of the cardiac silhouette and a haze obscuring the left costophrenic angle. FIGURE IB (lower). P-A chest picture one week later showing clear lung fields and marked decrease in size of the cardiac silhouette.
A 51-year-old white man was admitted to The Brookdale Hospital Center on July 26, 1968 because of increasingly severe anterior chest pain of one day's duration. One year earlier, he had had an uncomplicated inferior wall myocardial infarction. Physical examination revealed an acutely ill middle-aged white man. The blood pressure was 122/80, pulse 92 and regular and temperature 100AoF. There was no neck vein distention. Fine moist rail'S were heard in the lung bases, but no murmurs or mbs were audible, nor was a gallop rhythm described. The electrocardiogram showed both the old inferior wall infarction and changes of an acute anterior wall infarction. Serial enzyme determinations and electrocardiograms confirmed this diagno~is. Twenty-four hours after admission, the patient was digitalized because of pump failure manifested by dyspnea, a sinus tachycardia of 126 per minute and a summation gallop. After 48 hours, a pericardial friction mb was heard; one day later he began to complain of severe anterior and left lateral chest pain clearly wor.:ened by respiration. A chest x-ray examination revealed cardiomegaly and bilateral pleural effusion ( Fig 3A). On the fourth hospital day, because of the persistence of dyspnea, tachycardia and the friction rub, a pulmonary angiogram was obtained. Patency of all pulmonary arteries was demonstrated, but an unequivocal increase in the space between the left ventricular cavity and the outer left heart border was seen. Dressler's syndrome was diagnosed and prednisone in a dose of 80 mg daily administered.
CHEST, VOL. 63, NO.1, JANUARY, 1973
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POST MYOCARDIAL INFARCTION SYNDROME
Within 12 hours, the pain largely subsided. The patient became afebrile, (Fig 4) and his pulse fell below 100 for the first time. A chest x-ray picture obtained one week later showed clear lung fields and a striking decrease in cardiac size (Fig 3B). He remained asymptomatic until August 11, 1968 when, 12 hours after prednisone therapy was discontinued, he had a recurrence of fever and pleuropericardial pain. The reinstitution of prednisone therapy effected prompt relief and in 48 hours he was asymptomatic again. The patient was discharged on the 29th hospital day on 15 mg prednisone daily. Prednisone was subsequently discontinued, but a typical recurrence six months later again required the use of corticosteroids. CASE
FIGURE 3A (upper). P-A chest film demonstrating cardiomegaly and bilateral pleural effusions. FIGURE 3B (lower). P-A chest picture after one week of prednisone therapy.
104
A 50-year-old building inspector with no prior history of heart disease, was admitted to The Brookdale Hospital Center on November 8, 1970 because of burning retrosternal pain of three hours' duration. Physical examination revealed an acutely ill obese white man. The blood pressure was 150/90, pulse 60 per minute, temperahlre 98.6°F. The neck veins were not distended. Scattered rhonchi were audible over both lung bases. The heart was not enlarged. An S4 gallop was audible at the apex, but no murmur or rubs were heard. The rest of the examination was within normal limits. An electrocardiogram revealed changes of an acute inferolateral wall infarction. The white blood cell count was 16,630 per cubic millimeter with a predominance of neutrophils. The CPK and SCOT reached peak values 36 hours after admission of 80 and 250 IU, respectively. Anticoagulation with warfarin sodium (Coumadin) was started on admission and atropine was administered for ventricular premature contractions associated with a sinus bradycardia. Two days after admission, the patient began to complain of pleuropericardial pain; a friction rub was audible for the first time. On the third hospital day, pump failure, manifested by sinus tachycardia, alternans and gallop rhythm, was treated with parenteral ouabain. One day later, on November 12, 1970, an angiogram was obtained which was compatible with the presence of a pericardia! effusion (FigS).
DAYS OF HOSPITALIZATION 2 3 4 5 6 7 8 9 10 II 12 13 1415 16 17 18 19 20 0----0
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t-
99 98 97
CHEST, VOL. 63, NO, 1, JANUARY, 1973
FIGURE 4. Temperature curves demonstrating the prolonged febrile course in all five patients. Institution of prednisone therapy (in case 2) is denoted by the upward arrows and its withdrawal by the downward arrow.
38
KOSSOWSKY, EPSTEIN, LEVINE An electrocardiogram showed ehanges of an extensive acute anterior wall myocardial infaretion and an old inferior wall infarction. The CPK elevated on admission, rose to 1,386 IV on the second day. Rapid digitalization was accomplished with intravenous ouabain. Three days after admission the patient complained of pleuritic pain relieved by sitting up. His temperahire was elevated to 101°F and a pericardial friction mb was heard for th,· first time. An echoeardiogram was consistent with a small amount of pericardial fluid anteriorly (Fig 6). Five days after admission physical examination suggested the presence of a left pleural effusion. This was confirmed by a ehe~t film examination. A repeat x-ray examination in four days showed it~ complete resolution. The pericardial friction mb, pain and fever persisted through the 12th hospital day when he became afebrile and pain free for the first time. The remainder of the hospital course was unventful and he was discharged on the 21st hospital day on di~oxin. 0.25 mg PO daily.
FIC:UHE .5. An~iocardiogram compatible with the presence of pericardial effusion. At that time the prothrombin time was 12/18 seconds; warfarin sodium (Coumadin) was discontinued. The friction TIl!> persisted for another 24 hours, and the pain and fever for an additional 48 hours. The remainder of the patient's hospital course was uneventful and he was discharged on the 21st hospital day on maintenanee di~oxin. A chest x-ray picture obtained at time of diseharge was within normal limits. CASE 4 A 49-year-old laborer with maturity onset diabetes and prl'vious myocardial infarction was admitted to The Brookdale Hospital Center on April 6, 1971 with a three day history of increasingly severe chest pain. Physical examination revealed a well developed, obese, Negro man in respiratory distress. Blood pressure was 160/100. Heart rate was 130 per minute. Pulsus alternans was present. Neck veins were distended at 30° and a summation gallop was audible at the cardiac apex. The liver was not palpable and the remainder of the examination was unremarkable.
. , - _......- . . - . -......- ECG
.'--.::1=-__-..... PERICARDIUM PERICARDIAL FLUID R. V. WALL R. V. CAVITY
CASE 5 A 44-year-old Puerto Riean man with mahlrity onset of diabetes and a three year history of angina peetoris was admitted to The Brookdale Hospital Center on January 6. 1970 because of severe chest pain radiatin~ down both arms of four hours' duration. Physical examination revealed a diaphoretic man with blood pressure of 140/100, temperahlre of 98.8°F and pulse rate of 90 per minute. Rail'S were present at the right lun~ base. On examination of the heart, an S4 gallop was heard. The liver was not palpable and the remainder of the examination was unremarkable. An electrocardiogram revealed an acute extensive anterior wall myocardial infarction. CPK peaked to 1,600 IV and the SCOT to 315 IV on the second hospital day. Two days after admission, parenteral digoxin was given because of the development of signs of pump failure as manifested by sinus tachycardia, pulsus aItemans and summation gallop. A pericardial friction mb was clearly audible. The tachycardia persisted for the first two weeks of the patient's illness as did the pericardial friction mb. In addition, he had a temperature ranging from l00AOF to 103.2° during the entire period. Chest x-ray pichlre on the tenth hospital day showed a fine reticular pulmonary infiltrate involving the lower two-thirds of the right chest and left base. Repeat chest x-ray examination on day 13 showed clearing of the infiltrate. A pulmonary angiogram was obtained on the 14th day of hospitalization and demonstrated a 10 mm distance between the right atrial endocardium and the outer border of the heart, consistent with a significant pericardial effusion, and no evidence of pulmonary embolism. After the 16th hospital day, the patient was afebrile and pain free and his subsequent course was uneventful. Chest film just prior to discharge revealed an enlarged heart with left ventricular prominence. He was discharged on the 25th hospital day on digoxin, 0.25 mg and tolbutamide (Orinase), 500 mg PO daily. DISCUSSION
F1GUHE 6. Echocardiogram consistent with the presence of lwrieardial fluid. .
The postmyocardial infarction syndrome is a well recognized clinical entity of unknown etiology.'-4 Although a viral etiology has recently been proposed,6 the Dressler syndrome is generally thought CHEST, VOL. 63, NO.1, JANUARY, 1973
39
POST MYOCARDIAL INFARCTION SYNDROME
of as an immune disorder resulting from a hypersensitivity reaction to injured cardiac tissue. 3.7 Lending support to the concept of an altered immunity in the pathogenesis of this disorder are the similarity between the clinical features of the postinfarction syndrome and diseases commonly thought to have an immune basis/'s the frequent presence of circulating antibodies to heart tissue,9-11 and the response to both corticosteroids3 and antimetabolites. 12 A pericardial friction rub heard during the first days of acute myocardial infarction is characteristically evanescent and is generally thought to reflect transmural infarction. 13.14 The persistence of the rub, a prolonged febrile course (Fig 4), the presence of pleuropericardial effusion, or the appearance of the rub after the first week of illness, however, suggests a complication of myocardial infarction such as a pulmonary embolus, pneumonia, congestive heart failure or the postmyocardial infarction syndrome. 2.3.14 In patients receiving anticoagulants the appearance of a pericardial effusion may suggest the additional diagnosis of a drug related hemopericardium. ls' ls Angiocardiography was diagnostic for pleuropericardial effusion in three of our patients on the fourth day and in one patient on the 14th day of illness. In the fifth patient, the diagnosis of pericardial effusion was made echocardiographically on the fourth hospital day. In none of our patients did alternate explanations such as pulmonary emboli, severe congestive heart failure, pneumonia or anticoagulant-related hemorrhagic pericarditis prove to be diagnostically tenable. Neither progressive heart failure nor pulmonary emboli could be documented in any of our patients. Although a warfarin sodium (Coumadin) related hemopericardium was a consideration in two of our patients, this diagnosis was unlikely since hemorrhagic pericarditis complicating anticoagulant therapy in acute myocardial infarction is generally a late complication of therapy.IS.IS Furthermore, the pericarditis occurred after only two days of warfarin sodium therapy when the prothrombin time was not in a therapeutic range in either patient. Pericardial effusion due solely to the myocardial infarction was an additional consideration in all of our patients but this too seemed unlikely. The case described by NichoP9 of pericardial effusion complicating acute coronary thrombosis, and cited by Friedberg20 in his textbook, is that of a patient who satisfied all clinical criteria of the Dressler syndrome. The rarity of pericardial effusion complicating myocardial infarction is perhaps underlined by CHEST, VOL. 63, NO.1, JANUARY, 1973
the experience of Mintz and Katz 21 who failed to find evidence of such effusion in 572 patients with recent myocardial infarction. The clinical features in the patients described in this report were consistent with the postmyocardial infarction syndrome except for the very early appearance of pleuropericarditis. The spontaneous resolution of the fever, pleuropericardial and pulmonary findings in four of the five patients and the dramatic response to corticosteroids in the other is characteristic of the Dressler syndrome and adds support to this diagnosis. Our experience with the five patients reported here supports the observation that the postmyocardial infarction syndrome more frequently follows extensive infarction. 12.22 The observations add to the clinical spectrum of this syndrome by suggesting that a pericardial rub heard during the first days of acute myocardial infarction is sometimes a manifestation of the Dressler syndrome. REFERENCES
2 3 4 5
6 7 8 9 10
11
12
13
14 15
16
Dressler W: A post myocardial infarction syndrome. Preliminary report of a complication resemhling idiopathic recurrent benign pericarditis. JA~fA 160: 1379, 1956 Connolly DC, Burchell HB: Pericarditis: A ten year survey. Am J CardioI7:7, 1961 Dressler W: The post myocardial infarction syndrome. A report on 45 cases. Arch Intern Med 103:28, 1959 Levin JW, Bryk D: Dressler syndrome (post myocardial infarction syndrome). Radiology 87:731,1966 Hurst JW, Logue RB: The Heart (Arteries and Veins). Sec ed. New York, McGraw-Hili Book Company, The Blakiston Division, 1970, p 1966 Burch GE, Colcolough HL: Post cardiotomy and post infarction syndromes-a theory. Am Heart J 80:290, 1970 Kaplan \fH, Frengley JD: Autoimmunity to the heart in cardiac disease. Am J CardioI24:459, 1969 Davies A~f, Gery I: Autoimmunity in heart disease. Biochem Clin 1: 19, 1963 Davies AM, Gery I: The role of autoantihodies in heart disease. Am Heart J 60:669, 1960 Van Der Geld H: Antiheart antihodies in the post-pericardiotomy and the post myocardial infarction syndromes. Lancet 2:617, 1964 Faivre G, Gilgenkrantz JM, Duheille J, et al: Immunofluorescence et syndromes postcommissurotomie ou post infarctus. Arch ~fal Coeur 60:484, 1967 Kossow~ky WA, Kim KS, Tobin MS: Antimetabolite therapy in the post myocardial infarction syndrome. Am Heart J, in press Harvey WP: Some pertinent physical findings in the clinical evaluation of acute myocardial infarction. Circulation 40: (suppl IV) 175, 1969 Evans E: Introduction to symposium on pericarditis. Am J CardioI7:1,1961 Goldstein R, Wolff L: Hemorrhagic pericarditis in acute myocardial infarction treated with bishydroxycoumarin. JAt-1A 146:616, 1951 Anderson M, Christensen N, Edwards J: Hemopericar(Hum complicating myocardial infarction in the absence of
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KOSSOWSKY, EPSTEIN, LEVINE
cardiac rupture. Arch Intern Moo 90:634, 1952 17 Aarseth 5, Lange HF: The influence of anticoagulant therapy on the occurrence of cardiac rupture and hemopericardium following heart infarction. 1. A study of 89 cases of hemopericardium. Am Heart J 56:250, 1958 18 Lange HF, Aarseth 5: The influence of anticoagulant therapy on the occurrence of cardiac and hemopericar(lium following heart infarction. II. A controlled study of a selected treated group base on 1,044 autopsies. Am
Heart J 56:257, 1958 19 Nichol ES: Large pericardial effusion complicating acute coronary thrombosis. Ann Intern Med 11:1900, 1937 20 Friedberg CK: Disease of the heart. Philadelphia and London, WB Saunders Company, 1966, p 809 21 Mintz 55, Katz LN: Recent myocardial infarction. Analysis of 572 cases. Arch Intern Med 80:205, 1947 22 Ravnskov V: Aneurysm of the heart in the post-myocardial infarction syndrome. Acta Med Scand 183:393, 1968
Editorial Expression
their five patients to rule out pulmonary embolism, it is likely that echocardiography and pulmonary scanning would establish the diagnosis in many such patients. Why these patients manifest what is frequently considered an autoimmune response to myocardial necrosis so early in the course of their infarction is not clear, particularly since two of the five patients had no prior evidence of heart disease. Herbert J. Ledne
It has not been appreciated previously that the post myocardial infarction syndrome may develop during the first week of a coronary attack and sometimes blend imperceptibly with the pericarditis of transmural infarction. Fever and a pericardia! friction rub which outlasts that of acute myocardial necrosis are helpful signs. While the authors employed angiocardiography in four of
Boston
African Safari Vacations are desirable for getting away from the tension of business and professional responsibilities or from the drab monotony of every day routine. Years ago safaris had been accessible to the financial and social elite only. Hunting expeditions of this sort cost well over $6,000 for two for a thirty-day period, in addition to expenses for air travel and other requisites. Of course, bagging the "big five" (lion, leopard, rhinoceros, elephant, buffalo) means precious trophies and gives a tremendous boost to one's ego and social prestige. A great many people, however, prefer to go on a nonshooting safari. Currently this represents a major contingent of the tourist revenue of East Africa. Sightseers and those interested in wild life in its natural surroundings are not concerned with hair-raising encounters with wild animals or with demonstration of hunting skill or courage. Rather they are craving for relief from the tedium of customary living and want to escape from the city into aimless wanderings in exotic scenery and wrap themselves in a comforting sense of isolation. They follow the urge to roam around in the shades of massive forests, treading luminous arabesques of sunrays on the carpet of heavy grass. They enjoy being lulled into a strange, thoughtless enchantment by the exuberant vegetation, prodigious Howers, the sight and songs of colorful birds. Communing with nature in this manner is an enrichment of the soul, a grandiose experience in recreation, an amalgam of relaxation, langor and what the Italian so aptly calls "dolce far niente,"
meaning sweet doing nothing. The only dissonant note I am obliged to record is the remote possibility of illness acquired on a safari. Although the vector mosquito, Anopheles is not common in Africa, malaria may be acquired occasionally. Occurrence of pneumonia, bronchitis, asthma and pleurisy with effusion (serofibrinous or hemorrhagic) have been attributed to plasmodium. Confirming previous pertinent findings of others, Godard and Hansen observed a patient with x-ray evidence of diffuse interstitial pulmonary edema. It disappeared on intensive antimalarial treatment. In their view pulmonary hypersensitivity would best account for the local changes in the pulmonary capillaries resulting in malarial pulmonary edema (Radiology 101:523, 1971). In some instances, encephalitis, involvement of the abdominal organs may develop. Cardiovascular manifestations are infrequent; they vary from angina pectoris to fatty degeneration of the myocardium. During a brief stay in Africa, infection with Entamoeba histolytica may pose a serious problem. It may compromise not only the digestive system but also the lung, pleura and pericardium, either by direct extension from the liver or by hematogenous spread. A number of potent antimalarial drugs are available. In pneumonitis and other forms of extraintestinal forms of amebiasis, the administration of chloroquine and hydroxychloroquine is recommended by Krantz et al (Pharmacologic Principles in Medical Practice, Baltimore, Williams & Wilkins, 1969). Andrew L. Banyai, M.D.
CHEST, VOL. 63, NO.1, JANUARY, 1973