ATS
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Author home page(s):
Fritz J. Baumgartner
Bassam O. Omari
John M. Robertson
Ronald J. Nelson
Jeffrey C. Milliken
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Baumgartner, F. J.
Right arrow Articles by Milliken, J. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Baumgartner, F. J.
Right arrow Articles by Milliken, J. C.

Ann Thorac Surg 2000;70:442-447
© 2000 The Society of Thoracic Surgeons


Original articles: cardiovascular

Annular abscesses in surgical endocarditis: anatomic, clinical, and operative features

Fritz J. Baumgartner, MDa, Bassam O. Omari, MDa, John M. Robertson, MDa, Ronald J. Nelson, MDa, Avni Pandya, BSa, Andy Pandya, BSa, Jeffrey C. Milliken, MDa

a Division of Cardiothoracic Surgery, Harbor-UCLA Medical Center, Torrance, California, USA

Address reprint requests to Dr Baumgartner, Vascular Surgery Associates, 3791 Katella Ave, Suite 201, Los Alamitos, CA 90720


    Abstract
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 References
 
Background. The aim of this study was to determine patterns of anatomic, clinical, and operative features in surgical endocarditis (SE) with annular abscess (AA).

Methods. The study consisted of a retrospective analysis of SE cases with AA between 1981 and 1997.

Results. A total of 41 cases with AA were found in 106 consecutive SE cases. There was a higher incidence of AA in aortic (37 of 71 [52%]) (p < 0.01) compared to mitral (6 of 42 [14.3%]) or tricuspid (0 of 12) infections. However, the mitral abscesses had a greater tendency toward fistula or pseudoaneurysm formation (4 of 6 [67%]) than other valve abscess cavities (7 of 46 [15%]) (p < 0.01). Severe heart failure (p < 0.01), heart block (p < 0.05), and fistula/pseudoaneurysm (p < 0.001), were more often found in SE with AA than without. There were 46 separate aortic AA in 37 instances of aortic valve SE. Of these, 31 of 46 (67%) were less than 1 cm (group 1), 10 of 46 (22%) were large but confined to a given cusp annulus (group 2), 4 of 46 (8.6%) were large between multiple cusps (group 3), and 1 of 46 (2.2%) was circumferential (group 4). There were four instances of aortoventricular discontinuity. Group 1 abscesses were repaired by local closure without a patch significantly more often than the other groups. The mortality of SE with AA was significantly greater for larger AA (groups 3 and 4, 3 of 5 [60%]) than for smaller AA (groups 1 and 2, 0 of 36) (p < 0.001). There were six separate mitral AA in six instances of mitral SE, five requiring patch repair. The 30-day operative mortality for AA cases was 3 of 41 (7.3%) compared to 2 of 65 (3.1%) without AA. All AA mortalities involved large AA in the aortic valve position. Of 35 mechanical valves placed for AA, only one required subsequent removal for prosthetic endocarditis.

Conclusions. Annular abscesses are most frequent in aortic AA, but fistulas/pseudoaneurysms are more frequent in mitral AA. Small to moderate aortic AA can be managed by local closure without an increased mortality compared to SE without AA. Patients with large aortic AA have a higher operative mortality. Mechanical prostheses are safe and effective for the majority of patients with AA.


    Introduction
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 References
 
Annular abscesses (AA) are serious complications of infectious valvular endocarditis. It is well known that aortic valve endocarditis is much more frequently complicated by ring abscesses than mitral or tricuspid endocarditis [1, 2]. Nonetheless, specific anatomic details including annular location and extent have not been clearly catalogued. We wished to evaluate patterns of anatomic features in surgical endocarditis (SE) with AA, relate them to clinical parameters, and determine their effect on operative strategies and outcomes.


    Material and methods
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 References
 
A retrospective analysis was performed of SE cases with AA treated at Harbor-UCLA between 1981 and 1997 and compared with SE cases without AA treated during that time period. Antibiotic therapy was directed specifically at the offending organism if known; otherwise broad spectrum antibiotics were used. Echocardiographic evaluation was routinely performed; cardiac catheterization was generally reserved for patients more than 45 years of age. "Surgical endocarditis" (SE) was defined by appropriate indications for surgery, as previously described [3]. Intravenous antibiotics were routinely administered for 6 weeks postoperatively. All cases were treated using cardiopulmonary bypass with mild to moderate systemic hypothermia. Cardioplegic arrest was achieved using antegrade cold crystalloid cardioplegia alone, or both antegrade and retrograde cold blood cardioplegia. Surgery on the tricuspid valve was performed with the heart beating. Abscess cavities were thoroughly debrided with resection and currettage of necrotic tissue and thorough providone-iodine swabbing of affected areas. Pledgeted 2-0 Ethibond (Ethicon, Somerville, NJ) valve sutures were used in mattress fashion.

A specific organism is listed as the source of the endocarditis if it was cultured in blood or on the valve itself. A mixed infection was defined as multiple organisms cultured. Intravenous drug abuse(r) [IVDA] was defined as such either in the patient’s past history or at the time of the SE episode. "Dental involvement" was defined as either active caries or having received a dental procedure within 3 months of the SE episode. Active endocarditis was defined as such if the patient had positive blood or valve cultures, signs of ongoing sepsis, rapid progression of an abscess, or if the patient required surgery before completing a standard antibiotic regimin. The AA cavities were thus categorized as active or inactive. Severe heart failure is defined as New York Heart Association Class III or IV, either on admission or during hospitalization. Persistent sepsis was defined as persistent emboli, fever greater than 101.5°F, or positive blood culture despite intravenous antibiotics for at least 3 days. Aortoventricular discontinuity was defined as a separation between the aorta and left ventricle of more than one-third of its circumference. The term "fibrinous pericarditis" was only applied to extensive pericardial adhesions in a first-time, non-redo setting. All aortic abscess cavities were listed as group 1, 2, 3, or 4. Group 1 AA were less than 1 cm; group 2 AA were larger but still confined to a single cusp area; group 3 AA were larger and encompassed multiple cusps; and group 4 was circumferential. Statistical analyses were done using {chi}2 test, Yates correction, and Student’s t test.


    Results
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 References
 
Among 100 patients, there were 106 separate, consecutive SE cases. Of the 106 SE cases, 41 had AA (39%). The SE cases involved a total of 125 valves, of which the highest incidence of AA was found in aortic SE (37 of 71 [52%]). This was a significantly higher rate than AA found in mitral (6 of 42 [14.3%]) or tricuspid (0 of 12) infections (p < 0.01). There were 46 separate aortic AA cavities in 37 instances of aortic valve SE. There were six separate mitral AA cavities in six instances of mitral SE.

Table 1 tabulates the preoperative parameters studied for their relationship to SE with and without AA; Table 2 tabulates the operative and postoperative parameters. S aureus was the most frequently cultured organism in AA cases (13 of 36 [36%]). This was a higher frequency than in SE without AA, but barely missed statistical significance at the 0.05 p value level. Table 3 lists all of the organisms cultured in the 41 SE cases with AA. Large AA (groups 3 and 4) had a higher incidence of S aureus infection than groups 1 and 2 (3 of 5 [60%] vs 10 of 31 [32%]). The cultures in five instances of group 3 and four AA cases were S aureus in 3, S viridens in one, and no growth in one. There were no mixed infections in cases of SE with AA, and this was statistically significant when compared with seven instances of mixed infection in SE without AA.


View this table:
[in this window]
[in a new window]
 
Table 1. Preoperative Characteristics and Relationship to Surgical Endocarditis With and Without Annular Abscesses

 

View this table:
[in this window]
[in a new window]
 
Table 2. Intraoperative and Postoperative Characteristics of Surgical Endocarditis With and Without Annular Abscesses

 

View this table:
[in this window]
[in a new window]
 
Table 3. Blood or Valve Culture Results in 41 Instances of Surgical Endocarditis With Annular Abscesses

 
The most common predisposing factor in the development of SE was IVDA, with or without AA. Of SE with AA, IVDA was a predisposing factor in 49%, similar in frequency to SE without AA. Stated another way, of 48 instances of IVDA-related SE, AA were found in 20 instances (42%). The frequency with which a dental procedure was a predisposing factor was similar for SE with or without AA. Congenital anomalies of valves involved with SE occurred in about equal frequency with or without AA. All eight congenitally anomalous valves in the AA group involved bicuspid aortic valves.

The frequency of active endocarditis was higher in SE with AA than without, but this did not reach statistical significance (an AA in the presence of inactive SE was, in essence, a burned-out abscess cavity). Heart failure (New York Heart Association class III or IV) was significantly more frequent in SE cases with AA than without (84% vs 63%, respectively). Preoperative heart block was present with statistically higher frequency in cases of aortic valve SE with AA compared with cases without AA. Of the five preoperative heart blocks, all were in patients with aortic AA; three were first degree and two were third degree. Overall, AA were more commonly associated with young patients (age <= 40 years), which barely missed statistical significance.

Surgical endocarditis with or without AA both had septic emboli about half of the time. Surprisingly, persistent sepsis as an indication for surgery was found more commonly in patients without AA, although this barely missed statistical significance.

Surgical endocarditis with AA occurred far more frequently in the aortic position than other valve locations. Prosthetic endocarditis was found in 17% of instances of AA compared with 6.2% without AA. This did not reach statistical significance. Stated another way, 7 of 11 instances of prosthetic endocarditis involved an AA (64%). Of note, vegetations were found significantly more frequently in SE without AA (75%) than with AA (44%). Aortoventricular discontinuity was only found in instances in which AA was present, and constituted 11% of instances of AA.

Of 106 SE cases, six fistulas and three pseudoaneurysms were found. With the exception of one pseudoaneurysm arising from an aorta without AA, all arose from nine cases of AA. The overall incidence of a fistula or pseudoaneurysm complicating a case of AA was 9 of 41 (22%). Mitral abscesses had a greater tendency toward fistula or pseudoaneurysm formation than aortic abscesses (4 of 6 [67%] vs 5 of 46 [11%], p < 0.01). The fistulas included aorto–right atrial fistula, two aorto–right ventricular fistulas, right coronary–cameral fistula, and three cases of left ventriculo–atrial fistulas. Of the four pseudoaneurysms arising from AA, two arose from prior aortic suture lines (one from a Dacron patch) and two from posterior mitral annular abscesses eroding into the pericardium. No operative mortalities occurred in these fistula or pseudoaneurysm cases. S aureus was cultured in 5 of 8 (63%) of instances of AA complicated by fistula/pseudoaneurysm compared with 8 of 29 (29%) of instances of AA without fistula/pseudoaneurysm. In the four mitral AA associated with fistula/pseudoaneurysms, 100% cultured out S aureus.

Fibrinous pericarditis was found in 15% of instances of first-time, non-redo SE with AA, and this was significantly more frequent than instances without AA. The mean pump and crossclamp times were significantly higher for SE with AA than without.

The 30-day operative mortality was 7.3% in SE cases with AA, and was 3.1% in cases without AA. Major operative morbidity excluding mortality was significantly higher for SE with AA compared with SE without AA (32% vs 14.6%, respectively). Nonfatal postoperative complications of SE with AA included new third-degree block in patients who did not have a third-degree block preoperatively (four cases), stroke (two cases), tamponade or effusion (two cases), and renal failure (one case).

Of the 43 valves with AA, 40 were replaced. Three repairs were done without valve replacement. Two of these were patch repairs of mitral AA (one polytetrafluoroethylene [PTFE], one pericardial); one was a PTFE patch repair of an aortic suture line involved with an abscess and pseudoaneurysm. In all, 35 St. Jude valves were inserted in 33 instances of SE with AA. One of these 33 instances (3%) developed PVE and involved one St. Jude valve in the aortic position. Conversely, of 43 instances of SE without AA undergoing St. Jude valve insertion, PVE developed in one instance (2%) and involved two St. Jude valves (aortic and mitral valves in a single patient).

Anatomic location of aortic abscesses
There were 46 separate, distinct aortic annular abscesses found at surgery in 37 instances of aortic valve SE. Figure 1 depicts the location of these aortic AA. Of these, 31 of 46 (67%) were less than 1 cm (group 1), 10 of 46 (22%) were large but confined to a given cusp annulus (group 2), 4 of 46 (8.6%) were large between multiple cusps (group 3), and 1 of 46 (2.2%) was circumferential (group 4). Of all aortic annular sites involved with AA, the most common location was at the anterior commissure in 16 instances. The posterior commissure and intercoronary commissure were involved in 14 and 12 instances, respectively. Of the cusp regions of the annulus, the noncoronary cusp (NCC) was involved in 14, the left coronary cusp (LCC) in 13, and the right coronary cusp (RCC) in eight instances. A given aortic AA cavity had the greatest chance of being large (ie, group 2, 3, or 4) if it involved the RCC (6 of 8 [75%] of RCC abscesses were large; 40 of 69 [57%] of non-RCC abscesses were large).



View larger version (23K):
[in this window]
[in a new window]
 
Fig 1. Anatomic locations of 46 aortic annular abscesses (AA). Group 1 were localized, small (< 1 cm) AA (n = 31), Group 2 were larger AA that remained localized to one cusp area (n = 10). Group 3 were very large AA extending between cusp regions (n = 4). Group 4 was a circumferential AA (n = 1). (Gp. = group; L = left coronary cusp; N = noncoronary cusp; R = right coronary cusp.)

 
Group 1 AA were repaired by local closure without a patch or other maneuvers more often than the other groups (17 of 31 [55%] vs 0 of 15 [0%] p < 0.001). The 17 local closures were done using the pledgeted mattress valve sutures or as a separate repair. The remaining 14 group 1 AA repairs included a pericardial patch in seven, and a prosthetic patch less often than in the other groups (11 of 31 [36%] vs 11 of 15 [73%]). A homograft was used less frequently in group 1 compared with other groups (3 of 31 [9.7%] vs 4 of 15 [27%]).

Group 2 AA repairs included a pericardial patch in four, prosthetic patch in four, and homograft in two. Group 3 AA repairs included a pericardial patch in two, prosthetic patch in one, and homograft in one. The single circumferential group 4 abscess was repaired with a St. Jude Dacron valved conduit. There were four instances of aortoventricular discontinuity (two treated by homograft, one by prosthetic valved conduit replacement seated deep into the left ventricular outflow tract, and one by extensive pericardial patch reconstruction and prosthetic valve placement). Figure 2 depicts one such group 3 case with aortoventricular discontinuity.



View larger version (158K):
[in this window]
[in a new window]
 
Fig 2. Example of a group 3 annular abscesses after debridement. This 23-year-old man had staphyloccocus aureus aortic valve endocarditis with multiple septic emboli and heart block. An aortoventricular dehiscence was present, as were annular abscesses near the coronary orifices and into the interventricular septum. On debridement, the aorta was separated from the ventricle, the coronary orifices were left as buttons, and a high ventricular septal defect was created. Homograft repair was done and the patient did well, despite his complete heart block. (1 = left coronary orifice; 2 = right coronary orifice; 3 = right ventricle through a debrided necrotic septum; A = aorta.)

 
The three deaths in SE with AA were all in patients with group 3 AA. Two of these three deaths had S aureus on culture. The mortality of SE with AA was significantly greater for larger AA (group 3 and 4: 3 of 5 [60%]) than for smaller AA (groups 1 and 2: 0 of 41 [0%], p < 0.001).

Anatomic location of mitral abscesses
There were six separate, distinct mitral AA in six instances of mitral SE (Fig 2). Two involved the septal annulus and four the mural annulus. Pericardial and prosthetic patches were used in two and three instances, respectively. The pledgeted mattress valve sutures themselves were used to repair one abscess cavity located at the medial aspect of the septal annulus. As mentioned, mitral abscesses had a significantly higher incidence of fistula/pseudoaneurysm formation.

The mitral AA were repaired without mitral valve replacement in two of six instances. Both cases involved the posteromedial mitral annulus without leaflet involvement and resulted in left ventricular to left atrial fistulas. Repair was accomplished with pericardial patch in one case and PTFE patch in another. Two of the six patients with mitral AA also had aortic AA (33%). There were no operative mortalities in the patients with mitral AA.


    Comment
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 References
 
Perivalvular abscess is a serious complication of native or prosthetic endocarditis. Aside from the well-known finding of a higher incidence of ring abscesses in aortic SE (33% to 50%) compared with mitral SE (10% to 20%), there is a paucity of information detailing specific location, size, and extent of AA and relating this to other clinical and operative features. One such study in 95 necropsy patients with endocarditis showed that patients with annular abscess had a greater frequency of aortic valve involvement, acute valvular regurgitation, pericarditis, heart block, and short duration of symptoms before disability or death [1]. In another study, two independent parameters that significantly predicted AA among patients with native vave endocarditis were aortic valve involvement and IVDA [2].

In the present study, the parameters that were found significantly more frequently in SE with AA compared to SE without AA included severe heart failure, preoperative heart block, aortic location, aortoventricular discontinuity, fistula/pseudoaneurysm, fibrinous pericarditis, major morbidity, and longer crossclamp and pump times. S aureus infection, age 40 years or less, and mortality approached but did not reach a statistically significantly higher incidence in the AA group. The mean cross-clamp and pump times were significantly higher in SE with AA. The higher frequency of severe heart failure in the presence of AA speaks to the virulence of the offending organisms in their ability to cause valvular as well as perivalvular destruction, leading to severe regurgitation and AA. A frequent indication for urgent operation in this situation was acute, refractory heart failure.

The more frequent presence of heart block, aortoventricular discontinuity, fistula/pseudoaneurysm formation, and fibrinous pericarditis further speak to the virulence of an infection resulting in an AA. Previous studies have documented that periannular extension of endocarditis, particularly in the aortic position, can lead to preoperative atrioventricular block [4, 5]. Even if no heart block is present preoperatively, the appropriately radical debridement of infected, necrotic tissue may lead to permanent, complete atrioventricular block.

Aortoventricular discontinuity in our study was present in 5.6% of all instances of aortic SE and in 11% of aortic SE with AA. All methods that we used to repair aortoventricular discontinuity, including homograft, valve conduit, or pericardial patch and mechanical valve insertion, have documented success in the literature. David and colleagues [57] report the use of autologous pericardium in the extensive reconstruction of the left ventricular outflow tract and common annulus between the aortic and mitral valves in SE with AA. This was followed by insertion of a prosthetic valve alone or by a valved conduit with reimplantation of the coronary arteries. Others have successfully used prosthetic graft material rather than pericardium for major annular reconstruction in aorto–ventricular discontinuity [8] or fibrous skeleton AA within the aortic-mitral common annulus [9]. Homografts also have seen excellent results for complex aortic endocarditis [10].

Fistulas and pseudoaneurysms are the result of periannular extension of endocarditis with tissue necrosis and liquefaction leading to communication between, or external to, cardiac chambers. The incidence of fistulas/pseudoaneurysms in our patients was much higher for mitral AA than aortic AA (67% vs 11%, respectively).

The fibrinous pericarditis in our six patients, aside from previous sternotomy and pericardiotomy, represents an intrinsic inflammatory response from the endocarditis. In 5 of 6 instances of fibrinous pericarditis associated with SE, it occurred in the setting of AA. This bespeaks of the severe inflammation resulting in the AA, but even more ominously may represent extracardiac extension of the AA [1], as occurred in multiple instances in our series. A dense pericarditis found at the time of operation for SE should alert the surgeon to the probability of AA, possibly with pseudoaneurysm formation.

In our study, there was a higher operative mortality and major morbidity in SE with AA as compared to without, although only the latter was statistically significant. Although intuitively likely, various studies differ as to whether AA is indeed a significant risk factor for operative mortality. David and colleagues showed that AA was a significant risk factor for operative mortality in univariate, but not multivariate analysis [5]. Others [4, 11, 12] imply that AA is not a risk factor for mortality, and that radical debridement is the key to keeping the operative mortality low [4]. Although we agree that radical debridement is imperative and that this will lower the mortality, we nonetheless believe that the extensive reconstruction necessary to treat large AA will increase the operative mortality from increased cross-clamp and pump times alone, apart from repairing fistulas, pseudoaneurysms, and aortoventricular separation. Furthermore, the mere presence of AA in and of itself, particularly large group 3 or 4 AA, bespeaks of a more aggressive form of endocarditis.

Severe heart failure may be one manifestation of this more aggressive form of SE associated with AA. Previous studies have shown heart failure to be associated with AA, and the heart failure to be associated with increased operative mortality [1, 4]. The decreased incidence of vegetations and persistent sepsis in AA cases in our study may reflect a process that is more destructive to valve leaflets, necessitating earlier surgery.

Whether S aureus infections are more commonly found in SE with AA differs from study to study. In a previous review from our institution [2], S aureus was not found to be a predictive risk factor for periannular extension of native valve endocarditis. Several previous reports have emphasized the importance of virulent gram-positive cocci, especially S aureus, among cases of periannular extension of native valve endocarditis [1, 13, 14]. However, none showed a statistically significant difference in the incidence of S aureus infections with or without AA. More intriguing in our study is the finding of the greatest incidence of S aureus growth in the most aggressive AA, ie, those involving fistulas or pseudoaneurysm formation (particularly mitral AA) or those cases of large group 3 or 4 aortic AA.

In the current study of 106 instances of SE from 1981 to 1997, AA were found in 46% of aortic SE versus 14% of mitral SE. This is compared to several previous reports from our institution. In the earliest study [15], of 32 patients with SE from 1972 to 1977, AA were found in 10 of 25 (40%) aortic SE versus 1 of 10 (10%) of mitral SE. In another study [2], of 73 episodes of native SE between 1973 and 1987, AA were found in 25 of 53 (47%) aortic SE versus 7 of 28 (25%) of mitral SE.

The present study did not identify IVDA as a risk factor in the development of AA in SE. In two previous studies from our institution [2, 15], IVDA patients were found to have a higher incidence of periannular extension than non–drug abusers. The reason for the differences between the studies is unclear. However, the prior studies were from the 1970s and 1980s, and the present era may reflect earlier intervention for IVDA-related endocarditis before the development of AA.

There is considerable variance of opinion in the literature regarding the optimal valve to be used to replace an infected valve, particularly in the presence of an AA. Conceptually, homografts would seem more resistant to infection than mechanical prostheses, and there is some evidence in the literature to support this [16]. Although the results of homograft use in complex SE are excellent [10], homografts and even autografts are not immune to the development of endocarditis [17]. Furthermore, mechanical valves in the face of acute infective endocarditis are safe with a low incidence of recurrent endocarditis (2.2% in one series) as long as radical debridement of infective tissues is done [4]. In our current series, of the 40 valve replacements done in the presence of AA, St. Jude mechanical prostheses were used 35 times (88%). Only one of the 35 St. Jude valves placed for AA in our study required removal for prosthetic valve endocarditis. There was no greater risk for PVE in mechanical valves placed in SE with AA compared to without AA. We believe that the reasons for these good results is not only radical abscess debridement but swabbing of the area with providone iodine.

Previous studies detailing AA size and anatomic location have been scant. The present study grouped individual aortic abscesses into groups 1 to 4, of progressively increasing size and extent. Large AA had a general predilection for the annular region corresponding to the RCC. Predictably, the smaller abscesses could be managed with local closure about half the time, whereas the larger abscesses always needed additional repair techniques. Mortality was far greater for larger aortic AA in groups 3 and 4 (60%) compared with groups 1 and 2 (0%).

Mitral AA pose difficult management problems because of the proximity of the circumflex artery, coronary sinus, and ventricular free wall. Such cavities may rupture into the pericardial space [18], between the aorta and left atrium [19], or between the left atrium and ventricle [20]. For the mitral AA in our study, patching was the predominant mode of repair. David and colleagues have previously emphasized the importance of patch reconstruction of mitral AA as superior to primary closure [6].

The presence of AA is not a reported risk factor for mortality in mitral SE. The present study confirms the relatively low incidence of AA in mitral SE. In our six instances of mitral AA, there was concurrent aortic AA one-third of the time. This speaks to the virulence of infection that leads to mitral AA, and confirms that the aortic valve should be viewed with suspicion in cases of mitral AA [1]. Another finding in our study implying that mitral SE with AA is particularly virulent is the significantly higher frequency with which fistulas/pseudoaneurysms were found in mitral AA compared with aortic AA. Furthermore, of those mitral AA involving fistula/pseudoaneurysm formation, all grew S aureus as the offending organism.

Mitral valve repair techniques in SE have been advocated [21, 22]. We previously reported two patients from our present series who underwent repair of left ventriculoatrial fistulas because of posterior mitral AA [20].

With regard to AA in SE, we conclude that the aortic valve is most commonly involved with AA. However, the presence of mitral AA, S aureus infection, or fistula/pseudoaneurysm formation signifies a more aggressive AA infection. S aureus was more frequently involved in SE with AA than without, but was even more frequently found in aggressive cases involving fistula/pseudoaneurysm formation, especially of the mitral valve, or very large aortic AA. Operative mortality is increased in cases of large, aggressive aortic AA requiring extensive reconstruction. Mechanical prostheses in SE, even with AA, can be safe with a low risk of PVE.


    Acknowledgments
 
Funding for this work was supported in part by St. Jude Medical Inc, Minneapolis, MN.


    References
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 References
 

  1. Arnett E., Roberts W.C. Valve ring abscess in active infective endocarditis. Circulation 1976;54:140-145.[Abstract/Free Full Text]
  2. Omari B., Shapiro D., Ginzton L., et al. Predictive risk factors for periannular extension of native valve endocarditis. Chest 1989;96:1273-1279.[Abstract/Free Full Text]
  3. Cukingnan R.A., Carey J.S., Wittig J.H., Cimochowski G.E. Early valve replacement in active infective endocarditis—results and late survival. J Thorac Cardiovasc Surg 1983;85:163-173.[Abstract]
  4. Bauernschmitt R., Jakob H.G., Vahl C.F., Lange R., Hagl S. Operation for infective endocarditis. Ann Thorac Surg 1998;65:359-364.[Abstract/Free Full Text]
  5. David T.E., Bos J., Christakis G.T., Brofman P.R., Wong D., Feindel C.M. Heart valve operations in patients with active infective endocarditis. Ann Thorac Surg 1990;49:701-705.[Abstract]
  6. David T.E., Feindel C.M., Ropchan G.V. Reconstruction of the left ventricle with autologous pericardium. J Thorac Cardiovasc Surg 1987;94:710-714.[Abstract]
  7. David T.E., Komeda M. Surgical treatment of aortic root abscess. Circulation 1989;80(Suppl 1):269-274.
  8. Symbas P.N., Vlasis S.E., Zacharopoulos L., Hatcher C.R., Arensberg D. Immediate and long-term outlook for valve replacement in acute bacterial endocarditis. Ann Surg 1982;195:721-725.[Medline]
  9. Kameyama T., Ando F., Okamoto F., Hanada M., Sasahashi N. A brimmed valve conduit in repair of fibrous skeleton abscess. Ann Thorac Surg 1998;66:2108-2110.[Abstract/Free Full Text]
  10. Dearani J.A., Orszulak T.A., Schaff H.V., Daly R.C., Anderson B.J., Danielson G.K. Results of allograft aortic valve replacement for complex endocarditis. J Thorac Cardiovasc Surg 1997;113:285-291.[Abstract/Free Full Text]
  11. Lewis B.S., Agathangelou N.E., Colsen P.R., Antunes M., Kinsley R.H. Cardiac operation during active infective endocarditis—results of aortic, mitral, and double valve replacement in 94 patients. J Thorac Cardiovasc Surg 1982;84:579-584.[Abstract]
  12. Jault F., Gandjbakhch I., Rama A., et al. Active native valve endocarditis. Ann Thorac Surg 1997;63:1737-1741.[Abstract/Free Full Text]
  13. Mammano R.B., Levitsky S., Sernaque D., Bechman C.B., Silverman N.A. Valve replacement for left-sided endocarditis in drug addicts. Ann Thorac Surg 1983;35:436-441.[Abstract]
  14. Dinubile M.J. Surgery in active endocarditis. Ann Intern Med 1982;96:650-659.
  15. Hiratzka L.F., Nelson R.J., Oliver C.B., Jengo J.A. Operative experience with infective endocarditis—drug users compared with non-drug users. J Thorac Cardiovasc Surg 1979;3:355-361.
  16. Haydock D., Barratt-Boyes B., Macedo T., Kirklin J.W., Blackstone E. Aortic valve replacement for active infectious endocarditis in 108 patients. J Thorac Cardiovasc Surg 1992;103:130-139.[Abstract]
  17. Prat A., de Ibarra J.S., Vincentelli A., Decoene C., Savoye C., Goffin Y. Late autograft and homograft endocarditis after the Ross operation. J Thorac Cardiovasc Surg 1998;115:1388-1389.[Free Full Text]
  18. Weale A.E., Hutter J., Collins C.M.P Rupture of ventricular abscess after mitral valve replacement. Br Heart J 1992;67:271-272.[Abstract/Free Full Text]
  19. English T.A.H., Cleland W.P. Ruptured true aneurysm of mitral valve. Br Heart J 1972;34:434-436.[Free Full Text]
  20. Baumgartner F., Omari B., Milliken J. Repair of left ventricular-atrial fistulas due to posterior mitral annular abscesses. J Heart Valve Dis 1997;6:550-552.[Medline]
  21. Dreyfus G., Serraf A., Jebara V.A., et al. Valve repair in acute endocarditis. Ann Thorac Surg 1990;49:706-713.[Abstract]
  22. Hendren W.G., Morris A.S., Rosenkranz E.R., et al. Mitral valve repair for bacterial endocarditis. J Thorac Cardiovasc Surg 1992;103:124-129.[Abstract]
Accepted for publication February 4, 2000.




This article has been cited by other articles:


Home page
Anesth. Analg.Home page
S. Garneau, P. Demers, and A. Y. Denault
Unexpected Periaortic Cavity During Heart Surgery
Anesth. Analg., January 1, 2007; 104(1): 75 - 76.
[Full Text] [PDF]


Home page
Eur J EchocardiogrHome page
J. Walpot, C. Klazen, R. Hokken, J. Sorgedrager, M. Hoevenaar, and J. den Braber
Aorto-right ventricular fistula as an occasional finding
Eur J Echocardiogr, January 1, 2005; 6(1): 65 - 66.
[Abstract] [Full Text] [PDF]


Home page
Eur. J. Cardiothorac. Surg.Home page
R. Turkoz, O. Gulcan, E. Uguz, and H. B. Cihan
Mitral valve replacement after application of atrial appendix flap in endocarditis with posterior annular abscess
Eur. J. Cardiothorac. Surg., October 1, 2004; 26(4): 837 - 838.
[Abstract] [Full Text] [PDF]


Home page
NEJMHome page
A. W. Karchmer, D. F. Torchiana, C. U. Chae, N. A. Afridi, and S. L. Houser
Case 29-2004 - A 75-Year-Old Woman with Acute Onset of Chest Pain Followed by Fever
N. Engl. J. Med., September 16, 2004; 351(12): 1240 - 1248.
[Full Text] [PDF]


Home page
J. Thorac. Cardiovasc. Surg.Home page
T. Fukui, S. Suehiro, T. Shibata, K. Hattori, H. Hirai, and T. Aoyama
Aortic root replacement with Freestyle stentless valve for complex aortic root infection
J. Thorac. Cardiovasc. Surg., January 1, 2003; 125(1): 200 - 203.
[Full Text] [PDF]


Home page
NEJMHome page
E. Mylonakis and S. B. Calderwood
Infective Endocarditis in Adults
N. Engl. J. Med., November 1, 2001; 345(18): 1318 - 1330.
[Full Text] [PDF]


This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Author home page(s):
Fritz J. Baumgartner
Bassam O. Omari
John M. Robertson
Ronald J. Nelson
Jeffrey C. Milliken
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Baumgartner, F. J.
Right arrow Articles by Milliken, J. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Baumgartner, F. J.
Right arrow Articles by Milliken, J. C.


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
ANN THORAC SURG ASIAN CARDIOVASC THORAC ANN EUR J CARDIOTHORAC SURG
J THORAC CARDIOVASC SURG ICVTS ALL CTSNet JOURNALS