Background
The aim of this study was to identify the predisposing factors for pseudoaneurysm formation after aortic valve replacement without previous endocarditis.
Methods
Echocardiography was used to identify patients. Parameters with influence on the occurrence of pseudoaneurysms were analyzed, and the odds ratio for the influence of the type of valve was estimated. The χ 2 goodness-of-fit test was used to analyze whether location or underlying etiology was associated with an accumulated occurrence of a pseudoaneurysm. Fisher’s exact test was used to assess a possible relation between the occurrence of a pseudoaneurysm after composite graft implantation and etiology or location.
Results
Patients treated with composite grafts had a 27-fold increased risk for developing pseudoaneurysms (ψ MH = 27; 95% confidence interval, 1.61-454.19) in comparison with aortic valve replacement only. There was a significant difference for the probability of different etiologies to occur ( P = .032), with Stanford type A aortic dissection and aortic regurgitation being the most often occurring pathologies. Significant associations between the use of a composite graft and both the underlying etiology ( P = .002) and the location of the pseudoaneurysm ( P = .04) was found. Furthermore, patients with composite grafts had larger diameters of the aortic root compared with patients with aortic valve replacement only ( P = .03). Neither the diameter of the annulus of the aortic valve (95% confidence interval, 0.89-1.32; P = .41) nor the diameter of the ascending aorta (95% confidence interval, 0.27-1.97; P = .54) had any influence on pseudoaneurysm formation.
Conclusions
The underlying disorder, determining the surgical procedure, influences the risk for the development of pseudoaneurysms in patients without previous endocarditis. The location of most pseudoaneurysms at the level of the aortic root may be a consequence of its larger diameter.
Pseudoaneurysm (PA), or false aneurysm, formation is a potential late complication after aortic valve (AV) replacement (AVR) with potentially fatal consequences, including high rates of rupture, recurrence, and sepsis. Predisposing factors for PA formation are dissection of the native aorta, infection, connective tissue disorders, preoperative chronic hypertension, and aortic calcification. Echocardiography, computed tomography, and magnetic resonance imaging are the noninvasive investigations of choice to diagnose PA. Although PA formation is a well-known complication, no data exist on predisposing factors leading to noninfective PA development after AVR. Hence, the aim of the present study was to determine these factors in our collective of patients after AVR.
Methods
Definition of PA
PA was defined as a rupture of the aortic wall or rupture of the mitral-aortic intravalvular fibrosa, with the free wall of the PA being made of fibrous tissue and not the aortic wall per se. The communication between the perfused echo-free space within the native aortic wall due to partial dehiscence at the suture line and the left ventricular outflow tract was visualized as a systolic-diastolic color Doppler signal on transthoracic echocardiography ( Figures 1 A and 1 B). Typically, the onset of this signal within the echo-free space occurred before the onset of the systolic color Doppler signal within the aortic vessel wall.
Patient Population
We retrospectively evaluated all echocardiographic reports in adults (aged >16 years) performed in our echocardiography laboratory during a 15-year period (1992-2007) to identify patients with PA formation after AVR. Echocardiograms were carefully reviewed to confirm the diagnosis of PA before inclusion of the patients into the study. Criteria for inclusion into the study were preoperative echocardiography performed in our laboratory, the implantation of a biological or mechanical AV prosthesis and no evidence of endocarditis prior to or after AVR. In a case-control design, all patients with PA after AVR were matched with controls with respect to age, gender, and time of operation. To this end, a specifically designed computer program was used. Patients’ histories, preoperative and postoperative clinical data, and reports from the operations were obtained from the medical and surgical records in all patients and controls. The presence of a PA was compared with the type and size of the prosthesis implanted and the diameters of the ascending aorta, the aortic root, and the aortic annulus.
Color-Coded Doppler Echocardiography
Doppler echocardiography was performed according to standard techniques using a real-time phased-array sector scanner with integrated color Doppler facilities (3.5 MHz). Preoperative echocardiography included the determination of AV function and the measurement of the annular size of the AV and the diameters of the ascending aorta and the aortic root. Measurements of the annular size were performed in the 2-dimensional long-axis view of the left ventricle and of the left ventricular outflow tract. Measurements of the ascending aorta and the aortic root were performed in the 2-dimensional long-axis view of the aortic root and the ascending aorta, respectively, using M-mode echocardiography. The postoperative development of a PA was defined as a perfused, echo-free space communicating with the left ventricular outflow tract, as described above.
Operative Technique for AVR
The heart was exposed through a median sternotomy. After heparinization, the ascending aorta and right atrium were cannulated, and cardiopulmonary bypass was initiated. The patients were cooled to 30°C. The aorta was cross-clamped, and blood cardioplegia was infused antegradely and retrogradely. The AV was exposed through an oblique or transverse aortotomy. The native AV was excised and the annulus thoroughly decalcified. The selection of the correct size of the AV prosthesis was performed on the basis of the preoperatively measured annulus size and by sizing of the annulus using appropriate valve sizers. Valve implantation was typically in a supra-annular position, using a noneverting suture technique with 2.0 Ticron suture (Ethicon, Somerville, NJ). Rewarming was started, the aortotomy was closed, and the aorta was declamped. Patients were weaned from cardiopulmonary bypass, and the cannulae were removed. Protamine was administered, and the operation was terminated in a standardized fashion. The operative technique described here did not substantially change over the observation period of our study.
Statistical Analyses
Analyses were performed using the statistical software package R version 2.7.2 for Mac OS X (R Project for Statistical Computing, Vienna, Austria). A case-control study design with 1:1 matching for age, gender, and time of operation was selected. The influence of the type of valve on the development of PA was examined after grouping the implanted AVs into the following categories: mechanical prostheses, biologic prostheses, homografts, and composite grafts. The Mantel-Haenszel estimator was used to estimate the odds ratio for the influence of the type of valve. The diameters of the aortic root and the ascending aorta were compared between AVR and composite grafts using the nonparametric Mann-Whitney U test. Furthermore, differences in annular size, as determined preoperatively by echocardiography, and in the sizes of the implanted AV prostheses were compared between patients who developed PAs and controls using conditional logistic regression analysis. To analyze differences between the different locations and etiologies leading to PAs, the χ 2 goodness-of-fit test for equal probabilities was used. To assess if there was a relation between the occurrence of PA after composite graft implantation and the etiology or location of PA, Fisher’s exact test was used. A P value < .05 was regarded as statistically significant, and 95% confidence intervals (CIs) were calculated.
Results
Patient Population
During a 15-year period from 1992 to 2007, 24 patients fulfilling the inclusion criteria were identified and matched to controls. PAs were detected in 13% of the patients (n = 3) after the implantation of homografts, in 29% of the patients (n = 7) after the implantation of mechanical or biologic valve prostheses, and in 54% of the patients (n = 14) after the implantation of composite grafts. The mean age at diagnosis was 52 years (range, 20-87 years). Eighteen patients were men, and 6 were women ( Table 1 ). Thirty-eight percent of the patients (n = 9) had undergone previous AV surgery. There was no significant difference in the concomitant occurrence of arterial hypertension between patients (38% [n = 9]) and controls (25% [n = 6]) ( P = .16). Two patients in the case group had Marfan syndrome, whereas in the control group, 1 patient with Marfan syndrome and 1 patient with Shone’s complex could be identified. The mean time from operation to first documentation of PA was 705 ± 1482 days (range, 1-6289 days; median, 68 days).
| Patient | Gender | Age (y) | Number of AV cusps | AV annular diameter (mm) | Aortic root diameter (mm) | Ascending aortic diameter (mm) | Type of prosthesis | AV prosthesis diameter (mm) | Localization | Etiology | Time to PA (d) |
|---|---|---|---|---|---|---|---|---|---|---|---|
| 1 | M | 60 | 2 | 24 | 39 | 38 | CM | 23 | NC | Bicuspid † | 54 |
| 2 | M | 60 | 3 | 24 | NA | NA | SJM | 23 | NC | Tricuspid ‡ | 1 |
| 3 | M | 41 | 3 | 24 | 59 | 61 | CM (comp) | 23 | LC | AD | 63 |
| 4 | M | 57 | 3 | 27 | 74 | 30 | CM (comp) | 25 | AA | AD | 9 |
| 5 | F | 57 | 0 ∗ | 21 | 31 | 40 | Shelhigh § (comp) | 21 | RC | AV insufficiency | 73 |
| 6 | M | 39 | 0 ∗ | 31 | 50 | 37 | Homograft | 28 | LC | AV insufficiency | 216 |
| 7 | M | 20 | 0 ∗ | 23 | 26 | 40 | SJM (comp) | 25 | NC/LC | Unknown | 6289 |
| 8 | M | 47 | 3 | 30 | 59 | 29 | Shelhigh § (comp) | 27 | RC | AD | 21 |
| 9 | F | 66 | 0 ∗ | 29 | 31 | 29 | CE (comp) | 29 | NC | Sinus of Valsalva rupture | 2611 |
| 10 | F | 67 | 0 ∗ | 25 | 51 | 47 | CM (comp) | 25 | AA | AAA | 163 |
| 11 | M | 48 | 0 ∗ | 29 | NA | NA | SJM (comp) | 31 | NC | AV insufficiency | 1 |
| 12 | F | 65 | 3 | 21 | 35 | 38 | CE | 21 | NC | Tricuspid ‡ | 57 |
| 13 | M | 21 | 3 | 23 | 35 | NA | Homograft | 20 | NC/RC | AV insufficiency | 182 |
| 14 | M | 82 | 3 | 21 | 39 | 37 | ELS | 23 | NC | Tricuspid ‡ | 8 |
| 15 | M | 35 | 2 | 39 | 99 | NA | CM (comp) | 31 | RC | AD | 104 |
| 16 | M | 62 | 0 ∗ | 21 | 31 | 35 | Homograft | 19 | NC | AV insufficiency | 22 |
| 17 | F | 46 | 3 | 24 | 59 | 42 | SJM (comp) | 25 | RC/LC | AV insufficiency | 6 |
| 18 | M | 64 | 3 | 25 | 69 | 25 | Composite | 25 | RC | AD | 56 |
| 19 | M | 87 | 3 | 22 | 31 | 28 | CE | 21 | RC/NC | Tricuspid ‡ | 192 |
| 20 | M | 50 | 0 ∗ | 22 | 36 | 44 | Shelhigh § (comp) | 21 | NC | AV insufficiency | 15 |
| 21 | M | 30 | 2 | 27 | 38 | 42 | CM | 25 | LC | Bicuspid † | 1310 |
| 22 | F | 58 | 3 | 26 | 63 | 43 | Shelhigh § (comp) | 25 | NC | AD | 581 |
| 23 | M | 47 | 0 ∗ | 29 | 31 | 31 | CM | 25 | RC | AV insufficiency | 3425 |
| 24 | M | 62 | 3 | 24 | 67 | NA | SJM (comp) | 29 | RC | AD | 1440 |
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