CASE
REPORTS
Acute Coronary Embolism Complicating Bacterial
Endocarditis:
JAMES F. PFEIFER, MARTIN J. LIPTON,
MD, MD
Palo Alto and Stanford,
Treatment
A patient with bacterial endocarditis and no previous history of angina sustained an acute anterolateral myocardial infarction while awaiting surgery. Selective coronary arteriography revealed a filling defect in the left anterior descending coronary artery with limited flow beyond the area of occlusion. A calcific embolus from the infected aortic valve was removed at the time of valve replacement, and the patient had an uneventful immediate postoperative course. Late postoperatively paravalvular aortic regurgitation recurred before and after a second repair.
FACC
JAMES H. OURY, MD WILLIAM W. ANGELL, MD HERBERT N. HULTGREN, MD,
Operative
FACC
California
Coronary arterial occlusion complicating acute bacterial endocarditis was first described in 18.56 by Virch0w.l It was thought to be a fatal complication until Massafia diagnosed it in a living patient in 1948.2 Wenger and BaueS and later Cordeiro et al4 reviewed coronary arterial embolism and believed that it could be diagnosed during life although nearly every case was proved only at autopsy. This report illustrates use of selective coronary arteriography in diagnosis of an embolus due to bacterial endocarditis. The clinical findings, course and the patient’s subsequent management and recovery are discussed. Case Report
From the Cardiology,
Radiology and CardiovasDivisions, Veterans Administration Hospital, Palo Alto, Calif. and Stanford University, Stanford, Calif. Manuscript accepted January 29, 1975. Address for reprints: James F. Pfeifer, MD, 3300 Webster St., Suite 306, Oakland, Calif. cular
Surgery
94609.
920
May 1976
The American
Journal
A 48 year old steel worker was admitted to another hospital in the Southwest on January 12, 1972. During the previous September he became symptomatic with pyorrhea. In October he had fatigue and weight loss and in December he noted fever and chills. A course of quinacrine was given 1 month before this admission, since malaria was suspected. Physical examination on this admission revealed a confused acutely ill man with signs of severe aortic regurgitation and left ventricular failure. Splinter hemorrhages, petechiae, enlarged spleen and liver and right facial weakness were noted. The blood hemoglobin level was 9.8 g/l00 ml. Blood cultures grew Streptococcus viridans. The patient had a history of anaphylaxis to penicillin and was therefore treated with parenterally administered vancomycin and streptomycin. The organism was sensitive to vancomycin. The signs of left heart failure and disorientation decreased. On February 3 he was transferred to the Palo Alto Veterans Administration Hospital for evaluation for valve replacement. Three days after admission, he experienced severe substernal chest pain while at rest in bed. He had had no previous angina. During the next 24 hours signs of left heart failure developed, and a triphasic friction rub was heard along the left sternal border. In addition to the diastolic decrescendo murmur at the base, third and fourth sound gallops were heard. Bibasilar rales developed, and chest X-ray findings were compatible with pulmonary edema. Twelve hours after the onset of chest pain, the electrocardiogram (Fig. 1) and serum enzyme levels (Table I) were compatible with an acute anterolateral myocardial infarction. Because the patient did not respond to the usual therapy for congestive heart failure, surgery was believed indicated, but selective coronary arteriography was performed first to rule out the possibility of coronary embolism.
of CARDIOLOGY
Volume
37
CORONARY
Selective coronary angiography revealed a filling defect in the mid-portion of the left anterior descending coronary artery (Fig. 2); the other coronary arteries were normal. An aortic root injection revealed 4+ aortic regurgitation. At operation, the aortic valve was removed. It was calcified and covered with vegetations. There was a small area of purulent material around the base of the aorta. A no. 13 Starr-Edwards prosthesis was sewn into the valve ring. Subsequently, a small incision was made distal to the occluded area in the left anterior descending coronary artery. Minimal flow was seen when the artery was opened. A Fogarty catheter was passed in retrograde manner, and a small embolus was removed (Fig. 3). Excellent flow was established before closure of the arteriotomy.
EMBOLISM
IN
BACTERIAL
ENDOCARDITIS-PFEIFER
ET
AL.
Although the evolutionary changes of an acute anterior myocardial occurred, the patient had an uneventful postoperative course and was discharged in 3 weeks. However, a regurgitant murmur developed shortly after his return home and he had symptoms of mild congestive heart failure. He was readmitted, and an aortic root angiogram demonstrated a 3+ paravalvular regurgitant jet around the noncoronary cusp. At reoperation the valve was repaired with placement of an external Teflon@ bolster around the aorta. The patient was discharged 2 weeks later without evidence of endocarditis or a paravalvular leak, but returned 9 months later with recurrence of the paravalvular leak. Thirty months after the original valve replacement he continues to have symptoms of mild congestive failure and recurrent pleural effusions but has refused further surgical treatment.
Discussion The patient’s sudden severe chest pain and the apan acute myocardial pearance of Q waves suggested
2-3
2-6
2-6
(11.30)
2-3 MR
Z-6
FIGURE 2. Contrast injection of the left coronary artery in the right anterior oblique projection reveals a 4 to 5 cm long intraluminal filling defect in the mid portion of the left anterior descending artery created by an embolus originating from the diseased aortic valve. There is only partial occlusion, as evidenced by some filling of the distal segment of the vessel.
2-6
(11.30)
RW
FIGURE 1. Electrocardiograms obtained on February 3 and on February 6 at 11:30 AM (center) and 9:00 PM (right). Acute S-T segment elevation with Cl waves in leads I, aVL and V2 to Vs.
TABLE
I
Preoperative
Serum
Enzyme
Levels (units) Feb. 6
Serum Enzymes CPK GOT GPT LDH
9100 AM 10 30 4%
Feb. 7 5:30
PM
6100 AM 180
212 1’520
360 48 3015
CPK = creaune phosphokinase; LDH = lactic dehydrogenase; GOT = glutamic oxaloacetic transaminase; GPT = glutamic pyruv~c transaminase.
FIGURE 3. Fresh blood clot and calcific material, 1.5 cm long and 0.1 cm in diameter, taken from the left anterior descending coronary artery.
May 1976
The American
Journal
of CARDIOLOGY
Volume
37
921
CORONARY
EMBOLISM IN BACTERIAL ENDOCARDITIS-PFEIFER
ET AL.
infarction, which was confirmed by subsequent serum enzyme elevations. In addition, acute left ventricular failure with pulmonary edema developed. Urgent replacement of the regurgitant aortic valve was indicated since the patient’s condition deteriorated with medical management. Surgical replacement of heart valves in infectious endocarditis even when the disease is active is performed with increasing frequency.5-g It has been recommended particularly when there is recurrent peripheral embolism, congestive heart failure unrelieved by medical treatment, severe aortic or mitral regurgitation or resistant bacteremia despite adequate and appropriate antibiotic therapy.iO The diagnosis of coronary arterial embolism should be considered in a patient with known bacterial endocarditis who has the signs and symptoms of an acute myocardial infarction. Because acute myocardial ischemia has been shown to be reversible provided the period of acute occlusion is brief,i’ immediate complete embolectomy might be expected to restore adequate myocardial perfusion and perhaps prevent or limit myocardial infarction. The deleterious effects of reperfusion after coronary occlusion as described by Bresnahan et a1.12 apparently have two patterns. Extension of infarction with hemorrhage as well as reduction in infarct size were both seen when reperfusion was initiated 5 hours after occlusion. Cheanvechai et a1.13 suggested that most of the myocardium will be preserved if revascularization is carried out within 6 hours of the acute infarction. Cohn et al.‘” performed emergency coronary bypass grafting in eight patients with documented acute coronary obstruction that had usually occurred during coronary angiography. One patient in their group was observed for 36 hours before operation and although he had progressive enzymatic and electrocardiographic evidence of anterolateral infarction, his discharge electrocardiogram demonstrated no new infarct and only minor T wave changes over the anterior lateral precordium.
Our patient did not have an area of long-standing ischemia with attendant collateral development as would be the case in a patient with underlying coronary artery disease. Contrast medium was seen beyond the embolus in the left anterior descending coronary artery, and it is conceivable that there was an area of marginal perfusion in the surrounding area. A large zone of marginal ischemia around an acute infarct has been shown to decrease up to 4 hours in some cases in primate experiments.‘” Although 18 hours had elapsed since the pattern of acute infarction was apparent in the electrocardiogram, reperfusion of the ischemic area was accomplished by removing the obstructing embolus. Whether this resulted in extension or reduction of the infarct is not clear; however, the further elevation of serum enzyme levels suggests the former. This partially occluded area might have progressed to total occlusion as a result of thrombus formation on the embolus or a change in position of the embolus. These possibilities favored embolectomy. Finally, no adequate data are available on the mechanism of mycotic aneurysm formation, and it is conceivable that a bacterial embolism might later lead to the development of a coronary arterial aneurysm at its site with the attendant risks, including rupture.16 Coronary arteriography and surgery can be accomplished in a patient who has a pattern of an acute evolving injury in the electrocardiogram and, although arteriography causes significant added risk to the patient,17 we believe that the study is essential for complete evaluation and subsequent management. Addendum Since submission of this paper, we have learned that the patient was admitted to the referring Veterans Administration Hospital on November 10, 1974 with gastrointestinal symptoms, vomiting and loose stools. Several days after he was permitted out of bed, he apparently collapsed and was found dead. Autopsy was not permitted.
References 1. Virchow 2. 3.
4. 5. 6.
7. 8.
9.
922
10.
Wallace AG, Young GW, Osterhout S: Treatment of acute bacterial endocarditis by valve excision and replacement. Circulation 31:450-453, 1965 11. Cox JL, Daniel TM, Boineau JP: The electrophysiologic timecourse of acute myocardial ischemia and the effects of early coronary artery perfusion. Circulation 48:971-983, 1973 12. Bresnahan GF, Roberts R, Shell WE, et al: Deleterious effects due to hemorrhage after myocardial reperfusion. Am J Cardiol 33:82-86, 1974 C, Effler DB, Loop FD, et al: Emergency myocar13. Cheanvechai dial revascularization. Am J Cardiol 32:901-908, 1973 bypass 14. Cohn LH, Gorlin R, Herman MV, et al: Aorto-coronary for acute coronary occlusion. J Thorac Cardiovasc Surg 64: 503-513.1972 15. McNamara JJ, Smith GT, Suehiro GT, et al: Myocardial viability after transient ischemia in primates. J Thorac Cardiovasc Surg 68:248-256, 1974 16. Crook BR, Raftery EB, Oram S: Mycotic aneurysms of coronary arteries. Br Heart J 35:107-109, 1973 R, Moran J, et al: Accelerated angina 17. Scanlon P, Nemickas pectoris: clinical, hemodynamic, arteriographic and therapeutic experience in 85 patients. Circulation 47:19-26, 1973
R: uber capillare embolie. Virchows Arch Pathol Anat 9:307-308, 1856 Massafia A: Embolia coronarica in torso di endocardite batterica subacuta. Cuore Circolaz 32:91-95, 1948 Wenger NK, Bauer S: Coronary embolism. Review of the literature and presentation of fifteen cases. Am J Med 5499557, 1958 Cordeiro A, Pimentel C, Laginha F, et al: Coronary embolism. Am Heart J 29:91-95, 1967 Griffin FM, Jones G, Cobbs CG: Aortic insufficiency in bacterial endocarditis. Ann Intern Med 76:23-28, 1972 Kaiser GC, Willman VL, Thurmann M, et al: Valve replacement in cases of aortic insufficiency due to active endocarditis. J Thorac Cardiovasc Surg 54:491-502. 1967 Manhas DR, Hessel EA, Winterscheid LC, et al: Open heart surgery in infective endocarditis. Circulation 41:841-848, 1970 Neville WE, Magno M, Foxworthy DT, et al: Emergency aortic valve replacement in bacterial endocarditis. J Thorac Cardiovast Surg 61:916-923, 1971 Hancock EW, Shumway NE, Remington JS: Valve replacement in active bacterial endocarditis. J Infect Dis 123: 106-109, 1971
May 1976
The American
Journal
of CARDIOLOGY
Volume
37
REPORTS
Acute Coronary Embolism Complicating Bacterial
Endocarditis:
JAMES F. PFEIFER, MARTIN J. LIPTON,
MD, MD
Palo Alto and Stanford,
Treatment
A patient with bacterial endocarditis and no previous history of angina sustained an acute anterolateral myocardial infarction while awaiting surgery. Selective coronary arteriography revealed a filling defect in the left anterior descending coronary artery with limited flow beyond the area of occlusion. A calcific embolus from the infected aortic valve was removed at the time of valve replacement, and the patient had an uneventful immediate postoperative course. Late postoperatively paravalvular aortic regurgitation recurred before and after a second repair.
FACC
JAMES H. OURY, MD WILLIAM W. ANGELL, MD HERBERT N. HULTGREN, MD,
Operative
FACC
California
Coronary arterial occlusion complicating acute bacterial endocarditis was first described in 18.56 by Virch0w.l It was thought to be a fatal complication until Massafia diagnosed it in a living patient in 1948.2 Wenger and BaueS and later Cordeiro et al4 reviewed coronary arterial embolism and believed that it could be diagnosed during life although nearly every case was proved only at autopsy. This report illustrates use of selective coronary arteriography in diagnosis of an embolus due to bacterial endocarditis. The clinical findings, course and the patient’s subsequent management and recovery are discussed. Case Report
From the Cardiology,
Radiology and CardiovasDivisions, Veterans Administration Hospital, Palo Alto, Calif. and Stanford University, Stanford, Calif. Manuscript accepted January 29, 1975. Address for reprints: James F. Pfeifer, MD, 3300 Webster St., Suite 306, Oakland, Calif. cular
Surgery
94609.
920
May 1976
The American
Journal
A 48 year old steel worker was admitted to another hospital in the Southwest on January 12, 1972. During the previous September he became symptomatic with pyorrhea. In October he had fatigue and weight loss and in December he noted fever and chills. A course of quinacrine was given 1 month before this admission, since malaria was suspected. Physical examination on this admission revealed a confused acutely ill man with signs of severe aortic regurgitation and left ventricular failure. Splinter hemorrhages, petechiae, enlarged spleen and liver and right facial weakness were noted. The blood hemoglobin level was 9.8 g/l00 ml. Blood cultures grew Streptococcus viridans. The patient had a history of anaphylaxis to penicillin and was therefore treated with parenterally administered vancomycin and streptomycin. The organism was sensitive to vancomycin. The signs of left heart failure and disorientation decreased. On February 3 he was transferred to the Palo Alto Veterans Administration Hospital for evaluation for valve replacement. Three days after admission, he experienced severe substernal chest pain while at rest in bed. He had had no previous angina. During the next 24 hours signs of left heart failure developed, and a triphasic friction rub was heard along the left sternal border. In addition to the diastolic decrescendo murmur at the base, third and fourth sound gallops were heard. Bibasilar rales developed, and chest X-ray findings were compatible with pulmonary edema. Twelve hours after the onset of chest pain, the electrocardiogram (Fig. 1) and serum enzyme levels (Table I) were compatible with an acute anterolateral myocardial infarction. Because the patient did not respond to the usual therapy for congestive heart failure, surgery was believed indicated, but selective coronary arteriography was performed first to rule out the possibility of coronary embolism.
of CARDIOLOGY
Volume
37
CORONARY
Selective coronary angiography revealed a filling defect in the mid-portion of the left anterior descending coronary artery (Fig. 2); the other coronary arteries were normal. An aortic root injection revealed 4+ aortic regurgitation. At operation, the aortic valve was removed. It was calcified and covered with vegetations. There was a small area of purulent material around the base of the aorta. A no. 13 Starr-Edwards prosthesis was sewn into the valve ring. Subsequently, a small incision was made distal to the occluded area in the left anterior descending coronary artery. Minimal flow was seen when the artery was opened. A Fogarty catheter was passed in retrograde manner, and a small embolus was removed (Fig. 3). Excellent flow was established before closure of the arteriotomy.
EMBOLISM
IN
BACTERIAL
ENDOCARDITIS-PFEIFER
ET
AL.
Although the evolutionary changes of an acute anterior myocardial occurred, the patient had an uneventful postoperative course and was discharged in 3 weeks. However, a regurgitant murmur developed shortly after his return home and he had symptoms of mild congestive heart failure. He was readmitted, and an aortic root angiogram demonstrated a 3+ paravalvular regurgitant jet around the noncoronary cusp. At reoperation the valve was repaired with placement of an external Teflon@ bolster around the aorta. The patient was discharged 2 weeks later without evidence of endocarditis or a paravalvular leak, but returned 9 months later with recurrence of the paravalvular leak. Thirty months after the original valve replacement he continues to have symptoms of mild congestive failure and recurrent pleural effusions but has refused further surgical treatment.
Discussion The patient’s sudden severe chest pain and the apan acute myocardial pearance of Q waves suggested
2-3
2-6
2-6
(11.30)
2-3 MR
Z-6
FIGURE 2. Contrast injection of the left coronary artery in the right anterior oblique projection reveals a 4 to 5 cm long intraluminal filling defect in the mid portion of the left anterior descending artery created by an embolus originating from the diseased aortic valve. There is only partial occlusion, as evidenced by some filling of the distal segment of the vessel.
2-6
(11.30)
RW
FIGURE 1. Electrocardiograms obtained on February 3 and on February 6 at 11:30 AM (center) and 9:00 PM (right). Acute S-T segment elevation with Cl waves in leads I, aVL and V2 to Vs.
TABLE
I
Preoperative
Serum
Enzyme
Levels (units) Feb. 6
Serum Enzymes CPK GOT GPT LDH
9100 AM 10 30 4%
Feb. 7 5:30
PM
6100 AM 180
212 1’520
360 48 3015
CPK = creaune phosphokinase; LDH = lactic dehydrogenase; GOT = glutamic oxaloacetic transaminase; GPT = glutamic pyruv~c transaminase.
FIGURE 3. Fresh blood clot and calcific material, 1.5 cm long and 0.1 cm in diameter, taken from the left anterior descending coronary artery.
May 1976
The American
Journal
of CARDIOLOGY
Volume
37
921
CORONARY
EMBOLISM IN BACTERIAL ENDOCARDITIS-PFEIFER
ET AL.
infarction, which was confirmed by subsequent serum enzyme elevations. In addition, acute left ventricular failure with pulmonary edema developed. Urgent replacement of the regurgitant aortic valve was indicated since the patient’s condition deteriorated with medical management. Surgical replacement of heart valves in infectious endocarditis even when the disease is active is performed with increasing frequency.5-g It has been recommended particularly when there is recurrent peripheral embolism, congestive heart failure unrelieved by medical treatment, severe aortic or mitral regurgitation or resistant bacteremia despite adequate and appropriate antibiotic therapy.iO The diagnosis of coronary arterial embolism should be considered in a patient with known bacterial endocarditis who has the signs and symptoms of an acute myocardial infarction. Because acute myocardial ischemia has been shown to be reversible provided the period of acute occlusion is brief,i’ immediate complete embolectomy might be expected to restore adequate myocardial perfusion and perhaps prevent or limit myocardial infarction. The deleterious effects of reperfusion after coronary occlusion as described by Bresnahan et a1.12 apparently have two patterns. Extension of infarction with hemorrhage as well as reduction in infarct size were both seen when reperfusion was initiated 5 hours after occlusion. Cheanvechai et a1.13 suggested that most of the myocardium will be preserved if revascularization is carried out within 6 hours of the acute infarction. Cohn et al.‘” performed emergency coronary bypass grafting in eight patients with documented acute coronary obstruction that had usually occurred during coronary angiography. One patient in their group was observed for 36 hours before operation and although he had progressive enzymatic and electrocardiographic evidence of anterolateral infarction, his discharge electrocardiogram demonstrated no new infarct and only minor T wave changes over the anterior lateral precordium.
Our patient did not have an area of long-standing ischemia with attendant collateral development as would be the case in a patient with underlying coronary artery disease. Contrast medium was seen beyond the embolus in the left anterior descending coronary artery, and it is conceivable that there was an area of marginal perfusion in the surrounding area. A large zone of marginal ischemia around an acute infarct has been shown to decrease up to 4 hours in some cases in primate experiments.‘” Although 18 hours had elapsed since the pattern of acute infarction was apparent in the electrocardiogram, reperfusion of the ischemic area was accomplished by removing the obstructing embolus. Whether this resulted in extension or reduction of the infarct is not clear; however, the further elevation of serum enzyme levels suggests the former. This partially occluded area might have progressed to total occlusion as a result of thrombus formation on the embolus or a change in position of the embolus. These possibilities favored embolectomy. Finally, no adequate data are available on the mechanism of mycotic aneurysm formation, and it is conceivable that a bacterial embolism might later lead to the development of a coronary arterial aneurysm at its site with the attendant risks, including rupture.16 Coronary arteriography and surgery can be accomplished in a patient who has a pattern of an acute evolving injury in the electrocardiogram and, although arteriography causes significant added risk to the patient,17 we believe that the study is essential for complete evaluation and subsequent management. Addendum Since submission of this paper, we have learned that the patient was admitted to the referring Veterans Administration Hospital on November 10, 1974 with gastrointestinal symptoms, vomiting and loose stools. Several days after he was permitted out of bed, he apparently collapsed and was found dead. Autopsy was not permitted.
References 1. Virchow 2. 3.
4. 5. 6.
7. 8.
9.
922
10.
Wallace AG, Young GW, Osterhout S: Treatment of acute bacterial endocarditis by valve excision and replacement. Circulation 31:450-453, 1965 11. Cox JL, Daniel TM, Boineau JP: The electrophysiologic timecourse of acute myocardial ischemia and the effects of early coronary artery perfusion. Circulation 48:971-983, 1973 12. Bresnahan GF, Roberts R, Shell WE, et al: Deleterious effects due to hemorrhage after myocardial reperfusion. Am J Cardiol 33:82-86, 1974 C, Effler DB, Loop FD, et al: Emergency myocar13. Cheanvechai dial revascularization. Am J Cardiol 32:901-908, 1973 bypass 14. Cohn LH, Gorlin R, Herman MV, et al: Aorto-coronary for acute coronary occlusion. J Thorac Cardiovasc Surg 64: 503-513.1972 15. McNamara JJ, Smith GT, Suehiro GT, et al: Myocardial viability after transient ischemia in primates. J Thorac Cardiovasc Surg 68:248-256, 1974 16. Crook BR, Raftery EB, Oram S: Mycotic aneurysms of coronary arteries. Br Heart J 35:107-109, 1973 R, Moran J, et al: Accelerated angina 17. Scanlon P, Nemickas pectoris: clinical, hemodynamic, arteriographic and therapeutic experience in 85 patients. Circulation 47:19-26, 1973
R: uber capillare embolie. Virchows Arch Pathol Anat 9:307-308, 1856 Massafia A: Embolia coronarica in torso di endocardite batterica subacuta. Cuore Circolaz 32:91-95, 1948 Wenger NK, Bauer S: Coronary embolism. Review of the literature and presentation of fifteen cases. Am J Med 5499557, 1958 Cordeiro A, Pimentel C, Laginha F, et al: Coronary embolism. Am Heart J 29:91-95, 1967 Griffin FM, Jones G, Cobbs CG: Aortic insufficiency in bacterial endocarditis. Ann Intern Med 76:23-28, 1972 Kaiser GC, Willman VL, Thurmann M, et al: Valve replacement in cases of aortic insufficiency due to active endocarditis. J Thorac Cardiovasc Surg 54:491-502. 1967 Manhas DR, Hessel EA, Winterscheid LC, et al: Open heart surgery in infective endocarditis. Circulation 41:841-848, 1970 Neville WE, Magno M, Foxworthy DT, et al: Emergency aortic valve replacement in bacterial endocarditis. J Thorac Cardiovast Surg 61:916-923, 1971 Hancock EW, Shumway NE, Remington JS: Valve replacement in active bacterial endocarditis. J Infect Dis 123: 106-109, 1971
May 1976
The American
Journal
of CARDIOLOGY
Volume
37
