Myocardial abscess complicating healed myocardial infarction SAMUEL WEIsz, MD, FRCP[C], FACP; DONALD G. YOUNG, MD, FRCP[CI
An Isolated myocardial abscess due to Bacteroides fragilis developed In the scar of a myocardlal Infarction. Fever, chills and signs of pericarditis were the main clinical features. Mild enteritis I week prior to the onset of symptoms related to the abscess was the most likely cause of the bacteremia. The diagnosis was established at thoracotomy, performed because of cardiac tamponade. Thirteen other cases of isolated bacterial myocardial abscess accompanying myocardial infarction have been reported, but all the infarctions were recent. Surgical resection for a suspected myocardial abscess should be considered in view of the high mortality, largely from cardiac rupture. Un abcas isol6 du myocarde caus6 par las Bacteroides fragilis est apparu dans Ia tissu cicatriclel d'un infarctus du myocarde. La fievre, des frissons et des signes de p6ricardite constituent las principales manifestations cliniques observees. Une enterite b6nigne, qui est survenue I semaine avant le d6but des sympt8mes associ6s a l'abces myocardique, est Ia cause Ia plus probable de Ia bacteremie. Le diagnostic a ste pose au cours dune thoracotomie, rendue n6cessaire par l'apparition d'une tamponnade cardlaque. Treize autres cas d'abces bacteriens isoles du myocarde accompagnant un infarctus du myocarde ont 6te signal6s, mais ii s'agissait dans tous les cas d'infarctus recents. Vu Ia forte mortalit6 rencontr6e dans cette infection, due principalement A une rupture cardiaque, on devrait songer a Ia r6section chirurgicale lorsqu'un abcAs myocardique est soup9onn6.
The development of myocardial abscess has been considered to be rare. We were unable to find any reports of myocardial abscess associated with myocardial infarction diagnosed ante mortem. Murray1 reported survival in a case of suppurative pericarditis complicating myocardial infarction in which abscess of the myocardium was thought to have been the cause of the pericarditis, but no abscess was seen at the time of surgical drainage of the pericardium. The frequency of detection of myocardial abscess at autopsy has varied from 0.2' and 0.56%. to From the Misericordia Hospital, Edmonton Reprint requests to: Dr. S. weisz, 939 Professional Building, 10830 Jasper Ave., Edmonton, Alta. T5J 2B3
1.5% .. Sanson, Slodki and Gruhn4 noted that a recent surgical procedure was a frequent etiologic factor. Myocardial abscess most frequently occurs secondary to demonstrable bacterial infection at some other site, as a result of either contiguous spread from the cardiac valves or metastatic spread from a more distant site. In reviewing the literature we found 13 case reports of bacterial myocardial abscess complicating a recent myocardial infarction. There were no reports of an abscess occurring in a completely healed myocardial scar, the site of an old myocardial infarction; such a case is reported below. No primary source of infection could be found in almost half of the 14 cases.
Case report Clinical course
A 54-year-old man was admitted to hospital because of weakness and fever. One week prior to admission he had awakened with a violent chill, followed by nausea, vomiting and diarrhea for 24 hours. The day prior to admission he had noted recurrence of chills and profuse diaphoresis. He had been robust and had played professional football until age 27. Thereafter he remained very active, working as a salesman. At age 51 he began to have angina pectoris and suffered an acute myocardial infarction. He returned to work after recovery and had been well until his present illness. His temperature was 37.5 0C; pulse rate, 80 beats/mm; and blood pressure, 120/85 mm Hg. Apart from obesity no physical abnormalities were detected. The hemoglobin value was 13.8 g/dl. The leukocyte count was 12.6 x 10/l with 78% polymorphonuclear leukocytes, 5% lymphocytes, 7% monocytes and 10% bands. The erythrocyte sedimentation rate was 108 mm/h. An electrocardiogram was unchanged from one taken a year earlier; it showed Q waves in all precordial and standard leads, and in the aVF lead, indicating extensive anterolateral and inferior wall infarction. The chest radiograph showed a cardiothoracic ratio of 1:2. The spiking fever continued, with peaks of 410C, but the pulse rate remained between 70 and 90 beats/mm. On the 5th hospital day Bacteroides fragilis was isolated from two blood cultures. Intravenous administration of tetracycline was started and the fever remitted for 2 days, then spiked to 390C. On the 8th hospital day the patient ex-
perienced severe retrosternal chest pain that was accentuated with a deep breath and relieved by sitting upright. A pleural friction rub was heard on both sides but
1156 CMA JOURNAL/MAY 21, 1977/VOL. 116
was loudest on the left. Because the neck was short and thick the neck veins were difficult to see. Respirations became shallow, rapid and grunting. A chest radiograph showed a substantial increase in the size of the cardiac silhouette, and an electrocardiogram showed ST-segment elevation, with a downward convexity in leads 2, 3 and aVF. Myocardial blood pool and pericardial scanning with radioactive technetium suggested the presence of a large pericardial effusion. Antibiotic therapy was changed to clindamycin and penicillin given intravenously, and gentamicin given intramuscularly. On the 9th hospital day the patient's condition appeared grave. While he was breathing room air his arterial blood pH was 7.48, the Pco, was 27 mm Hg and the Po2 was 49 mm Hg. Pericardiocentesis was attempted but only a few millilitres of fibrinosanguinous fluid was obtained. Central venous pressure increased from 20.5 to 23.0 cm H20 within 2 hours. At this time the pulse rate was 115 beats! mm, the extremities were cold and clammy, the systolic blood pressure had decreased to 80 mm Hg and the urinary output had become scant. A diagnosis of suppurative pericarditis causing cardiac tamponade prompted an immediate thoracotomy, which revealed 500 ml of turbid fluid in the left chest cavity. Aspiration of the pericardial cavity yielded 600 ml of sanguinous fluid. When the pericardium was opened 300 ml of friable fibrinous exudate was found; its removal revealed an anteroapical, creamcoloured abscess of the myocardium, 1.5 cm in diameter, with a central, 0.1-cm perforation that was exuding pus. Relief of the pressure in the pericardial cavity resulted in rapid improvement in blood pressure and urine output. Culture of pus from the myocardial abscess, as well as the pericardial fluid and pencardium, yielded B. fragilis. Postoperatively the patient was given the same antibiotics plus cloxacillin. The fever subsided and the cardiovascular status improved. On the 6th postoperative day shortness of breath occurred, a pleural - rub was heard on the left side and the patient's temperature increased to 38 0C. Antibiotic therapy was changed to chloramphenicol and crystalline penicillin administered intravenously. The patient continued to have a low-grade fever with intermittent elevation of temperature to 38 0C. He remained weak and listless and suddenly became apneic and unresponsive; he died on the 15th postoperative day. Autopsy findings Cardiac rupture with hemopericardium was found, the 300 to 400 ml of fluid being a mixture of clotted blood and fibrinopurulent exudate. Rupture had occurred through a full-thickness, aneurysmal myocardial scar involving the lower
two thirds of the anterior left ventricular myocardium at the apex. The endocardial surface of the scar was covered by a recent fibrinous, unorganized mural thrombus, 1 to 3 cm in thickness. The site of the rupture was an abscess in the scar, composed of a polymorphonuclear exudate surrounded by granulation tissue, which was beginning to involve the overlying mural thrombus (Fig. 1). The site of the abscess and rupture corresponded to that of the abscess seen at thoracotomy. The heart weighed 620 g. No recent infarction was found but the coronary arteries showed three-vessel atherosclerotic narrowing, most pronounced in the left anterior descending vessel, and there was a recent thrombotic occlusion of the right coronary artery. The liver showed chronic passive congestion, more accentuated in the right lobe, which had centrilobular necrosis and an old organized thrombotic occlusion of its branch of the hepatic artery.
Bacteriologic findings The organism isolated from the abscess and pericardium was an anaerobic gramnegative rod identified as B. fragilis, subspecies distasonis by its fermentation and biochemical reactions.5 Discussion The 13 reported cases of myocardial abscess associated with a recent myocardial infarction are detailed in Table I. There were five women and eight men; most were in the 5th or 6th decade. Bronchopneumonia was the source of infection in four cases, and acute pyelonephritis, empyema of the gallbladder, small intestinal necrosis and gangrene of the leg underlay one case each. No primary focus of infection was found in five of these cases or in our case. In one of the cases re-
FIG. 1-Rupture through abscess in myocardlal scar, Indicated by probe.
ported by Katz1 the patient had had a tooth extracted 1 week prior to the onset of symptoms. The 28-year-old
woman described by Lewis14 had given birth 2 weeks before the onset of symptoms related to myocardial abscess. Our patient had had acute viral enteritis 1 week prior to the onset of symptoms related to the abscess.
The infecting organism was Staphylococcus aureus in four cases, Clostridium pertingens in three cases, Escherichia coli in two cases, 16-hemolytic streptococcus in one case and Streptococcus pneumoniae in one case. In two recently reported cases14'15 the organism was B. fragilis, the same organism isolated from our patient. Thus, anaerobic bacteria were the causative organisms in five of the more recently reported cases, their isolation occurring at a time when the prevalence of anaerobic infections was generally increased.17 Signs and symptoms included chills, fever, coma and, in some patients, localized findings suggestive of pencarditis. Leakage of exudate from the myocardial abscess into the pericardial space, resulting in fibrinopurulent pencarditis, was reported in five cases. In two cases7 a thin fibrinous exudate was found on the pericardium. Therefore, myocardial abscess must be considered in the differential diagnosis of pencarditis, associated with fever and chills, occurring in any patient after the onset of myocardial infarction. Including ours, five (36%) of the reported cases terminated in cardiac rupture; in contrast, the frequency of cardiac rupture in myocardial infarction is 5% 18 and in myocardial abscess alone, 5 to 1O%4.16.19 Our case is unique in that the development of cardiac tamponade due to fibrinopurulent pencarditis prompted surgical intervention, whereby the diagnosis was established and the patient's condition improved. Preoperative suspicion of myocardial abscess may allow for its surgical resection and possible survival of the patient. Survival of a patient after surgical treatment of myocardial abscess associated with bacterial endocarditis has been reportedY' In the previously reported cases the myocardial abscess occurred between approximately 1 week and 2 months after the onset of myocardial infarction. Six of the patients also had scars from previous myocardial infarctions. Our patient's abscess developed in a scar 3 years after myocardial infarction, and at autopsy no evidence of recent myocardial infarction was found. The old hepatic artery occlusion and centriobular necrosis in the right lobe of the liver of our patient suggests that the filtering function of the liver for CMA JOURNAL/MAY 21, 1977/VOL. 116 1157
the portal circulation was impaired. This could have allowed B. fragilis from the gut to escape to the systemic circulation during the episode of enteritis, prior to the onset of symptoms of the myocardial abscess. Impaired circulation at the site of the myocardial scar would reduce the chances of the body's humoral and celluhir defence mechanisms eradicating the infection and would also reduce the effectiveness of antibiotic therapy. The large accumulation of recent mural thrombus over the abscess in the scar was secondary to the subendocardial inflammatory reaction that eventually included the inner layer of the mural thrombus. Surgical resection of a myocardial abscess complicating myocardial infarction or a myocardial scar, when the diagnosis is made before death, would be logical therapy.
References 1. MURRAY M: Suppurative pericarditis complicating myocardial infarction. Br I Med 1: 223, 1968 2. FLAXMAN N: Myocardial abscess formation in myocardial infarction. N Engi J Med 243: 1024, 1950 3. SAPHIR 0: Myocarditis; general review, with analysis of 240 cases. Arch Pathol 33: 88, 1942 4. SANSON J, Ssooici 5, GRUHN JG: Myocardial abscesses. Am Heart 1 66: 301, 1963 5. LENNEiTE EH, SPAULDING EH, TRUANT JP:
Manual ol Clinical Microbiology, 2nd ed, Washington, Am Soc Microbiol, 1974, p 393 6. Cossso P. BERCON5KY I: Abseco parietal del coraz6n e infarcto del miocardio. Sem Med 2: 1691, 1933
7. TEDESCHI CG, STEVENSON TD JR. LEVENSON
HM: Abscess formation in myocardial infarction. N Engi I Med 243: 1024, 1950 8. MILLER RD, EDWARDS JE: Abscess formation in an acute myocardial infarct: report of a case. Mayo Clin Proc 26: 178, 1951 9. TENNANT R, PARKS HW: Myocardial abscesses. Arch Pathol 68: 456, 1959 10. KATZ A: Abscess of the myocardium camplicating infarction: report of two cases. Can Med Assoc 1 91: 1225, 1964
11. KORNS ME: Suppuration within an acute myocardial infarction with rupture and tamponade. Am / Cardiol 18: 124, 1966 12. MARGOLIS J, WEST D, ARGANARUS E: Abscess formation complicating myocardial infarction. Texas Med 63: 54, 1967 13. CANNING BS, MULCAHY R, TOWERS R: Ab-
scess formation in an acute cardiac infarct. Br J Med 1: 164, 1969 14. LEwis JF: Myocardial infarction during pregnancy: with associated myocardial Bacteroides abscess. South Med J 66: 379, 1973 15. VIANNA NJ: Myocardial abscess and infarction: report of a case and review of the literature. J Med Soc NJ 70: 931, 1973 16. GUNERATNE F: Gas gangrene (abscess) of heart. NY State J Med 75: 1766, 1975 17. MARCOUX
JA,
ZABRANSKY
RJ,
WASHINGTON
JA ii, et al: Bacteroides bacteremia. Minn Med 53: 1169, 1970 18. FRIEDBERG CK: Diseases of the Heart, 3rd ed, Philadelphia, Saunders, 1966, p 854 19. WEISS 5, WILKINS RW: Myocardial abscess with perforation of the heart. Am I Med Sci 194: 199, 1937 20. DANIELSON
GK,
TITUS JL,
DUSHANE
JW:
Successful treatment of aortic valve endocarditis and aortic root abscesses by insertion of prosthetic valve in ascending aorta and placement of bypass grafts to coronary arteries. I Thorac Cardaovasc Surg 67: 443, 1974
Thrombosis of Bjork-Shiley aortic valve prosthesis: report of three cases ALBERTO G. DE LA ROCHA,* MD; STEPHEN K. PLUME,* MD; RONALD J. BAIRD,t MD
Un d6r.glement dO a une thrombose d'une valvule aortique Bjork-Shiley
est survenu chez trois patients entre 6 et 16 mois apres l'operation. Aucun des patients ne prenalent d'antlcoagulants. Bien quo ce d6regloment so soit pr6sent6 do faqon aigu, des sympt6mes prodromiquos ont Pu 6tre identifies r6trospectivoment chez doux patients. Deux patients ont survecu a Ia thrombectomie. Un traitement postop6ratoire aux anticoagulants est recommande chez los patients porteurs do ces valvules prosthetiques en depit des facteurs qui rendent ce traitement plus rlsqu6 chez certains patients. Une attention portee au caractere des murmures et au bruit do fermeture do Ia valvule prosthetique devrait faire partie des examens do rappel habituel. Dans une situation d'urgence, quand los delais doivent 6tre evites, Ia cathet6risation et l'angiographie no sont pas necessaires. L'abord operatoire consiste a realiser une thrombectomie complete sans remplacer Ia valvule ni aucune do SOS places & moms quil n'y alt une fuite 6vidente autour do Ia protheso ou une usure do Ia protheso.
From the department of surgery, University of Toronto and Toronto Western Hospital *Resident in cardiovascular surgery tProfessor of surgery, University of Toronto and chief of cardiovascular surgery, Toronto Western Hospital Reprint requests to: Dr. RJ. Baird, 399 Bathurst St., Ste. 304, Toronto, Ont. MST 2S8
Malfunction of a prosthetic heart valve because of thrombosis is an unusual, potentially lethal complication. Design factors meant to minimize the risk of thrombosis are incorporated in the Bjork-Shiley aortic valve prosthesis. The free-floating, tilting disc provides
Thrombotic malfunction of a Bjork-Shiley aortic valve prosthesis occurred in three patients 6 to 16 months postoperatively. None of the patients had been taking anticoagulants. Although the presentation was acute, prodromal symptoms could be identified retrospectively in two of the patients. Two patients survived thrombectomy. Postoperative anticoagulant therapy is recommended in patients with these prostheses despite factors that may make such therapy riskier in specific patients. Attention to the character of murmurs and of the closure sound of the prosthetic valve must be part of the routine follow-up. In the emergency situation, when delay must be avoided, catheterization and angiography are unnecessary. The operative approach consists of complete thrombectomy without replacement of the valve or any of its components unless there is obvious periprosthetic leak or prosthetic wear.
1158 CMA JOURNAL/MAY 21, 1977/VOL. 116
central, laminar flow and good hemodynamic performance. Made of pyrolytic carbon, the disc is physiologically inert, thromboresistant and electronegative in blood, and has excellent wear characteristics.1' This valve has been used in over 200 patients at our institution. Because of the reported low incidence of thromboembolic episodes3 we withheld sodium warfarin anticoagulants from a few selected patients in whom their use was thought to be contraindicated. This report describes three patients not taking anticoagulants who returned to hospital between 6 and 16 months postoperatively with thrombotic malfunction of the aortic valve prosthesis.
Case reports Case 1 In July 1975 a 43-year-old, non-Englishspeaking immigrant underwent replacement of a stenotic and incompetent aortic valve with a no. 29 Pyrolite disc prosthesis (Shiley Laboratories, Santa Ana, California). Postoperative anticoagulant therapy was omitted because of the language barrier, the absence of an established relationship with a family doctor and the patient's refusal to attend a follow-up clinic. Six months after operation the patient presented in the emergency ward following the acute onset of shortness of breath. A loud systolic ejection murmur and a
An Isolated myocardial abscess due to Bacteroides fragilis developed In the scar of a myocardlal Infarction. Fever, chills and signs of pericarditis were the main clinical features. Mild enteritis I week prior to the onset of symptoms related to the abscess was the most likely cause of the bacteremia. The diagnosis was established at thoracotomy, performed because of cardiac tamponade. Thirteen other cases of isolated bacterial myocardial abscess accompanying myocardial infarction have been reported, but all the infarctions were recent. Surgical resection for a suspected myocardial abscess should be considered in view of the high mortality, largely from cardiac rupture. Un abcas isol6 du myocarde caus6 par las Bacteroides fragilis est apparu dans Ia tissu cicatriclel d'un infarctus du myocarde. La fievre, des frissons et des signes de p6ricardite constituent las principales manifestations cliniques observees. Une enterite b6nigne, qui est survenue I semaine avant le d6but des sympt8mes associ6s a l'abces myocardique, est Ia cause Ia plus probable de Ia bacteremie. Le diagnostic a ste pose au cours dune thoracotomie, rendue n6cessaire par l'apparition d'une tamponnade cardlaque. Treize autres cas d'abces bacteriens isoles du myocarde accompagnant un infarctus du myocarde ont 6te signal6s, mais ii s'agissait dans tous les cas d'infarctus recents. Vu Ia forte mortalit6 rencontr6e dans cette infection, due principalement A une rupture cardiaque, on devrait songer a Ia r6section chirurgicale lorsqu'un abcAs myocardique est soup9onn6.
The development of myocardial abscess has been considered to be rare. We were unable to find any reports of myocardial abscess associated with myocardial infarction diagnosed ante mortem. Murray1 reported survival in a case of suppurative pericarditis complicating myocardial infarction in which abscess of the myocardium was thought to have been the cause of the pericarditis, but no abscess was seen at the time of surgical drainage of the pericardium. The frequency of detection of myocardial abscess at autopsy has varied from 0.2' and 0.56%. to From the Misericordia Hospital, Edmonton Reprint requests to: Dr. S. weisz, 939 Professional Building, 10830 Jasper Ave., Edmonton, Alta. T5J 2B3
1.5% .. Sanson, Slodki and Gruhn4 noted that a recent surgical procedure was a frequent etiologic factor. Myocardial abscess most frequently occurs secondary to demonstrable bacterial infection at some other site, as a result of either contiguous spread from the cardiac valves or metastatic spread from a more distant site. In reviewing the literature we found 13 case reports of bacterial myocardial abscess complicating a recent myocardial infarction. There were no reports of an abscess occurring in a completely healed myocardial scar, the site of an old myocardial infarction; such a case is reported below. No primary source of infection could be found in almost half of the 14 cases.
Case report Clinical course
A 54-year-old man was admitted to hospital because of weakness and fever. One week prior to admission he had awakened with a violent chill, followed by nausea, vomiting and diarrhea for 24 hours. The day prior to admission he had noted recurrence of chills and profuse diaphoresis. He had been robust and had played professional football until age 27. Thereafter he remained very active, working as a salesman. At age 51 he began to have angina pectoris and suffered an acute myocardial infarction. He returned to work after recovery and had been well until his present illness. His temperature was 37.5 0C; pulse rate, 80 beats/mm; and blood pressure, 120/85 mm Hg. Apart from obesity no physical abnormalities were detected. The hemoglobin value was 13.8 g/dl. The leukocyte count was 12.6 x 10/l with 78% polymorphonuclear leukocytes, 5% lymphocytes, 7% monocytes and 10% bands. The erythrocyte sedimentation rate was 108 mm/h. An electrocardiogram was unchanged from one taken a year earlier; it showed Q waves in all precordial and standard leads, and in the aVF lead, indicating extensive anterolateral and inferior wall infarction. The chest radiograph showed a cardiothoracic ratio of 1:2. The spiking fever continued, with peaks of 410C, but the pulse rate remained between 70 and 90 beats/mm. On the 5th hospital day Bacteroides fragilis was isolated from two blood cultures. Intravenous administration of tetracycline was started and the fever remitted for 2 days, then spiked to 390C. On the 8th hospital day the patient ex-
perienced severe retrosternal chest pain that was accentuated with a deep breath and relieved by sitting upright. A pleural friction rub was heard on both sides but
1156 CMA JOURNAL/MAY 21, 1977/VOL. 116
was loudest on the left. Because the neck was short and thick the neck veins were difficult to see. Respirations became shallow, rapid and grunting. A chest radiograph showed a substantial increase in the size of the cardiac silhouette, and an electrocardiogram showed ST-segment elevation, with a downward convexity in leads 2, 3 and aVF. Myocardial blood pool and pericardial scanning with radioactive technetium suggested the presence of a large pericardial effusion. Antibiotic therapy was changed to clindamycin and penicillin given intravenously, and gentamicin given intramuscularly. On the 9th hospital day the patient's condition appeared grave. While he was breathing room air his arterial blood pH was 7.48, the Pco, was 27 mm Hg and the Po2 was 49 mm Hg. Pericardiocentesis was attempted but only a few millilitres of fibrinosanguinous fluid was obtained. Central venous pressure increased from 20.5 to 23.0 cm H20 within 2 hours. At this time the pulse rate was 115 beats! mm, the extremities were cold and clammy, the systolic blood pressure had decreased to 80 mm Hg and the urinary output had become scant. A diagnosis of suppurative pericarditis causing cardiac tamponade prompted an immediate thoracotomy, which revealed 500 ml of turbid fluid in the left chest cavity. Aspiration of the pericardial cavity yielded 600 ml of sanguinous fluid. When the pericardium was opened 300 ml of friable fibrinous exudate was found; its removal revealed an anteroapical, creamcoloured abscess of the myocardium, 1.5 cm in diameter, with a central, 0.1-cm perforation that was exuding pus. Relief of the pressure in the pericardial cavity resulted in rapid improvement in blood pressure and urine output. Culture of pus from the myocardial abscess, as well as the pericardial fluid and pencardium, yielded B. fragilis. Postoperatively the patient was given the same antibiotics plus cloxacillin. The fever subsided and the cardiovascular status improved. On the 6th postoperative day shortness of breath occurred, a pleural - rub was heard on the left side and the patient's temperature increased to 38 0C. Antibiotic therapy was changed to chloramphenicol and crystalline penicillin administered intravenously. The patient continued to have a low-grade fever with intermittent elevation of temperature to 38 0C. He remained weak and listless and suddenly became apneic and unresponsive; he died on the 15th postoperative day. Autopsy findings Cardiac rupture with hemopericardium was found, the 300 to 400 ml of fluid being a mixture of clotted blood and fibrinopurulent exudate. Rupture had occurred through a full-thickness, aneurysmal myocardial scar involving the lower
two thirds of the anterior left ventricular myocardium at the apex. The endocardial surface of the scar was covered by a recent fibrinous, unorganized mural thrombus, 1 to 3 cm in thickness. The site of the rupture was an abscess in the scar, composed of a polymorphonuclear exudate surrounded by granulation tissue, which was beginning to involve the overlying mural thrombus (Fig. 1). The site of the abscess and rupture corresponded to that of the abscess seen at thoracotomy. The heart weighed 620 g. No recent infarction was found but the coronary arteries showed three-vessel atherosclerotic narrowing, most pronounced in the left anterior descending vessel, and there was a recent thrombotic occlusion of the right coronary artery. The liver showed chronic passive congestion, more accentuated in the right lobe, which had centrilobular necrosis and an old organized thrombotic occlusion of its branch of the hepatic artery.
Bacteriologic findings The organism isolated from the abscess and pericardium was an anaerobic gramnegative rod identified as B. fragilis, subspecies distasonis by its fermentation and biochemical reactions.5 Discussion The 13 reported cases of myocardial abscess associated with a recent myocardial infarction are detailed in Table I. There were five women and eight men; most were in the 5th or 6th decade. Bronchopneumonia was the source of infection in four cases, and acute pyelonephritis, empyema of the gallbladder, small intestinal necrosis and gangrene of the leg underlay one case each. No primary focus of infection was found in five of these cases or in our case. In one of the cases re-
FIG. 1-Rupture through abscess in myocardlal scar, Indicated by probe.
ported by Katz1 the patient had had a tooth extracted 1 week prior to the onset of symptoms. The 28-year-old
woman described by Lewis14 had given birth 2 weeks before the onset of symptoms related to myocardial abscess. Our patient had had acute viral enteritis 1 week prior to the onset of symptoms related to the abscess.
The infecting organism was Staphylococcus aureus in four cases, Clostridium pertingens in three cases, Escherichia coli in two cases, 16-hemolytic streptococcus in one case and Streptococcus pneumoniae in one case. In two recently reported cases14'15 the organism was B. fragilis, the same organism isolated from our patient. Thus, anaerobic bacteria were the causative organisms in five of the more recently reported cases, their isolation occurring at a time when the prevalence of anaerobic infections was generally increased.17 Signs and symptoms included chills, fever, coma and, in some patients, localized findings suggestive of pencarditis. Leakage of exudate from the myocardial abscess into the pericardial space, resulting in fibrinopurulent pencarditis, was reported in five cases. In two cases7 a thin fibrinous exudate was found on the pericardium. Therefore, myocardial abscess must be considered in the differential diagnosis of pencarditis, associated with fever and chills, occurring in any patient after the onset of myocardial infarction. Including ours, five (36%) of the reported cases terminated in cardiac rupture; in contrast, the frequency of cardiac rupture in myocardial infarction is 5% 18 and in myocardial abscess alone, 5 to 1O%4.16.19 Our case is unique in that the development of cardiac tamponade due to fibrinopurulent pencarditis prompted surgical intervention, whereby the diagnosis was established and the patient's condition improved. Preoperative suspicion of myocardial abscess may allow for its surgical resection and possible survival of the patient. Survival of a patient after surgical treatment of myocardial abscess associated with bacterial endocarditis has been reportedY' In the previously reported cases the myocardial abscess occurred between approximately 1 week and 2 months after the onset of myocardial infarction. Six of the patients also had scars from previous myocardial infarctions. Our patient's abscess developed in a scar 3 years after myocardial infarction, and at autopsy no evidence of recent myocardial infarction was found. The old hepatic artery occlusion and centriobular necrosis in the right lobe of the liver of our patient suggests that the filtering function of the liver for CMA JOURNAL/MAY 21, 1977/VOL. 116 1157
the portal circulation was impaired. This could have allowed B. fragilis from the gut to escape to the systemic circulation during the episode of enteritis, prior to the onset of symptoms of the myocardial abscess. Impaired circulation at the site of the myocardial scar would reduce the chances of the body's humoral and celluhir defence mechanisms eradicating the infection and would also reduce the effectiveness of antibiotic therapy. The large accumulation of recent mural thrombus over the abscess in the scar was secondary to the subendocardial inflammatory reaction that eventually included the inner layer of the mural thrombus. Surgical resection of a myocardial abscess complicating myocardial infarction or a myocardial scar, when the diagnosis is made before death, would be logical therapy.
References 1. MURRAY M: Suppurative pericarditis complicating myocardial infarction. Br I Med 1: 223, 1968 2. FLAXMAN N: Myocardial abscess formation in myocardial infarction. N Engi J Med 243: 1024, 1950 3. SAPHIR 0: Myocarditis; general review, with analysis of 240 cases. Arch Pathol 33: 88, 1942 4. SANSON J, Ssooici 5, GRUHN JG: Myocardial abscesses. Am Heart 1 66: 301, 1963 5. LENNEiTE EH, SPAULDING EH, TRUANT JP:
Manual ol Clinical Microbiology, 2nd ed, Washington, Am Soc Microbiol, 1974, p 393 6. Cossso P. BERCON5KY I: Abseco parietal del coraz6n e infarcto del miocardio. Sem Med 2: 1691, 1933
7. TEDESCHI CG, STEVENSON TD JR. LEVENSON
HM: Abscess formation in myocardial infarction. N Engi I Med 243: 1024, 1950 8. MILLER RD, EDWARDS JE: Abscess formation in an acute myocardial infarct: report of a case. Mayo Clin Proc 26: 178, 1951 9. TENNANT R, PARKS HW: Myocardial abscesses. Arch Pathol 68: 456, 1959 10. KATZ A: Abscess of the myocardium camplicating infarction: report of two cases. Can Med Assoc 1 91: 1225, 1964
11. KORNS ME: Suppuration within an acute myocardial infarction with rupture and tamponade. Am / Cardiol 18: 124, 1966 12. MARGOLIS J, WEST D, ARGANARUS E: Abscess formation complicating myocardial infarction. Texas Med 63: 54, 1967 13. CANNING BS, MULCAHY R, TOWERS R: Ab-
scess formation in an acute cardiac infarct. Br J Med 1: 164, 1969 14. LEwis JF: Myocardial infarction during pregnancy: with associated myocardial Bacteroides abscess. South Med J 66: 379, 1973 15. VIANNA NJ: Myocardial abscess and infarction: report of a case and review of the literature. J Med Soc NJ 70: 931, 1973 16. GUNERATNE F: Gas gangrene (abscess) of heart. NY State J Med 75: 1766, 1975 17. MARCOUX
JA,
ZABRANSKY
RJ,
WASHINGTON
JA ii, et al: Bacteroides bacteremia. Minn Med 53: 1169, 1970 18. FRIEDBERG CK: Diseases of the Heart, 3rd ed, Philadelphia, Saunders, 1966, p 854 19. WEISS 5, WILKINS RW: Myocardial abscess with perforation of the heart. Am I Med Sci 194: 199, 1937 20. DANIELSON
GK,
TITUS JL,
DUSHANE
JW:
Successful treatment of aortic valve endocarditis and aortic root abscesses by insertion of prosthetic valve in ascending aorta and placement of bypass grafts to coronary arteries. I Thorac Cardaovasc Surg 67: 443, 1974
Thrombosis of Bjork-Shiley aortic valve prosthesis: report of three cases ALBERTO G. DE LA ROCHA,* MD; STEPHEN K. PLUME,* MD; RONALD J. BAIRD,t MD
Un d6r.glement dO a une thrombose d'une valvule aortique Bjork-Shiley
est survenu chez trois patients entre 6 et 16 mois apres l'operation. Aucun des patients ne prenalent d'antlcoagulants. Bien quo ce d6regloment so soit pr6sent6 do faqon aigu, des sympt6mes prodromiquos ont Pu 6tre identifies r6trospectivoment chez doux patients. Deux patients ont survecu a Ia thrombectomie. Un traitement postop6ratoire aux anticoagulants est recommande chez los patients porteurs do ces valvules prosthetiques en depit des facteurs qui rendent ce traitement plus rlsqu6 chez certains patients. Une attention portee au caractere des murmures et au bruit do fermeture do Ia valvule prosthetique devrait faire partie des examens do rappel habituel. Dans une situation d'urgence, quand los delais doivent 6tre evites, Ia cathet6risation et l'angiographie no sont pas necessaires. L'abord operatoire consiste a realiser une thrombectomie complete sans remplacer Ia valvule ni aucune do SOS places & moms quil n'y alt une fuite 6vidente autour do Ia protheso ou une usure do Ia protheso.
From the department of surgery, University of Toronto and Toronto Western Hospital *Resident in cardiovascular surgery tProfessor of surgery, University of Toronto and chief of cardiovascular surgery, Toronto Western Hospital Reprint requests to: Dr. RJ. Baird, 399 Bathurst St., Ste. 304, Toronto, Ont. MST 2S8
Malfunction of a prosthetic heart valve because of thrombosis is an unusual, potentially lethal complication. Design factors meant to minimize the risk of thrombosis are incorporated in the Bjork-Shiley aortic valve prosthesis. The free-floating, tilting disc provides
Thrombotic malfunction of a Bjork-Shiley aortic valve prosthesis occurred in three patients 6 to 16 months postoperatively. None of the patients had been taking anticoagulants. Although the presentation was acute, prodromal symptoms could be identified retrospectively in two of the patients. Two patients survived thrombectomy. Postoperative anticoagulant therapy is recommended in patients with these prostheses despite factors that may make such therapy riskier in specific patients. Attention to the character of murmurs and of the closure sound of the prosthetic valve must be part of the routine follow-up. In the emergency situation, when delay must be avoided, catheterization and angiography are unnecessary. The operative approach consists of complete thrombectomy without replacement of the valve or any of its components unless there is obvious periprosthetic leak or prosthetic wear.
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central, laminar flow and good hemodynamic performance. Made of pyrolytic carbon, the disc is physiologically inert, thromboresistant and electronegative in blood, and has excellent wear characteristics.1' This valve has been used in over 200 patients at our institution. Because of the reported low incidence of thromboembolic episodes3 we withheld sodium warfarin anticoagulants from a few selected patients in whom their use was thought to be contraindicated. This report describes three patients not taking anticoagulants who returned to hospital between 6 and 16 months postoperatively with thrombotic malfunction of the aortic valve prosthesis.
Case reports Case 1 In July 1975 a 43-year-old, non-Englishspeaking immigrant underwent replacement of a stenotic and incompetent aortic valve with a no. 29 Pyrolite disc prosthesis (Shiley Laboratories, Santa Ana, California). Postoperative anticoagulant therapy was omitted because of the language barrier, the absence of an established relationship with a family doctor and the patient's refusal to attend a follow-up clinic. Six months after operation the patient presented in the emergency ward following the acute onset of shortness of breath. A loud systolic ejection murmur and a
