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Original Articles: Adult Cardiac

Mitral Valve Surgery for Functional Mitral Regurgitation: Should Moderate-or-More Tricuspid Regurgitation Be Treated? A Propensity Score Analysis

^a Department of Cardiac Surgery, University of Catania, Ferrarotto Hospital, Catania, Italy
^b Department of Cardiology, University of Chieti, Chieti, Italy

Accepted for publication November 12, 2008.

^_* Address correspondence to Dr Calafiore, Division of Cardiac Surgery, University of Catania, Ferarrotto Hospital, Via Citelli, Catania, 95124, Italy (Email: calafiore{at}unich.it).

	Abstract

Top Abstract Introduction Material and Methods Results Comment References

 
Background: The aim of this retrospective study was to evaluate the clinical outcome of treating or not treating moderate-or-more functional tricuspid regurgitation in patients with functional mitral regurgitation undergoing mitral valve surgery.

Methods: From January 1988 to March 2003, 110 patients with functional mitral regurgitation undergoing mitral valve surgery showed moderate-or-more functional tricuspid regurgitation, which was treated (group T) in 51 and untreated in 59 (group UT) patients. Propensity score was used to adjust midterm results. The tricuspid valve was always repaired using the DeVega technique. The mitral valve was repaired in 84 and replaced in 26 patients; no residual moderate-or-more functional mitral regurgitation was assessed at hospital discharge.

Results: Thirty-day mortality was 5.5% (8.5% for group UT versus 2% for group T; p= 0.245). Adjusted 5-year survival was 45.0% ± 6.1% in group UT and 74.5% ± 5.1% in group T (p= 0.004), whereas the possibility to be alive in New York Heart Association class I or II was 39.8% ± 6.0% in group UT versus 60.0% ± 6.5% in group T (p= 0.044). Proportional Cox analysis, forcing propensity score into the model, demonstrated that untreated moderate-or-more tricuspid regurgitation was a risk factor for lower midterm survival (hazard ratio, 2.7; 95% confidence interval, 1.3 to 5.4) and survival in New York Heart Association class I or II (hazard ratio, 1.9; 95% confidence interval, 1.1 to 3.4). Follow-up functional tricuspid regurgitation progression rate (3+/4+) was 5% in group T versus 40% in group UT (p < 0.001). The progression of functional tricuspid regurgitation grade at follow-up was a risk factor for worse survival and the possibility to be alive in New York Heart Association class I or II.

Conclusions: Tricuspid annuloplasty is an easy and safe procedure, mandatory in case of at least moderate functional tricuspid regurgitation to achieve better mid-term outcome in patients with functional mitral regurgitation undergoing mitral valve surgery.

	Introduction

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The presence of any grade of functional tricuspid regurgitation (FTR) is a very common finding in the presence of mitral valve (MV) disease [1, 2]. Its degree increases in the presence of right ventricular dilatation and dysfunction, left ventricular dysfunction, and pulmonary hypertension [3]. Functional tricuspid regurgitation can be defined as the incompetence of the tricuspid valve (TV) in the absence of any structural leaflet disease [4]. Recent insights from three-dimensional echocardiographic and sonometric studies [4–6] helped us to better understand the mechanisms underlying FTR. The tricuspid annulus (TA) is a nonplanar shape with the posteroseptal portion deeper in the right ventricle and the anteroseptal portion higher in the right atrium. In healthy subjects the TA has a homogeneous contraction, reaching the minimum and maximum area during mid and late diastole, respectively [4]. Moreover, the height of the TA increases during annular contraction [6]. In patients with FTR, the TA enlarges in the septolateral direction, in correspondence of the free wall, and at the same time, has a trend to become more planar shaped [4, 5]. Along with these annular changes, papillary muscle displacement contributes to cause FTR [7–9].

For several years, FTR was not treated, as the common thinking was that it could be relieved simply by treating the MV disease. Long-term outcomes, however, did not support this hypothesis. Positive TA remodeling is not routine after MV surgery, and most patients increase their tricuspid regurgitation (TR) degree years after surgery [1, 10, 11]. Furthermore, being TR functional, surgery cannot be scheduled on the basis of TR degree, which can vary according to preload, afterload, and right ventricular function. Hence, TR has to be surgically treated also on anatomic bases [10], even if it is of low degree.

Some studies focused on the natural history of uncorrected TR showed that FTR can worsen with time, significantly impairing long-term outcomes in this group of patients [3, 10, 11]. On the other hand, the high rate of TR recurrence after TV annuloplasty, independent of the surgical technique used, seems to reduce the enthusiasm of many surgeons to treat FTR [12–17].

Thus, this retrospective propensity-matched study was aimed at comparing clinical and echocardiographic results of two groups of patients either undergoing TV annuloplasty or not.

	Material and Methods

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Population
From January 1988 to March 2003, 110 patients with functional MV regurgitation (MVR) undergoing MV surgery showed moderate-or-more FTR; it was treated (group T) in 51 and untreated in 59 (group UT) patients. A nonparsimonious regression model (c statistic = 0.83; Hosmer-Lemeshow p = 0.76; bootstrapping = 500 samples) was built to obtain the propensity score (Appendix A). Differences between the two groups are reported in Table 1. Patients with organic mitral or tricuspid valve disease were excluded.

Echocardiography
A preoperative routine transthoracic echocardiogram was performed by the same operator (S.G.). Methods used to assess MVR, MV apparatus changes, biventricular dimensions, and function have been already reported [18]. The severity of TR assessed by Doppler echocardiography was graded on a scale from 1 to 4 (1 mild, 2 moderate, 3 moderate to severe, 4 severe) [19, 20].

Surgery
Surgical details stratified by groups are listed in Table 1. Both cavae were cannulated, and myocardial protection was achieved with intermittent antegrade warm blood cardioplegia [21].

Mitral valve surgical techniques have been described previously [21]. The success of surgical correction in terms of reduction of MVR was assessed by means of intraoperative transesophageal echocardiography. It was achieved in all investigated patients. Moderate-to-severe and severe TR was always treated except for in 6 patients. Most of the moderate TR (88%) was not surgically corrected. The decision of performing TV repair was mainly related to a personal choice of the surgeon and reflects our ongoing understanding of the prognostic role of FTR. Tricuspid valve repair was always performed by means of the De Vega technique [22]. All patients showed mild or less TR at postoperative transesophageal echocardiography.

Postoperative Course and Follow-Up
After surgery, all patients were admitted to the intensive care unit and from there moved to the surgery and, later, cardiology wards, where oral treatment with β-blockers and angiotensin-converting enzyme inhibitor was started between the second and fourth postoperative days. Follow-up started in March 2007 and ended in June 2007, and it was 100% completed. All patients were clinically followed up in our outpatient clinic 3, 6, and 12 months after surgery and thereafter at yearly intervals. The more recent information was obtained by calling the patient or the referring cardiologists. Median follow-up time was 68 months (25th and 75th percentiles, 59 to 90 months); 85 months (25th and 75th percentiles, 70 to 120 months) in group UT and 66 months (25th and 75th percentiles, 59 to 83 months) in group T (p = 0.159). An echocardiographic control was performed by the same echocardiographer (S.G.) in 77 (74.0%) of 104 patients surviving the first month, after a median interval of 12 months (25th and 75th percentiles, 5 to 38 months).

Statistical Methods
Results are expressed as mean and standard deviation in cases of normally distributed continuous variables, and as median and 25th and 75th percentiles in cases of nonnormally distributed continuous variables. The Kolmogorov-Smirnov statistic with a Lilliefors significance level was used for testing normality. In cases of categorical variables, counts and percentages were reported. Statistical analysis comparing the two groups was performed with unpaired two-tailed Student's t test for continuous normally distributed variables, with the Mann-Whitney U test for continuous nonnormally distributed variables and with Pearson ² test (or Fisher's exact test) for categorical variables. A nonparsimonious regression model was solved to generate a propensity score for each patient, representing the retrospective probability of being in group UT (Appendix A) [23]. The model fit and predictive power were evaluated using the Hosmer-Lemeshow goodness-of-fit and c statistic, respectively. The model was validated in 500 bootstrap samples [24]. Five-year survival curves were obtained with the Kaplan–Meier method; significant differences between groups were evaluated with a log-rank test. Survival curves were adjusted for propensity score. Time-to-event analysis was performed by a multivariable Cox proportional-hazard regression adjusted for propensity score. Final models were validated in 500 bootstrap samples. Factors appearing in 50% or more of the analyses were considered reliably statistically significant. The results were reported as hazard ratio (HR) and 95% confidence interval (CI). For all tests, a probability value of less than 0.05 was considered significant. The SPSS software (SPSS Inc, Chicago, IL) was used.

	Results

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Thirty-day mortality was 5.5% (6 patients), 2.0% in group T (1 patient) versus 8.5% in group UT (5 patients; p = 0.213). Three patients (2.7%) died because of low output syndrome; all of them were in group UT (p = 0.245). Forty-six of 104 survivors died (16 in group T versus 30 in group UT); in 40 cases death was cardiac-related (13 in group T versus 27 in group UT). Cardiac death occurred because of heart failure in 22 cases, sudden death in 12, myocardial infarction in 3, complications after heart transplantation in 2, and endocarditis in 1. Non–cardiac-related deaths were caused by respiratory failure in 3 patients and hemolytic crisis, lung malignancy, and sepsis in the remaining 3. Among 48 survivors, functional status (New York Heart Association [NYHA] class) improved from 3.3 ± 0.6 to 2.3 ± 0.7 (p < 0.001); an improvement of at least one NYHA class was recorded in 38 (66.7%) patients. Functional status was unchanged in 15 (26.3%) and impaired in 5 (8.8%) patients, without any significant difference between groups. After adjusting Kaplan–Meier curves for propensity score, 5-year survival was 45.0% ± 6.1% in group UT and 74.5% ± 5.1% in group T (p = 0.004), whereas the possibility of being alive in NYHA class I or II was 39.8% ± 6.0% in group UT versus 60.0% ± 6.5% in group T (p = 0.044; Figs 1 and 2). Proportional Cox analysis, forcing propensity score into the model, demonstrated that untreated moderate-or-more TR was a risk factor for lower midterm survival (HR, 2.7; 95% CI, 1.3 to 5.4) and survival in NYHA class I or II (HR, 1.9; 95% CI, 1.1 to 3.4).

View larger version (14K): [in this window] [in a new window]   Fig 1. Adjusted 5-year survival stratified by groups. Group T (solid line) and Group UT (dashed line).

View larger version (12K): [in this window] [in a new window]   Fig 2. Adjusted 5-year possibility to be alive in I-II New York Heart Association class stratified by groups. Group T (solid line) and Group UT (dashed line).

View larger version (12K): [in this window] [in a new window]   Fig 3. Variation of average tricuspid regurgitation grade from preoperative to postoperative and follow up period. Group UT (square) and Group T (triangle). Results are expressed as mean ± standard deviation.

View larger version (20K): [in this window] [in a new window]   Fig 4. Distribution of different tricuspid regurgitation grade from preoperative to postoperative and follow up period, in Group UT (A) and in Group T (B). Results are expressed as percentage of patients having each tricuspid regurgitation (TR) grade.

	Comment

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The presence of TR has been clearly demonstrated to impair survival; Nath and associates [3] evaluated survival of 5,223 patients undergoing echocardiography at one of three Veterans Affairs Medical Center laboratories during a 4-year period. The 1-year survival rate for patients without TR was 91.7%, with mild TR 90.3%, with moderate TR 78.9%, and with severe TR 63.9% (p < 0.001). Four years after, patients with moderate-to-severe TR showed survival lower than 50% whereas those with no or mild TR had a survival higher than 70%. Moderate or greater TR was associated with increased mortality regardless of pulmonary hypertension or low ejection fraction (HR, 1.31). This study, focused on the natural history of patients with or without TR, provides a new insight: the forgotten valve can play a key role in survival determination. The reasons why moderate-or-more TR is correlated with higher mortality rate have not been clarified, but TR is commonly associated with right ventricular dysfunction and pulmonary hypertension, which are two great determinants of worse outcome [18]; and, even in the absence of a clear picture of right ventricular dysfunction, it is very likely that TR might mask the decreased right ventricular contractility as MVR does for the left ventricle. However, FTR is often associated with left-side valve disease, mostly the MV. Thus, the following step to really understand the prognostic importance of TR is to establish whether MV surgery alone can reduce FTR. For several years, surgeons believed that FTR could be relieved simply as a side effect of MV surgery. Dreyfus and colleagues [10] compared two groups of patients having moderate-or-less TR beside MVR; 163 patients underwent MV repair alone and 148 MV repair plus TV annuloplasty. Although the authors failed to demonstrate any difference after 10 years in terms of survival (90.3% MV repair + TV repair versus 85.5% MV repair alone, not significant) and of cardiac-related event-free survival (92.8% MV repair + TV repair versus 90.5% MV repair alone, not significant), they reported a significant improvement of NYHA class along with lower TR grade when TR was treated; in particular patients having TV annuloplasty showed a reduction of TR grade equal to 52%, whereas those having MV repair alone had a TR progression of 135%. Moreover, TR increased by more than two grades in 48% of patients in the MVR group and only in 2% of patients in the MV repair + TV repair (p < 0.001). Matsuyama and coworkers [11] demonstrated that, in a series of 174 patients with moderate-or-less TR undergoing MV surgery alone, uncorrected moderate TR (HR, 3.9) was a predictor for TR worsening with time.

The present study demonstrates that moderate-or-more FTR, if untreated, can impair both midterm survival and functional status, even if it seems not to affect early outcome. To overcome any selection bias, the two groups were matched by propensity score; afterward they were similar for all preoperative and operative characteristics. Moreover, in our series, among 31 patients in group UT who received both postoperative and follow-up echocardiographic controls, 17 patients (54.8%) had an improvement soon after MV surgery, but TR was still moderate in 45.2% of cases. In the midterm period, only 6 (19.4%) patients showed mild TR, whereas the remaining 25 (80.6%) had moderate-or-more TR; furthermore, the rate of patients with progression of TR grade to 3 or 4 was 45.1%. Nowadays, it is well known that FTR is related to annular dilatation along with loss of three-dimensional shape and contractility. Likewise, displacement of the papillary muscles, occurring as a consequence of RV dilatation, contributes to reduce TV leaflet coaptation [4–9]. Therefore, reversal of TV remodeling cannot be expected with MV surgery alone.

On the contrary, the main drawback of TV annuloplasty seems to be the high rate of residual TR [12, 14, 26]. Kuwaki and colleagues [12] reported a rate of TV annuloplasty failure (residual TR grade 2 or 3) by the first postoperative month of 25% using the De Vega technique [22]; the presence of residual TR soon after the procedure may lead to a vicious cycle, causing volume overloading of the right ventricle and further right ventricular dilatation and dysfunction, resulting in more TR [13]. Data from the Cleveland Clinic [14] show that the rate of residual TR grade 3 or 4 after a De Vega annuloplasty increases with time from 13.6% at the first month to 18.0%, 28%, and 33% at 1, 5, and 8 years, respectively. Use of a ring provided similar 1-month results (residual TR grade 3 or 4, 15.2% for Carpentier-Edwards ring and 15.3% for the Cosgrove band) that, however, remained stable with time (at 5 years, 17.0% and 18.0%, respectively).

The surgical technique can then influence the late results of TR correction. Although the De Vega annuloplasty is a simple, short, and inexpensive procedure, there are many evidences that it is related to an increased rate of residual TR more than ring implantation [12, 14–17]. Matsuyama and associates [17] reported long-term freedom from residual TR grade 2 or 3 was significantly higher in patients having ring implantation than in those undergoing De Vega annuloplasty (p = 0.027). The same finding was confirmed by Tang and coworkers [16], who demonstrated freedom from residual TR at 15 years was significantly lower in the De Vega group than in the prosthesis group (p = 0.003), and this influenced both survival and event-free survival. McCarhty and associates [14] showed that severity of regurgitation rose more rapidly with the De Vega procedure than with ring implantation (p = 0.002). This might be caused by different reasons: centripetal migration of sutures or shrinkage of the valve tissue with increased right ventricular pressure [17, 27].

However, in our series, despite the use of the De Vega technique, a very low rate of residual TR was achieved at early and midterm times; among 41 patients having both postoperative and midterm echocardiography, mild-or-less TR was found in 39 (95.1%) before hospital discharge and in 33 (80.5%) at follow-up. Hence, at a median interval of 1 year after surgery, only 8 (19.5%) patients showed moderate-or-more residual TR with a fraction of patients having TR grade 3 equal to 4.9%, which was significantly lower than the rate in the untreated TR group. This is an important finding, as residual TR grade 3 or 4 at follow-up was found to negatively impact survival (1.09 ± 0.46; p = 0.019) and quality of life (0.80 ± 0.39; p = 0.037).

Limitations of This Study
Besides the retrospective nature of this study, there are some other limitations that should be addressed. No information about preoperative right atrial and ventricular dimensions, tricuspid annular size, degree of leaflet tethering, intrinsic lung disease, and hemodynamic conditions are provided. Another important drawback is the relatively small sample size. Furthermore, the time course of changes in TR is not provided.

Conclusions
Despite these limitations, the results of this study offer an undeniable rationale to be more aggressive in the presence of TR, confirming that moderate-or-more TR should not be left untreated at the time of MV surgery to achieve a better midterm clinical outcome. In the near future, more efforts should be addressed to search for surgical guidelines that clearly identify the proper technique to schedule for each case, on the basis of severity of TV annular dilatation, TV tethering, and right ventricular dilatation and dysfunction. To achieve this goal, studies on larger series are surely mandatory.

In conclusion, our findings support the hypothesis that, in patients with functional MVR, contemporary treatment of FTR, if of moderate-or-more degree, is able to improve long-term outcome in terms of survival and survival in NYHA class I or II.

	References

Top Abstract Introduction Material and Methods Results Comment References

 

1. Colombo T, Russo C, Ciliberto GR, et al. Tricuspid regurgitation secondary to mitral valve disease: tricuspid annulus function as guide to tricuspid valve repair Cardiovasc Surg 2001;9:369-377.[Medline]
2. Cohn LH. Tricuspid regurgitation secondary to mitral valve disease: when and how to repair J Card Surg 1994;9:237-241.[Medline]
3. Nath J, Foster E, Heidenreich PA. Impact of tricuspid regurgitation on long-term survival J Am Coll Cardiol 2004;43:405-409.[Abstract/Free Full Text]
4. Fukuda S, Saracino G, Matsumura Y, et al. Three-dimensional geometry of the tricuspid annulus in healthy subjects and in patients with functional tricuspid regurgitation: a real-time, 3-dimensional echocardiographic study Circulation 2006;114(1 Suppl):I-492-I-498.[Medline]
5. Ton-Nu TT, Levine RA, Handschumacher, MD, et al. Geometric determinants of functional tricuspid regurgitation: insights from 3-dimensional echocardiography Circulation 2006;114:143-149Epub 2006 Jul 3.[Abstract/Free Full Text]
6. Jouan J, Pagel MR, Hiro ME, Lim KH, Lansac E, Duran CM. Further information from a sonometric study of the normal tricuspid valve annulus in sheep: geometric changes during the cardiac cycle J Heart Valve Dis 2007;16:511-518.[Medline]
7. Mikami T, Kudo T, Sakurai N, Sakamoto S, Tanabe Y, Yasuda H. Mechanisms for development of functional tricuspid regurgitation determined by pulsed Doppler and two-dimensional echocardiography Am J Cardiol 1984;53:160-163.[Medline]
8. Come PC, Riley MF. Tricuspid annular dilatation and failure of tricuspid leaflet coaptation in tricuspid regurgitation Am J Cardiol 1985;55:599-601.[Medline]
9. Sagie A, Schwammenthal E, Padial LR, et al. Determinants of functional tricuspid regurgitation in incomplete tricuspid valve closure: Doppler color flow study of 109 patients J Am Coll Cardiol 1994;24:446-453.[Abstract]
10. Dreyfus GD, Corbi PJ, Chan KM, Bahrami T. Secondary tricuspid regurgitation or dilatation: which should be the criteria for surgical repair? Ann Thorac Surg 2005;79:127-132.[Abstract/Free Full Text]
11. Matsuyama K, Matsumoto M, Sugita T, Nishizawa J, Tokuda Y, Matsuo T. Predictors of residual tricuspid regurgitation after mitral valve surgery Ann Thorac Surg 2003;75:1826-1828.[Abstract/Free Full Text]
12. Kuwaki K, Morishita K, Tsukamoto M, Abe T. Tricuspid valve surgery for functional tricuspid valve regurgitation associated with left-sided valvular disease Eur J Cardiothorac Surg 2001;20:577-582.[Abstract/Free Full Text]
13. Fukuda S, Gillinov AM, McCarthy PM, et al. Determinants of recurrent or residual functional tricuspid regurgitation after tricuspid annuloplasty Circulation 2006;114(1 Suppl):I-582-I-587.[Medline]
14. McCarthy PM, Bhudia SK, Rajeswaran J, et al. Tricuspid valve repair: durability and risk factors for failure J Thorac Cardiovasc Surg 2004;127:674-685.[Abstract/Free Full Text]
15. Ghanta RK, Chen R, Narayanasamy N, et al. Suture bicuspidization of the tricuspid valve versus ring annuloplasty for repair of functional tricuspid regurgitation: midterm results of 237 consecutive patients J Thorac Cardiovasc Surg 2007;133:117-126.[Abstract/Free Full Text]
16. Tang GH, David TE, Singh SK, Maganti, MD, Armstrong S, Borger MA. Tricuspid valve repair with an annuloplasty ring results in improved long-term outcomes Circulation 2006;114(1 Suppl):I-577-I-581.[Medline]
17. Matsuyama K, Matsumoto M, Sugita T, et al. De Vega annuloplasty and Carpentier-Edwards ring annuloplasty for secondary tricuspid regurgitation J Heart Valve Dis 2001;10:520-524.[Medline]
18. Di Mauro M, Calafiore AM, Penco M, Romano S, Di Giammarco G, Gallina S. Mitral valve repair for dilated cardiomyopathy: predictive role of right ventricular dysfunction Eur Heart J 2007;28:2510-2516.[Abstract/Free Full Text]
19. González Vílchez F, Zarauza J, Vázquez de Prada JA, et al. Assessment of tricuspid regurgitation by Doppler color flow imaging: angiographic correlation Int J Cardiol 1994;44:275-283.[Medline]
20. Zoghbi WA, Enriquez-Sarano M, Foster E, et al. Recommendations for evaluation of the severity of native valvular regurgitation with two-dimensional and Doppler echocardiography J Am Soc Echocardiogr 2003;16:777-802.[Medline]
21. Calafiore AM, Di Mauro M, Gallina S, et al. Mitral valve surgery for chronic ischemic mitral regurgitation Ann Thorac Surg 2004;77:1989-1997.[Abstract/Free Full Text]
22. De Vega NG. La anuloplastia selective regulable y permanente Rev Esp Cardiol 1972;25:555-556.[Medline]
23. Rosenbaum PR, Rubin DB. The central role of the propensity score in observational studies for causal effects Biometrika 1983;70:41-55.[Abstract/Free Full Text]
24. Breiman L. Bagging predictors J Mach Learn Res 1996;24:123-140.
25. Mihaljevic T, Lam BK, Rajeswaran J, et al. Impact of mitral valve annuloplasty combined with revascularization in patients with functional ischemic mitral regurgitation J Am Coll Cardiol 2007;49:2191-2201.[Abstract/Free Full Text]
26. Roques F, Nashef SAM, Michel P, et al. Risk factors and outcome in European cardiac surgery: analysis of the EuroSCORE multinational database of 19030 patients Eur J Cardiothorac Surg 1999;15:816-823.[Abstract/Free Full Text]
27. Holper K, Haehnel JC, Augustin N, Sebening F. Surgery for tricuspid insufficiency: long-term follow-up after De Vega annuloplasty Thorac Cardiovasc Surg 1993;41:1-8.[Medline]

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This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Antonio M. Calafiore Antonio Bivona Michele Di Mauro Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Calafiore, A. M. Articles by Di Mauro, M. Search for Related Content PubMed PubMed Citation Articles by Calafiore, A. M. Articles by Di Mauro, M. Related Collections Valve disease