Editorial Fourth Decade After Repair of Tetralogy of Fallot Taking Aim at Moving Targets David P. Bichell, MD
T
his year marks the 60th year since the first successful intracardiac repair of tetralogy of Fallot (TOF).1 The repair, largely unchanged over decades, consists of ventricular septal defect closure and the relief of variable forms of right ventricular (RV) obstruction, usually with a transannular patch (TAP), and usually resulting in free pulmonary insufficiency (PI). Early in the experience with TOF repair, attention was on quantity of life---lifting the early dip in the survival curve. Palliative shunts were widely used to permit repair at a safer, older age. The dividends from a full relief of obstruction included excellent function for decades for patients formerly suffering from morbid or lethal disease. In this issue of Circulation, Cuypers and colleagues2 report findings of the third decennial follow-up of a cohort of early TOF repairs, the longest prospective study of this population to date. As such longitudinal evidence accrues, we are continually called on to reexamine both ends of the treatment timeline, although it is a wobbly yardstick that attempts to inform today’s best practices by measuring the sequelae of yesterday’s.
Article see p 1944 Early mortality after TOF repair is now very low, and the 10- to 20-year follow-up was encouraging. However, in the third postrepair decade, the Kaplan–Meier curve droops with progressive exercise intolerance, arrhythmia, right heart failure, and sudden death. Evidence points to ventricular scarring, chronic PI, RV hypertrophy, and declining left ventricular and RV performance as interrelated contributing factors. Some late risk may be modified at the front end, during infant repair. The progression of late sequelae also pushes the question of how to do a better job at the back end, with proactive strategies to preempt the onset of late morbidity.
At the Front End Early- and long-term evidence supports the modern practice of repair in infancy, with nearly 0% mortality and excellent early physiology, regardless of a higher incidence of TAP with earlier repair.3,4 Echoing prior studies,5,6 Cuypers et al2 show that older age at primary repair and prior shunt are independent predictors of The opinions expressed in this article are not necessarily those of the editors or of the American Heart Association. From the Department of Cardiac Surgery, Vanderbilt University, Nashville, TN. Correspondence to David P. Bichell, MD, Cornelius Vanderbilt Chair in Surgery, Professor, Cardiac Surgery, Monroe Carell Jr Children’s Hospital, Vanderbilt University Medical Center, 2200 Children’s Way, Nashville, TN 37232–9292. E-mail [email protected] (Circulation. 2014;130:1931-1932.) © 2014 American Heart Association, Inc. Circulation is available at http://circ.ahajournals.org DOI: 10.1161/CIRCULATIONAHA.114.013270
late morbidity or death. Of note, very few patients were repaired in infancy in the Rotterdam cohort. Among other 3- to 4-decade series, the youngest age at repair was beyond infancy, and a palliative shunt was used for up to 40% of cases, compared with contemporary series when repair is seldom performed beyond the first half of infancy and the shunt has all but vanished.6,7 The populations are not comparable. In fact, by age and method of repair, they are nearly mutually exclusive, challenging a meaningful translation of 40-year data to the present. Repair in early infancy still awaits data on the third postrepair decade. Strategies to avoid TAP and to spare the pulmonary valve have enjoyed variable enthusiasm and mixed outcomes. Early successes are reported, but durable valve competence is limited to valves with milder dysplasia at the outset, and valvesparing approaches yield shorter freedom from reintervention than TAP.8 Twenty-year data are emerging for a valve-sparing approach, with encouraging freedom from ventricular arrhythmia, but era differences make comparison difficult.9 The Rotterdam data strengthen evidence that TAP is a factor predicting late dysfunction, arrhythmia, or death, which finds support in some but not all series.2,7,10
At the Back End Whereas the 40-year data presented today may questionably foresee the fate of today’s infants, they represent what is exactly relevant to today’s adults, who make up the drooping tail of the Kaplan–Meier curve and who account for a large proportion of adult congenital interventions today. Neither morbidity nor mortality plateaus in the fourth decade. Cuyper’s group shows a cumulative incidence of all events (death, cardiac reintervention, symptomatic arrhythmia, stroke, heart failure, endocarditis), continuing to worsen in the third decade, with event-free survival of only 25% at 40 years, consistent with other series.2 Although PI itself is not an independent predictor of functional status, decompensated chronic volume load likely underlies the progression of ventricular dysfunction and associated late arrhythmia and mortality.5,11 In addition to fueling valve-sparing approaches at the front end, these findings underlie a controversial examination of timing for pulmonary valve replacement (PVR) in the adult with chronic PI. Does an asymptomatic patient with 25-year freedom from PVR count as a success or as a failure to intervene in time to forestall the decline that is already silently underway? In the absence of symptoms, heart failure, or arrhythmia, there is not a clear consensus on PVR indications. PVR is a treatment that can both cause and prevent a cardiac event. Is preventive maintenance a justified risk? Are there any patients who will never need PVR? The criteria justifying PVR are reasonably moving in the direction of earlier intervention. A QRS duration of >180 milliseconds predicts ventricular tachycardia, and QRS duration
Downloaded from http://circ.ahajournals.org/ at CONS 1931 CALIFORNIA DIG LIB on December 3, 2014
1932 Circulation November 25, 2014 stabilizes after PVR.11 Reasoned thresholds for PVR based on QRS prolongation have moved from 180 toward 140 milliseconds.12 Functional recovery of the RV after PVR is less likely if the preoperative RV end-diastolic volume is >170 mL/m2, and that threshold is moving toward 150 mL/m2.12 Exercise criteria, RV mass-to-volume ratio, and other metrics support lowering the threshold.13 The Rotterdam data report results of a conservative strategy, with PVR reserved for those with symptoms.14 The threshold for asymptomatic patients with PI has moved earlier in recent years, but long-term data on the effect of proactive intervention remain incomplete. Competing risks of a more aggressive approach to PVR include an uncertain benefit and the higher risk of reinterventions after earlier PVR. Overall, the mortality for PVR is low and getting lower, and durable improvement in symptoms and functional class after PVR has been shown, although a survival advantage has so far not.15,16 Further complicating the question are the unknowns about the long-term fate of catheter-based PVR. Clarity awaits long-term results of the current more aggressive strategies and their effect on the tail of the Kaplan–Meier curve. Late overall data on chronic PI show cause for concern that we may be intervening too late, and earlier PVR seems a reasonable direction to continue leaning. Patient-tailored, evidence-based strategies for determining the threshold for PVR are maturing in sophistication and point to earlier intervention.12 The Rotterdam group and others show self-perceived health status among TOF patients to be generally good, despite declining cardiac function.2,17 Self-assessment may be a misleading portrait of the disease state and may delay the presentation for treatment. This points to the importance of improving the follow-up systems for adults with congenital heart disease, who commonly disappear from surveillance after they transition out of pediatric care, unless specific transition programs are developed. The goal of health care is to optimize both quantity and quality of life for patients. Challenging evidence-based medicine is the fact that evidence commonly comes from groups, but medicine is applied to individuals. The challenge broadens when our evidence from yesterday’s groups is all we have to gauge what is best for today’s individual. As our experience with TOF repair enters a fifth decade, the steady progression of functional decline justifies earlier intervention at both ends of the treatment timeline, with encouraging early results that await the test of coming decades. Positive patient self-assessments in the face of declining physiological status should alert us to the need to further refine the threshold for PVR and to devise systematic surveillance systems to identify earlier progression of silent disease.
Disclosures None.
References 1. Lillehei CW, Cohen M, Warden HE, Read RC, Aust JB, Dewall RA, Varco RL. Direct vision intracardiac surgical correction of the tetralogy of Fallot,
pentalogy of Fallot, and pulmonary atresia defects; report of first ten cases. Ann Surg. 1955;142:418–442. 2. Cuypers JAAE, Menting ME, Konings EEM, Opić P, Utens EMWJ, Helbing WA, Witsenburg M, van den Bosch AE, Ouhlous M, van Domburg RT, Rizopoulos D, Meijboom FJ, Boersma E, Bogers AJJC, Roos-Hesselink JW. The unnatural history of tetralogy of Fallot: prospective follow-up of 40 years after surgical correction. Circulation. 2014;130:1944–1953. 3. Van Arsdell GS, Maharaj GS, Tom J, Rao VK, Coles JG, Freedom RM, Williams WG, McCrindle BW. What is the optimal age for repair of tetralogy of Fallot? Circulation. 2000;102(suppl 3):III123–III129. 4. Munkhammar P, Cullen S, Jögi P, de Leval M, Elliott M, Norgård G. Early age at repair prevents restrictive right ventricular (RV) physiology after surgery for tetralogy of Fallot (TOF): diastolic RV function after TOF repair in infancy. J Am Coll Cardiol. 1998;32:1083–1087. 5. Geva T, Sandweiss BM, Gauvreau K, Lock JE, Powell AJ. Factors associated with impaired clinical status in long-term survivors of tetralogy of Fallot repair evaluated by magnetic resonance imaging. J Am Coll Cardiol. 2004;43:1068–1074. 6. Murphy JG, Gersh BJ, Mair DD, Fuster V, McGoon MD, Ilstrup DM, McGoon DC, Kirklin JW, Danielson GK. Long-term outcome in patients undergoing surgical repair of tetralogy of Fallot. N Engl J Med. 1993;329:593–599. 7. Nollert G, Fischlein T, Bouterwek S, Böhmer C, Klinner W, Reichart B. Long-term survival in patients with repair of tetralogy of Fallot: 36-year follow-up of 490 survivors of the first year after surgical repair. J Am Coll Cardiol. 1997;30:1374–1383. 8. Vida VL, Guariento A, Castaldi B, Sambugaro M, Padalino MA, Milanesi O, Stellin G. Evolving strategies for preserving the pulmonary valve during early repair of tetralogy of Fallot: mid-term results. J Thorac Cardiovasc Surg. 2014;147:687–694. 9. Hoashi T, Kagisaki K, Meng Y, Sakaguchi H, Kurosaki K, Shiraishi I, Yagihara T, Ichikawa H. Long-term outcomes after definitive repair for tetralogy of Fallot with preservation of the pulmonary valve annulus. J Thorac Cardiovasc Surg. 2014;148:802–808. 10. Hickey EJ, Veldtman G, Bradley TJ, Gengsakul A, Webb G, Williams WG, Manlhiot C, McCrindle BW. Functional health status in adult survivors of operative repair of tetralogy of Fallot. Am J Cardiol. 2012;109:873–880. 11. Gatzoulis MA, Balaji S, Webber SA, Siu SC, Hokanson JS, Poile C, Rosenthal M, Nakazawa M, Moller JH, Gillette PC, Webb GD, Redington AN. Risk factors for arrhythmia and sudden cardiac death late after repair of tetralogy of Fallot: a multicentre study. Lancet. 2000;356:975–981. 12. Geva T. Is MRI the preferred method for evaluating right ventricular size and function in patients with congenital heart disease? MRI is the preferred method for evaluating right ventricular size and function in patients with congenital heart disease. Circ Cardiovasc Imaging. 2014;7:190–197. 13. Valente AM, Gauvreau K, Assenza GE, Babu-Narayan SV, Schreier J, Gatzoulis MA, Groenink M, Inuzuka R, Kilner PJ, Koyak Z, Landzberg MJ, Mulder B, Powell AJ, Wald R, Geva T. Contemporary predictors of death and sustained ventricular tachycardia in patients with repaired tetralogy of Fallot enrolled in the INDICATOR cohort. Heart. 2014;100:247–253. 14. Meijboom FJ, Roos-Hesselink JW, McGhie JS, Spitaels SE, van Domburg RT, Utens LM, Simoons ML, Bogers AJ. Consequences of a selective approach toward pulmonary valve replacement in adult patients with tetralogy of Fallot and pulmonary regurgitation. J Thorac Cardiovasc Surg. 2008;135:50–55. 15. Babu-Narayan SV, Diller GP, Gheta RR, Bastin AJ, Karonis T, Li W, Pennell DJ, Uemura H, Sethia B, Gatzoulis MA, Shore DF. Clinical outcomes of surgical pulmonary valve replacement after repair of tetralogy of Fallot and potential prognostic value of preoperative cardiopulmonary exercise testing. Circulation. 2014;129:18–27. 16. Sabate Rotes A, Eidem BW, Connolly HM, Bonnichsen CR, Rosedahl JK, Schaff HV, Dearani JA, Burkhart HM. Long-term follow-up after pulmonary valve replacement in repaired tetralogy of Fallot. Am J Cardiol. 2014;114:901–908. 17. Knowles R, Veldtman G, Hickey EJ, Bradley T, Gengsakul A, Webb GD, Williams WG, McCrindle BW. Functional health status of adults with tetralogy of Fallot: matched comparison with healthy siblings. Ann Thorac Surg. 2012;94:124–132. Key Words: Editorials ◼ tetralogy of Fallot
Downloaded from http://circ.ahajournals.org/ at CONS CALIFORNIA DIG LIB on December 3, 2014
Fourth Decade After Repair of Tetralogy of Fallot: Taking Aim at Moving Targets David P. Bichell Circulation. 2014;130:1931-1932; originally published online October 23, 2014; doi: 10.1161/CIRCULATIONAHA.114.013270 Circulation is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231 Copyright © 2014 American Heart Association, Inc. All rights reserved. Print ISSN: 0009-7322. Online ISSN: 1524-4539
The online version of this article, along with updated information and services, is located on the World Wide Web at: http://circ.ahajournals.org/content/130/22/1931
Permissions: Requests for permissions to reproduce figures, tables, or portions of articles originally published in Circulation can be obtained via RightsLink, a service of the Copyright Clearance Center, not the Editorial Office. Once the online version of the published article for which permission is being requested is located, click Request Permissions in the middle column of the Web page under Services. Further information about this process is available in the Permissions and Rights Question and Answer document. Reprints: Information about reprints can be found online at: http://www.lww.com/reprints Subscriptions: Information about subscribing to Circulation is online at: http://circ.ahajournals.org//subscriptions/
Downloaded from http://circ.ahajournals.org/ at CONS CALIFORNIA DIG LIB on December 3, 2014
T
his year marks the 60th year since the first successful intracardiac repair of tetralogy of Fallot (TOF).1 The repair, largely unchanged over decades, consists of ventricular septal defect closure and the relief of variable forms of right ventricular (RV) obstruction, usually with a transannular patch (TAP), and usually resulting in free pulmonary insufficiency (PI). Early in the experience with TOF repair, attention was on quantity of life---lifting the early dip in the survival curve. Palliative shunts were widely used to permit repair at a safer, older age. The dividends from a full relief of obstruction included excellent function for decades for patients formerly suffering from morbid or lethal disease. In this issue of Circulation, Cuypers and colleagues2 report findings of the third decennial follow-up of a cohort of early TOF repairs, the longest prospective study of this population to date. As such longitudinal evidence accrues, we are continually called on to reexamine both ends of the treatment timeline, although it is a wobbly yardstick that attempts to inform today’s best practices by measuring the sequelae of yesterday’s.
Article see p 1944 Early mortality after TOF repair is now very low, and the 10- to 20-year follow-up was encouraging. However, in the third postrepair decade, the Kaplan–Meier curve droops with progressive exercise intolerance, arrhythmia, right heart failure, and sudden death. Evidence points to ventricular scarring, chronic PI, RV hypertrophy, and declining left ventricular and RV performance as interrelated contributing factors. Some late risk may be modified at the front end, during infant repair. The progression of late sequelae also pushes the question of how to do a better job at the back end, with proactive strategies to preempt the onset of late morbidity.
At the Front End Early- and long-term evidence supports the modern practice of repair in infancy, with nearly 0% mortality and excellent early physiology, regardless of a higher incidence of TAP with earlier repair.3,4 Echoing prior studies,5,6 Cuypers et al2 show that older age at primary repair and prior shunt are independent predictors of The opinions expressed in this article are not necessarily those of the editors or of the American Heart Association. From the Department of Cardiac Surgery, Vanderbilt University, Nashville, TN. Correspondence to David P. Bichell, MD, Cornelius Vanderbilt Chair in Surgery, Professor, Cardiac Surgery, Monroe Carell Jr Children’s Hospital, Vanderbilt University Medical Center, 2200 Children’s Way, Nashville, TN 37232–9292. E-mail [email protected] (Circulation. 2014;130:1931-1932.) © 2014 American Heart Association, Inc. Circulation is available at http://circ.ahajournals.org DOI: 10.1161/CIRCULATIONAHA.114.013270
late morbidity or death. Of note, very few patients were repaired in infancy in the Rotterdam cohort. Among other 3- to 4-decade series, the youngest age at repair was beyond infancy, and a palliative shunt was used for up to 40% of cases, compared with contemporary series when repair is seldom performed beyond the first half of infancy and the shunt has all but vanished.6,7 The populations are not comparable. In fact, by age and method of repair, they are nearly mutually exclusive, challenging a meaningful translation of 40-year data to the present. Repair in early infancy still awaits data on the third postrepair decade. Strategies to avoid TAP and to spare the pulmonary valve have enjoyed variable enthusiasm and mixed outcomes. Early successes are reported, but durable valve competence is limited to valves with milder dysplasia at the outset, and valvesparing approaches yield shorter freedom from reintervention than TAP.8 Twenty-year data are emerging for a valve-sparing approach, with encouraging freedom from ventricular arrhythmia, but era differences make comparison difficult.9 The Rotterdam data strengthen evidence that TAP is a factor predicting late dysfunction, arrhythmia, or death, which finds support in some but not all series.2,7,10
At the Back End Whereas the 40-year data presented today may questionably foresee the fate of today’s infants, they represent what is exactly relevant to today’s adults, who make up the drooping tail of the Kaplan–Meier curve and who account for a large proportion of adult congenital interventions today. Neither morbidity nor mortality plateaus in the fourth decade. Cuyper’s group shows a cumulative incidence of all events (death, cardiac reintervention, symptomatic arrhythmia, stroke, heart failure, endocarditis), continuing to worsen in the third decade, with event-free survival of only 25% at 40 years, consistent with other series.2 Although PI itself is not an independent predictor of functional status, decompensated chronic volume load likely underlies the progression of ventricular dysfunction and associated late arrhythmia and mortality.5,11 In addition to fueling valve-sparing approaches at the front end, these findings underlie a controversial examination of timing for pulmonary valve replacement (PVR) in the adult with chronic PI. Does an asymptomatic patient with 25-year freedom from PVR count as a success or as a failure to intervene in time to forestall the decline that is already silently underway? In the absence of symptoms, heart failure, or arrhythmia, there is not a clear consensus on PVR indications. PVR is a treatment that can both cause and prevent a cardiac event. Is preventive maintenance a justified risk? Are there any patients who will never need PVR? The criteria justifying PVR are reasonably moving in the direction of earlier intervention. A QRS duration of >180 milliseconds predicts ventricular tachycardia, and QRS duration
Downloaded from http://circ.ahajournals.org/ at CONS 1931 CALIFORNIA DIG LIB on December 3, 2014
1932 Circulation November 25, 2014 stabilizes after PVR.11 Reasoned thresholds for PVR based on QRS prolongation have moved from 180 toward 140 milliseconds.12 Functional recovery of the RV after PVR is less likely if the preoperative RV end-diastolic volume is >170 mL/m2, and that threshold is moving toward 150 mL/m2.12 Exercise criteria, RV mass-to-volume ratio, and other metrics support lowering the threshold.13 The Rotterdam data report results of a conservative strategy, with PVR reserved for those with symptoms.14 The threshold for asymptomatic patients with PI has moved earlier in recent years, but long-term data on the effect of proactive intervention remain incomplete. Competing risks of a more aggressive approach to PVR include an uncertain benefit and the higher risk of reinterventions after earlier PVR. Overall, the mortality for PVR is low and getting lower, and durable improvement in symptoms and functional class after PVR has been shown, although a survival advantage has so far not.15,16 Further complicating the question are the unknowns about the long-term fate of catheter-based PVR. Clarity awaits long-term results of the current more aggressive strategies and their effect on the tail of the Kaplan–Meier curve. Late overall data on chronic PI show cause for concern that we may be intervening too late, and earlier PVR seems a reasonable direction to continue leaning. Patient-tailored, evidence-based strategies for determining the threshold for PVR are maturing in sophistication and point to earlier intervention.12 The Rotterdam group and others show self-perceived health status among TOF patients to be generally good, despite declining cardiac function.2,17 Self-assessment may be a misleading portrait of the disease state and may delay the presentation for treatment. This points to the importance of improving the follow-up systems for adults with congenital heart disease, who commonly disappear from surveillance after they transition out of pediatric care, unless specific transition programs are developed. The goal of health care is to optimize both quantity and quality of life for patients. Challenging evidence-based medicine is the fact that evidence commonly comes from groups, but medicine is applied to individuals. The challenge broadens when our evidence from yesterday’s groups is all we have to gauge what is best for today’s individual. As our experience with TOF repair enters a fifth decade, the steady progression of functional decline justifies earlier intervention at both ends of the treatment timeline, with encouraging early results that await the test of coming decades. Positive patient self-assessments in the face of declining physiological status should alert us to the need to further refine the threshold for PVR and to devise systematic surveillance systems to identify earlier progression of silent disease.
Disclosures None.
References 1. Lillehei CW, Cohen M, Warden HE, Read RC, Aust JB, Dewall RA, Varco RL. Direct vision intracardiac surgical correction of the tetralogy of Fallot,
pentalogy of Fallot, and pulmonary atresia defects; report of first ten cases. Ann Surg. 1955;142:418–442. 2. Cuypers JAAE, Menting ME, Konings EEM, Opić P, Utens EMWJ, Helbing WA, Witsenburg M, van den Bosch AE, Ouhlous M, van Domburg RT, Rizopoulos D, Meijboom FJ, Boersma E, Bogers AJJC, Roos-Hesselink JW. The unnatural history of tetralogy of Fallot: prospective follow-up of 40 years after surgical correction. Circulation. 2014;130:1944–1953. 3. Van Arsdell GS, Maharaj GS, Tom J, Rao VK, Coles JG, Freedom RM, Williams WG, McCrindle BW. What is the optimal age for repair of tetralogy of Fallot? Circulation. 2000;102(suppl 3):III123–III129. 4. Munkhammar P, Cullen S, Jögi P, de Leval M, Elliott M, Norgård G. Early age at repair prevents restrictive right ventricular (RV) physiology after surgery for tetralogy of Fallot (TOF): diastolic RV function after TOF repair in infancy. J Am Coll Cardiol. 1998;32:1083–1087. 5. Geva T, Sandweiss BM, Gauvreau K, Lock JE, Powell AJ. Factors associated with impaired clinical status in long-term survivors of tetralogy of Fallot repair evaluated by magnetic resonance imaging. J Am Coll Cardiol. 2004;43:1068–1074. 6. Murphy JG, Gersh BJ, Mair DD, Fuster V, McGoon MD, Ilstrup DM, McGoon DC, Kirklin JW, Danielson GK. Long-term outcome in patients undergoing surgical repair of tetralogy of Fallot. N Engl J Med. 1993;329:593–599. 7. Nollert G, Fischlein T, Bouterwek S, Böhmer C, Klinner W, Reichart B. Long-term survival in patients with repair of tetralogy of Fallot: 36-year follow-up of 490 survivors of the first year after surgical repair. J Am Coll Cardiol. 1997;30:1374–1383. 8. Vida VL, Guariento A, Castaldi B, Sambugaro M, Padalino MA, Milanesi O, Stellin G. Evolving strategies for preserving the pulmonary valve during early repair of tetralogy of Fallot: mid-term results. J Thorac Cardiovasc Surg. 2014;147:687–694. 9. Hoashi T, Kagisaki K, Meng Y, Sakaguchi H, Kurosaki K, Shiraishi I, Yagihara T, Ichikawa H. Long-term outcomes after definitive repair for tetralogy of Fallot with preservation of the pulmonary valve annulus. J Thorac Cardiovasc Surg. 2014;148:802–808. 10. Hickey EJ, Veldtman G, Bradley TJ, Gengsakul A, Webb G, Williams WG, Manlhiot C, McCrindle BW. Functional health status in adult survivors of operative repair of tetralogy of Fallot. Am J Cardiol. 2012;109:873–880. 11. Gatzoulis MA, Balaji S, Webber SA, Siu SC, Hokanson JS, Poile C, Rosenthal M, Nakazawa M, Moller JH, Gillette PC, Webb GD, Redington AN. Risk factors for arrhythmia and sudden cardiac death late after repair of tetralogy of Fallot: a multicentre study. Lancet. 2000;356:975–981. 12. Geva T. Is MRI the preferred method for evaluating right ventricular size and function in patients with congenital heart disease? MRI is the preferred method for evaluating right ventricular size and function in patients with congenital heart disease. Circ Cardiovasc Imaging. 2014;7:190–197. 13. Valente AM, Gauvreau K, Assenza GE, Babu-Narayan SV, Schreier J, Gatzoulis MA, Groenink M, Inuzuka R, Kilner PJ, Koyak Z, Landzberg MJ, Mulder B, Powell AJ, Wald R, Geva T. Contemporary predictors of death and sustained ventricular tachycardia in patients with repaired tetralogy of Fallot enrolled in the INDICATOR cohort. Heart. 2014;100:247–253. 14. Meijboom FJ, Roos-Hesselink JW, McGhie JS, Spitaels SE, van Domburg RT, Utens LM, Simoons ML, Bogers AJ. Consequences of a selective approach toward pulmonary valve replacement in adult patients with tetralogy of Fallot and pulmonary regurgitation. J Thorac Cardiovasc Surg. 2008;135:50–55. 15. Babu-Narayan SV, Diller GP, Gheta RR, Bastin AJ, Karonis T, Li W, Pennell DJ, Uemura H, Sethia B, Gatzoulis MA, Shore DF. Clinical outcomes of surgical pulmonary valve replacement after repair of tetralogy of Fallot and potential prognostic value of preoperative cardiopulmonary exercise testing. Circulation. 2014;129:18–27. 16. Sabate Rotes A, Eidem BW, Connolly HM, Bonnichsen CR, Rosedahl JK, Schaff HV, Dearani JA, Burkhart HM. Long-term follow-up after pulmonary valve replacement in repaired tetralogy of Fallot. Am J Cardiol. 2014;114:901–908. 17. Knowles R, Veldtman G, Hickey EJ, Bradley T, Gengsakul A, Webb GD, Williams WG, McCrindle BW. Functional health status of adults with tetralogy of Fallot: matched comparison with healthy siblings. Ann Thorac Surg. 2012;94:124–132. Key Words: Editorials ◼ tetralogy of Fallot
Downloaded from http://circ.ahajournals.org/ at CONS CALIFORNIA DIG LIB on December 3, 2014
Fourth Decade After Repair of Tetralogy of Fallot: Taking Aim at Moving Targets David P. Bichell Circulation. 2014;130:1931-1932; originally published online October 23, 2014; doi: 10.1161/CIRCULATIONAHA.114.013270 Circulation is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231 Copyright © 2014 American Heart Association, Inc. All rights reserved. Print ISSN: 0009-7322. Online ISSN: 1524-4539
The online version of this article, along with updated information and services, is located on the World Wide Web at: http://circ.ahajournals.org/content/130/22/1931
Permissions: Requests for permissions to reproduce figures, tables, or portions of articles originally published in Circulation can be obtained via RightsLink, a service of the Copyright Clearance Center, not the Editorial Office. Once the online version of the published article for which permission is being requested is located, click Request Permissions in the middle column of the Web page under Services. Further information about this process is available in the Permissions and Rights Question and Answer document. Reprints: Information about reprints can be found online at: http://www.lww.com/reprints Subscriptions: Information about subscribing to Circulation is online at: http://circ.ahajournals.org//subscriptions/
Downloaded from http://circ.ahajournals.org/ at CONS CALIFORNIA DIG LIB on December 3, 2014
