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Surgical Therapy for Infective Endocarditis
Editorial Surgical Therapy for Infective Endocarditis In recent years, considerable advances have been made in the ability to diagnose various aspects of cardiac valvular dysfunction and in operative strategies for cardiac disease. Developments in the understanding and applications of antimicrobial treatment have also advanced. Despite this progress, infective endocarditis remains a major cause of morbidity and mortality. In this issue of the Mayo Clinic Proceedings (pages 517 to 525), Mullany and colleagues describe a 30year experience with culture-positive endocarditis in Mayo Clinic patients who underwent surgical treatment. The clinical spectrum of endocarditis is changing. In comparison with the past, rheumatic heart disease occurs less commonly in the young population, and endocarditis is being seen more frequently in older patients. Cardiac surgical procedures have contributed to this phenomenon because they have prolonged the lives of many patients with valvular heart disease. In addition, the aging of the general population has presented an increased opportunity for the clinical expression of structural valvular abnormalities. Increasingly, the organisms involved in endocarditis are nosocomial and more resistant to antibiotics, and more patients have multiple infecting organisms.' Most likely, the incidence of endocarditis will increase in the future because, despite the decline in rheumatic heart disease, the number of patients with prosthetic heart valves and the use of indwelling catheters and pacing wires are increasing. Moreover, intravenous drug abusers and patients with immunosuppression or immunodeficiency are constituting an enlarging population. Before the use of antibiotics and cardiac surgical procedures, 95% of cases of endocarditis were caused by viridans streptococci. Currently, numerous organisms are encountered, and staphylococci are the most common in hospitalacquired infections, although most infections from the community remain streptococcal.P This trend is confirmed in the current review of the Mayo Clinic series. Staphylococcal were more common that streptococcal infections, although the commonest organism in native valve endocarditis remained viridans streptococci. To some extent, this pattern accounts for the increased likelihood of a cure with antibiotics in native valve endocarditis. Address reprint requests to Dr. S. W. Jamieson, Division of Cardiothoracic Surgery, University of California, San Diego, 200 West Arbor Drive, MC 8892, San Diego, CA 92103-8892. Mayo Clin Proc 1995; 70:598-600
Unlike infections of the native heart valve, which are often cured by appropriate antibiotic therapy, prosthetic valve endocarditis usually necessitates an operative approach for adequate treatment. Prosthetic valve endocarditis is associated with a greater mortality and morbidity than is native valve endocarditis, and this relationship is attributable to the increased likelihood of annular destruction and the increased complexity of surgical repair. The risk of prosthetic valvular disease is greatest early after operation, and affected patients are also more likely to have hospital-based virulent and destructive organisms, which are less responsive to antibiotic therapy. Fortunately, the frequency of occurrence of prosthetic valvular endocarditis is only approximately 2 to 4%.4 Although endocarditis remains a devastating and often lethal condition, there have been recent advances in its diagnosis and therapy. The evolution of transesophageal echocardiography has led to its increasing application in the assessment of cardiac valvular abnormalities. Operative treatment has improved with a firmer understanding of the need for the complete removal of all devitalized and infected tissue, if necessary in combination with major surgical reconstruction, and an increased use of homograft tissue valves. Echocardiography.-Echocardiography is helpful in detecting various cardiac lesions in endocarditis, including valvular regurgitation, annular ring abscesses, and vegetations. Transesophageal is better than transthoracic echocardiography in finding evidence of vegetations, quantifying valvular dysfunction, and diagnosing the spread of infection.' This advantage is especially noted in prosthetic valve endocarditis, in which shielding by the prosthesis may prevent adequate transthoracic diagnosis of vegetations or abscess cavities. What is the significance of finding vegetations on echocardiography? Although seemingly large and loose vegetations may be a daunting phenomenon when discovered echocardiographically, no firm evidence suggests that this appearance, in itself, should trigger surgical intervention. As pointed out in the article by Mullany and associates, although one series showed that mitral vegetations or large vegetations were more likely than others to embolize," this finding did not necessarily prevail in treated patients at the Mayo Clinic," Of interest, antibiotic treatment rather than anticoagulation has been noted to inhibit embolization." Nevertheless, emboli are common (25% of patients in the current series) and usually involve the brain. The frequency of emboli is the same with both native and prosthetic valve endocarditis. Antibiotic treatment should be with bacteri-
598
© 1995 Mayo Foundation/or Medical Education and Research
For personal use. Mass reproduce only with permission from Mayo Clinic Proceedings.
Mayo Clin Proc, June 1995, Vol 70
cidal agents, often in combination, and surgical intervention need not be delayed because of cerebral events, which are usually ischemic rather than hemorrhagic (although cerebral mycotic aneurysms are possible). Of note, the presence of emboli did not emerge as a risk factor in this series. OperativeIntervention.-When antibiotics fail to control native valve endocarditis, surgical treatment is indicated. Evidence may be persistent sepsis; signs of progressive invasion of the surrounding myocardium with abscess formation, heart block, or development of fistulas; progressive hemodynamic instability as a result of destruction of valve leaflets; or repeated emboli of vegetations. With prosthetic valve endocarditis, the indications will be the same; however, in this situation, hemodynamic instability may be due to progressive dehiscence of the valve, and the organisms may be more resistant to treatment. With fungal endocarditis, a surgical cure offers the only hope9 - t o a lesser extent, this is also true for Staphylococcus aureus and gramnegative endocarditis. The surgical results in acute endocarditis depend on the valve affected, whether it is a prosthesis, the organism involved, and the stage of the disease. Aortic endocarditis is associated with the worst prognosis, but the principles of aggressively removing all devitalized and infected tissue, reconstructing cardiac defects, and replacing valvular integrity are dependable. This approach often necessitates extensive debridement, and subsequent reconstruction should be performed by using as little foreign material as possible. Increasing confidence with techniques of myocardial protection have prompted wide resection of damaged tissue, even to the point of transecting the superior vena cava for complete exposure of the aortic outflow tract and rebuilding the entire aortic-mitral area to accommodate two new valves. The use of bovine pericardium, rather than other patches, is favored to reconstruct septal defects or the aortic outflow tract. Monofilament nylon or polypropylene should perhaps be used whenever possible instead of braided sutures. Investigators have extensively discussed the issue of whether valve replacement should be with tissue or mechanical prostheses; Mullany and colleagues found no striking difference, a conclusion confirmed in other published series.'? However, enthusiasm for use of homografts in the aortic position has been increasing, as emphasized in a recent Mayo Clinic report. II The subcoronary position can be used when the annulus has not been extensively eroded;" when the aortic root is widely destroyed, replacement can be accomplished with a homograft conduit," and the coronary arteries can subsequently be reimplanted. When the mitral valve is affected, a repair is sometimes possible by excision of the involved segment of the leaflet
EDITORIAL
599
and subsequent repair with or without a pericardial patch. In severe infections with destruction of the annulus, a mitral prosthesis can be inserted away from the annulus, in an intraatrial site." Results.-Because the operation takes place in an infected anatomic site and all infection clearly cannot always be eradicated surgically, recurrence of disease is not as common as might be expected. Periprosthetic leaks, however, occur frequently-although often without recurrent infection (when the aortic root has been replaced with a homograft, periprosthetic leaks obviously cannot occur). In the series of patients described by Mullany and coworkers, although reoperation was required in 30 patients, only 4 reoperations were for recurrent endocarditis. Patients should receive high-dose antibiotic therapy intravenously for at least 6 weeks. Recurrent infection, should it occur, is most common early after replacement with a prosthetic valve. Homografts are not associated with this early peak of infection" but rather with a steady linear rate of infection. 15 A mortality rate of 20 to 50% for surgical treatment of culture-positive acute endocarditis has been reported. In the current series, the operative mortality was 26%, which is well within this range, especially because isolated rightsided endocarditis (which is associated with less risk) was encountered in only two cases, and the investigators have been careful to include only patients with active infection at the time of surgical treatment. The exceptionally low incidence of tricuspid endocarditis perhaps represents the historical population of Rochester, Minnesota. Mullany and associates point out that operative mortality was related to the presence of an abscess at operation or to renal failure. Formation of an abscess cavity (the only factor related to hospital mortality on multivariate analysis) was most commonly noted with staphylococcal infections, prosthetic valve infections, and the aortic site, all elements that are classically believed to be associated with increased risk. The onset of renal failure is also usually multifactorial; factors such as poor cardiac output, sepsis, possible emboli, and antibiotic therapy can be contributory. One aspect that perhaps is not widely appreciated is that renal impairment is common in conjunction with severe aortic regurgitation, which produces a low diastolic pressure. The presence of deteriorating renal function in patients with endocarditis associated with severe aortic regurgitation should, in itself, stimulate urgent operation.
Stuart W. Jamieson, M.B. Division of Cardiothoracic Surgery University of California, San Diego San Diego, California
For personal use. Mass reproduce only with permission from Mayo Clinic Proceedings.
600
Mayo Clin Proc, June 1995, Vol 70
EDITORIAL
REFERENCES 1. Baddour LM, Meyer J, Henry B. Polymicrobial infective endocarditis in the 1980s. Rev Infect Dis 1991; 13:963970 2. Dwyer DE, Chen SC, Wright EJ, Crimmins D, Collignon PJ, Sorrell TC. Hospital practices influence the pattern of infective endocarditis. Med J Aust 1994; 160:709-713; 716-718 3. Lim MC, Tan TZ, Choo M, Lim YT, Soo CS, Ling LH. Review of patients with infective endocarditis of native valves over a five-year period. Ann Acad Med Singapore 1993; 22:296-299 4. Baumgartner WA, Miller DC, Reitz BA, Oyer PE, Jamieson SW, Stinson EB, et al. Surgical treatment of prosthetic valve endocarditis. Ann Thorac Surg 1983; 35:87-104 5. Leung DY, Cranney GB, Hopkins AP, Walsh WF. Role of transoesophageal echocardiography in the diagnosis and management of aortic root abscess. Br Heart J 1994; 72:175181 6. Rohmann S, Erbel R, Gorge G, Makowski T, Mohr-Kahaly S, Nixdorff D, et al. Clinical relevance of vegetation localization by transoesophagea1 echocardiography in infective endocarditis. Eur Heart J 1992; 13:446-452 7. Steckelberg JM, Murphy JG, Ballard D, Bailey K, Tajik AJ, Taliercio CP, et al. Emboli in infective endocarditis: the prognostic value of echocardiography. Ann Intern Med 1991; 114:635-640 8. Davenport J, Hart RG. Prosthetic valve endocarditis 19761987: antibiotics, anticoagulation, and stroke. Stroke 1990; 21:993-999
9.
Denning DW, Stevens DA. Antifungal and surgical treatment of invasive aspergillosis: review of 2,121 published cases. Rev Infect Dis 1990; 12:1147-1201 10. Grover FL, Cohen DJ, Oprian C, Henderson WG, Sethi G, Hammermeister KE. Determinants of the occurrence of and survival from prosthetic valve endocarditis: experience of the Veterans Affairs Cooperative Study on Valvular Heart Disease. J Thorac Cardiovasc Surg 1994; 108:207-214 11. Tuna IC, Orszulak TA, Schaff HV, Danielson GK. Results of homograft aortic valve replacement for active endocarditis. Ann Thorac Surg 1990; 49:619-624 12. Albertucci M, Wong K, Petrou M, Mitchell A, Somerville J, Theodoropoulos S, et al. The use of unstented homograft valves for aortic valve reoperations: review of a twentythree-year experience. J Thorac Cardiovasc Surg 1994; 107:152-161 13. Glazier JJ, Verwilghen J, Donaldson RM, Ross DN. Treatment of complicated prosthetic aortic valve endocarditis with annular abscess formation by homograft aortic root replacement. J Am ColI Cardiol 1991; 17:1177-1182 14. NatafP, Pavie A, Jault F, Bors V, Cabro1C, Gandjbakhch I. Intraatrial insertion of a mitral prosthesis in a destroyed or calcified mitral annulus. Ann Thorac Surg 1994; 58:163167 15. Haydock D, Barratt-Boyes B, Macedo T, Kirklin JW, Blackstone E. Aortic valve replacement for active infectious endocarditis in 108 patients: a comparison of freehand allograft valves with mechanical prostheses and bioprostheses. J Thorac Cardiovasc Surg 1992; 103:130-139
For personal use. Mass reproduce only with permission from Mayo Clinic Proceedings.
Unlike infections of the native heart valve, which are often cured by appropriate antibiotic therapy, prosthetic valve endocarditis usually necessitates an operative approach for adequate treatment. Prosthetic valve endocarditis is associated with a greater mortality and morbidity than is native valve endocarditis, and this relationship is attributable to the increased likelihood of annular destruction and the increased complexity of surgical repair. The risk of prosthetic valvular disease is greatest early after operation, and affected patients are also more likely to have hospital-based virulent and destructive organisms, which are less responsive to antibiotic therapy. Fortunately, the frequency of occurrence of prosthetic valvular endocarditis is only approximately 2 to 4%.4 Although endocarditis remains a devastating and often lethal condition, there have been recent advances in its diagnosis and therapy. The evolution of transesophageal echocardiography has led to its increasing application in the assessment of cardiac valvular abnormalities. Operative treatment has improved with a firmer understanding of the need for the complete removal of all devitalized and infected tissue, if necessary in combination with major surgical reconstruction, and an increased use of homograft tissue valves. Echocardiography.-Echocardiography is helpful in detecting various cardiac lesions in endocarditis, including valvular regurgitation, annular ring abscesses, and vegetations. Transesophageal is better than transthoracic echocardiography in finding evidence of vegetations, quantifying valvular dysfunction, and diagnosing the spread of infection.' This advantage is especially noted in prosthetic valve endocarditis, in which shielding by the prosthesis may prevent adequate transthoracic diagnosis of vegetations or abscess cavities. What is the significance of finding vegetations on echocardiography? Although seemingly large and loose vegetations may be a daunting phenomenon when discovered echocardiographically, no firm evidence suggests that this appearance, in itself, should trigger surgical intervention. As pointed out in the article by Mullany and associates, although one series showed that mitral vegetations or large vegetations were more likely than others to embolize," this finding did not necessarily prevail in treated patients at the Mayo Clinic," Of interest, antibiotic treatment rather than anticoagulation has been noted to inhibit embolization." Nevertheless, emboli are common (25% of patients in the current series) and usually involve the brain. The frequency of emboli is the same with both native and prosthetic valve endocarditis. Antibiotic treatment should be with bacteri-
598
© 1995 Mayo Foundation/or Medical Education and Research
For personal use. Mass reproduce only with permission from Mayo Clinic Proceedings.
Mayo Clin Proc, June 1995, Vol 70
cidal agents, often in combination, and surgical intervention need not be delayed because of cerebral events, which are usually ischemic rather than hemorrhagic (although cerebral mycotic aneurysms are possible). Of note, the presence of emboli did not emerge as a risk factor in this series. OperativeIntervention.-When antibiotics fail to control native valve endocarditis, surgical treatment is indicated. Evidence may be persistent sepsis; signs of progressive invasion of the surrounding myocardium with abscess formation, heart block, or development of fistulas; progressive hemodynamic instability as a result of destruction of valve leaflets; or repeated emboli of vegetations. With prosthetic valve endocarditis, the indications will be the same; however, in this situation, hemodynamic instability may be due to progressive dehiscence of the valve, and the organisms may be more resistant to treatment. With fungal endocarditis, a surgical cure offers the only hope9 - t o a lesser extent, this is also true for Staphylococcus aureus and gramnegative endocarditis. The surgical results in acute endocarditis depend on the valve affected, whether it is a prosthesis, the organism involved, and the stage of the disease. Aortic endocarditis is associated with the worst prognosis, but the principles of aggressively removing all devitalized and infected tissue, reconstructing cardiac defects, and replacing valvular integrity are dependable. This approach often necessitates extensive debridement, and subsequent reconstruction should be performed by using as little foreign material as possible. Increasing confidence with techniques of myocardial protection have prompted wide resection of damaged tissue, even to the point of transecting the superior vena cava for complete exposure of the aortic outflow tract and rebuilding the entire aortic-mitral area to accommodate two new valves. The use of bovine pericardium, rather than other patches, is favored to reconstruct septal defects or the aortic outflow tract. Monofilament nylon or polypropylene should perhaps be used whenever possible instead of braided sutures. Investigators have extensively discussed the issue of whether valve replacement should be with tissue or mechanical prostheses; Mullany and colleagues found no striking difference, a conclusion confirmed in other published series.'? However, enthusiasm for use of homografts in the aortic position has been increasing, as emphasized in a recent Mayo Clinic report. II The subcoronary position can be used when the annulus has not been extensively eroded;" when the aortic root is widely destroyed, replacement can be accomplished with a homograft conduit," and the coronary arteries can subsequently be reimplanted. When the mitral valve is affected, a repair is sometimes possible by excision of the involved segment of the leaflet
EDITORIAL
599
and subsequent repair with or without a pericardial patch. In severe infections with destruction of the annulus, a mitral prosthesis can be inserted away from the annulus, in an intraatrial site." Results.-Because the operation takes place in an infected anatomic site and all infection clearly cannot always be eradicated surgically, recurrence of disease is not as common as might be expected. Periprosthetic leaks, however, occur frequently-although often without recurrent infection (when the aortic root has been replaced with a homograft, periprosthetic leaks obviously cannot occur). In the series of patients described by Mullany and coworkers, although reoperation was required in 30 patients, only 4 reoperations were for recurrent endocarditis. Patients should receive high-dose antibiotic therapy intravenously for at least 6 weeks. Recurrent infection, should it occur, is most common early after replacement with a prosthetic valve. Homografts are not associated with this early peak of infection" but rather with a steady linear rate of infection. 15 A mortality rate of 20 to 50% for surgical treatment of culture-positive acute endocarditis has been reported. In the current series, the operative mortality was 26%, which is well within this range, especially because isolated rightsided endocarditis (which is associated with less risk) was encountered in only two cases, and the investigators have been careful to include only patients with active infection at the time of surgical treatment. The exceptionally low incidence of tricuspid endocarditis perhaps represents the historical population of Rochester, Minnesota. Mullany and associates point out that operative mortality was related to the presence of an abscess at operation or to renal failure. Formation of an abscess cavity (the only factor related to hospital mortality on multivariate analysis) was most commonly noted with staphylococcal infections, prosthetic valve infections, and the aortic site, all elements that are classically believed to be associated with increased risk. The onset of renal failure is also usually multifactorial; factors such as poor cardiac output, sepsis, possible emboli, and antibiotic therapy can be contributory. One aspect that perhaps is not widely appreciated is that renal impairment is common in conjunction with severe aortic regurgitation, which produces a low diastolic pressure. The presence of deteriorating renal function in patients with endocarditis associated with severe aortic regurgitation should, in itself, stimulate urgent operation.
Stuart W. Jamieson, M.B. Division of Cardiothoracic Surgery University of California, San Diego San Diego, California
For personal use. Mass reproduce only with permission from Mayo Clinic Proceedings.
600
Mayo Clin Proc, June 1995, Vol 70
EDITORIAL
REFERENCES 1. Baddour LM, Meyer J, Henry B. Polymicrobial infective endocarditis in the 1980s. Rev Infect Dis 1991; 13:963970 2. Dwyer DE, Chen SC, Wright EJ, Crimmins D, Collignon PJ, Sorrell TC. Hospital practices influence the pattern of infective endocarditis. Med J Aust 1994; 160:709-713; 716-718 3. Lim MC, Tan TZ, Choo M, Lim YT, Soo CS, Ling LH. Review of patients with infective endocarditis of native valves over a five-year period. Ann Acad Med Singapore 1993; 22:296-299 4. Baumgartner WA, Miller DC, Reitz BA, Oyer PE, Jamieson SW, Stinson EB, et al. Surgical treatment of prosthetic valve endocarditis. Ann Thorac Surg 1983; 35:87-104 5. Leung DY, Cranney GB, Hopkins AP, Walsh WF. Role of transoesophageal echocardiography in the diagnosis and management of aortic root abscess. Br Heart J 1994; 72:175181 6. Rohmann S, Erbel R, Gorge G, Makowski T, Mohr-Kahaly S, Nixdorff D, et al. Clinical relevance of vegetation localization by transoesophagea1 echocardiography in infective endocarditis. Eur Heart J 1992; 13:446-452 7. Steckelberg JM, Murphy JG, Ballard D, Bailey K, Tajik AJ, Taliercio CP, et al. Emboli in infective endocarditis: the prognostic value of echocardiography. Ann Intern Med 1991; 114:635-640 8. Davenport J, Hart RG. Prosthetic valve endocarditis 19761987: antibiotics, anticoagulation, and stroke. Stroke 1990; 21:993-999
9.
Denning DW, Stevens DA. Antifungal and surgical treatment of invasive aspergillosis: review of 2,121 published cases. Rev Infect Dis 1990; 12:1147-1201 10. Grover FL, Cohen DJ, Oprian C, Henderson WG, Sethi G, Hammermeister KE. Determinants of the occurrence of and survival from prosthetic valve endocarditis: experience of the Veterans Affairs Cooperative Study on Valvular Heart Disease. J Thorac Cardiovasc Surg 1994; 108:207-214 11. Tuna IC, Orszulak TA, Schaff HV, Danielson GK. Results of homograft aortic valve replacement for active endocarditis. Ann Thorac Surg 1990; 49:619-624 12. Albertucci M, Wong K, Petrou M, Mitchell A, Somerville J, Theodoropoulos S, et al. The use of unstented homograft valves for aortic valve reoperations: review of a twentythree-year experience. J Thorac Cardiovasc Surg 1994; 107:152-161 13. Glazier JJ, Verwilghen J, Donaldson RM, Ross DN. Treatment of complicated prosthetic aortic valve endocarditis with annular abscess formation by homograft aortic root replacement. J Am ColI Cardiol 1991; 17:1177-1182 14. NatafP, Pavie A, Jault F, Bors V, Cabro1C, Gandjbakhch I. Intraatrial insertion of a mitral prosthesis in a destroyed or calcified mitral annulus. Ann Thorac Surg 1994; 58:163167 15. Haydock D, Barratt-Boyes B, Macedo T, Kirklin JW, Blackstone E. Aortic valve replacement for active infectious endocarditis in 108 patients: a comparison of freehand allograft valves with mechanical prostheses and bioprostheses. J Thorac Cardiovasc Surg 1992; 103:130-139
For personal use. Mass reproduce only with permission from Mayo Clinic Proceedings.