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Salmonella Pericarditis: An Unusual Complication of Myocardial Infarction
Salmonella Pericarditis: An Unusual Complication of Myocardial Infarction* John W. Schatz, M.D.; Leslie Wiener, M.D.; Hugh S. Gallagher, M.D.; and Richard/. Eberly, M.D.
A cue of Salmonella pericwditis is reported as • infectious complication of acute myocardial Infarction. A review of the literature reveals 15 other cases of postmyocardial infarction septic myocarditis, with or without pericarditis, and establishes this syndrome as an uncommon sequelae of myocardial Infarction. The appropriate diagnosis was made by WJe of ecbocardiograpby and pericardiocentesis. These diagnostic tools are useful in making a heretofore seldom recognized premortem diagnosis. complications at the site of acute myocardial Septic infarction are seldom recognized during life. Accu-
mulated case reports suggest that occasionally infections directly involving the heart may contribute to the morbidity of acute myocardial infarction. A case is presented describing the unusual complication of Salmonella pericarditis following acute myocardial infarction. CASE REPORT
This 62-year-old Caucasian man sustained an acute diaphragmatic myocardial infarction on July 27, 1970. Serial electrocardiograms and enzyme studies confirmed this diagnosis. With the exception of transient bradycardia and premature ventricular contractions, his course was uneventful. Twenty-one days after admission, he was discharged on oral anticoagulant therapy (sodium warfarin). °From the Division of Cardiology, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania. YK 308311
Pertinent past medical history included a subtotal gastrectomy performed in 1967 for a peptic ulcer. Three weelcs after discharge, he was hospitalized again for temperature elevation and cough. Hepatomegaly, ascites, and an elevated venous pressure were observed. A pericardia! friction rub was audible. Echocardiography was performed verifying the presence of pericardia! effusion (Fig 1 ) . A diagnosis of postmyocardial infarction syndrome was considered. Treatment consisted of digoxin and furosemide. Sodium warfarin was discontinued. One week after discharge, November 11, 1970, he was readmitted with fever, breathlessness and suprapubic pain. Physical examination revealed left costovertebral angle tenderness and hepatomegaly. Salicylates and, subsequently, prednisone were added to the therapeutic regimen. Soon after admission, evidence of cardiac tamponade appeared. Three hundred milliliters of sanguineous fluid were removed by pericardiocentesis on November 16, 1970. Roentgenograms, before and after this procedure, revealed a thickened pericardium ( Fig 2a and 2b). Culture of the pericardia! aspirate was positive for Salmonella typhimurium. Urine culture at this time was also positive for the same organism. The paratyphoid B titer was 1:1280. Chloramphenicol therapy was instituted and prednisone stopped on November 18, 1970. Temperature of 100.4•F dropped to normal. Clinical signs of cardiac constriction failed to abate. On December 1, 1970, he was transferred to Thomas Jefferson University Hospital, Philadelphia. On the day of transfer, blood pressure was 100/70, pulse rate 100 per minute and regular, respiratory rate 18 per minute and temperature 97•F orally. Pulsus paradoxus was present. Jugular venous distention was prominent at 45 degrees. Kussmaul's sign could not be elicited. Dullness was demonstrable at both bases. A gallop rhythm was present without murmurs or rubs. The liver was distended below the ri~t costal margin. Electrocardiogram showed Q waves in 2, 3, and a VF and ST-segment depression consistent with ischemia. Echocardiography again revealed the presence of pericardia! effusion. A pericardia! window was created at thoracotomy. At the time of surgery, a fibrotic, poorly contractile area of myocardium was present. Two days after surgery, the patient sustained a cardiorespiratory arrest. Resuscitation was unsuccessful.
B£FDRE PERICAROIDCENTESIS
CHEST WALL 4 LSB
FiGURE
effusion.
CHEST, VOL. 64, NO. 2, AUGUST, 1973
1. Echocardiogram of pericardia!
267
268
SCHATZ ET AL
FIGURE 2a. Chest x-ray film ( posteroanterior and lateral), prior to pericardiacentesis.
2b. Chest x-ray film ( posteroanterior and lateral), after pericardiocentesis and air injection. FIGURE
DISCUSSION
In 1933, Cossio and Berconsky described the course of a 64-year-old man with signs and symptoms of a myocardial infarction. He was hospitalized on the fourth day of his illness, developed pneumococcal pneumonia and died on the 14th hospital day. Cultures from the necrotic myocardial focus and the lungs were positive for Pneumococcus. Since then, 15 other cases, including the present case,2· 12 of myocardial infarction complicated by abscess formation have been reported (Table 1). All patients were elderly and had experienced recent myocardial infarction as determined from electrocardiograms or from autopsy. In most cases, manifestations of cardiac infection evolved acutely (within two weeks) or subacutely ( 3 weeks to 18 weeks) after myocardial infarction. Most commonly, Staphylococcus aureus was involved (five cases), but Pneumococcus, Bacteroides, E coli, Clostridia perfringens and SalmoneUa typhimurium have been reported. A concomitant infectious process involving the same organism in another site was demonstrated in eight of 16 cases. In ten out of 16 patients, the pericardium was involved. All but one patient died and, in most cases, diagnosis was not appreciated before death. Clinical recognition of this entity is dependent upon 1
pericardia! involvement and formation of effusion. Other causes of pericardia! effusion in the setting of acute myocardial infarction include transmural myocardial infarction with extension to the pericardium, postinfarction pericarditis (Dressler's syndrome), and congestive heart failure. The use of echocardiography and pericardiocentesis are suggested as appropriate measures to make the diagnosis. Infectious pericarditis following myocardial infarction is a potentially correctable lesion. An aggressive diagnostic approach is therefore warranted. This case was unusual in that cardiac involvement after myocardial infarction was due to Salmonella. The necrotic tissue of myocardium present after infarction seems to be a preferential site for organisms to settle during bacteremia. It was speculated that an indolent infectious site such as the gallbladder predisposes to recurrent bacteremia, ultimately taking hold in target organs when conditions become suitable. ACKNOWLEDGMENT: We wish to thank Miss Carol Hemelt for her assistance in preparing this report. REFERENCES
1 Cossio P, Berconsky 1: Absceso parietal del corazon e infarto del miocardio. Sem Med (B Aires) 2:1691-1698, 1933 2 Tedeschi C, Stevenson T, Levenson H: Abscess formation
CHEST, VOL 64, NO. 2, AUGUST, 1973
269
CONTINUOUS HEART MURMUR AFTER BYPASS· SURGERY
3 4 5 6 7 8 9 10 11 12
in myocardial infarction. N Eng! J Med 243:1024-1027, 1950 Miller R, Edwards J: Abscess formation in an acute myocardial infarct: Report of a case. Proc Staff Meet Mayo Clin 26:178-184, 1957 Weiss S, Wilkins R: Myocardial abscess with perforation of the heart. Am J Med Sci 194:199-205, 1937 Tennant R, Parks H: Myocardial abscesses. Arch Path 68:456-460, 1959 Katz A: Abscess of the myocardium complicating infarction: Report of two cases. Canad Med Assoc J 91:12251227, 1964 Korns M: Suppuration with rupture and tamponade. Am J Cardiol18:124-126, 1966 Murray M: Suppurative pericarditis complicating myocardial infarction. Br Med J 1:223-224, 1968 Canning B, Mulcahy R, Towers R: Abscess formation in an acute cardiac infarct. Br Med J 1: 164, 1969 Joffe S, Feil H: Subacute bacterial endocarditis arising in mural thrombi following a myocardial infarction: a case report. Circulation 12:242-246, 1955 Case Records of the Massachusetts General Hospital (Case 45-1970): N Eng! J Med 283:982-990, 1970 Case Records of the Massachusetts General Hospital (Case 27-1970): N Eng! J Med 282:1477-1485, 1970
Continuous Heart Murmur following Aorto-Coronary Bypass Surgery* Dennis}. Bauman, M.D., and Theofilos }. Tsagaris, M.D.
A patient is described with a continuous heart murmur which appeared following aort&coronary bypass graft surgery. Previously reported causes of a continuous murmur were virtually excluded by cOnical, BDgiograpbic and hemodynamic data. We speculate that the murmur is produced by turbulent flow related to the patent graft. he detection of a continuous murmur in a patient T who had undergone aorto-coronary bypass surgery stimulated the following case report.
CASE REPORT
A 55-year-old man was first seen in September, 1968 because of increasing angina pectoris. He had well documented myocardial infarctions in 1965 and again in early 1968, and began to note angina pectoris in 1966. A coronary arteriogram performed in May, 1969 was interpreted as showing severe obstruction of both the right and left anterior descending coronary arteries. The distal portions of these vessels were considered unsuitable for bypass grafting, and because of incapacitating angina both internal mammary arteries were implanted into the left ventricle ( Vineberg procedure) in July, 1969. Postoperatively, the patient was unimproved. High grade obstruction of the distal right and proximal obtuse marginal arteries was again noted on coronary arteriography on January 19, 1971, and, in addition, the proximal portion of the anterior descending artery was completely occluded. Attempts to visualize the internal mammary °From the Department of Medicine, University of Utah College of Me
CHEST, VOL. 64, NO. 2, AUGUST, 1973
implants arteriographically were unsuccessful. The left ventricular cavity was judged by ventriculography to be slightly enlarged with a small area of paradoxic pulsation in the anterior wall. On reevaluation of the patient's coronary lesions bypass grafting was thought to be feasible, and on November 16, 1971 saphenous vein bypass grafts were interposed between the ascending aorta and the distal portions of the right and left anterior descending coronary arteries. The right internal mammary implant was found to be occluded, and this vessel was ligated and divided. No trace of the left internal mammary implant could be found in the myocardium, and it is postulated that the vessel pulled out of the ventricle and retracted. Between September, 1968 and his bypass graft surgery in November, 1971 the patient had a total of 28 cardiovascular examinations recorded by 25 different observers, three of whom were senior staff cardiologists. A short grade 1/6 systolic ejection murmur at the apex and lower left sternal border was recorded on approximately one-third of these examinations. In no case was a diastolic or continuous murmur described. Following recovery from bypass graft surgery, the patient noted a definite decrease in the frequency of his angina. Upon admission to the Veterans Administration Hospital for follow-up study in April, 1972, he had a regular pulse of 82/minute and a brachial blood pressure of 146/80 mm Hg. The first and second heart sounds were normal, with physiologic splitting of the second sound. A continuous murmur of grade 1-2/6 intensity was quite well localized to the apex and heard best in the left lateral position. The murmur was heard by three different observers and was high-pitched and blowing in quality, beginning in the middle third of systole, reaching a peak at the second heart sound and continuing approximately half the way through diastole. At cardiac catheterization on April 27, 1972, both bypass grafts were selectively catheterized and shown to be patent. The site of distal anastomosis appeared significantly narrowed for the graft to the right, but not to the left anterior descending coronary artery. The ratio of the diameter of the graft to that of the anastomosis and the artery distal to the anastomosis was approximately 3:1:2 for the right and 2:1:1 for the left anterior descending. coronary artery. Contrast material injected into the anterior descending graft filled this artery in both an antegrade and retrograde fashion. Retrograde filling occurred across an area of severe narrowing adjacent to the anastomosis. The angiographically estimated site of anastomosis was at the level of the fourth intercostal space anteriorly for both grafts, and appeared to be approximately 3 em to the right of the mid sternal line for the right and 7 em to the left of the mid sternal line for the anterior descending graft. The location of the murmur thus corresponded closely to the estimated site of anastomosis of the anterior descending graft. The coronary arteriograms were unchanged from the study of January, 1971. There was no evidence of a coronary arteriovenous fistula or communication between a coronary artery or sinus of Valsalva and any other cardiac chamber. Slight dilatation of the left ventricular cavity and a small aneurysm of the anterior wall were still present. Resting pulmonary artery wedge pressure was 11 mm Hg and there were no valvular gradients. The contour of indicator dilution curves obtained by injecting indocyanine green dye into the pulmonary artery and sampling from the brachial artery was normal. DISCUSSION
There have been several case reports'·• of diastolic
A cue of Salmonella pericwditis is reported as • infectious complication of acute myocardial Infarction. A review of the literature reveals 15 other cases of postmyocardial infarction septic myocarditis, with or without pericarditis, and establishes this syndrome as an uncommon sequelae of myocardial Infarction. The appropriate diagnosis was made by WJe of ecbocardiograpby and pericardiocentesis. These diagnostic tools are useful in making a heretofore seldom recognized premortem diagnosis. complications at the site of acute myocardial Septic infarction are seldom recognized during life. Accu-
mulated case reports suggest that occasionally infections directly involving the heart may contribute to the morbidity of acute myocardial infarction. A case is presented describing the unusual complication of Salmonella pericarditis following acute myocardial infarction. CASE REPORT
This 62-year-old Caucasian man sustained an acute diaphragmatic myocardial infarction on July 27, 1970. Serial electrocardiograms and enzyme studies confirmed this diagnosis. With the exception of transient bradycardia and premature ventricular contractions, his course was uneventful. Twenty-one days after admission, he was discharged on oral anticoagulant therapy (sodium warfarin). °From the Division of Cardiology, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania. YK 308311
Pertinent past medical history included a subtotal gastrectomy performed in 1967 for a peptic ulcer. Three weelcs after discharge, he was hospitalized again for temperature elevation and cough. Hepatomegaly, ascites, and an elevated venous pressure were observed. A pericardia! friction rub was audible. Echocardiography was performed verifying the presence of pericardia! effusion (Fig 1 ) . A diagnosis of postmyocardial infarction syndrome was considered. Treatment consisted of digoxin and furosemide. Sodium warfarin was discontinued. One week after discharge, November 11, 1970, he was readmitted with fever, breathlessness and suprapubic pain. Physical examination revealed left costovertebral angle tenderness and hepatomegaly. Salicylates and, subsequently, prednisone were added to the therapeutic regimen. Soon after admission, evidence of cardiac tamponade appeared. Three hundred milliliters of sanguineous fluid were removed by pericardiocentesis on November 16, 1970. Roentgenograms, before and after this procedure, revealed a thickened pericardium ( Fig 2a and 2b). Culture of the pericardia! aspirate was positive for Salmonella typhimurium. Urine culture at this time was also positive for the same organism. The paratyphoid B titer was 1:1280. Chloramphenicol therapy was instituted and prednisone stopped on November 18, 1970. Temperature of 100.4•F dropped to normal. Clinical signs of cardiac constriction failed to abate. On December 1, 1970, he was transferred to Thomas Jefferson University Hospital, Philadelphia. On the day of transfer, blood pressure was 100/70, pulse rate 100 per minute and regular, respiratory rate 18 per minute and temperature 97•F orally. Pulsus paradoxus was present. Jugular venous distention was prominent at 45 degrees. Kussmaul's sign could not be elicited. Dullness was demonstrable at both bases. A gallop rhythm was present without murmurs or rubs. The liver was distended below the ri~t costal margin. Electrocardiogram showed Q waves in 2, 3, and a VF and ST-segment depression consistent with ischemia. Echocardiography again revealed the presence of pericardia! effusion. A pericardia! window was created at thoracotomy. At the time of surgery, a fibrotic, poorly contractile area of myocardium was present. Two days after surgery, the patient sustained a cardiorespiratory arrest. Resuscitation was unsuccessful.
B£FDRE PERICAROIDCENTESIS
CHEST WALL 4 LSB
FiGURE
effusion.
CHEST, VOL. 64, NO. 2, AUGUST, 1973
1. Echocardiogram of pericardia!
267
268
SCHATZ ET AL
FIGURE 2a. Chest x-ray film ( posteroanterior and lateral), prior to pericardiacentesis.
2b. Chest x-ray film ( posteroanterior and lateral), after pericardiocentesis and air injection. FIGURE
DISCUSSION
In 1933, Cossio and Berconsky described the course of a 64-year-old man with signs and symptoms of a myocardial infarction. He was hospitalized on the fourth day of his illness, developed pneumococcal pneumonia and died on the 14th hospital day. Cultures from the necrotic myocardial focus and the lungs were positive for Pneumococcus. Since then, 15 other cases, including the present case,2· 12 of myocardial infarction complicated by abscess formation have been reported (Table 1). All patients were elderly and had experienced recent myocardial infarction as determined from electrocardiograms or from autopsy. In most cases, manifestations of cardiac infection evolved acutely (within two weeks) or subacutely ( 3 weeks to 18 weeks) after myocardial infarction. Most commonly, Staphylococcus aureus was involved (five cases), but Pneumococcus, Bacteroides, E coli, Clostridia perfringens and SalmoneUa typhimurium have been reported. A concomitant infectious process involving the same organism in another site was demonstrated in eight of 16 cases. In ten out of 16 patients, the pericardium was involved. All but one patient died and, in most cases, diagnosis was not appreciated before death. Clinical recognition of this entity is dependent upon 1
pericardia! involvement and formation of effusion. Other causes of pericardia! effusion in the setting of acute myocardial infarction include transmural myocardial infarction with extension to the pericardium, postinfarction pericarditis (Dressler's syndrome), and congestive heart failure. The use of echocardiography and pericardiocentesis are suggested as appropriate measures to make the diagnosis. Infectious pericarditis following myocardial infarction is a potentially correctable lesion. An aggressive diagnostic approach is therefore warranted. This case was unusual in that cardiac involvement after myocardial infarction was due to Salmonella. The necrotic tissue of myocardium present after infarction seems to be a preferential site for organisms to settle during bacteremia. It was speculated that an indolent infectious site such as the gallbladder predisposes to recurrent bacteremia, ultimately taking hold in target organs when conditions become suitable. ACKNOWLEDGMENT: We wish to thank Miss Carol Hemelt for her assistance in preparing this report. REFERENCES
1 Cossio P, Berconsky 1: Absceso parietal del corazon e infarto del miocardio. Sem Med (B Aires) 2:1691-1698, 1933 2 Tedeschi C, Stevenson T, Levenson H: Abscess formation
CHEST, VOL 64, NO. 2, AUGUST, 1973
269
CONTINUOUS HEART MURMUR AFTER BYPASS· SURGERY
3 4 5 6 7 8 9 10 11 12
in myocardial infarction. N Eng! J Med 243:1024-1027, 1950 Miller R, Edwards J: Abscess formation in an acute myocardial infarct: Report of a case. Proc Staff Meet Mayo Clin 26:178-184, 1957 Weiss S, Wilkins R: Myocardial abscess with perforation of the heart. Am J Med Sci 194:199-205, 1937 Tennant R, Parks H: Myocardial abscesses. Arch Path 68:456-460, 1959 Katz A: Abscess of the myocardium complicating infarction: Report of two cases. Canad Med Assoc J 91:12251227, 1964 Korns M: Suppuration with rupture and tamponade. Am J Cardiol18:124-126, 1966 Murray M: Suppurative pericarditis complicating myocardial infarction. Br Med J 1:223-224, 1968 Canning B, Mulcahy R, Towers R: Abscess formation in an acute cardiac infarct. Br Med J 1: 164, 1969 Joffe S, Feil H: Subacute bacterial endocarditis arising in mural thrombi following a myocardial infarction: a case report. Circulation 12:242-246, 1955 Case Records of the Massachusetts General Hospital (Case 45-1970): N Eng! J Med 283:982-990, 1970 Case Records of the Massachusetts General Hospital (Case 27-1970): N Eng! J Med 282:1477-1485, 1970
Continuous Heart Murmur following Aorto-Coronary Bypass Surgery* Dennis}. Bauman, M.D., and Theofilos }. Tsagaris, M.D.
A patient is described with a continuous heart murmur which appeared following aort&coronary bypass graft surgery. Previously reported causes of a continuous murmur were virtually excluded by cOnical, BDgiograpbic and hemodynamic data. We speculate that the murmur is produced by turbulent flow related to the patent graft. he detection of a continuous murmur in a patient T who had undergone aorto-coronary bypass surgery stimulated the following case report.
CASE REPORT
A 55-year-old man was first seen in September, 1968 because of increasing angina pectoris. He had well documented myocardial infarctions in 1965 and again in early 1968, and began to note angina pectoris in 1966. A coronary arteriogram performed in May, 1969 was interpreted as showing severe obstruction of both the right and left anterior descending coronary arteries. The distal portions of these vessels were considered unsuitable for bypass grafting, and because of incapacitating angina both internal mammary arteries were implanted into the left ventricle ( Vineberg procedure) in July, 1969. Postoperatively, the patient was unimproved. High grade obstruction of the distal right and proximal obtuse marginal arteries was again noted on coronary arteriography on January 19, 1971, and, in addition, the proximal portion of the anterior descending artery was completely occluded. Attempts to visualize the internal mammary °From the Department of Medicine, University of Utah College of Me
CHEST, VOL. 64, NO. 2, AUGUST, 1973
implants arteriographically were unsuccessful. The left ventricular cavity was judged by ventriculography to be slightly enlarged with a small area of paradoxic pulsation in the anterior wall. On reevaluation of the patient's coronary lesions bypass grafting was thought to be feasible, and on November 16, 1971 saphenous vein bypass grafts were interposed between the ascending aorta and the distal portions of the right and left anterior descending coronary arteries. The right internal mammary implant was found to be occluded, and this vessel was ligated and divided. No trace of the left internal mammary implant could be found in the myocardium, and it is postulated that the vessel pulled out of the ventricle and retracted. Between September, 1968 and his bypass graft surgery in November, 1971 the patient had a total of 28 cardiovascular examinations recorded by 25 different observers, three of whom were senior staff cardiologists. A short grade 1/6 systolic ejection murmur at the apex and lower left sternal border was recorded on approximately one-third of these examinations. In no case was a diastolic or continuous murmur described. Following recovery from bypass graft surgery, the patient noted a definite decrease in the frequency of his angina. Upon admission to the Veterans Administration Hospital for follow-up study in April, 1972, he had a regular pulse of 82/minute and a brachial blood pressure of 146/80 mm Hg. The first and second heart sounds were normal, with physiologic splitting of the second sound. A continuous murmur of grade 1-2/6 intensity was quite well localized to the apex and heard best in the left lateral position. The murmur was heard by three different observers and was high-pitched and blowing in quality, beginning in the middle third of systole, reaching a peak at the second heart sound and continuing approximately half the way through diastole. At cardiac catheterization on April 27, 1972, both bypass grafts were selectively catheterized and shown to be patent. The site of distal anastomosis appeared significantly narrowed for the graft to the right, but not to the left anterior descending coronary artery. The ratio of the diameter of the graft to that of the anastomosis and the artery distal to the anastomosis was approximately 3:1:2 for the right and 2:1:1 for the left anterior descending. coronary artery. Contrast material injected into the anterior descending graft filled this artery in both an antegrade and retrograde fashion. Retrograde filling occurred across an area of severe narrowing adjacent to the anastomosis. The angiographically estimated site of anastomosis was at the level of the fourth intercostal space anteriorly for both grafts, and appeared to be approximately 3 em to the right of the mid sternal line for the right and 7 em to the left of the mid sternal line for the anterior descending graft. The location of the murmur thus corresponded closely to the estimated site of anastomosis of the anterior descending graft. The coronary arteriograms were unchanged from the study of January, 1971. There was no evidence of a coronary arteriovenous fistula or communication between a coronary artery or sinus of Valsalva and any other cardiac chamber. Slight dilatation of the left ventricular cavity and a small aneurysm of the anterior wall were still present. Resting pulmonary artery wedge pressure was 11 mm Hg and there were no valvular gradients. The contour of indicator dilution curves obtained by injecting indocyanine green dye into the pulmonary artery and sampling from the brachial artery was normal. DISCUSSION
There have been several case reports'·• of diastolic