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J Thorac Cardiovasc Surg 1994;108:207-214
© 1994 Mosby, Inc.
SURGERY FOR ACQUIRED HEART DISEASE |
Denver Colo., San Antonio, Tex., Hines, Ill., and Tucson, Ariz.
Supported by the Cooperative Studies Program of the Department of Veterans Affairs Medical Research Service.
Address for reprints: Frederick L. Grover, MD, Surgical Service (112), Department of Veterans Affairs Medical Center, 1055 Clermont, Denver, CO 80220.
Abstract
For the determination of the risk factors associated with the development of and death caused by prosthetic valve endocarditis, data were reviewed from 66 patients who were prospectively entered into the Veterans Affairs Cooperative Study on Valvular Heart Disease and in whom prosthetic valve endocarditis subsequently developed. Data were recorded at 13 medical centers between October 1977 and September 1982 in patients randomized to receive a mechanical valve (Björk-Shiley spherical disc, n = 510 patients) or a bioprosthetic valve (Hancock porcine heterograft, n = 522 patients). The average rate of prosthetic valve endocarditis development was 0.8% per year over an average follow-up period of 7.7 years. Of the 66 patients in whom prosthetic valve endocarditis developed (5.8%), 15 cases occurred within 2 months of operation (early) and 51 occurred after operation (late). The most significant preoperative predictor of prosthetic valve endocarditis was active endocarditis at the time of operation (7.4% versus 0.9%) (p = 0.001). Early prosthetic valve endocarditis occurred more frequently in patients who underwent operation for multivalvular disease (p = 0.023). Significantly related perioperative variables were coma, prolonged mechanical ventilation, deep postoperative wound infection, postoperative jaundice, ventricular tachycardia, ventricular fibrillation, and replacement of more than one valve (p < 0.05). Multivariate predictors were hypoxia (p = 0.001), preoperative endocarditis (p = 0.003), preoperative valve lesion (p = 0.020), and resident surgeon (p = 0.05). Significant preoperative variables predictive of late prosthetic valve endocarditis were mitral stenosis and mixed mitral stenosis-regurgitation. The only multivariate predictor of late prosthetic valve endocarditis was superficial wound infection (p = 0.004). Of deaths attributable to prosthetic valve endocarditis, 41% occurred in patients treated with antibiotics alone, 48% occurred in patients treated with surgical intervention and antibiotics, and death resulted in both patients who received no treatment. No difference was found in the risk of early or late postoperative prosthetic valve endocarditis developing in patients receiving the mechanical valve versus those receiving the bioprosthetic valve. (J THORAC CARDIOVASC SURG 1994;108;207-14)
Despite the apparent decrease in occurrence of prosthetic valve endocarditis (PVE) since the 1960s, 
1 the mortality in mostseries reported in the 1980s remains 30% or more. 2-7 Generally, PVE within 2 months after valve replacement (early) carries a higher mortality (65% to 80%) than does PVE more than 2 months after valve replacement (late) (30% to 50%). Several reports have emphasized a more favorable outcome of PVE with prompt surgical therapy, particularly with replacement of the infected valve. 5,6,8 Nevertheless, PVE continues to be a highly lethal disease. Thus, there is a need to identify patients at risk and institute appropriate preventive measures. It is the purpose of this article to examine the univariate and multivariate risk factors for development of and death resulting from PVE on the basis of 66 such patients from the Veterans Affairs (VA) Cooperative Study on Valvular Heart Disease.
METHODS
The 13 medical centers participating in the Department of Veterans Affairs Cooperative Study on Valvular Heart Disease entered 1482 patients at the time of clinically indicated diagnostic cardiac catheterization between October 1977 and September 1982 to achieve two principal goals: (1) to identify variables predictive of survival in patients with valvular heart disease and (2) to compare death and valve-related complication rates between patients undergoing single aortic or mitral valve replacement randomized to receive a mechanical (Björk-Shiley spherical disc; Shiley, Inc., Irvine, Calif.) or a bioprosthetic (Hancock porcine heterograft; Johnson & Johnson Cardiovascular, King of Prussia, Pa.) valve. 9 The 5-, 7.5-, and 11-year results of the 575 patients in the randomized trial have been published. 9-11
Patient population
The present report is based on the 1137 of the 1482 patients in the registry who underwent replacement of one or more cardiac valves with or without other concomitant cardiac procedures. Of these 1137 patients, 510 received a Björk-Shiley spherical disc valve, and 522 received the Hancock porcine heterograft; the remaining 105 received an assortment of other prosthetic valves. There were 735 patients with aortic valve replacement (356 Björk-Shiley, 345 Hancock, 44 other), 274 patients with mitral valve replacement (117 Björk-Shiley, 154 Hancock, 3 other), 94 patients with multiple valve replacement (47 Björk-Shiley, 23 Hancock, 24 other), and 34 with missing data. All patients were male; the mean age at entry was 59.9 years. None had undergone previous valve replacement.
Data collection
Although the detailed study design has been published, 12 a summary relevant to the present report will be given here. Over 300 baseline variables from the history, physical examination, routine laboratory evaluation including chest roentgenogram and electrocardiogram, exercise tolerance test, and cardiac catheterization with quantitative left ventricular angiography and coronary arteriography were recorded on standardized data forms at the time of cardiac catheterization. The present analyses were limited to 14 preoperative variables and 20 perioperative variables selected for possible relevance to development of or survival from PVE. Preoperative variables were as follows: age, valve lesion, New York Heart Association functional class, congestive heart failure, diabetes, prior heart surgery, body surface area, preoperative endocarditis, arterial oxygen tension, serum creatinine, serum bilirubin, arteriographic evidence of coronary artery disease, and left ventricular ejection fraction. Perioperative variables were as follows: valve position, mechanical or bioprosthetic valve, valve size, concomitant coronary artery bypass grafting, left ventricular aneurysectomy, surgical priority, total crossclamp time, total operative duration, use of the intraaortic balloon pump, sustained intraoperative arrhythmia, attending physician versus resident physician as principal surgeon, superficial wound infection, deep wound infection, postoperative ventricular tachycardia or ventricular fibrillation, postoperative unconsciousness for more than 48 hours, postoperative jaundice, postoperative hypoxia, causative organism, medical versus medical plus surgical therapy, and time from diagnosis of endocarditis to surgical therapy.
PVE was diagnosed if the following criteria were met: (1) if there was fever and two or more blood cultures were positive for the same organism in the absence of another obvious focus of infection, (2) if bacteria was cultured from or identified histologically in pus or vegetation on or near the prosthetic valve, or (3) if bacteria was cultured from or identified histologically in septic emboli. Early PVE was defined as that developing 2 months after the operation or before, and late PVE was defined as that occurring more than 2 months after the operation.
Patients were followed up at 6-month intervals at the participating cardiac surgical center through October 1985, at which time detailed follow-up of the nonrandomized patients was terminated. Mean follow-up duration of patients in this report was 7.7 years. At each follow-up visit, a standardized data form containing objective questions relevant to the definitions of the valve-related complications (including endocarditis) was completed. If a data form suggested a possible valve-related complication, the data form, supplemented by the narrative medical record, was reviewed by a subcommittee blinded to valve type for final determination of occurrence of a valve-related complication. A similar procedure was followed for classification of cause of death.
Data analysis
Continuous variables were transformed into clinically meaningful categorical variables (e.g., age 
60 or >60); the univariate relation to development of or survival from PVE was assessed by the 
2 test (Fisher's exact test for dichotomous variables with expected frequences less than 5). For the identification of independent predictors of early PVE, variables with p < 0.2 on univariate testing were entered into a logistic regression analysis. Cox's regression analysis was used to determine independent predictors of late endocarditis and survival from endocarditis. Kaplan-Meier survival curves were used to compare the risk of PVE developing for patients with a mechanical valve versus a bioprosthetic valve and to compare survival after development of early versus late PVE.
RESULTS
Sixty-six of the 1137 (5.8%) patients had PVE over the 7.5-year average follow-up; fifteen cases occurred within 2 months of operation (early PVE), whereas late PVE occurred in 51 patients. As shown in Fig. 1, the rate of development of endocarditis was relatively constant over the entire period of follow-up—approximately 0.8% per year.
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Table I summarizes the data on the relationship between preoperative variables and the development of early postoperative PVE. The most significant predictor was the presence of active endocarditis at the time of valve replacement; PVE developed in 7.4% (5 of 68) of patients with preoperative endocarditis, but only 0.9% (10 of 1066) of patients who did not have endocarditis at the time of operation (p = 0.001). Early PVE occurred more frequently in patients who underwent operation for multivalvular disease (p < 0.023) compared with those patients with single valve lesions. An S3 gallop, congestive heart failure, preoperative hypoxemia, chronic renal failure, and increased jugular venous pressure exhibited relationships to early PVE of borderline statistical significance (p = 0.05 to 0.2). The preoperative variables not significantly associated (p > 0.2) with the development of early PVE were of interest: more than 60 years of age (8 of 461; 1.7%), New York Heart Association functional class III or IV (12 of 757; 1.6%), diabetes (0 of 40; 0%), previous heart surgery (1 of 82; 1.2%), serum bilirubin level more than 1.5 mg/dl (1 of 73; 1.4%), and arteriographic evidence or coronary artery disease (8 of 462; 1.7%).
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Table I). Perioperative variables with a borderline statistically significant relationship (p = 0.05 to 0.2) to early PVE were resident physician as the primary surgeon, emergency operation, intraoperative arrhythmia, left ventricular aneurysectomy, superficial wound infection, and aortic valve size of 23 mm or less. No difference was found in the risk of developing early postoperative PVE between patients receiving the Björk-Shiley spherical disc valve (1.4%) and those receiving the Hancock porcine heterograft valve (1.2%). Other relevant perioperative variables that were not significantly (p > 0.2) related to early PVE included mitral valve size of 29 mm or less (1 of 131; 1.5%), concomitant coronary artery bypass grafting (7 of 417; 1.7%), total crossclamp time 2 hours or more (1 of 142; 0.7%), total operative duration of 4 hours of more (11 of 639; 1.1%), and use of the intraaortic balloon pump (3 of 143; 2.1%).
Multivariate predictors of early PVE.
Table II shows the results of the logistic regression analysis of the preoperative and perioperative variables in Table I, with p < 0.2. Preoperative hypoxia (arterial oxygen tension less than 80 mm Hg) and active endocarditis at the time of operation were the most powerful independent predictors of early PVE; patients with preoperative hypoxemia and active endocarditis at the time of operation had adjusted relative risks of 7.9 (p = 0.001) and 6.8 (p = 0.003), respectively, for the development of early postoperative endocarditis compared with patients without these risk characteristics. Other significant predictors were preoperative valve lesion (p = 0.020) and operation by resident physician (adjusted relative risk = 3.2; p = 0.050).
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Table III). However, late PVE occurred about twice as often in patients with preoperative valve lesions of mitral stenosis (8.1%) and mixed mitral stenosis and regurgitation (8.6%) compared with patients with other valve lesions (4.0%; p = 0.073). Preoperative hypoxia was also of borderline statistical significance (p = 0.191). No other preoperative variable approached statistical significance, including the following: age greater than 60 years (26 of 479; 5.4%), diabetes (3 of 43; 6.7%), preoperative endocarditis (2 of 63; 3.2%), serum creatinine level greater than 1.5 mg/dl (4 of 146; 2.7%), and serum bilirubin level greater than 1.5 mg/dl (4 of 76; 5.3%).
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Table III). As with early PVE, the prevalence of late endocarditis is virtually identical in patients with a Björk-Shiley prosthesis (5.0%) and those with a Hancock porcine heterograft (4.9%).
Multivariate predictors of late PVE.
With the use of the multivariate Cox regression analysis, the only variable significantly (p < 0.05) independently predictive of the development of late endocarditis was superficial wound infection (risk ratio = 3.5; p = 0.004) (Table IV). Valve position (aortic, mitral, and multiple) was of borderline statistical significance (p = 0.0809), with mitral being higher risk.
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Late endocarditis. Again, Staphylococcus epidermidis was the most common organism with 12 cases (24%); seven (14%) patients were infected with Staphylococcus aureus. Other organisms included Streptococcal viridans (four cases), Enterobacter aerogenes (three cases), Streptococcus bovis (two cases), and Enterococcus (two cases). There were no instances of late fungal endocarditis.
Outcome from PVE
Forty-two of the 66 patients with PVE died: 30 (46%) as a direct result of their PVE, nine (14%) as a result of other causes, and three unclassified (5%). The mortality was similar to that with gram-positive organisms (48%, 24 of 51) and gram-negative organisms (36%, 4 of 11). Similarly, no difference in mortality was found between patients with early (47%) or late (45%) PVE.
Predictors of death resulting from PVE.
The only preoperative variable predictive of death caused by PVE was New York Heart Association functional class, with 57% of patients in functional class III and IV dying compared with 30% in class I or II (p = 0.048, Table V). No difference in rates of death from PVE was found for patients with the Björk-Shiley valve (47%) compared with patients with the Hancock porcine heterograft valve (50%). We also examined the relationship between certain risk characteristics present within the month after the diagnosis of late PVE and death caused by endocarditis. Weak associations were found between New York Heart Association functional class (9 of 16 in class III or IV died compared with 5 of 18 in class I or II; p = 0.163) and pulse rate greater than 100 beats/min (7 of 12 with pulse >100 beats/min died compared with 8 of 24 with pulse 100 beats/min; p = 0.175), but no association was found (p > 0.2) between mortality and exertional dyspnea, paroxysmal nocturnal dyspnea, increased venous pressure, rales, S3 gallop, or a diagnosis of congestive heart failure.
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Only about one third of patients (n = 23) received operative treatment for their PVE: six for early endocarditis and 17 for late endocarditis. Death directly attributable to the endocarditis occurred in 41% (17 of 41) of those treated with antibiotics alone, 48% (11 of 23) of those treated with operation plus antibiotics, and in both patients who received no treatment. The high mortality rate among surgically treated patients with PVE could not be attributed to delay in operation. For the 20 patients with a known interval from diagnosis of endocarditis to reoperation, the mortality rate from endocarditis was 67% (8 of 12) in those who underwent operation within 7 days of diagnosis but only 13% (1 of 8) in those who underwent operation more than 7 days after diagnosis.
DISCUSSION
In a cohort of 1137 patients with prosthetic valves prospectively followed up from the time of entry at initial diagnostic catheterization into the VA Cooperative Study on Valvular Heart Disease, PVE developed at a constant rate of approximately 0.8% per year. The development of early PVE was significantly related to coma for more than 48 hours in the postoperative period, postoperative hypoxia, presence of active endocarditis before the operation, deep wound infection, postoperative jaundice, preoperative valve lesion (multivalvular disease more so than mitral stenosis and regurgitation more so than other valve lesions), postoperative ventricular tachycardia or ventricular fibrillation, and prosthetic valve replaced (multiple more so than mitral more so than aortic). The only variable associated with the development of late endocarditis was postoperative superficial wound infection. No difference was found in susceptibility of mechanical versus bioprosthetic valves to development of endocarditis; nor was any difference found in mortality once endocarditis developed. The mortality from PVE was high (45%, 30 of 66) with no apparent favorable impact from reoperation.
Early postoperative PVE
Preoperative predictors.
Although the most powerful preoperative predictor of early PVE was active endocarditis at the time of operation, it is notable that only 7% of patients (5 of 68) had PVE.
Early PVE developed in patients with regurgitant valve lesions several times more frequently than in those with stenotic lesions (Table I); this finding was probably not a result of preoperative active endocarditis causing the regurgitation because both preoperative endocarditis and valve lesion were statistically significant in the multivariate analysis.
Equally important were the variables not associated with the development of early PVE: age, New York Heart Association functional class, diabetes, previous heart operation, and elevated serum bilirubin level.
Several previous reports have also noted the increased risk of PVE in patients with active endocarditis at the time of valve replacement. 13,14 The sevenfold increase in risk of PVE in patients with preoperative endocarditis reported by Arvay and Lengyel 13 is identical to our adjusted risk ratio of 6.8 (Table II). Similarly, an increased risk of PVE has been previously reported for multiple valve replacement 8 and for mitral valve replacement 15; however, others have reported an increased frequency of PVE in the aortic position. 13,14
Perioperative variables.
The most striking finding is that we did not find an association between early PVE and five important measures of operative complexity: prior heart operation, concomitant coronary artery bypass grafting, intraoperative use of the intraaortic balloon pump, total aortic crossclamp time, and total operative duration. However, a weak association was found with emergency priority of operation (p = 0.078). The weak association with left ventricular aneurysectomy may be a chance observation because only eight patients had this procedure, one of whom had early PVE.
Conflicting data exist in the literature regarding whether a bioprosthetic or mechanical valve has a lower risk of developing PVE and achieving a better outcome once PVE develops. Arvay and Lengyel 13 report about a fourfold increase in actuarial prevalence of PVE in patients with a bioprosthesis. However, data from both of the randomized trials comparing outcomes of patients after valve replacement with a mechanical prosthesis versus a bioprosthesis show no difference in risk of PVE developing. 11,16 Furthermore, the data in the present report combining patients in the randomized trial and registry of the VA Cooperative Study on Valvular Heart Disease show identical survival after development of mechanical valve endocarditis or bioprosthetic valve endocarditis (Fig. 2).
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17
Although early endocarditis appeared to develop more frequently if the resident physician (2.0%) and not the attending physician (0.7%) was the primary surgeon, our previously published analyses have shown no differences in either operative mortality 18 or morbidity 19 between resident and attending surgeons.
Late postoperative PVE
If the hypothesis that late PVE is the result of transient bacteremia associated with antecedent procedures or illnesses 20,21 is correct, then it is not surprising that we found few associations between preoperative variables and late PVE. Furthermore, the absence of associations between age and comorbid conditions not likely to be corrected by valve replacement (preoperative hypoxia, diabetes, elevated creatinine, increased bilirubin, and left ventricular dysfunction) lends support to the concept that the inciting bacteremia has a preventable cause. Unfortunately, compliance with the American Heart Association recommendations for endocarditis prophylaxis has been less than optimal. 22
Outcomes after PVE
Limited evidence exists that survival after PVE may be improving; some have reported survival rates of greater than 75% 23—particularly with surgicaltherapy. 24,25 On the other hand, our data and many other reports 2-7 indicate that PVE is a disease with a distressingly high fatality rate. The persistently high mortality is not surprising given the location of the infection between the prosthetic valve sewing ring and the fibrous valve anulus for all mechanical prosthetic valve infections and many bioprosthetic valve infections. This infection results in a burrowing abscess into the myocardium and conduction system and destruction of the fibrous anulus. Furthermore, septic embolization is common. 26
Although our search for patient characteristics that were present the month preceding late PVE diagnosis and were related to endocarditis death was unsuccessful by conventional criteria (p < 0.05), the mortality from late PVE was about twice as high in patients in New York Heart Association functional class III or IV (56%) compared with those in class I or II (28%), in patients with a pulse rate of 100 beats/min or greater (58%) compared with those with a pulse rate of less than 100 beats/min (33%), and in patients with increased venous pressure (71%) compared with those without (38%). These data support the current recommendations for early operative therapy in patients with congestive heart failure. 6,27
Conclusions and clinical implications
We undertook this investigation with the intent of identifying subgroups of patients susceptible to the development of PVE so that specific preventive measures could be recommended. We were able to identify only active preoperative endocarditis and postoperative deep wound infection as causative factors for early PVE and perioperative superficial wound infection as a possible causative factor for late PVE. No difference was found in the prevalence of early or late PVE between Björk-Shiley and Hancock prostheses. Our data and much of the current literature indicate a persistently high mortality with PVE.
Appendix: APPENDIX
Participants in the Department of Veterans Affairs (DVA) Cooperative Study on Valvular Heart Disease
Co-chairman's Office (DVA Medical Center, Denver, Colo) K. E. Hammermeister, MD, Medical Co-chairman; Randall Johnson, MS, Computer Specialist; Anita Birdwell, Data Analyst
Co-chairman's Office (DVA Medical Center, Tucson, Ariz.) Gulshan K. Sethi, MD, Surgical Co-chairman; Martin Haluza, Data Technician
Hines DVA Cooperative Studies Program Coordinating Center (DVA Medical Center, Hines,Ill.) William G. Henderson, PhD, Chief; Charles Oprian, PhD, Study Biostatistician; Tai Kim, Study Programmer; Mary Ellen Vitek, Study Coordinator
Participating Investigators Michael Crawford, MD (University of New Mexico, Albuquerque)Edward D. Folland, MD (University of Massachusetts, Worcester, Mass.); Frederick L. Grover, MD (DVA Medical Center, San Antonio, Tex.); Shukri Khuri, MD (DVA Medical Center, West Roxbury, Mass.); Ming Hwang, MD (DVA Medical Center, Hines, Ill.); D. Craig Miller, MD (DVA Medical Center, Palo Alto, Calif.)
Consultant Shahbudin Rahimtoola, MD (University of Southern California, Los Angeles, Calif.)
DVA Central Office Daniel Deykin, MD, Chief, Cooperative Studies Program (DVA Medical Center, Boston, Mass.); Janet Gold, Administrative Office (DVA Medical Center, Boston, Mass.); Ping Huang, PhD, Staff Assistant (Washington, D.C.)
Footnotes
From the Cardiothoracic Surgery and Cardiology Sections of the Denver Department of Veterans Affairs Medical Center, University of Colorado Health Sciences Center, Denver, Colo. a; Audie L. Murphy Memorial Veterans Administration Hospital and the University of Texas Health Science Center, San Antonio, Tex. b; the Cooperative Studies Program Coordinating Center, Department of Veterans Affairs Medical Center, Hines, Ill. c; and the Department of Veterans Affairs Medical Center, University of Arizona Health Sciences Center, Tucson, Ariz. d 
Read at the Seventeenth Annual Meeting of the Western Thoracic Surgical Association, Seattle, Wash., June 16-29, 1991.
*See Appendix for personnel listing.
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