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):
Farkas B. Vánky
Eva Tamás
Rolf Svedjeholm
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 Vánky, F. B.
Right arrow Articles by Svedjeholm, R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Vánky, F. B.
Right arrow Articles by Svedjeholm, R.
Related Collections
Right arrow Valve disease

Ann Thorac Surg 2006;81:1297-1304
© 2006 The Society of Thoracic Surgeons


Original article: Cardiovascular

Risk Factors for Postoperative Heart Failure in Patients Operated on for Aortic Stenosis

Farkas B. Vánky, MD a , Erik Håkanson, MD, PhD b , Eva Tamás, MD a , Rolf Svedjeholm, MD, PhD a , *

a Department of Cardiothoracic Surgery, University Hospital, Linköping, Sweden
b Department of Cardiothoracic Anesthesia, Linköping Heart Center, Linköping, Sweden

Accepted for publication November 22, 2005.

* Address correspondence to Dr Svedjeholm, Department of Cardiothoracic Surgery, University Hospital, SE-581 85 Linköping, Sweden (Email: rolf.svedjeholm{at}lio.se).


    Abstract
 Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
BACKGROUND: Risk factors for postoperative heart failure (PHF) have not been specifically studied in valve surgery although it has been acknowledged that patient variables may have a more profound influence on postoperative outcome than valve-related factors.

METHODS: All patients undergoing isolated aortic valve replacement for aortic stenosis from January 1995 to December 2000 in the southeast region of Sweden were studied (n = 398). Forty-five patients with aortic valve replacement required treatment for PHF. Univariate and multivariate logistic regression analysis was carried out to identify risk factors for PHF.

RESULTS: Thirty-day mortality was 6.7% versus 1.4% for patients with and without PHF, respectively (p = 0.05). With regard to clinical presentation of aortic stenosis, angina was associated with reduced risk, whereas history of congestive heart failure increased the risk for PHF. Five preoperative (hypertension, history of congestive heart failure, severe systolic left ventricular dysfunction, pulmonary hypertension, preoperative hemodynamic instability) and two intraoperative (aortic cross-clamp time, intraoperative myocardial infarction) variables were identified as independent risk factors for PHF. Patient–prosthesis mismatch did not influence the risk of PHF significantly.

CONCLUSIONS: Postoperative heart failure was associated with a marked increase in postoperative mortality and morbidity. Risk factors for PHF were variables indicating preexisting myocardial dysfunction, increased right or left ventricular afterload, and intraoperative myocardial injury. Our results highlight issues concerning cross-clamp time and myocardial protection, particularly for patients with preoperatively compromised myocardial function. Asymptomatic patients with significant aortic stenosis should be considered for surgery before substantial echocardiographic evidence of left ventricular dysfunction or increased pulmonary artery pressure develops.


    Introduction
 Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
Postoperative heart failure (PHF) is a major determinant for adverse outcome in cardiac surgery [1–3]. However, little attention has been paid to this complication in valve surgery. In a recent study this issue was addressed in patients undergoing isolated aortic valve replacement (AVR) for aortic stenosis (AS), representing the largest subgroup of valve patients in our surgical practice [4]. Substantial differences in characteristics of PHF were found between patients undergoing coronary surgery and those undergoing isolated AVR for AS. In contrast to coronary surgery, PHF after AVR was less clearly related to preoperative ischemia and intraoperative myocardial infarction. A potentially eliciting event could be identified in only one third of the patients with PHF after surgery for AS. To shed further light on the mechanisms behind PHF in these patients, we decided to analyze risk factors for PHF within the total cohort of patients undergoing surgery for isolated AS.


    Material and Methods
 Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
Patients
The University Hospital in Linköping is the only referral center in the southeast region of Sweden, serving a population of approximately 1 million. Demographic and periprocedural data including complications were registered prospectively in a computerized institutional database (Summit Vista for Windows; Version 1.98.1, Summit Medical Systems Inc, Minneapolis, MN). All fields were defined in a data dictionary. Missing data were completed by scrutinizing the patient records. Completeness of mortality data was checked with the Swedish Civil Registry.

From January 1, 1995, to December 31, 2000, 4,806 patients underwent cardiac surgery. There were 398 patients operated on with isolated AVR because of AS without clinically significant regurgitation or associated coronary disease. Redo procedures were not included. From this cohort, 45 patients undergoing AVR (11.3%) were treated for PHF. Univariate and multivariate logistic regression analysis was performed to identify risk factors for PHF.

Clinical Management
The patients underwent surgery using standard techniques with cardiopulmonary bypass and aortic cross-clamping. Ringer's acetate solution and mannitol was used for priming the extracorporeal circuit. Moderate hemodilution (hematocrit 20% to 25%) and mild hypothermia (33° to 36°C) were usually used. Antegrade or combined antegrade and retrograde delivery of a cold crystalloid cardioplegic solution (Plegisol, Abbot, North Chicago, IL) supplemented with procaine hydrochloride was used for myocardial protection. Weaning from cardiopulmonary bypass was started at a rectal temperature of 35° to 36°C. Heparin was neutralized with protamine chloride. Ringer's acetate solution was used for volume substitution postoperatively. Shed mediastinal blood was routinely retransfused in the intensive care unit. Postoperative rewarming was facilitated by radiant heat provided by a thermal ceiling. Details of hemodynamic monitoring have been given previously [4].

Definitions
Postoperative heart failure was defined as a hemodynamic state secondary to pump failure unable to meet systemic demands, usually manifested as inability to wean from cardiopulmonary bypass without supportive measures or hemodynamic deterioration after weaning from cardiopulmonary bypass that required active treatment other than correction of volume or vascular resistance. Supportive measures or treatment consisted of intraaortic balloon pump, inotropic treatment, and metabolic support with glucose–insulin–potassium or intravenous glutamate [5]. Inotropic treatment was defined as continuous infusion for more than 30 minutes of catecholamines (epinephrine, dobutamine) or phosphodiesterase inhibitor (milrinone). A low cardiac output can be sufficient to supply the body demands in an anesthetized or sedated patient, and hence, reliance on markers for adequate circulation, in particular mixed venous oxygen saturation (SvO 2), and echocardiographic evaluation rather than fixed hemodynamic criteria were used to diagnose PHF [6–8]. Hemodynamic measures such as atrial filling pressures, systemic pressure, and Swan-Ganz data were used to aid the interpretations. In the majority of patients, PHF was evident at weaning from cardiopulmonary bypass, with rapidly deteriorating circulation and increasing filling pressures. In the remaining patients, echocardiographic evidence of left ventricular or right ventricular dysfunction associated with signs of inadequate circulation was used to diagnose PHF. Although the diagnosis was dependent on the judgment of individual anesthesiologists and surgeons, the following relationships between SvO 2 and systolic arterial pressure (SAP) (SvO 2 < 50% and SAP < 130 mm Hg; SvO 2 < 55% and SAP < 110 mm Hg; SvO 2 < 60% and SAP < 90 mm Hg; SvO 2 < 65% and SAP < 70 mm Hg—after correction of benign causes of low SvO 2 such as shivering and hypovolemia) provide our guidelines to recognize inadequate circulation. Hemodynamic results for patients who were sufficiently stable to permit recordings when PHF presented are given under results.

Emergency operation was defined as a procedure that could not be postponed to the following day and was therefore usually performed immediately but not later than 24 hours from acceptance. Urgent operations were defined as scheduled procedures within 1 week for patients unable to leave the hospital because of clinical condition. These procedures were usually performed in the daytime, as soon as possible. The effective orifice area for the different prostheses used in this study are based on in vivo Doppler echocardiographic measurements reported in the literature [9–17].

Complications presented refer to in-hospital events occurring at our institution. Intraoperative myocardial infarction was diagnosed by biochemical markers of myocardial injury or by findings at autopsy. Aspartate aminotransferase exceeding 3.0 µkat/L with alanine aminotransferase less than half of the aspartate aminotransferase value, supported by MB isozyme of creatine kinase in excess of 70 µg/L on the first postoperative morning or by a sustained elevation of troponin-T greater than 2.0 µg/L on the fourth postoperative day, was considered diagnostic for intraoperative myocardial infarction [18]. Stroke was defined as a permanent or transient central neurologic deficit. The majority of patients with suspected neurologic injury were examined by computed tomographic scan. Cognitive dysfunction was not included in the assessment.

Preoperative left ventricular function was evaluated by a few cardiologists dedicated to echocardiography and categorized as normal, mildly depressed, moderately depressed, or severe depressed systolic left ventricular function. Severe systolic left ventricular dysfunction corresponds to an ejection fraction of 0.30 or less. Hospital stay refers to hospital stay at the University Hospital including preoperative stay (the majority of patients were discharged to the referring hospitals). Preoperative unstable hemodynamics was defined as a circulatory state requiring either inotropic treatment or mechanical circulatory assist immediately before surgery. The other variables in the database were defined according to the Society of Thoracic Surgeons Cardiac and Thoracic Databases definitions.

Statistical Analysis
Data are presented as mean ± standard deviation. Nonparametric tests (Mann-Whitney U test and Fisher's exact test) were used for comparison of patients with and without PHF. For evaluation of independent risk factors for PHF, univariate logistic regression was first used. Variables were tested in a stepwise forward multivariate logistic regression model if the univariate p value was less than 0.25. Furthermore, variables that previously have been shown to influence postoperative outcome were tested in the model. Statistical significance was defined as p less than 0.05. Hosmer-Lemeshow goodness-of-fit statistics was calculated for the final model [19]. Statistical analyses were performed with computerized statistical packages (Statistica 5.5, StatSoft Inc, Tulsa, OK, and MINITAB 13, Minitab Inc, State College, PA).

Ethical Aspects
The study was performed according to the principles of the Helsinki Declaration of Human Rights and was approved by the ethics committee for medical research at the University Hospital of Linköping.


    Results
 Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
The average age of patients undergoing AVR for AS was 69.6 ± 6.7 years, and 48% were women. Postoperative heart failure occurred in 11.3% (45 of 398 patients) and presented at weaning from cardiopulmonary bypass in 73.3% of the patients. Mixed venous oxygen saturation was 53.7% ± 11.0% in the 23 patients sufficiently stable to allow recordings at presentation of PHF, and in these patients SAP was 84 ± 16 mm Hg. Treatment of PHF consisted of intraaortic balloon pump (2.2%), inotropic treatment (93.3%), and metabolic support with glucose–insulin–potassium or intravenous glutamate (42.2%).

Preoperative and intraoperative data for patients with and without PHF is given in Tables 1 and 2. Go The postoperative course was more complicated, with extended intensive care unit care and higher 30-day mortality (6.7% versus 1.4%) in patients with PHF (Table 3).


View this table:
[in this window]
[in a new window]
 
Table 1. Preoperative Data a
 

View this table:
[in this window]
[in a new window]
 
Table 2. Intraoperative Data a
 

View this table:
[in this window]
[in a new window]
 
Table 3. Postoperative Data a
 
Univariate association between different variables and PHF after AVR are given in Table 4. In the forward stepwise multiple logistic regression analysis, hypertension, history of congestive heart failure, severe systolic left ventricular dysfunction preoperatively, systolic pulmonary pressure of 60 mm Hg or greater, preoperatively unstable hemodynamics, cross-clamp time, and intraoperative myocardial infarction emerged as independent risk factors for PHF (Table 5).


View this table:
[in this window]
[in a new window]
 
Table 4. Univariate Analysis of Risk Factors for Postoperative Heart Failure a
 

View this table:
[in this window]
[in a new window]
 
Table 5. Multivariate Analysis of Risk Factors for Postoperative Heart Failure a
 
In the PHF group intraoperative surgical problems were reported in 7 of the 45 patients. These consisted of paravalvular leak requiring additional sutures (n = 2), prosthesis reimplantation because of leaflet impingement (n = 1) or choice of oversized prosthesis (n = 1), repair of right coronary ostium (n = 1), exploration of the mitral valve through the left atrium (n = 1), and suture of the anterior mitral leaflet after decalcification (n = 1). Average aortic cross-clamp time was 133 ± 46 minutes in PHF patients with intraoperative problems compared with 89 ± 23 minutes in PHF patients without reported problems (p = 0.015).


    Comment
 Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
Postoperative heart failure after AVR for AS was associated with an almost fivefold increase in postoperative mortality, a substantial increase in postoperative morbidity, and subsequently increased utilization of intensive care unit resources. Multivariate logistic regression analysis identified seven variables as independent risk factors for PHF after surgery for isolated AS, five preoperative (hypertension, history of congestive heart failure, severe systolic left ventricular dysfunction, pulmonary hypertension, hemodynamic instability preoperatively) and two intraoperative (aortic cross-clamp time, intraoperative myocardial infarction).

Studies on patients undergoing AVR have generally focused on the prosthesis. The size and choice of prosthesis, echocardiographic evaluation, myocardial mass reduction, freedom from reoperation, and thromboembolic complications have been the main topics of these studies. Valuable information has been gained that has contributed to the development of current treatment of aortic valve disease. However, the Ad Hoc Liaison Committee for Standardizing Definitions of Prosthetic Heart Valve Morbidity has acknowledged that patient variables may be more responsible for outcome than valve-related factors. They have also pointed out the lack of data on this issue and encouraged investigators to identify relevant patient factors in addition to factors related to replacement valves [20]. A substantial contribution was provided by the Northern New England Cardiovascular Disease study group in a recent paper on risk factors for in-hospital mortality in association with valve surgery [21]. Furthermore, this group has previously identified PHF as the most important cause of mortality in association with cardiac surgery [1]. To add to the picture, we have focused on PHF in patients undergoing surgery for AS inasmuch as increased knowledge about this issue could aid efforts to improve the management of these patients and, hence, outcome.

The study cohorts were selected from the complete number of patients undergoing surgery for AS within an area of Sweden with 1 million inhabitants during 1995 through 2000. Therefore, no referral selection bias should be present. The subgroup chosen represents the largest homogenous group of valve patients in our surgical practice. Redo procedures are a recognized risk group for postoperative mortality after valve surgery, but they constitute a small fraction of our patients undergoing AVR. Therefore, and to avoid heterogeneity, redo procedures were not included. Certain study limitations deserve to be acknowledged. Our database provided information about the severity of AS by aortic valve area rather than valve gradients. This prevented evaluation of the combination of low gradient and poor left ventricular function, which has been identified as a risk factor for postoperative mortality [22]. Virtually all patients coming to surgery for AS have some degree of left ventricular hypertrophy and diastolic dysfunction, but these variables were not sufficiently quantified to permit evaluation of their influence on PHF. However, it is conceivable that the severity of these variables were to some extent reflected in the pulmonary artery pressures.

Prosthesis size and patient–prosthesis mismatch have been shown to play a role for postoperative hemodynamics and regression of left ventricular mass, whereas there are conflicting data on its impact on clinical outcome and survival [23–31]. We did not find a significant association between PHF and patient–prosthesis mismatch in our study. It can be argued that our material was not large enough to detect such a relationship. However, it is evident that other variables emerged as risk factors of greater importance for PHF [20].

Pulmonary hypertension, hemodynamic instability before anesthesia, intraoperative myocardial infarction, and severe systolic left ventricular dysfunction preoperatively had the highest odds ratios for PHF. However, the hazard associated with them was not matched by their explanatory role in the final model. In contrast, aortic cross-clamp time emerged as the statistically most significant risk factor and also demonstrated the highest explanatory role according to the multivariate analysis. Our data suggest that the prolonged aortic cross-clamp times were partly explained by intraoperative surgical problems. However, the nature of surgical problems did not by themselves provide obvious explanations to PHF, and hence the role of cross-clamp time per se remains to be considered a major risk factor. Hypertension and history of congestive heart failure also emerged as a significant risk factor in the final model.

Multivariate analyses provide variables that can be used to predict an increased risk for a certain outcome. Such variables do not necessarily have a mechanistic relationship with the outcome studied, and it can be debated whether a mechanistic variable such as intraoperative myocardial infarction for PHF should have been included. However, the aim of this study was to identify not only predictive variables but also factors with a mechanistic relationship to PHF. It seems that our final model met these aims as it provided variables with both predictive and explanatory value. Basically these variables seem to indicate either preoperatively existing or intraoperatively acquired myocardial dysfunction. Furthermore, arterial and pulmonary hypertension indicating increased left and right ventricular afterload, respectively, emerged as independent risk factors. The latter variable is also a marker of left ventricular dysfunction.

In contrast to what has been found in coronary artery bypass grafting, population variables such as female sex, diabetes mellitus, and older age did not emerge as independent risk factors for PHF after surgery for AS [2, 32]. The EuroSCORE was significantly associated with PHF in the univariate analysis although not developed for this purpose, but for predicting risk for postoperative mortality [33]. This is in agreement with the role suggested for PHF as the major cause of postoperative mortality [1]. In our study PHF was associated with a marked increase in postoperative mortality and morbidity. The long-term consequences of PHF in patients undergoing AVR remain to be described.

Currently, surgery is indicated mainly for symptomatic AS. Interestingly, angina pectoris had a protective influence regarding the risk for PHF in contrast to history of congestive heart failure according to the univariate analysis. Our database did not include information about the history of syncope. Small orifice area of the stenotic aortic valve, a marker of advanced valvular disease, was associated with an increased risk of PHF in the univariate analysis.

To summarize, limitations of preoperative myocardial functional reserve, increased afterload, and intraoperatively acquired myocardial depression or injury seem to be the issues to consider with regard to PHF after AVR in AS. Our results highlight the importance of addressing myocardial protection and minimizing cross-clamp time, particularly for patients with preoperatively compromised myocardial function. Furthermore, we suggest that aortic valve surgery should be considered in asymptomatic patients before substantial secondary myocardial dysfunction or pulmonary hypertension develops.


    Acknowledgments
 Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
We are grateful to Olle Eriksson, Division of Statistics at the Department of Mathematics, Linköping University, for professional assistance with statistical analyses. The study was financially supported by research grants from The Swedish Heart Lung Foundation (grant 20050241), Lions Research Foundation, Östergötlands Läns Landsting, and Linköping University Hospital.


    References
 Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 

  1. O'Connor GT, Birkmeyer JD, Dacey LJ, et al. Northern New England Cardiovascular Disease Study Group Results of a regional study of modes of death associated with coronary artery bypass grafting Ann Thorac Surg 1998;66:1323-1328.[Abstract/Free Full Text]
  2. Surgenor SD, O'Connor GT, Lahey SJ, et al. Predicting the risk of death from heart failure after coronary artery bypass graft surgery Anesth Analg 2001;92:596-601.[Abstract/Free Full Text]
  3. Jarvinen A. Low-output syndrome as a complication of open-heart surgery in 85 patients Ann Clin Res 1975;7:379-393.[Medline]
  4. Vanky F, Hakanson E, Maros T, Svedjeholm R. Different characteristics of postoperative heart failure after surgery for aortic stenosis and coronary disease Scand Cardiovasc J 2004;38:152-158.[Medline]
  5. Svedjeholm R, Huljebrant I, Hakanson E, Vanhanen I. Glutamate and high-dose glucose-insulin-potassium (GIK) in the treatment of severe cardiac failure after cardiac operations Ann Thorac Surg 1995;59(Suppl):S23.[Medline]
  6. Hakanson E, Svedjeholm R, Vanhanen I. Physiologic aspects in postoperative cardiac patients Ann Thorac Surg 1995;59(Suppl):S12-S14.[Medline]
  7. Svedjeholm R, Hakanson E, Szabo Z. Routine SvO2 measurement after CABG surgery with a surgically introduced pulmonary artery catheter Eur J Cardiothorac Surg 1999;16:450-457.[Abstract/Free Full Text]
  8. Reichert CL, Visser CA, Koolen JJ, et al. Transesophageal echocardiography in hypotensive patients after cardiac operations. Comparison with hemodynamic parameters J Thorac Cardiovasc Surg 1992;104:321-326.[Abstract]
  9. Aupart MR, Sirinelli AL, Diemont FF, Meurisse YA, Dreyfus XB, Marchand MA. The last generation of pericardial valves in the aortic positionten-year follow-up in 589 patients. Ann Thorac Surg 1996;61:615-620.[Abstract/Free Full Text]
  10. Dumesnil JG, LeBlanc MH, Cartier PC, et al. Hemodynamic features of the freestyle aortic bioprosthesis compared with stented bioprosthesis Ann Thorac Surg 1998;66(Suppl):S130-S133.[Medline]
  11. Chafizadeh ER, Zoghbi WA. Doppler echocardiographic assessment of the St. Jude Medical prosthetic valve in the aortic position using the continuity equation Circulation 1991;83:213-223.[Abstract/Free Full Text]
  12. Bernal JM, Martin-Duran R, Rabasa JM, Revuelta JM. The CarboMedics "Top-Hat" supraannular prosthesis Ann Thorac Surg 1999;67:1299-1303.[Abstract/Free Full Text]
  13. De Paulis R, Sommariva L, De Matteis GM, et al. Hemodynamic performances of small diameter CarboMedics and St. Jude valves J Heart Valve Dis 1996;5(Suppl 3):S339-S343.[Medline]
  14. Zingg U, Aeschbacher B, Seiler C, Althaus U, Carrel T. Early experience with the new Masters series of St. Jude Medical heart valvein vivo hemodynamic and clinical results in patients with narrowed aortic annulus. J Heart Valve Dis 1997;6:535-541.[Medline]
  15. Chambers J, Cross J, Deverall P, Sowton E. Echocardiographic description of the CarboMedics bileaflet prosthetic heart valve J Am Coll Cardiol 1993;21:398-405.[Abstract]
  16. Chambers J, Ely JL. Early postoperative echocardiographic hemodynamic performance of the On-X prosthetic heart valvea multicenter study. J Heart Valve Dis 1998;7:569-573.[Medline]
  17. Chambers JB. Studies on the use of Doppler ultrasound in the assessment of prosthetic cardiac valve function [MD thesis]. Cambridge: Cambridge University; 2000.
  18. Dahlin LG, Kagedal B, Nylander E, Olin C, Rutberg H, Svedjeholm R. Early identification of permanent myocardial damage after coronary surgery is aided by repeated measurements of CK-MB Scand Cardiovasc J 2002;36:35-40.[Medline]
  19. Hosmer DW, Lemeshow S. Applied logistic regression. New York: Wiley; 1989.
  20. Edmunds Jr LH, Clark RE, Cohn LH, Grunkemeier GL, Miller DC, Weisel RD. Guidelines for reporting morbidity and mortality after cardiac valvular operations. The American Association for Thoracic Surgery, Ad Hoc Liaison Committee for Standardizing Definitions of Prosthetic Heart Valve Morbidity Ann Thorac Surg 1996;62:932-935.[Abstract/Free Full Text]
  21. Nowicki ER, Birkmeyer NJ, Weintraub RW, et al. Multivariable prediction of in-hospital mortality associated with aortic and mitral valve surgery in Northern New England Ann Thorac Surg 2004;77:1966-1977.[Abstract/Free Full Text]
  22. Smucker ML, Manning SB, Stuckey TD, Tyson DL, Nygaard TW, Kron IL. Preoperative left ventricular wall stress, ejection fraction, and aortic valve gradient as prognostic indicators in aortic valve stenosis Cathet Cardiovasc Diagn 1989;17:133-143.[Medline]
  23. Ruel M, Rubens FD, Masters RG, Pipe AL, Bedard P, Mesana TG. Late incidence and predictors of persistent or recurrent heart failure in patients with mitral prosthetic valves J Thorac Cardiovasc Surg 2004;128:278-283.[Abstract/Free Full Text]
  24. Blais C, Dumesnil JG, Baillot R, Simard S, Doyle D, Pibarot P. Impact of valve prosthesis-patient mismatch on short-term mortality after aortic valve replacement Circulation 2003;108:983-988.[Abstract/Free Full Text]
  25. Pibarot P, Dumesnil JG. Hemodynamic and clinical impact of prosthesis-patient mismatch in the aortic valve position and its prevention J Am Coll Cardiol 2000;36:1131-1141.[Abstract/Free Full Text]
  26. Rao V, Jamieson WR, Ivanov J, Armstrong S, David TE. Prosthesis-patient mismatch affects survival after aortic valve replacement Circulation 2000;102(Suppl 3):III-5-III-9.[Medline]
  27. Milano AD, De Carlo M, Mecozzi G, et al. Clinical outcome in patients with 19-mm and 21-mm St. Jude aortic prosthesescomparison at long-term follow-up. Ann Thorac Surg 2002;73:37-43.[Abstract/Free Full Text]
  28. Ruel M, Kulik A, Lam BK, et al. Long-term outcomes of valve replacement with modern prostheses in young adults Eur J Cardiothorac Surg 2005;27:425-433.[Abstract/Free Full Text]
  29. Medalion B, Blackstone EH, Lytle BW, White J, Arnold JH, Cosgrove DM. Aortic valve replacementis valve size important?. J Thorac Cardiovasc Surg 2000;119:963-974.[Abstract/Free Full Text]
  30. Blackstone EH, Cosgrove DM, Jamieson WR, et al. Prosthesis size and long-term survival after aortic valve replacement J Thorac Cardiovasc Surg 2003;126:783-796.[Abstract/Free Full Text]
  31. Hanayama N, Christakis GT, Mallidi HR, et al. Patient prosthesis mismatch is rare after aortic valve replacementvalve size may be irrelevant. Ann Thorac Surg 2002;73:1822-1829.[Abstract/Free Full Text]
  32. Rao V, Ivanov J, Weisel RD, Ikonomidis JS, Christakis GT, David TE. Predictors of low cardiac output syndrome after coronary artery bypass J Thorac Cardiovasc Surg 1996;112:38-51.[Abstract/Free Full Text]
  33. Roques F, Nashef SA, Michel P, et al. Risk factors and outcome in European cardiac surgeryanalysis of the EuroSCORE multinational database of 19030 patients. Eur J Cardiothorac Surg 1999;15:816-822.[Abstract/Free Full Text]



This article has been cited by other articles:


Home page
HeartHome page
J Mascherbauer, R Rosenhek, C Fuchs, E Pernicka, U Klaar, C Scholten, M Heger, G Wollenek, G Maurer, and H Baumgartner
Moderate patient-prosthesis mismatch after valve replacement for severe aortic stenosis has no impact on short-term and long-term mortality
Heart, December 1, 2008; 94(12): 1639 - 1645.
[Abstract] [Full Text] [PDF]


Home page
Ann. Thorac. Surg.Home page
F. B. Vanky, E. Hakanson, and R. Svedjeholm
Long-Term Consequences of Postoperative Heart Failure After Surgery for Aortic Stenosis Compared With Coronary Surgery
Ann. Thorac. Surg., June 1, 2007; 83(6): 2036 - 2043.
[Abstract] [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):
Farkas B. Vánky
Eva Tamás
Rolf Svedjeholm
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 Vánky, F. B.
Right arrow Articles by Svedjeholm, R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Vánky, F. B.
Right arrow Articles by Svedjeholm, R.
Related Collections
Right arrow Valve disease


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