Keywords
INTRODUCTION
The mortality associated with repeat valve repair is 4.7% to 6.8% for scheduled surgery1,2 and as high as 25% to 41% for emergency reoperations, as in the case of prosthetic heart valve thrombosis.3 However, the long-term natural history of patients who require various reoperations for prosthetic mitral valve dysfunction is not well understood. The purpose of this retrospective study is to analyze the early and long-term outcome of patients who require repeat operations for prosthetic mitral valve dysfunction.
METHODS
Between 1974 and 2006, 1535 isolated mitral valve replacements (MVR) were performed in our hospital (879 bioprosthetic, 656 mechanical). The mean age of patients at the time of the first operation was 56.2 (13.9) years and the causes were rheumatic valve disease (57.7%), degenerative disease (35.9%), or other (6.4%). The in-hospital mortality in this group was 5% (cardiac, 50; infectious, 7; respiratory, 3; renal, 2; hemorrhagic, 5; neurologic, 3).
During follow-up, 369 (24%) patients required a second MVR operation (119 bioprosthetic, 250 mechanical), after an average of 7.9 years. At that time, the mean age was 58.1 (11.2) years. The main reasons for the second operation were structural deterioration of the bioprosthesis (82.7%), paravalvular leak (9%), infective endocarditis (5.1%), and prosthetic thrombosis (3.2%). Inhospital mortality was 8.1% (cardiac, 20; infectious, 4; respiratory, 3; renal 2; hemorrhagic, 1). The study included 80 patients (45 women, 35 men) who required a third mitral valve operation an average of 5.5 years after the previous operation and 13.4 years after the first operation involving the native valve. All patients underwent surgery consecutively and no one was excluded for clinical, emergency, or other reasons. The mean age was 59.8 (11.4) years. At the time of the third MVR, 39% of patients were in functional class IV and 61% in class II-III. Left ventricular function on ventriculography was <35 in 11 1 35 -50 66 7 and 50% in 22.2%. Mean pulmonary artery systolic pressure was 65.2 (25) mm Hg. The surgical indication was established as structural deterioration (72.5%), paravalvular leak (20%), infective endocarditis (6.3%), and prosthetic thrombosis (1.2%). Two etiologic groups were considered: structural deterioration of the bioprosthesis (n=58) and annular disease (endocarditis or paravalvular leak, n=21). The main perioperative data are shown in Table.
The operation was performed as usual, with on-pump circulation and moderate hypothermia. Myocardial protection consisted of anterograde crystalloid cardioplegia before 1991 and anterograde and/or retrograde hematic cardioplegia thereafter. In the first operation on the native valve, the ischemia time was 53.8 (26.7) minutes and the on-pump time was 93 (41.2) minutes. In the second operation, the times were 62.6 (31.4) and 81.2 (37.7) minutes, respectively, and in the third, 74 (34) and 117 (50.9) minutes. The procedure consisted of a new valve replacement with a mechanical prosthesis in 49 patients and biological prosthesis in 31. The procedures were associated with aortic valve replacement in 12 and tricuspid valve annuloplasty in 16.
Follow-up
Follow-up was handled by the outpatient service and by contact with the patients or their relatives. The information was completed by contacting the hospitals and consulting the databases of the health services of the various autonomous communities of origin, the admission and clinical documentation services, and in some cases, the health centers. All patients were followed up after the third operation, although 2 patients were lost to follow-up at 7.8 and 14.2 years. The maximum follow-up possible was 5398 months and the actual follow-up obtained was 5306 months; hence, the follow-up was complete at 98.3%, with a mean follow-up of 17.8 (range, 2-32) years.
Statistical Analysis
The values are expressed as the mean (SD). The Student t test was used to compare quantitative variables, and survival and event-free curves were calculated using the actuarial method. Stata Intercooled, version 6 (Stata Corporation, College Station, Texas, United States), was used for the statistical calculations.
RESULTS
In-hospital Mortality
Fifteen patients died in hospital (18.8%) after the third operation. This figure is statistically significant (P<.05) when compared to the in-hospital mortality of the first and the second operation (5% and 8.1%, respectively). The cause of death was cardiac in 8 patients, hemorrhagic in 3, infectious in 2, and neurologic in 2. Late mortality comprised 38 (58.5%) deaths, mainly cardiovascular (35 patients), including 8 in successive reoperations; 2 were due to cancer and 1 to a traffic accident. In-hospital mortality was 17.8% and late mortality 55.4% when the lesion was structural deterioration of a bioprosthesis, and 14.3% (nonsignificant) and 61.9% (P=.07) when the etiology was annular disease (endocarditis or valvular leak). The actuarial survival rate was 40.7% (5.7%) at 6 years, 24.6% (5.4%) at 12 years, and 15.4% (5.4%) at 18 years (Figure 1).
Figure 1. Actuarial survival rate for the group of patients with 3 mitral operations.
Subsequent Reoperations
Of the 65 survivors, 19 (29.2%) required a fourth mitral operation, 42.1% for structural deterioration, 42.1% for paravalvular leak, and 15.8% for endocarditis; in-hospital mortality was 42.1% and late mortality 26.3%. The actuarial reoperation-free rate (Figure 2) was 65.8% (6.8%) at 6 years, 50.3% (10.9%) at 14 years, and 40.1% (13.8%) at 20 years. A statistically significant relationship was observed between the need for reoperation and etiology. New reoperations were required for structural deterioration of the bioprosthesis in 21.4%, and for annular disease (endocarditis or valvular leak) in 42.9% (P=.035).
Figure 2. Actuarial reoperation-free rate for the group of patients with 3 mitral operations.
DISCUSSION
Prosthetic valve dysfunction is an acquired condition that presents in up to 10% of patients after the first MVR.1,2 A decrease in early mortality from 7%-20%1-3 to 4%-5% has been reported in recent publications.3 The long-term natural history, however, is not well defined. Nonetheless, it is understood that the outcome for patients with repeat reoperations is not necessarily satisfactory.3 The literature on repeat reoperations is scanty and often mixes several types of reoperations. The main reason for the initial reoperation for prosthetic dysfunction is structural deterioration of the bioprosthesis. The widespread use of bioprostheses in our series can be explained by the difficulties encountered to ensure adequate anticoagulation in our population during the earlier years of this experience.4 Repeat replacements were associated with high mortality in our experience, with early mortality at 18.8% and late mortality at 58.5% over a mean follow-up of 18 years. Certain approach routes, such as left thoracotomy or the Heart Port technique, can help reduce high early mortality. In addition, 19 patients required a fourth operation, with an actuarial reoperation rate of 40% at 16 years. The risk in the first elective reoperation is low and, therefore, the indication of bioprosthesis has been extended to populations of young patients.3 However, inhospital mortality progressively increases with each new reoperation. This study showed that the mean age of the patient groups was very similar in the successive operations, likely because the durability of the bioprosthesis is lower in young patients and in the mitral position, as we have reported previously.5 In subsequent reoperations, annulus involvement (endocarditis or valvular leak) gradually becomes more important than the structural deterioration of the bioprosthesis, and is associated with higher mortality. In conclusion, repeat prosthetic mitral valve dysfunction has a poor early and late prognosis and high associated mortality. Annular disease (valvular leak or endocarditis) results in a high incidence of reoperations. The indication for a repeat valve surgery should be assessed on an individual basis because the associated surgical risk is very high.
Correspondence: Dr. V. Expósito García.
Servicio de Cardiología. Hospital Universitario Marqués de Valdecilla. Avda. de Valdecilla, s/n. 39008 Santander. Cantabria. España.
E-mail: vicast79@hotmail.com
Received July 1, 2008.
Accepted for publication November 12, 2008.