Ann Thorac Surg 1995;60:1686-1693
© 1995 The Society of Thoracic Surgeons
Original Articles: Cardiovascular
Atrioventricular Valve Insufficiency and Atrial Geometry After Orthotopic Heart Transplantation
Raffaele De Simone, MD,
Rüdiger Lange, MD,
Falk-Udo Sack, MD,
Hormoz Mehmanesh, MD,
Siegfried Hagl, MD
Department of Cardiac Surgery, University of Heidelberg, Heidelberg, Germany
Accepted for publication July 17, 1995.
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Abstract
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Background. The etiology of tricuspid and mitral valve regurgitation (TR and MR) after heart transplantation is still controversial.
Methods. We studied 25 patients undergoing transplantation and intraoperative transesophageal echocardiography to evaluate the incidence, the degree, and the cause of TR and MR. The degree of valve regurgitation was assessed by color Doppler echocardiography. Cross-sectional areas of the recipient (R) and donor (D) portions of the atria and their ratio (R/D) were measured to assess the distortion of atrial geometry. Tricuspid and mitral valve annuli, their systolic shortening, and hemodynamic indices were measured preoperatively and perioperatively.
Results. Tricuspid valve regurgitation was found in 21 of 25 patients (84%) and MR in 12 of 25 (48%). The degree of MR was mild, whereas TR was mild to moderate. Mitral valve regurgitation did not show any correlation with the studied indices; TR showed no correlation with the hemodynamic indices but a significant correlation with R/D ratio (r = 0.90; standard error of the estimate = 0.2). An inverse correlation was found between the degree of TR and systolic shortening of tricuspid annulus (r = -0.88; standard error of the estimate = 0.03) and between R/D ratio and systolic shortening of tricuspid annulus (r = -0.85; standard error of the estimate = 0.04).
Conclusions. Tricuspid valve regurgitation has a higher incidence than MR and occurs immediately after transplantation; MR is mild and correlates with neither hemodynamic indices nor atrial distortion. An increased R/D ratio, and hence distortion of right atrial geometry, may lead to a reduction in systolic annulus shortening, which in turn causes TR. Surgical attempts to reduce the R/D ratio may decrease the incidence and the degree of TR after heart transplantation.
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Introduction
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Orthotopic heart transplantation is mostly performed according to the technique described by Shumway and associates in 1966 [1]. Atrioventricular valve insufficiency (Fig 1
), probably due to the distortion of atrial geometry, occurs very frequently in patients who have undergone orthotopic heart transplantation [2, 3]. The incidence and the etiology of tricuspid and mitral valve regurgitation are still open questions [4–8].
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Fig 1. . Color Doppler transesophageal echocardiography, four-chamber view, shows atrioventricular valve insufficiency in a patient just after orthotopic heart transplantation. Mitral and tricuspid regurgitant jets in the left and the right atrium are displayed as a mosaic. (LA = left atrium; LV = left ventricle; RA = right atrium; RV = right ventricle.)
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The aims of this study were to evaluate the incidence, degree, and cause of atrioventricular valve insufficiency immediately after heart transplantation and to identify factors eventually correlated with the degree of valve regurgitation.
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Material and Methods
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Patients
Twenty-five patients (mean age, 47.9 ± 11.8 years) with heart failure in New York Heart Association class IV underwent orthotopic heart transplantation with the technique described by Shumway and associates [1]. Intraoperative transesophageal color Doppler echocardiography was performed during the surgical procedure.
Echocardiography
All examinations were performed with commercially available equipment (Aloka SSD 870 color flow mapping system) provided with pulsed, continuous, and two-dimensional Doppler echocardiography (color Doppler flow imaging). The transesophageal probe used was an Aloka UST-5228-5 with a 5-MHz phased-array system fitted to the distal end. All data were recorded on high-fidelity videotape for later review. Two-dimensional echocardiography showed a typical ``hourglass'' configuration of the atria, due to the anastomoses protruding into the atrial cavity (Fig 2). The degree of mitral and tricuspid valve regurgitation was assessed with color Doppler flow imaging by direct planimetry of the systolic regurgitant jet flow area (JA) [9, 10]. The areas of the mitral (JAm; cm2) and the tricuspid (JAt; cm2) regurgitant jet were assessed by planimetry of the jets at their major extensions in systole. Because regurgitant jets are associated with turbulence and high velocity, we measured by planimetry only the flow area with a ``mosaic'' pattern. Grading of tricuspid and mitral valve regurgitation was assessed semiquantitatively, by color Doppler imaging, on a scale (grade 0 to 4+) according to the systolic length of the regurgitant jet in the right atrium [11]. The areas of the left and right atria were measured by two-dimensional echocardiography [12]. Atrial anastomoses of the transplanted heart appear as prominent structures protruding into the atrial cavities (see Fig 2). The areas of the recipient (R) and donor (D) atrial portions were measured by tracing a line between the atrial anastomoses, as shown in Figure 3. In addition, the diameters of the tricuspid and mitral valve annulus and the percentage of systolic shortening of each were assessed by two-dimensional echocardiography to evaluate the degree of ``sphincteric'' effect of the mitral and tricuspid valve annuli in systole [13]. Echocardiographic examinations were performed during the surgical procedure, before cardiopulmonary bypass and just after, and until up to 10 minutes after closure of the chest.
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Fig 2. . Two-dimensional transesophageal echocardiography, four-chamber view, shows atrial anatomy of the transplanted heart. The arrows show the anastomoses between recipient and donor portions of the atria. (M = mitral valve; T = tricuspid valve; other abbreviations as in Fig 1 .)
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Fig 3. . Two-dimensional transesophageal echocardiography, four-chamber view, shows planimetry of recipient (R) and donor (D) portions of the right atrium. (A) The arrows show the sites of the anastomoses. (B) Cross-sectional area of each portion has been assessed by tracing a line between the anastomoses and by measuring the area delimited by these contours.
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Hemodynamic Data
All patients underwent conventional heart catheterization before operation. The following indices were evaluated: cardiac index (L•min-1•m-2), systemic arterial pressure (mm Hg), mean systemic arterial pressure (mm Hg), pulmonary arterial pressure (mm Hg), mean pulmonary arterial pressure (mm Hg), and pulmonary vascular resistance (dynes• s • cm-5) (Table 1).
Statistics
All data are reported as mean ± standard deviation. Correlation coefficients (r) and the linear regression equations (y = a + bx) were calculated with the method of least squares. Student's unpaired t test was used to compare the data of subgroups. A p value less than 0.01 was taken as statistically significant.
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Results
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Tricuspid valve regurgitation was found in 21 of 25 patients (84%), and mitral regurgitation was found in 12 (48%). The degree of mitral regurgitation was mild, whereas the degree of tricuspid regurgitation ranged from mild to moderate. The area of the tricuspid regurgitant jet was significantly higher than the area of the mitral regurgitant jet (JAt = 4.3 ± 3.9 cm2; JAm = 1.2 ± 1.5 cm2). Hemodynamic and echocardiographic indices are shown in Tables 2 and 3. The degree of mitral regurgitation, as assessed by JAm, did not show any correlation with the hemodynamic and echocardiographic indices. The equation correlations of mitral regurgitation are shown in Table 4. The degree of tricuspid regurgitation, as assessed by JAt, did not show any correlation with the hemodynamic indices of pulmonary circulation (Table 5). A significant correlation was found between JAt and R and between JAt and R/D (Fig 4). The equation correlations of tricuspid regurgitation are shown in Table 5. The JAm did not show any correlation with systolic shortening of the mitral annulus (Table 6). An inverse correlation was found between JAt and systolic shortening of the tricuspid annulus and between R/D and systolic shortening of the tricuspid annulus (Table 6; Fig 5). In patients 20 to 25, a slight modification of the surgical technique was performed to reduce the recipient atrium to as small an area as possible. The data related to tricuspid valve regurgitation of patients 1 to 19 were compared with the data from patients 20 to 25. Patients 20 to 25 showed a significantly lower degree of tricuspid regurgitation than patients 1 to 19 (Table 7).
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Fig 4. . Regression analysis of tricuspid valve regurgitation and echocardiographic indices. (A) Correlation between tricuspid valve regurgitation and recipient (R) portion of the right atrium (r = 0.89; y = 1.7 + 0.895x; standard error of the estimate = 1.86; p < 0.001). (B) Correlation between tricuspid valve regurgitation and recipient/donor ratio (R/D) (r = 0.90; y = 0.2 + 0.102x; standard error of the estimate = 0.20; p < 0.001). (JAt = jet flow area of tricuspid regurgitation.)
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Fig 5. . Regression analysis of tricuspid valve regurgitation and echocardiographic indices. (A) Correlation between tricuspid valve regurgitation and systolic annulus shortening (r = -0.88; y = 0.2 - 0.016x; standard error of the estimate = 0.03; p < 0.001). (B) Correlation between systolic annulus shortening and recipient/donor ratio (R/D) (r = -0.85; y = 0.2 - 0.131x; standard error of the estimate = 0.04; p < 0.001). (JAt = jet flow area of tricuspid regurgitation; TVA% = systolic shortening of tricuspid annulus.)
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Comment
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Incompetence of the atrioventricular valves is a common finding in patients who have undergone orthotopic heart transplantation, but the cause of this phenomenon is still controversial [4–8]. The present study examined the degree of atrioventricular valve regurgitation immediately after the surgical procedure by means of intraoperative transesophageal echocardiography. This technique provides optimal visualization of the anatomic characteristics of the transplanted heart, as well as of the atrioventricular valves and the anastomoses of recipient to donor atria [12–15]. In addition, color Doppler flow imaging allows reliable assessment and quantification of valve regurgitation [16–19]. Angermann and colleagues [14] first examined and described the anatomic characteristics of the transplanted heart by transesophageal echocardiography; however, this study did not analyze the extent of atrioventricular valve regurgitation and its possible relation with other etiologic factors. In the present study, mitral valve regurgitation occurred in about 50% of the transplanted hearts and was usually mild. These observations are in accordance with previous reports [3, 14]. However, Stevenson and associates [2] found a higher prevalence of mitral valve regurgitation (88% of patients) after heart transplantation. In our series of patients, analysis of the hemodynamic and echocardiographic data related to mitral regurgitation did not show any correlation with the extent of valve regurgitation.
The data from the present study show that tricuspid valve regurgitation is usually moderate to severe and occurs in almost all patients after heart transplantation. Many hypotheses have been proposed to explain the high prevalence of tricuspid valve regurgitation in the transplanted heart. Young and co-workers [4] showed a correlation between high pulmonary vascular resistance and the degree of tricuspid regurgitation. These findings have not been confirmed either by later studies [3, 8] or by the analysis of data in the present study. Other authors [5, 6, 20] reported that a restrictive dysfunction of the right ventricle, due to a progressive interstitial edema, may be a major factor in the pathogenesis of tricuspid regurgitation. However, this theory is in contrast with the finding that tricuspid regurgitation occurs immediately after transplantation. This observation was confirmed also in the present study. Other studies reported that tricuspid regurgitation was related to the preexisting pulmonary hypertension and consequently to right ventricular dilatation [5, 7, 21] or to abnormal atrial size and geometry [14]. Analysis of the data in the present study, in accordance with other reports [5, 6], showed the lack of significant correlation between pulmonary pressure, or resistance, and the extent of tricuspid regurgitation. The cause of tricuspid regurgitation might be explained by the distortion of right atrial geometry. A significant correlation was found between the extent of tricuspid regurgitation and the R/D, ratio, an index of the degree of atrial distortion. No correlation could be demonstrated between the size of the right atrium and the degree of tricuspid regurgitation. The pathogenesis of tricuspid regurgitation after cardiac transplantation may involve the reduction of tricuspid annulus shortening in systole caused by the atrial distortion due to the right atrial anastomoses. Patients with a higher R/D ratio, ie, greater atrial distortion, showed impaired tricuspid annulus shortening. In addition, we found a significant inverse correlation between systolic shortening of the tricuspid annulus and the extent of tricuspid regurgitation. These last findings confirm the central role of atrial distortion and impairment of annulus shortening in the etiology of tricuspid regurgitation after heart transplantation. An increased R/D ratio, and hence higher distortion of right atrial geometry, may lead to a reduction in systolic annulus shortening, which in turn is a major factor in determining tricuspid valve regurgitation.
The relatively lower prevalence of mitral regurgitation than of tricuspid valve regurgitation after transplantation may be explained by the surgical technique itself. According to the technique of Shumway and associates [1], the atrial anastomoses create a distortion of atrial geometry. Because the left atrium anastomoses are performed before the right atrial anastomoses, the degree of adaptation of the left atrial walls is better than of the right side, and hence the mismatch between donor and recipient is more evident at the right atrial side than at the left. Haverich and colleagues [22] reported a significant correlation between the degree of donor-recipient mismatch and tricuspid regurgitation. In our series of patients, more severe tricuspid regurgitation has been found in patients with higher R/D ratio (Fig 6). This finding was constant in the first 19 patients of our series. In the last group of patients, particular care was devoted to the surgical technique in an attempt to reduce the R/D ratio. In this series of patients, the prevalence and the degree of tricuspid regurgitation were lower than in the earlier patients (Table 7). Recently, we performed two cardiac transplantations using direct bicaval anastomoses and direct pulmonary vein to left atrial anastomoses. Color Doppler echocardiography showed absence of pronounced tricuspid valve regurgitation. Our observation has been confirmed by the recent study of Blanche and colleagues [23], who found a significantly lower incidence of tricuspid regurgitation in patients who had undergone orthotopic heart transplantation using bicaval end to end anastomoses. Although alternative techniques of bicaval anastomoses for orthotopic heart transplantation [23, 24] promise lower degrees of tricuspid valve regurgitation, this issue requires further investigation in longer follow-up studies.
In conclusion, the data from the present study show that tricuspid valve regurgitation has a higher incidence than mitral valve regurgitation and occurs immediately after heart transplantation. The degree of mitral valve regurgitation is only mild and correlates with neither hemodynamic indices nor atrial distortion. An increased R/D ratio, and hence higher distortion of right atrial geometry, may lead to a reduction in systolic annulus shortening, which in turn is a major factor in the pathogenesis of tricuspid valve regurgitation. Surgical attempts to reduce the R/D ratio may decrease the incidence and the degree of tricuspid valve regurgitation after heart transplantation.
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Acknowledgments
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We thank Mr Manfred Heinen for invaluable technical assistance.
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Footnotes
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Address reprint requests to Dr De Simone, Department of Cardiac Surgery, University of Heidelberg, Im Neuenheimer Feld 110, D-69120 Heidelberg, Germany.
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References
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Abstract
Introduction
