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Suppuration within an acute myocardial infarct with rupture and tamponade
Suppuration Within an Acute Myocardial Infarct with Rupture and Tamponade* MICHARI . E . HORNS, . .D M
Iowa City, Iowa
infarction block and lateral wall ischernia . The next day there was rhythmic bigeminy . "I 'he last electrocardiogram, which was made on this day (January 29), after the administration of procainamide, was similar to the first except that there was no peri-infarction block . At noon January 30, a pericardial friction rub suddenly developed, accompanied by profuse sweating . Despite the administration of metaraminol intravenously, the blood pressure fell slowly and steadily, and she died that night .
BSCESSES of the myocardium are uncommon .
A
Because abscess formation within an acute myocardial infarct is even more uncommon,' this case is reported . CASE REPORT
A 70 year old white woman was admitted to University Hospitals Jan . 28, 1965, because of severe pain in the left side of the chest anteriorly. The pain began that day when she climbed the basement steps, and it was not relieved by resting . "There was transient radiation of the pain into the left arm . She was not nauseated but vomited several times . In November 1964, she was said to have had thrombophlebitis in the deep veins of the left leg, followed by pulmonary embolism and infarction, A diagnosis of hypertension had been made 25 years before ; also, she was said to have an old myocardial infarct . In addition, there was a history of peptic ulcer and glaucoma . Her father died of a stroke . Her mother, one brother and one sister were said to have died of myocardial infarction . On physical examination, the patient was acutely ill . The skin was pale and clammy . The blood pressure was 115 ;'60 mm . Hg. She had grunting respirations . The lungs were normal except for dullness at both bases posteriorly, The arterial pulses were normal in volume and contour ; the heart rate was 52 per minute . The heart was not enlarged . The heart sounds were faint, and there was a grade 2, apical, pansystolic murmur which radiated to the left axilla . Laboratory Data : The urine was normal . The hemoglobin was 16 gm . % ; the hematocrit, 50% ; and the leukocyte count, 25,400 per cu . mm . The serum glutamic oxaloacetic transaminase was 16 units on the first day ; the next day it rose to 94 and then to 152 units . The serum lactic acid dehydrogenase was 530 units the first day and it rose to 1,450 and then to 2,150 units the next day . A roentgenogram of the chest showed congestive changes in the lungs . An electrocardiogram on the day of admission showed acute inferior wall infarction with peri-
NECROPSY
Necropsy was done nine hours after death . The principal abnormalities involved the cardiovascular system . The pericardial sac was distended by approximately 250 cc, of blood . The posterior wall of the left ventricle was the seat of an acute, massive, transmural infarct ; it extended from the annulus of the initial valve to the apex and into the anterior wall of the left ventricle for a distance of 2 cm . In the center of the infarct was a large, irregularly shaped hole which measured 5 cm . in greatest dimension . The myocardium adjacent to the perforation did not exceed 0 .3 cm . in thickness, whereas the remainder of the myocardium of the left ventricle averaged 1 .1 cm . The endocardium was the seat of mural thrombi, the distribution of which corresponded to that of the necrotic muscle . 'I here was an old infarct in the anterolateral wall of the left ventricle, The anterior descending branch of the left coronary artery and the proximal segment of the right coronary artery contained recent thrombi which occluded the lumina . The valves were normal . The heart weighed 370 gm . Bilateral pleural effusion, acute pulmonary edema and severe, generalized visceral stasis were regarded as manifestations of congestive heart failure, as was patchy centrolobular hepatic necrosis . Microscopically, in addition to extensive coagulation necrosis, there was frank suppuration in the myocardial infarct (Fig . 1)- There were many chains of gram-positive bacteria which contained spores (Fig. 2), and a few clomps of gram-positive cocci .
*From the Department of Pathology, State University of Iowa, College of Medicine, Iowa City, Ia . This study was supported by graduate training grant 5T1 GM-168-06, National Institutes of Health, Bethesda, Md . 124
THE AMERICAN JOURNAL OF CARDIOLOGY
Suppuration Within Acute Myocardial Infarct
Fte . 1 . Margin of uryocardial abscess . X200, reduced by 7% .)
The fibers at the right are necrotic .
The former resembled a species of Clostridium, and, in fact, cultures showed large numbers of Clostridium perfringeru, Streptococcus faecalis and a few colonies of pseudomonads and Proteu.r mirobilis . The thrombi in the coronary ateries did not contain microorganisms . There were a few patchy areas of mucosal necrosis in the small intestine ; the exudate contained Cl . perfringens. This organism caused a septicemia and was also present in the edematous lungs and in a small, acute splenic infarct .
125
i IIcmatosvIin and eosin stain,
The general subject of nivocardial abscesses has been reviewed in admirable papers by Weiss and Wilkins,' and Saphir . 7 In view of the fact that necrotic tissue is an ideal culture atedium and that a focus of infection, regardless of the size or location, is often found among patients who die of acute myocardial infarction and congestive heart
COMMENT
The patchy areas of ruucosal necrosis in the bowel were caused by a severe degree of stasis or shock, or b oth . CL perfringens, which is a normal inhabitant of the bowel, thus converted a bland myocardial infarct into a septic infarct . I have been able to find reports of only 7 cases in which there has been formation of an abscess within a myocardial infarct . Some features of these are listed in Table i . Most myocardial abscesses are caused by Staphylococcus aureus . It is somewhat unusual for Clostridium perfringens to produce suppurative inflammation, as in this case, and that of Tennant and Parks .' In regard to the report by Tennant and Parks, however, there is some doubt that Cl . perfringens was, in fact, the organism which caused the abscess, inasmuch as the bacteria did riot contain spores . VOLUME 18, JULY 1966
Ftc . 2 . Chains of Clostridium perfringens in myocardial exudate . (liematnxylin and eosin stain, X800, reduced by 43°ic .)
126
Korns TABLE I Reported Cases of Abscess Formation Within a Myocardial Infarct
Year
Authors
No . of Cases
1933 1950
Cossio & Berconsky% "rcdcschi, ct al.s
1 2
1951 1959
Miller & Edwards , Temtant & Parksl
64 69 75 76 67
M F M M
1964
Katzz
2
63 66
M M
Patient Age sex
failure, it is somewhat surprising that more instances of abscess formation within my=ocardial infarcts have not been observed . SUMMARY
The eighth case in which there was suppuration within an acute myocardial infarct is presented, and some features of the other cases are reviewed . In this case there was a large, acute infarct in the posterior wall, and the patientdied of myocardial rupture and ran ponade . Necropsy showed large numbers of Clostridium( perfringens in the infarct, as well as fewer numbers in the lungs and spleen . The portal of entry was the small bowel . In only one other instance has Cl. perfringens been the causative organism .
Organism
Origin
Pneumococcus Slaph . across Steep/ . .wrens E. en! : Ciwbidmm perjrzngvo .r roll Stop/, . (00'14r
Bronchopneumonia Bronchopneumonia Bronchopneumonia Pyelonephritis Empyema of gallbladder Unknown CnkI ow I
Myocardial Rupture
No Yes No No Yes No No
REFERENCES 1 . TENNANT, R . and PARKS, 11 . W . Myocardial abscesses_ Arch . Path ., 68 : 456, 1959 . 2 . Cossio, P . and BERCONSEy, I . Absceso parietal del corazon c infarto del mincardin . Senana toed. (B . Aires), 2 : 1691, 1933 . 3. LL,ESeaI, C. G ., S'1'EVENSON, r. 1) ., be . and LEVENsote, It . M . Abscess formation in myocardial infarction . Sew England .L _Lied . . 243 : 1024, 1950 . 4 . MILLER, R . D . and EDWARDS, J . E . Abscess formation in an acute myocardial infarct Report of case . Proc . Staff Meet . Mayo Chn ., 26 : 178, 1951 . Abscess of the nryocardiunl eo,nplieating 5 . KATZ, A . infarction : Report of two cases . Canad . .H . A . J., 91 : 1225, 1964 . 6 . WErss, S . and WILIONS, R . W . Myocardial abscess With perforation of the heart Am . J. _M . Se ., 194 : 199, 1937 . 7 . SAPHIR, O . Myocarditis : A general review, with analysis of two hundred and forty cases . arch . Path ., 32 : 1000, 1941 ; 33 : 88, 1942 .
THE AMERICAN JOURNAL OF CARDIOLOGY
Iowa City, Iowa
infarction block and lateral wall ischernia . The next day there was rhythmic bigeminy . "I 'he last electrocardiogram, which was made on this day (January 29), after the administration of procainamide, was similar to the first except that there was no peri-infarction block . At noon January 30, a pericardial friction rub suddenly developed, accompanied by profuse sweating . Despite the administration of metaraminol intravenously, the blood pressure fell slowly and steadily, and she died that night .
BSCESSES of the myocardium are uncommon .
A
Because abscess formation within an acute myocardial infarct is even more uncommon,' this case is reported . CASE REPORT
A 70 year old white woman was admitted to University Hospitals Jan . 28, 1965, because of severe pain in the left side of the chest anteriorly. The pain began that day when she climbed the basement steps, and it was not relieved by resting . "There was transient radiation of the pain into the left arm . She was not nauseated but vomited several times . In November 1964, she was said to have had thrombophlebitis in the deep veins of the left leg, followed by pulmonary embolism and infarction, A diagnosis of hypertension had been made 25 years before ; also, she was said to have an old myocardial infarct . In addition, there was a history of peptic ulcer and glaucoma . Her father died of a stroke . Her mother, one brother and one sister were said to have died of myocardial infarction . On physical examination, the patient was acutely ill . The skin was pale and clammy . The blood pressure was 115 ;'60 mm . Hg. She had grunting respirations . The lungs were normal except for dullness at both bases posteriorly, The arterial pulses were normal in volume and contour ; the heart rate was 52 per minute . The heart was not enlarged . The heart sounds were faint, and there was a grade 2, apical, pansystolic murmur which radiated to the left axilla . Laboratory Data : The urine was normal . The hemoglobin was 16 gm . % ; the hematocrit, 50% ; and the leukocyte count, 25,400 per cu . mm . The serum glutamic oxaloacetic transaminase was 16 units on the first day ; the next day it rose to 94 and then to 152 units . The serum lactic acid dehydrogenase was 530 units the first day and it rose to 1,450 and then to 2,150 units the next day . A roentgenogram of the chest showed congestive changes in the lungs . An electrocardiogram on the day of admission showed acute inferior wall infarction with peri-
NECROPSY
Necropsy was done nine hours after death . The principal abnormalities involved the cardiovascular system . The pericardial sac was distended by approximately 250 cc, of blood . The posterior wall of the left ventricle was the seat of an acute, massive, transmural infarct ; it extended from the annulus of the initial valve to the apex and into the anterior wall of the left ventricle for a distance of 2 cm . In the center of the infarct was a large, irregularly shaped hole which measured 5 cm . in greatest dimension . The myocardium adjacent to the perforation did not exceed 0 .3 cm . in thickness, whereas the remainder of the myocardium of the left ventricle averaged 1 .1 cm . The endocardium was the seat of mural thrombi, the distribution of which corresponded to that of the necrotic muscle . 'I here was an old infarct in the anterolateral wall of the left ventricle, The anterior descending branch of the left coronary artery and the proximal segment of the right coronary artery contained recent thrombi which occluded the lumina . The valves were normal . The heart weighed 370 gm . Bilateral pleural effusion, acute pulmonary edema and severe, generalized visceral stasis were regarded as manifestations of congestive heart failure, as was patchy centrolobular hepatic necrosis . Microscopically, in addition to extensive coagulation necrosis, there was frank suppuration in the myocardial infarct (Fig . 1)- There were many chains of gram-positive bacteria which contained spores (Fig. 2), and a few clomps of gram-positive cocci .
*From the Department of Pathology, State University of Iowa, College of Medicine, Iowa City, Ia . This study was supported by graduate training grant 5T1 GM-168-06, National Institutes of Health, Bethesda, Md . 124
THE AMERICAN JOURNAL OF CARDIOLOGY
Suppuration Within Acute Myocardial Infarct
Fte . 1 . Margin of uryocardial abscess . X200, reduced by 7% .)
The fibers at the right are necrotic .
The former resembled a species of Clostridium, and, in fact, cultures showed large numbers of Clostridium perfringeru, Streptococcus faecalis and a few colonies of pseudomonads and Proteu.r mirobilis . The thrombi in the coronary ateries did not contain microorganisms . There were a few patchy areas of mucosal necrosis in the small intestine ; the exudate contained Cl . perfringens. This organism caused a septicemia and was also present in the edematous lungs and in a small, acute splenic infarct .
125
i IIcmatosvIin and eosin stain,
The general subject of nivocardial abscesses has been reviewed in admirable papers by Weiss and Wilkins,' and Saphir . 7 In view of the fact that necrotic tissue is an ideal culture atedium and that a focus of infection, regardless of the size or location, is often found among patients who die of acute myocardial infarction and congestive heart
COMMENT
The patchy areas of ruucosal necrosis in the bowel were caused by a severe degree of stasis or shock, or b oth . CL perfringens, which is a normal inhabitant of the bowel, thus converted a bland myocardial infarct into a septic infarct . I have been able to find reports of only 7 cases in which there has been formation of an abscess within a myocardial infarct . Some features of these are listed in Table i . Most myocardial abscesses are caused by Staphylococcus aureus . It is somewhat unusual for Clostridium perfringens to produce suppurative inflammation, as in this case, and that of Tennant and Parks .' In regard to the report by Tennant and Parks, however, there is some doubt that Cl . perfringens was, in fact, the organism which caused the abscess, inasmuch as the bacteria did riot contain spores . VOLUME 18, JULY 1966
Ftc . 2 . Chains of Clostridium perfringens in myocardial exudate . (liematnxylin and eosin stain, X800, reduced by 43°ic .)
126
Korns TABLE I Reported Cases of Abscess Formation Within a Myocardial Infarct
Year
Authors
No . of Cases
1933 1950
Cossio & Berconsky% "rcdcschi, ct al.s
1 2
1951 1959
Miller & Edwards , Temtant & Parksl
64 69 75 76 67
M F M M
1964
Katzz
2
63 66
M M
Patient Age sex
failure, it is somewhat surprising that more instances of abscess formation within my=ocardial infarcts have not been observed . SUMMARY
The eighth case in which there was suppuration within an acute myocardial infarct is presented, and some features of the other cases are reviewed . In this case there was a large, acute infarct in the posterior wall, and the patientdied of myocardial rupture and ran ponade . Necropsy showed large numbers of Clostridium( perfringens in the infarct, as well as fewer numbers in the lungs and spleen . The portal of entry was the small bowel . In only one other instance has Cl. perfringens been the causative organism .
Organism
Origin
Pneumococcus Slaph . across Steep/ . .wrens E. en! : Ciwbidmm perjrzngvo .r roll Stop/, . (00'14r
Bronchopneumonia Bronchopneumonia Bronchopneumonia Pyelonephritis Empyema of gallbladder Unknown CnkI ow I
Myocardial Rupture
No Yes No No Yes No No
REFERENCES 1 . TENNANT, R . and PARKS, 11 . W . Myocardial abscesses_ Arch . Path ., 68 : 456, 1959 . 2 . Cossio, P . and BERCONSEy, I . Absceso parietal del corazon c infarto del mincardin . Senana toed. (B . Aires), 2 : 1691, 1933 . 3. LL,ESeaI, C. G ., S'1'EVENSON, r. 1) ., be . and LEVENsote, It . M . Abscess formation in myocardial infarction . Sew England .L _Lied . . 243 : 1024, 1950 . 4 . MILLER, R . D . and EDWARDS, J . E . Abscess formation in an acute myocardial infarct Report of case . Proc . Staff Meet . Mayo Chn ., 26 : 178, 1951 . Abscess of the nryocardiunl eo,nplieating 5 . KATZ, A . infarction : Report of two cases . Canad . .H . A . J., 91 : 1225, 1964 . 6 . WErss, S . and WILIONS, R . W . Myocardial abscess With perforation of the heart Am . J. _M . Se ., 194 : 199, 1937 . 7 . SAPHIR, O . Myocarditis : A general review, with analysis of two hundred and forty cases . arch . Path ., 32 : 1000, 1941 ; 33 : 88, 1942 .
THE AMERICAN JOURNAL OF CARDIOLOGY