Indications for Pulmonary Valve Replacement in Repaired Tetralogy of Fallot
2013; Lippincott Williams & Wilkins; Volume: 128; Issue: 17 Linguagem: Inglês
10.1161/circulationaha.113.005878
ISSN1524-4539
Autores Tópico(s)Coronary Artery Anomalies
ResumoHomeCirculationVol. 128, No. 17Indications for Pulmonary Valve Replacement in Repaired Tetralogy of Fallot Free AccessEditorialPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessEditorialPDF/EPUBIndications for Pulmonary Valve Replacement in Repaired Tetralogy of FallotThe Quest Continues Tal Geva, MD Tal GevaTal Geva From the Department of Cardiology, Boston Children's Hospital, Boston, MA, and Department of Pediatrics, Harvard Medical School, Boston, MA. Originally published24 Sep 2013https://doi.org/10.1161/CIRCULATIONAHA.113.005878Circulation. 2013;128:1855–1857Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: October 22, 2013: Previous Version 1 Until Blalock and Taussig developed the first palliative systemic-to-pulmonary shunt operation in 1945,1 tetralogy of Fallot (TOF) was a nearly uniformly lethal congenital cardiac anomaly. In the 5 decades since Lillehei and his colleagues at the University of Minnesota reported the first successful intracardiac repair in 1955,2 early mortality has decreased markedly from 50% to <2%.2–4 In the modern surgical era, most infants with TOF survive the initial surgical repair and reach adulthood. More recently, the excellent results in the pediatric age group have led the field to shift its attention to late sequelae of repaired TOF in the rapidly growing population of adult patients, including the increasing rates of morbidity and mortality.Article see p 1861Despite many advances in surgical repair during the past 6 decades, the majority of TOF patients continue to experience residual hemodynamic and electrophysiological abnormalities.5,6 To effectively relieve the obstructed right ventricular outflow tract (RVOT), the surgeon must often disrupt the integrity of the pulmonary valve, which results in pulmonary regurgitation. The ensuing chronic right ventricular (RV) volume overload and akinesis or dyskinesis of the RVOT wall, along with conduction delay from the nearly universal right bundle-branch block, initiate a cascade of pathophysiological abnormalities that lead to RV dilatation and ultimately dysfunction.7 Left ventricular dysfunction, arrhythmias, exercise intolerance, heart failure symptoms, and death may follow.8 Residual intracardiac shunts, tricuspid regurgitation, RVOT or pulmonary artery stenosis, impaired diastolic properties, atrial enlargement, RV hypertension, intraventricular and interventricular dyssynchrony, and diffuse myocardial fibrosis are some of the factors that might accelerate the adverse cardiac remodeling and lead to worse clinical outcomes. Indeed, the adverse remodeling that leads to electromechanical cardiomyopathy manifests in increasing rates of morbidity and mortality beginning during the third decade of life.9Pulmonary valve replacement (PVR) is increasingly used to treat the chronic volume overload from pulmonary regurgitation. The procedure can be performed by a transcatheter technique or surgically, using one of the many available bioprosthetic valves. The procedural mortality is low, usually 150 mL/m2 or z score >4. In patients whose body surface area falls outside published normal data: RV/LV end-diastolic volume ratio >210, 12 b. RV end-systolic volume index >80 mL/m211, 13 c. RV ejection fraction <47%11, 15, 16 d. LV ejection fraction 160 ms11 g. Sustained tachyarrhythmia related to right-sided heart volume load6 h. Other hemodynamically significant abnormalities: • RVOT obstruction with RV systolic pressure ≥0.7 systemic19 • Severe branch pulmonary artery stenosis (<30% flow to affected lung) not amenable to transcatheter therapy • Greater than or equal to moderate tricuspid regurgitation19 • Left-to-right shunt from residual atrial or ventricular septal defects with pulmonary-to-systemic flow ratio ≥1.519 • Severe aortic regurgitation19II. Symptomatic patients fulfilling ≥1 of the quantitative criteria detailed above. Examples of symptoms and signs include: a. Exercise intolerance not explained by extracardiac causes (eg, lung disease, musculoskeletal anomalies, genetic anomalies, obesity), with documentation by exercise testing with metabolic cart (≤70% predicted peak o2 for age and sex not explained by chronotropic incompetence) b. Signs and symptoms of heart failure (eg, dyspnea with mild effort or at rest not explained by extracardiac causes, peripheral edema)19 c. Syncope attributable to arrhythmiaIII. Special considerations: a. Because of higher risk of adverse clinical outcomes in patients who underwent TOF repair at ≥3 years of age, PVR may be considered if they fulfill ≥1 of the quantitative criteria in section I16 b. Women with severe PR and RV dilatation or dysfunction may be at risk for pregnancy-related complications. Although no evidence is available to support benefit from prepregnancy PVR, the procedure may be considered if fulfilling ≥1 of the quantitative criteria in section I20LV indicates left ventricular; PR, pulmonary regurgitation; PVR, pulmonary valve replacement; RV, right ventricular; RVOT, right ventricular outflow tract; and TOF, tetralogy of Fallot.The study by Frigiola et al14 raises intriguing questions about our ability to identify patients with good outcomes late after TOF repair and, conversely, those at risk of poor outcomes. Simultaneously, though, the authors illustrate that even in a center with a large patient volume, our current ability to prognosticate remains poor, as highlighted by the 2 patients who were included in the good outcome group only to require subsequent PVR. Furthermore, as illustrated above, many controversies about optimal management of this growing population remain contentious. Thus, further progress in resolving these disagreements will only be achieved through large multicenter collaborative studies. Ideally, this will be performed with standardized, prospectively acquired clinical, imaging, exercise, electrocardiographic, and laboratory data. Such a large multicenter investigation would allow us to create an evidence-based consensus on the optimal timing and indications for PVR, as well as for refinement of surgical techniques. A collaborative endeavor such as that will help to overcome the relatively short duration of time that the procedure has been performed routinely (less than a decade in many institutions), the low rate of hard outcomes (eg, death, resuscitated cardiac arrest, sustained ventricular tachycardia), the reliance on surrogate outcomes of unclear clinical importance, and the ongoing evolution in treatment options. Such a prospective multicenter study would help generate hypotheses on optimal management that can then be tested in future randomized clinical trials.Sources of FundingThis work was supported in part by National Institutes of Health/National Heart, Lung, and Blood Institute grant 1 R01 HL089269-01A2 and by the Higgins Family Noninvasive Research Fund.DisclosuresDr Geva is a Screening Committee member, Native Transcatheter Pulmonary Valve Study, Medtronic.FootnotesThe opinions expressed in this editorial are not necessarily those of the editors or of the American Heart Association.Correspondence to Tal Geva, MD, Department of Cardiology, Children's Hospital Boston, 300 Longwood Ave, Boston, MA 02115. E-mail [email protected]References1. Blalock A, Taussig HB. The surgical treatment of malformations of the heart in which there is pulmonary stenosis or pulmonary atresia.JAMA. 1945; 128:189–202.CrossrefGoogle Scholar2. 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