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Clinical and echocardiographic observations in pulmonary valve endocarditis
Clinical and Echocardiographic Observations in Pulmonary Valve Endocarditis ANNE-CLAUDE CREMIEUX, MD, SERGE WlTCHITZ, MD, MARIE-CHRISTINE MALERGUE, MD, MICHEL WOLFF, MD, DANIEL VITTECOCQ, MD, JEAN-LOUIS VILDE, MD, JACQUES FROTTIER, MD, PIERRE ETIENNE VALERE, MD, CLAUDE GIBERT, MD, and ADRIEN G. SAIMOT, MD
Candida guillermondii in 1. M-mode and P-dimensional echocardiography was performed in 10 patients and revealed vegetations in 8. Pulsed Doppler echocardiography was performed in 6 patients and revealed pulmonary regurgitation in all 6. Seven patients had pulmonary emboli. Four patients underwent surgery. Four patients died, including 1 after cardiac surgery. Five patients, including the patient infected with Candida guillermondii, recovered with antibiotic treatment. (Am J Cardiol 1985;56:610-613)
Clinical and echocardiographic data from 12 patients with pulmonary valve endocarditis are described. Seven patients had isolated pulmonary endocarditis and in 5 patients other valves were infected (aortic, tricuspid, mitral or all 3). Two patients were heroin addicts and 4 had underlying heart disease (congenital heart disease in 3 and aortic regurgitation in 1 patient). The organisms involved were alpha sfrepfococci in 3 patients (all with underlying heart disease), Sfaphylococcus aureus in 4, Sfrepfococcus D bovis in 1 patient and
were systematically examined using the usual methods. Several recordings were made during follow-up. Diagnosis of vegetations was made when abnormal, shaggy, irregular echoes were seen on or near 1 or 2 pulmonary cusps and the motion of the cusps was not restricted. Six patients underwent 2-D pulsed Doppler echocardiographic examinations with an ATL Mark 500 mechanical scanner. The sample volume (2 mm) was positioned along an M-mode line simultaneously with the 2-D image. For the PV examination, the sample volume was placed just below the pulmonary cusps in a short-view axis. PV regurgitation was demonstrated when abnormal positive diastolic turbulence was recorded toward the transducer and the pulmonary ejection signal moved away from the transducer.
Pulmonary valve (PV) endocarditis is rare. Only 47 cases have been reported since 1960,1-2g most of these being 1 or 2 cases of drug addicts or patients with congential heart disease. We report 12 patients with PV endocarditis.
Methods Twelve cases of PV endocarditis were observed at Claude Bernard and Bichat Hospitals between 1972 and 1984. The diagnosis of PV endocarditis was made on the basis that septicemia was present and the PV was affected. PV involvement was confirmed by anatomic examination (surgery or autopsy), echocardiographic images of vegetations or by recent PV regurgitation diagnose by auscultation or pulsed Doppler echocardiography. Echocardiography: Ten patients had echocardiographic examinations (M-mode and 2-dimensional[2-D] in 9 patients and M-mode alone in 1 patient). The echocardiographic examination was done either with a phased-array sector scanner (RT 400) with an M-mode type Irex II or with a mechanical sector scanner (ATL Mark 500) with a 3 MHz in-line transducer. PV recording was done in the short-axis view and the transducer was placed on the third or fourth intercostal space in a parasternal view visualizing the pulmonary outflow tract. The valves, the size of the right ventricle and septal motion
Results The clinical and bacteriologic results are summarized in Table I. Clinical findings: The patients were 3 to 61 years old (mean 34). Eleven patients were men (92%). The patients were separated into 2 groups. Group I included 4 patients with underlying heart disease (congenital in 3). Group II included 8 patients with primitive PV endocarditis (2 heroin addicts, 2 alcoholics and 4 with no predisposing factors). Seven patients (59%) had isolated PV endocarditis and in 5 patients other valves were infected (aortic in 1 patient, tricuspid in 2 patients, mitral in 1 and all 3 valves in 1). Fever was present in all cases. A typical PV regurgitation murmur was found in only 3 patients (25%), all in group II. Associated aortic regurgitation masked the pulmonary auscultation in 2 other patients. One patient
From the Departments of Infectious and Tropical Diseases and the Intensive Care Unit, Claude Bernard Hospital, and the Departments of Cardiology and the Intensive Care Unlt, Bichat Hospital, Paris, France. Manuscript received November 26, 1984; revised manuscript received May 1, 1985, accepted May 2, 1985. Address for reprints: Anne-Claude Cremieux, MD, lnstitut de Medetine et d’Epidemiologie Tropicales, Hopital Claude Bernard, 10 avenue Porte d’Aubervilliers, 75019 Paris, France. 610
had right-sided congestive heart failure and 1 had left-sided heart failure. Seven patients (59%) had septic pulmonary emboli. The other signs of endocarditis were splenomegaly in 5 patients, arthralgia in 2, arthritis in 1 patient, purpura in 1 and proteinuria in 4. The portal of entry was found in 7 patients (Table I). Bacteriologic findings: Positive blood cultures were found in 9 cases: coagulase-positive staphylococci in 4 patients, including 1 methicillin-resistant case; alpha streptococci in 3; Streptococcus D bovis in 1; and Candida guillermondii in 1. Negative blood cultures were found in 3 patients who had taken antibiotics before hospitalization. M-mode, 2-dimensional and pulsed Doppler echocardiography: Echocardiography revealed PV vegetations in 8 of 10 patients. However, for patients 3, 4,7 and 8, the first echocardiogram, done on days 31,14, 5 and 10, respectively, of the illness, yielded normal findings, although a typical diastolic murmur had been noted previously in patient 7. In addition, tricuspid valve fluttering was observed in patients 9,10 and 11, and paradoxical septal motion with right ventricular hypertrophy in patients 9 and 10. Echocardiography did not reveal vegetations in patients 11 or 12. Patient 11 had only an M-mode echocardiogram, which did not visualize the PV. In patient 12 the 2-D echocardiogram was normal, but the M-mode echocardiogram revealed diastolic vibrations, suggesting valve impairment. The M-mode and 2-D echocardiographic results for patient 9 are shown in Figure 1. On day 30, the PV vegetation was visible; 48 hours later, the abnormal echoes had disappeared. This patient had had several episodes of pulmonary emboli. Images of PV vegetation disappeared in patient 2, and remained unchanged in the others. Six patients had pulsed Doppler echocardiographic examinations. PV regurgitation was diagnosed in all 6. Figure 2 shows the pulsed Doppler echocardiogram from patient 12; a considerable diastolic flow suggestive of pulmonary regurgitation is visible. Anatomic findings: Anatomic study was possible in 6 patients (2 autopsies and 4 operations). PV vegetations were found in all 6. Vegetations were also found on the right ventricle in patient 2, the tricuspid valve in patients 2 and 11, the mitral valve in patients 6 and 11 and the aortic valve in patients 4 and 11. The anterior pulmonary leaflet was destroyed in patient 1. Treatment and clinical outcome: The illness lasted from 8 to 90 days (average 45). All patients were first treated with antibiotics 2 to 90 days (average 18) after the onset of illness. In group I, 3 patients had cardiac surgery: patients 1 and 4 were cured with antibiotics and underwent surgery several months later to correct underlying heart disease; patient 2 had surgery after a 40-day course of antibiotic treatment, to correct heart disease, persistent large vegetations and repeated pulmonary emboli, and she recovered; patient 3 had leukemia and also mycotic endocarditis, which was cured by antibiotic therapy. In group II only 1 patient (no. 11) had surgery, for left-sided heart failure owing to aortic regurgitation, but
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PULMONARY VALVE ENDOCARDITIS
TABLE II
Surgery involved insertion of bioprostheses on the pulmonary and aortic valves for patient 4, resection of the PV in patient 1 and resection of PV vegetations in patients 2 and 11.
Pulmonary Valve Endocarditis: Comparsion of Current Study Group with Published Cases Our Group (12 Cases)
Category Incidence PV IE/TotallE Mean age (yr) Primitive PV alone Congenital heart disease Opiate addiction PR murmur Pulmonary embolism Right-sided CHF Recovery
=
1.5% 34 5(42%) 25%
17% 25% 59%
8% 67%
=
Published Cases (47 Cases) 1.7% (Roberts). 2% (Johnson) 35 9(19%) 51% 32% 61% 61% 12% 59%
CHF congestive heart failure; IE infective endocarditis; PR pulmonary regurgitation; PV = pulmonary valve.
=
he died of cardiac tamponade 14 days later. PV endocarditis was diagnosed at autopsy in patients 5 and 6. Patient 10 died suddenly after 24 days of antibiotic therapy, but autopsy was not possible. Four other patients were successfully treated with antibiotic therapy.
FIGURE 1. Two-dimensional and M-mode echocardiograms from patient 9. Top, day 30. A shaggy abnormal echo is present on the posterior pulmonary cusp. BoHom, day 32. The vegetation has disappeared. AO aorta; LPA left pulmonary artery; PV pulmonary valve; RPA right pulmonary artery; RV = right ventricle.
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Discussion The PV is the valve the least often involved in infective endocarditis. We found 47 reported cases since 1960 (Table II). However, the frequency of PV endocarditis apparently has increased. In our series, 10 of 12 cases were observed between 1982 and 1984, and the number of reported cases increases regularly. This is probably partly because of better diagnosis. In our study, PV endocarditis accounts for 1.5% of patients admitted for infective endocarditis. Roberts and Buchbinder21 estimated that PV endocarditis accounts for 1.7% of fatal endocarditis caseSi Johnson et all reported that PV endocarditis accounts for 2% of endocarditis in subjects younger than 25 years. In addition, necropsy studies of endocarditis in heroin addicts 2,15,3o show that the PV is involved one-tenth as often as the tricuspid valve. Five of our patients (42%) had PV involvement alone without underlying heart disease. Only 9 patients (19%) so affected have been reported previously.I6-18,22-26 PV endocarditis was more common in patients with congenital heart disease l - 14 and in heroin addicts 2- 11 ,15-20 than in our series (Table II). When PV endocarditis affected a healthy heart, a virulent organism, often Staphylococcus, was usually found. However, when patients with congenital heart disease were affected, the causative organism was often alpha Streptococcus. Gonococcus, formerly considered to be a frequent organism in PV endocarditis,31 is now seldom found; 2 cases have been reported since 1960.25,26 To our knowledge, our patient 11 is the first case of myocotic PV endocarditis.
FIGURE 2. Pulsed Doppler echocardiogram from patient 12. Abnormal diastolic turbulence is recorded just below the pulmonary cusps.
October 1, 1985
More than half of the patients had pulmonary emboli (Table II). Diastolic murmur due to pulmonary regurgitation was not always detected; it may be masked by the murmur because of aortic regurgitation. Right-sided congestive heart failure was found in only 5 patients. 5,7,8,12 In 4 patients this was a result of partial or total obstruction of the PV caused by a large vegetation. The first echocardiographic diagnosis ofPV vegetation was by Kramer et apo in 1977. Since then, 16 cases have been reported,2,13,14,17,18,20,25,26 10 of which were confirmed by histopathologic study. In 2 of our patients the echocardiographic examination did not detect PV vegetations. Patient 9 did not undergo 2-D echocardiographic examination. Two-dimensional echocardiography is more sensitive than M-mode echocardiography for detecting PV vegetations. 14 PV vegetations were not visualized in patient 10, but valve impairment was. Vegetations can be observed a few days after the onset of symptoms, and often remain after the endocarditis has been cured. In our study, tricuspid valve fluttering was not always observed in the diagnosis of pulmonary regurgitation (3 of 10 patients), but pulsed Doppler echocardiography was extremely sensitive (all 6 cases). The clinical course of PV endocarditis depends mainly on which valves are associated. In other reports, the 10 patients with PV endocarditis and left-sided heart involvement6,8,l1,14,15,20,21,27-29 and the 7 patients with PV endocarditis and congenital heart disease3,4,6,8,l1,14 who did not undergo surgery died. However, 7 of 8 patients who received drug treatment for primitive PV endocarditis, whether isolated or associated with tricuspid endocarditis, recovered.2,16,17,22,23,26 In PV endocarditis without left-sided cardiac involvement or congenital heart disease, drug treatment usually suffices; surgery is advisable in the case of failure to treat bacterial infection or in right-sided heart failure (usually owing to obstruction of the PV). Pulmonary emboli do not, in our experience, justify surgery in PV endocarditis or in tricuspid endocarditis. 32 Surgery of the PV either involves excision of the vegetations or partial or total excision of the PV if it is destroyed. Residual pulmonary regurgitation is generally well tolerated. 23 Valve replacements are rarely carried out. Acknowledgment: We thank Jane Alix for translating and typing the manuscript.
References 1. Johnson DH, Rosenthal A, Nadas AS. A forty year review of bacterial endocarditis In Infancy and childhood. Circulation 1975;51:581-588.
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2. Sheikh MU, All N, Covarrubias E, Fox LM, Mor/arla M, De/o J. Right-sided infective endocarditis; an echocardlographlc study. Am J Med 1979;66: 283-287. 3. Bashour FA, Winchell CPo Right-sided bacterial endocarditis. Am J Med Sci 1960;240:411-416. 4. Griffiths SP. Bacterial endocarditis associated with atrial septal defect of the ostium secundum type. Am Heart J 1961;61:543-547. 5. Dubourg G, Broustet P, Brlcaud H, Fontan F, Trarleux M, Besse P. Guerlson chlrurglcale d'une endocardlte bacterlenne du coeur droit. Arch Mal Coeur 1963;56:772-781. 6. Froment R, DallQz C, Descours C, Age C, Verneyre H, Syrlmis A. L'Insufflsance slgmoldlenne pulmonalre: types etio-pathologlques, evolution et diagnostic. Arch Mal Coeur 1965;58: 1-32. 7. Garcia R, Taber RE. Bacterial endocarditis of the pulmonic valve. Association with atrial septal defect of the ostium secundum type. Am J Cardlol 1966; 18:275-280. 8. Cherrier F, Adamec R, PetHier H, Dodlnot B. Endocardlte bacterlenne sur coeur droit. Ann Med Nancy 1967;6:315-323. 9. Jaffe RB, Koschmann EB. Septic pulmonary emboli. Radiology 1970;96: 527-532. 10. Berrada M, Pauly-Laubry C, Nguyen G, Gandjbakhch J, Benomar M, Cabrol C, Maurice P. A propos d'une complication rare de la perslstance due canal arterlell'Insufflsance pulmonalre d'orlgine oslerlenne. Coeur Mad Interne 1975;14:341-345. 11. Laurent M, Dratwa M. Endocardite pulmonalre et mltrale Staphylococcus aureus chez un patient herolnomane. Acta Clin Belg 1976;31:144151. 12. Oakley GOG, Carson PHM, Sanderson JM. Right-sided endocarditis Involving both tricuspid and pulmonary valves In a patient with ventricular septal defect. Br Heart J 1977;38:323-325. 13. Dander B. Righetti B, Poppl A. Echocardlographlc diagnosis of Isolated pulmonary valve endocarditis. Br Heart J 1982;47:298-300. 14. Nakamura K, Satoml G, Sakal T, Ando M, Hashimoto A, Koyanagi H, Hlrosawa K, Takao A. Clinical and echocardlographlc features of pulmonary valve endocarditis. Circulation 1983;67:198-204. 15. Banks T, Fletcher R, All N. Infective endocarditis In heroin addicts. Am J Med 1973;55:444-451. 16. Massumi RA, Just H, Tawakkol A. Pulmonary valve regurgitation secondary to bacterial endocarditis in heroin addicts. Am Heart J 1967;73:308316. 17. Berger M, Delfin LA, Jelveh M, Goldberg E. Two-dImensional echocardlographlc findings In right-sided Infective endocarditis. Circulation 1980;61:855-861. 18. Melvin ET, Berger M, Lutzker LG, Goldberg E, Mlldvan D. Non-Invasive methods for detection of valve vegetations In Infective endocarditis. Am J Cardlol 1981;47:271-278. 19. Reyes MP, Palukte WA, Wylln RF, Lerner AM. Pseudomonas endocarditis In the Detroit Medical Center, 1969-1972. Medicine 1973;52:173194. 20. Kramer NE, Gill SS, Patel R, Towne WD. Pulmonary valve vegetations detected with echocardiography. Am J Cardiol 1977;39:1064-1067. 21. Roberts WC, Buchbinder NA. Right-sided valvular Infective endocarditis. A clinicopathologic study of twelve necropsy patients. Am J Med 1972; 53:7-19. 22. Levin HS, Runco V, Wooley F, Ryan JM. Pulmonic regurgitation following staphylococcal endocarditis. Circulation 1964;30:411-415. 23. Holmes JC, Fowler NO, Kaplan S. Pulmonary valvular Insufficiency. Am J Med 1968;44:851-862. 24. Laniado S, Frater RWM, Jordan A, Kafka EC, Kadish AS, Zelefsky M. Endocarditis of the pulmonic valve simulating cardiac tumor Chest 1971; 59:464-467. 25. Dzlndzlo BS, Meyer LR, Osterholm R, Hopeman A, Wolt/en J, Forker AD. Isolated gonoccal pulmonary valve endocarditis: diagnosis by echocardlography. Circulation 1979;59:1319-1324. 26. Rosof MH, Cohen MV, Jacquette G. Pulmonary valve gonoccal endocarditis. A forgotten disease. Br Heart J 1983;50:290-292. 27. Bastin R, Acar JF, Guibert J, Vilde JL. Les endocardltes bacteriennes du coeur droit (a propos de trois observations). Bull Mem Soc Med Hop Paris 1966;117:545-557. 28. Laine JL, Morand P, Poltler N, Lhulntre Y, Raynaud R. Endocardlte bacterlenne de I'orlfice pulmonalre sans attelnte trlcuspldlenne. Sem Hop Paris 1972;48:565-570. 29. Morand P, Radaoul H, Casenave J. L'Insufflsance pulmonalre valvulalre. Ann Cardlol Angelol 1974;23:491-500. 30. Ramsey RG, Gunnar RM, Robin JR. Endocarditis In the drug addict. Am J Cardlol 1970;25:608-618. 31. Thayer WS. On the cardiac complications of gonorrhea. Johns Hopkins Hospital Bull 1922;33:361-372. 32. Graham DY, Reul GJ, Martin R, Morton J, Kennedy JH. Infective endocarditis In drug addicts. Experiences with medical and surgical treatment. Circulation 1973;48:suppl 111:111-37-111-41.
a
Candida guillermondii in 1. M-mode and P-dimensional echocardiography was performed in 10 patients and revealed vegetations in 8. Pulsed Doppler echocardiography was performed in 6 patients and revealed pulmonary regurgitation in all 6. Seven patients had pulmonary emboli. Four patients underwent surgery. Four patients died, including 1 after cardiac surgery. Five patients, including the patient infected with Candida guillermondii, recovered with antibiotic treatment. (Am J Cardiol 1985;56:610-613)
Clinical and echocardiographic data from 12 patients with pulmonary valve endocarditis are described. Seven patients had isolated pulmonary endocarditis and in 5 patients other valves were infected (aortic, tricuspid, mitral or all 3). Two patients were heroin addicts and 4 had underlying heart disease (congenital heart disease in 3 and aortic regurgitation in 1 patient). The organisms involved were alpha sfrepfococci in 3 patients (all with underlying heart disease), Sfaphylococcus aureus in 4, Sfrepfococcus D bovis in 1 patient and
were systematically examined using the usual methods. Several recordings were made during follow-up. Diagnosis of vegetations was made when abnormal, shaggy, irregular echoes were seen on or near 1 or 2 pulmonary cusps and the motion of the cusps was not restricted. Six patients underwent 2-D pulsed Doppler echocardiographic examinations with an ATL Mark 500 mechanical scanner. The sample volume (2 mm) was positioned along an M-mode line simultaneously with the 2-D image. For the PV examination, the sample volume was placed just below the pulmonary cusps in a short-view axis. PV regurgitation was demonstrated when abnormal positive diastolic turbulence was recorded toward the transducer and the pulmonary ejection signal moved away from the transducer.
Pulmonary valve (PV) endocarditis is rare. Only 47 cases have been reported since 1960,1-2g most of these being 1 or 2 cases of drug addicts or patients with congential heart disease. We report 12 patients with PV endocarditis.
Methods Twelve cases of PV endocarditis were observed at Claude Bernard and Bichat Hospitals between 1972 and 1984. The diagnosis of PV endocarditis was made on the basis that septicemia was present and the PV was affected. PV involvement was confirmed by anatomic examination (surgery or autopsy), echocardiographic images of vegetations or by recent PV regurgitation diagnose by auscultation or pulsed Doppler echocardiography. Echocardiography: Ten patients had echocardiographic examinations (M-mode and 2-dimensional[2-D] in 9 patients and M-mode alone in 1 patient). The echocardiographic examination was done either with a phased-array sector scanner (RT 400) with an M-mode type Irex II or with a mechanical sector scanner (ATL Mark 500) with a 3 MHz in-line transducer. PV recording was done in the short-axis view and the transducer was placed on the third or fourth intercostal space in a parasternal view visualizing the pulmonary outflow tract. The valves, the size of the right ventricle and septal motion
Results The clinical and bacteriologic results are summarized in Table I. Clinical findings: The patients were 3 to 61 years old (mean 34). Eleven patients were men (92%). The patients were separated into 2 groups. Group I included 4 patients with underlying heart disease (congenital in 3). Group II included 8 patients with primitive PV endocarditis (2 heroin addicts, 2 alcoholics and 4 with no predisposing factors). Seven patients (59%) had isolated PV endocarditis and in 5 patients other valves were infected (aortic in 1 patient, tricuspid in 2 patients, mitral in 1 and all 3 valves in 1). Fever was present in all cases. A typical PV regurgitation murmur was found in only 3 patients (25%), all in group II. Associated aortic regurgitation masked the pulmonary auscultation in 2 other patients. One patient
From the Departments of Infectious and Tropical Diseases and the Intensive Care Unit, Claude Bernard Hospital, and the Departments of Cardiology and the Intensive Care Unlt, Bichat Hospital, Paris, France. Manuscript received November 26, 1984; revised manuscript received May 1, 1985, accepted May 2, 1985. Address for reprints: Anne-Claude Cremieux, MD, lnstitut de Medetine et d’Epidemiologie Tropicales, Hopital Claude Bernard, 10 avenue Porte d’Aubervilliers, 75019 Paris, France. 610
had right-sided congestive heart failure and 1 had left-sided heart failure. Seven patients (59%) had septic pulmonary emboli. The other signs of endocarditis were splenomegaly in 5 patients, arthralgia in 2, arthritis in 1 patient, purpura in 1 and proteinuria in 4. The portal of entry was found in 7 patients (Table I). Bacteriologic findings: Positive blood cultures were found in 9 cases: coagulase-positive staphylococci in 4 patients, including 1 methicillin-resistant case; alpha streptococci in 3; Streptococcus D bovis in 1; and Candida guillermondii in 1. Negative blood cultures were found in 3 patients who had taken antibiotics before hospitalization. M-mode, 2-dimensional and pulsed Doppler echocardiography: Echocardiography revealed PV vegetations in 8 of 10 patients. However, for patients 3, 4,7 and 8, the first echocardiogram, done on days 31,14, 5 and 10, respectively, of the illness, yielded normal findings, although a typical diastolic murmur had been noted previously in patient 7. In addition, tricuspid valve fluttering was observed in patients 9,10 and 11, and paradoxical septal motion with right ventricular hypertrophy in patients 9 and 10. Echocardiography did not reveal vegetations in patients 11 or 12. Patient 11 had only an M-mode echocardiogram, which did not visualize the PV. In patient 12 the 2-D echocardiogram was normal, but the M-mode echocardiogram revealed diastolic vibrations, suggesting valve impairment. The M-mode and 2-D echocardiographic results for patient 9 are shown in Figure 1. On day 30, the PV vegetation was visible; 48 hours later, the abnormal echoes had disappeared. This patient had had several episodes of pulmonary emboli. Images of PV vegetation disappeared in patient 2, and remained unchanged in the others. Six patients had pulsed Doppler echocardiographic examinations. PV regurgitation was diagnosed in all 6. Figure 2 shows the pulsed Doppler echocardiogram from patient 12; a considerable diastolic flow suggestive of pulmonary regurgitation is visible. Anatomic findings: Anatomic study was possible in 6 patients (2 autopsies and 4 operations). PV vegetations were found in all 6. Vegetations were also found on the right ventricle in patient 2, the tricuspid valve in patients 2 and 11, the mitral valve in patients 6 and 11 and the aortic valve in patients 4 and 11. The anterior pulmonary leaflet was destroyed in patient 1. Treatment and clinical outcome: The illness lasted from 8 to 90 days (average 45). All patients were first treated with antibiotics 2 to 90 days (average 18) after the onset of illness. In group I, 3 patients had cardiac surgery: patients 1 and 4 were cured with antibiotics and underwent surgery several months later to correct underlying heart disease; patient 2 had surgery after a 40-day course of antibiotic treatment, to correct heart disease, persistent large vegetations and repeated pulmonary emboli, and she recovered; patient 3 had leukemia and also mycotic endocarditis, which was cured by antibiotic therapy. In group II only 1 patient (no. 11) had surgery, for left-sided heart failure owing to aortic regurgitation, but
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PULMONARY VALVE ENDOCARDITIS
TABLE II
Surgery involved insertion of bioprostheses on the pulmonary and aortic valves for patient 4, resection of the PV in patient 1 and resection of PV vegetations in patients 2 and 11.
Pulmonary Valve Endocarditis: Comparsion of Current Study Group with Published Cases Our Group (12 Cases)
Category Incidence PV IE/TotallE Mean age (yr) Primitive PV alone Congenital heart disease Opiate addiction PR murmur Pulmonary embolism Right-sided CHF Recovery
=
1.5% 34 5(42%) 25%
17% 25% 59%
8% 67%
=
Published Cases (47 Cases) 1.7% (Roberts). 2% (Johnson) 35 9(19%) 51% 32% 61% 61% 12% 59%
CHF congestive heart failure; IE infective endocarditis; PR pulmonary regurgitation; PV = pulmonary valve.
=
he died of cardiac tamponade 14 days later. PV endocarditis was diagnosed at autopsy in patients 5 and 6. Patient 10 died suddenly after 24 days of antibiotic therapy, but autopsy was not possible. Four other patients were successfully treated with antibiotic therapy.
FIGURE 1. Two-dimensional and M-mode echocardiograms from patient 9. Top, day 30. A shaggy abnormal echo is present on the posterior pulmonary cusp. BoHom, day 32. The vegetation has disappeared. AO aorta; LPA left pulmonary artery; PV pulmonary valve; RPA right pulmonary artery; RV = right ventricle.
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Discussion The PV is the valve the least often involved in infective endocarditis. We found 47 reported cases since 1960 (Table II). However, the frequency of PV endocarditis apparently has increased. In our series, 10 of 12 cases were observed between 1982 and 1984, and the number of reported cases increases regularly. This is probably partly because of better diagnosis. In our study, PV endocarditis accounts for 1.5% of patients admitted for infective endocarditis. Roberts and Buchbinder21 estimated that PV endocarditis accounts for 1.7% of fatal endocarditis caseSi Johnson et all reported that PV endocarditis accounts for 2% of endocarditis in subjects younger than 25 years. In addition, necropsy studies of endocarditis in heroin addicts 2,15,3o show that the PV is involved one-tenth as often as the tricuspid valve. Five of our patients (42%) had PV involvement alone without underlying heart disease. Only 9 patients (19%) so affected have been reported previously.I6-18,22-26 PV endocarditis was more common in patients with congenital heart disease l - 14 and in heroin addicts 2- 11 ,15-20 than in our series (Table II). When PV endocarditis affected a healthy heart, a virulent organism, often Staphylococcus, was usually found. However, when patients with congenital heart disease were affected, the causative organism was often alpha Streptococcus. Gonococcus, formerly considered to be a frequent organism in PV endocarditis,31 is now seldom found; 2 cases have been reported since 1960.25,26 To our knowledge, our patient 11 is the first case of myocotic PV endocarditis.
FIGURE 2. Pulsed Doppler echocardiogram from patient 12. Abnormal diastolic turbulence is recorded just below the pulmonary cusps.
October 1, 1985
More than half of the patients had pulmonary emboli (Table II). Diastolic murmur due to pulmonary regurgitation was not always detected; it may be masked by the murmur because of aortic regurgitation. Right-sided congestive heart failure was found in only 5 patients. 5,7,8,12 In 4 patients this was a result of partial or total obstruction of the PV caused by a large vegetation. The first echocardiographic diagnosis ofPV vegetation was by Kramer et apo in 1977. Since then, 16 cases have been reported,2,13,14,17,18,20,25,26 10 of which were confirmed by histopathologic study. In 2 of our patients the echocardiographic examination did not detect PV vegetations. Patient 9 did not undergo 2-D echocardiographic examination. Two-dimensional echocardiography is more sensitive than M-mode echocardiography for detecting PV vegetations. 14 PV vegetations were not visualized in patient 10, but valve impairment was. Vegetations can be observed a few days after the onset of symptoms, and often remain after the endocarditis has been cured. In our study, tricuspid valve fluttering was not always observed in the diagnosis of pulmonary regurgitation (3 of 10 patients), but pulsed Doppler echocardiography was extremely sensitive (all 6 cases). The clinical course of PV endocarditis depends mainly on which valves are associated. In other reports, the 10 patients with PV endocarditis and left-sided heart involvement6,8,l1,14,15,20,21,27-29 and the 7 patients with PV endocarditis and congenital heart disease3,4,6,8,l1,14 who did not undergo surgery died. However, 7 of 8 patients who received drug treatment for primitive PV endocarditis, whether isolated or associated with tricuspid endocarditis, recovered.2,16,17,22,23,26 In PV endocarditis without left-sided cardiac involvement or congenital heart disease, drug treatment usually suffices; surgery is advisable in the case of failure to treat bacterial infection or in right-sided heart failure (usually owing to obstruction of the PV). Pulmonary emboli do not, in our experience, justify surgery in PV endocarditis or in tricuspid endocarditis. 32 Surgery of the PV either involves excision of the vegetations or partial or total excision of the PV if it is destroyed. Residual pulmonary regurgitation is generally well tolerated. 23 Valve replacements are rarely carried out. Acknowledgment: We thank Jane Alix for translating and typing the manuscript.
References 1. Johnson DH, Rosenthal A, Nadas AS. A forty year review of bacterial endocarditis In Infancy and childhood. Circulation 1975;51:581-588.
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2. Sheikh MU, All N, Covarrubias E, Fox LM, Mor/arla M, De/o J. Right-sided infective endocarditis; an echocardlographlc study. Am J Med 1979;66: 283-287. 3. Bashour FA, Winchell CPo Right-sided bacterial endocarditis. Am J Med Sci 1960;240:411-416. 4. Griffiths SP. Bacterial endocarditis associated with atrial septal defect of the ostium secundum type. Am Heart J 1961;61:543-547. 5. Dubourg G, Broustet P, Brlcaud H, Fontan F, Trarleux M, Besse P. Guerlson chlrurglcale d'une endocardlte bacterlenne du coeur droit. Arch Mal Coeur 1963;56:772-781. 6. Froment R, DallQz C, Descours C, Age C, Verneyre H, Syrlmis A. L'Insufflsance slgmoldlenne pulmonalre: types etio-pathologlques, evolution et diagnostic. Arch Mal Coeur 1965;58: 1-32. 7. Garcia R, Taber RE. Bacterial endocarditis of the pulmonic valve. Association with atrial septal defect of the ostium secundum type. Am J Cardlol 1966; 18:275-280. 8. Cherrier F, Adamec R, PetHier H, Dodlnot B. Endocardlte bacterlenne sur coeur droit. Ann Med Nancy 1967;6:315-323. 9. Jaffe RB, Koschmann EB. Septic pulmonary emboli. Radiology 1970;96: 527-532. 10. Berrada M, Pauly-Laubry C, Nguyen G, Gandjbakhch J, Benomar M, Cabrol C, Maurice P. A propos d'une complication rare de la perslstance due canal arterlell'Insufflsance pulmonalre d'orlgine oslerlenne. Coeur Mad Interne 1975;14:341-345. 11. Laurent M, Dratwa M. Endocardite pulmonalre et mltrale Staphylococcus aureus chez un patient herolnomane. Acta Clin Belg 1976;31:144151. 12. Oakley GOG, Carson PHM, Sanderson JM. Right-sided endocarditis Involving both tricuspid and pulmonary valves In a patient with ventricular septal defect. Br Heart J 1977;38:323-325. 13. Dander B. Righetti B, Poppl A. Echocardlographlc diagnosis of Isolated pulmonary valve endocarditis. Br Heart J 1982;47:298-300. 14. Nakamura K, Satoml G, Sakal T, Ando M, Hashimoto A, Koyanagi H, Hlrosawa K, Takao A. Clinical and echocardlographlc features of pulmonary valve endocarditis. Circulation 1983;67:198-204. 15. Banks T, Fletcher R, All N. Infective endocarditis In heroin addicts. Am J Med 1973;55:444-451. 16. Massumi RA, Just H, Tawakkol A. Pulmonary valve regurgitation secondary to bacterial endocarditis in heroin addicts. Am Heart J 1967;73:308316. 17. Berger M, Delfin LA, Jelveh M, Goldberg E. Two-dImensional echocardlographlc findings In right-sided Infective endocarditis. Circulation 1980;61:855-861. 18. Melvin ET, Berger M, Lutzker LG, Goldberg E, Mlldvan D. Non-Invasive methods for detection of valve vegetations In Infective endocarditis. Am J Cardlol 1981;47:271-278. 19. Reyes MP, Palukte WA, Wylln RF, Lerner AM. Pseudomonas endocarditis In the Detroit Medical Center, 1969-1972. Medicine 1973;52:173194. 20. Kramer NE, Gill SS, Patel R, Towne WD. Pulmonary valve vegetations detected with echocardiography. Am J Cardiol 1977;39:1064-1067. 21. Roberts WC, Buchbinder NA. Right-sided valvular Infective endocarditis. A clinicopathologic study of twelve necropsy patients. Am J Med 1972; 53:7-19. 22. Levin HS, Runco V, Wooley F, Ryan JM. Pulmonic regurgitation following staphylococcal endocarditis. Circulation 1964;30:411-415. 23. Holmes JC, Fowler NO, Kaplan S. Pulmonary valvular Insufficiency. Am J Med 1968;44:851-862. 24. Laniado S, Frater RWM, Jordan A, Kafka EC, Kadish AS, Zelefsky M. Endocarditis of the pulmonic valve simulating cardiac tumor Chest 1971; 59:464-467. 25. Dzlndzlo BS, Meyer LR, Osterholm R, Hopeman A, Wolt/en J, Forker AD. Isolated gonoccal pulmonary valve endocarditis: diagnosis by echocardlography. Circulation 1979;59:1319-1324. 26. Rosof MH, Cohen MV, Jacquette G. Pulmonary valve gonoccal endocarditis. A forgotten disease. Br Heart J 1983;50:290-292. 27. Bastin R, Acar JF, Guibert J, Vilde JL. Les endocardltes bacteriennes du coeur droit (a propos de trois observations). Bull Mem Soc Med Hop Paris 1966;117:545-557. 28. Laine JL, Morand P, Poltler N, Lhulntre Y, Raynaud R. Endocardlte bacterlenne de I'orlfice pulmonalre sans attelnte trlcuspldlenne. Sem Hop Paris 1972;48:565-570. 29. Morand P, Radaoul H, Casenave J. L'Insufflsance pulmonalre valvulalre. Ann Cardlol Angelol 1974;23:491-500. 30. Ramsey RG, Gunnar RM, Robin JR. Endocarditis In the drug addict. Am J Cardlol 1970;25:608-618. 31. Thayer WS. On the cardiac complications of gonorrhea. Johns Hopkins Hospital Bull 1922;33:361-372. 32. Graham DY, Reul GJ, Martin R, Morton J, Kennedy JH. Infective endocarditis In drug addicts. Experiences with medical and surgical treatment. Circulation 1973;48:suppl 111:111-37-111-41.
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