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ERROR: type should be string, got "https://profreg.medscape.com/px/getpracticeprofile.do?method=getProfessionalProfile&urlCache=aHR0cHM6Ly9lbWVkaWNpbmUubWVkc2NhcGUuY29tL2FydGljbGUvOTA0MTM3LW92ZXJ2aWV3\nDrugs & Diseases > Pediatrics: Cardiac Disease and Critical Care Medicine\nSurgical Treatment of Pediatric Hypoplastic Left Heart Syndrome\nAuthor: Ming-Sing Si, MD; Chief Editor: Stuart Berger, MD more...\nSections Surgical Treatment of Pediatric Hypoplastic Left Heart Syndrome\nHistory of the Procedure\nRelevant Anatomy\nIntraoperative Details\nPostoperative Details\nOutcome and Prognosis\nFuture and Controversies\nHypoplastic left heart syndrome (HLHS) is a spectrum of congenital heart defects that is characterized by hypoplasia of the left ventricle and multilevel obstruction of systemic cardiac output from the level of the mitral valve to the proximal descending thoracic aorta. Other closely related functional single right ventricle lesions include double-outlet right ventricle with mitral atresia and unbalanced atrioventricular septal defect. A common physiology of HLHS is that the systemic circulation is driven by the right ventricle via a patent ductus arteriosus. Without intervention, HLHS is fatal.\nIn most cases, there is no cure for HLHS; however, surgical palliation, also referred to as staged reconstruction, can be undertaken in a series of surgical procedures that ultimately result in the right ventricle supporting the cardiac output to both the systemic and pulmonary circuits that are connected in series. Staged reconstruction, including a Norwood plus right ventricle–to–pulmonary artery shunt (RVPAS) or modified Blalock-Taussig shunt (MBTS) procedure at the time of birth, a stage II superior cavopulmonary connection, and a completion Fontan, remain the mainstay of the treatment of functional single right ventricle lesions.\nCardiac transplantation is an alternative therapy; however, because of the shortage of neonatal donor organs, the need for immunosuppression, and the limited durability of the transplant, this modality is not sufficient for the entire population of infants born with HLHS each year.\nA multi-institutional, prospective, randomized, controlled trial (Single Ventricle Reconstruction or SVR trial) in 2005 compared the RVPAS to the MBTS. [1] This trial has continued to yield a wealth of valuable insight into the management and outcomes of infants with HLHS. In this review, the anatomical and clinical considerations of HLHS, the medical and surgical management, and the outcomes of these patients, with special emphasis on the new knowledge gained from the SVR trial, is summarized.\nThe term hypoplastic left heart syndrome (HLHS) was introduced by Noonan and Nadas in 1958 to describe the morphologic features of combined aortic atresia and mitral atresia. [2] This followed Lev's description in 1952 of congenital cardiac malformations associated with underdevelopment of the chambers on the left side and a small ascending aorta and arch. [3]\nThe first successful palliation of hypoplastic left heart syndrome was reported by Norwood et al in a series of infants who underwent surgery from 1979-1981. [4] The procedure has been technically refined over the years, but the essential components remain (1) atrial septectomy, (2) anastomosis of the proximal pulmonary artery to the aorta with homograft augmentation of the aortic arch, and (3) aortopulmonary (modified Blalock-Taussig shunt [MBTS]) shunt or right ventricle–to–pulmonary artery shunt (RVPAS) to provide restricted pulmonary blood flow. Staged surgical palliation of HLHS with a Fontan operation using the right ventricle as the systemic ventricle was first reported in 1983 by Norwood et al. [5] More contemporary experience has demonstrated an improvement in short- and long-term survival rates.\nNorwood’s strategy of creating a functional single right ventricle circulation initially involved an aortic-to-pulmonary artery connection with patch aortic arch reconstruction to form a neoaorta and controlled pulmonary blood flow with a RVPAS. [4] The RVPASs used in these initial efforts were either 8- or 12-mm nonvalved polytetrafluoroethylene (PTFE) grafts, and all of these patients died because of pulmonary overcirculation or right ventricular failure. Norwood then achieved better results with either an MBTS or an aortopulmonary shunt, usually a 4-mm PTFE graft, yielding initial survival that allowed progression to a second-stage operation. This early experience strongly favored the systemic-to-pulmonary artery shunt; however, it now seems evident that it was the large size of the RVPAS rather than the RVPAS strategy itself that resulted in failure of this approach. [6]\nSince Norwood’s initial experience, the MBTS has been adopted as the preferred source of pulmonary blood flow in the Norwood procedure. [7, 8, 9, 10, 11] Kishimoto and colleagues from Osaka, Japan revisited the use of RVPAS in the Norwood procedure in the current era. [12, 13, 14] The presumed advantage of the RVPAS as compared with the MBTS was the increased systemic diastolic blood pressure and the potential for improved coronary perfusion. [15]\nSubsequent to these early descriptions of the use of the RVPAS, several small nonrandomized case series demonstrated improved hemodynamics, branch pulmonary artery growth, and overall results with the RVPAS that extended into the later stages of surgical palliation for HLHS. [16, 17, 18, 19, 20, 21]\nOthers centers, generally those experienced centers with a record of good results with the MBTS, demonstrated no benefit of the RVPAS in single-institution, nonrandomized studies. [22, 23, 24]\nHypoplastic left heart syndrome is a relatively common form of congenital heart disease, occurring in 7-9% of neonates in whom heart disease is diagnosed in the first year of life. Without surgical intervention, this condition is fatal, accounting for 25% of cardiac deaths in the first week of life.\nAt birth, systemic and pulmonary circulation depends on the cardiac output from the right ventricle via the main pulmonary artery and the patent ductus arteriosus. The amount of systemic and pulmonary flow depends on cardiac output of the right ventricle and the systemic and pulmonary vascular resistances. Obligatory mixing of pulmonary and systemic venous blood occurs in the right atrium and mixed saturated blood is ejected by the right ventricle. Since the mitral valve is either atretic or stenotic, the major outflow from the left atrium is into the right atrium via an atrial septal defect. Sometimes, a restrictive atrial septal defect is present and obstructs pulmonary venous return into the right atrium.\nWhole genome sequencing has demonstrated defects in cardiomyopathy-associated genes, potentially indicating impaired functional reserve of the single-ventricle circulation in patients with hypoplastic left heart syndrome. [25]\nAlthough the etiology of hypoplastic left heart syndrome (HLHS) is unknown, Lev has postulated that premature narrowing of the foramen ovale leads to a faulty transfer of blood from the inferior vena cava (IVC) to the left atrium during fetal life. [26] Thus, altered intrauterine hemodynamics may be the physiologic cause of HLHS. Other authors have postulated that the embryologic cause is severe underdevelopment of the left ventricular outflow in the form of isolated aortic valve atresia. This aortic atresia results in abnormal development of the remaining cardiac structures, resulting from the associated blood flow patterns.\nA linkage analysis of left ventricular outflow tract malformations (aortic valve stenosis, coarctation of the aorta, and HLHS) identified a significant peak on 2p15 for HLHS, although the exact gene(s) involved were not identified. [27] In an earlier report, these authors also identified a possible role for Notch1 signaling in left ventricular outflow tract malformation (including HLHS). [28] Another study identified seasonal variation of the incidence of HLHS, with a preponderance in summer months compared with other types of congenital heart defects. [29]\nHypoplastic left heart syndrome (HLHS) is often diagnosed in patients during the newborn period because of tachypnea and cyanosis within 24-48 hours of birth. When the ductus arteriosus begins to close, diminished systemic perfusion rapidly occurs, with pallor, lethargy, and diminished pulses. Cardiac examination reveals a dominant right ventricular impulse, a single second heart sound, and a nonspecific soft systolic murmur at the left sternal border. Ductal closure results in diminished systemic perfusion with the development of metabolic acidosis and renal failure.\nThe presence of hypoplastic left heart syndrome (HLHS) is an indication for therapy. Without intervention, HLHS is essentially universally fatal within the first month of life. As survival rates for both staged repair and transplantation have improved, the continued role of comfort-measures-only therapy can be questioned. Certainly, both pediatric and adult patients routinely undergo therapy for conditions with far worse prognosis than HLHS.\nHypoplastic left heart syndrome (HLHS) refers to a constellation of congenital cardiac anomalies characterized by marked hypoplasia or absence of the left ventricle and severe hypoplasia of the ascending aorta.\nPathologic findings by Bharati et al in a series of 230 patients with HLHS included 105 with aortic atresia and mitral stenosis (45%), 95 with aortic and mitral atresia (41%), and 30 with severe aortic and mitral stenosis (13%). [30] The dilated and hypertrophied right ventricle is the dominant ventricle and forms the apex of the heart. The tricuspid valve annulus is invariably dilated, and significant anomalies in morphology have been described in 5-7% of patients. Clinically significant tricuspid regurgitation has been reported by both Barber and Chang in 8-10% of patients studied and has been identified as a significant risk factor in short-term and long-term survival. [31, 32]\nIn 95% of these infants, the ventricular septum is intact and the left ventricular cavity is only a small slit with thick endocardial fibroelastosis. The ascending aorta is usually very small, ranging in size from 1-8 mm as measured using 2-dimensional echocardiography; mean diameter is 3.8 mm, and, in 55% of patients, the ascending aorta is smaller than 3 mm. The portion of ascending aorta between the atretic valve and the innominate artery serves only as a conduit for the retrograde flow of blood into the coronary arteries. The main pulmonary artery is very large and is the origin of a large ductus arteriosus that carries blood from the right ventricle into the aorta. A localized coarctation of the aorta is present in 80% of patients.\nOther than the presence of a lethal chromosomal anomaly, other anomalies, or an extremely poor clinical condition, no absolute contraindications to surgical repair are recognized. However, several factors have been noted to convey higher surgical risk. Patients older than 1 month undergoing the Norwood procedure, patients with severe obstruction to pulmonary venous return, patients with significant noncardiac congenital conditions (eg, prematurity, low birth weight, chromosomal anomalies), and patients with the anatomic subtype of HLHS with aortic atresia are at increased risk. Details of the outcomes for patients who are at standard-risk and those who are at high-risk are outlined in Outcome and Prognosis.\nOhye RG, Sleeper LA, Mahony L, Newburger JW, Pearson GD, Lu M, et al. Comparison of shunt types in the Norwood procedure for single-ventricle lesions. N Engl J Med. 2010 May 27. 362(21):1980-92. [Medline]. 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Management of 239 patients with hypoplastic left heart syndrome and related malformations from 1993 to 2007. Ann Thorac Surg. 2008 May. 85(5):1691-6; discussion 1697. [Medline].\nAshburn DA, McCrindle BW, Tchervenkov CI, et al. Outcomes after the Norwood operation in neonates with critical aortic stenosis or aortic valve atresia. J Thorac Cardiovasc Surg. 2003 May. 125(5):1070-82. [Medline].\nDaebritz SH, Nollert GD, Zurakowski D, et al. Results of Norwood stage I operation: comparison of hypoplastic left heart syndrome with other malformations. J Thorac Cardiovasc Surg. 2000 Feb. 119(2):358-67. [Medline].\nIshino K, Stümper O, De Giovanni JJ, et al. The modified Norwood procedure for hypoplastic left heart syndrome: early to intermediate results of 120 patients with particular reference to aortic arch repair. J Thorac Cardiovasc Surg. 1999 May. 117(5):920-30. [Medline].\nBove EL. Current status of staged reconstruction for hypoplastic left heart syndrome. Pediatr Cardiol. 1998 Jul-Aug. 19(4):308-15. [Medline].\nKishimoto H, Kawahira Y, Kawata H, Miura T, Iwai S, Mori T. The modified Norwood palliation on a beating heart. J Thorac Cardiovasc Surg. 1999 Dec. 118(6):1130-2. [Medline].\nSano S, Ishino K, Kado H, et al. Outcome of right ventricle-to-pulmonary artery shunt in first-stage palliation of hypoplastic left heart syndrome: a multi-institutional study. Ann Thorac Surg. 2004 Dec. 78(6):1951-7; discussion 1957-8. [Medline].\nSano S, Ishino K, Kawada M, Honjo O. Right ventricle-pulmonary artery shunt in first-stage palliation of hypoplastic left heart syndrome. Semin Thorac Cardiovasc Surg Pediatr Card Surg Annu. 2004. 7:22-31. [Medline].\nMalec E, Januszewska K, Kolcz J, Mroczek T. Right ventricle-to-pulmonary artery shunt versus modified Blalock-Taussig shunt in the Norwood procedure for hypoplastic left heart syndrome - influence on early and late haemodynamic status. 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The surgical anatomy of hypoplasia of aortic tract complex. J Thorac Cardiovasc Surg. 1984 Jul. 88(1):97-101. [Medline].\nBarber G, Helton JG, Aglira BA, et al. The significance of tricuspid regurgitation in hypoplastic left-heart syndrome. Am Heart J. 1988 Dec. 116(6 Pt 1):1563-7. [Medline].\nChang AC, Farrell PE Jr, Murdison KA, et al. Hypoplastic left heart syndrome: hemodynamic and angiographic assessment after initial reconstructive surgery and relevance to modified Fontan procedure. J Am Coll Cardiol. 1991 Apr. 17(5):1143-9. [Medline].\nLi J, Zhang G, Holtby H, et al. Carbon dioxide--a complex gas in a complex circulation: its effects on systemic hemodynamics and oxygen transport, cerebral, and splanchnic circulation in neonates after the Norwood procedure. J Thorac Cardiovasc Surg. 2008 Nov. 136(5):1207-14. [Medline].\nSano S, Ishino K, Kawada M, et al. Right ventricle-pulmonary artery shunt in first-stage palliation of hypoplastic left heart syndrome. 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J Thorac Cardiovasc Surg. 2008 Oct. 136(4):968-75. [Medline]. [Full Text].\nGalantowicz M, Cheatham JP. Lessons learned from the development of a new hybrid strategy for the management of hypoplastic left heart syndrome. Pediatr Cardiol. 2005 Mar-Apr. 26(2):190-9. [Medline].\nGalantowicz M, Cheatham JP, Phillips A, Cua CL, Hoffman TM, Hill SL, et al. Hybrid approach for hypoplastic left heart syndrome: intermediate results after the learning curve. Ann Thorac Surg. 2008 Jun. 85(6):2063-70; discussion 2070-1. [Medline].\nGoldberg CS, Bove EL, Devaney EJ, Mollen E, Schwartz E, Tindall S, et al. A randomized clinical trial of regional cerebral perfusion versus deep hypothermic circulatory arrest: outcomes for infants with functional single ventricle. J Thorac Cardiovasc Surg. 2007 Apr. 133(4):880-7. [Medline].\nVisconti KJ, Rimmer D, Gauvreau K, del Nido P, Mayer JE Jr, Hagino I. Regional low-flow perfusion versus circulatory arrest in neonates: one-year neurodevelopmental outcome. 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J Matern Fetal Neonatal Med. 2020 Nov 18. 1-12. [Medline].\nChristmann M, Valsangiacomo Buchel ER, Dave H, Klauwer D, Cavigelli-Brunner A. Prognostic value of troponin in infants with hypoplastic left heart syndrome between Stage I and II of palliation. Ann Pediatr Cardiol. 2018 Jan-Apr. 11 (1):56-9. [Medline]. [Full Text].\nBove EL, Lloyd TR. Staged reconstruction for hypoplastic left heart syndrome. Contemporary results. Ann Surg. 1996 Sep. 224(3):387-94; discussion 394-5. [Medline].\nNorwood WI Jr. Hypoplastic left heart syndrome. Ann Thorac Surg. 1991 Sep. 52(3):688-95. [Medline].\nJonas RA, Hanson D, Cook N. Anatomical subtype of hypoplastic left heart syndrome influences survival after palliative reconstruction. Paper presented at: The American Association for Thoracic Surgery; 1992. Los Angeles, Calif.\nTweddell JS, Hoffman GM, Mussato KA, et al. 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Early results of the fontan procedure in one hundred consecutive patients with hypoplastic left heart syndrome. J Thorac Cardiovasc Surg. 2000 Jun. 119(6):1110-8. [Medline].\nTabbutt S, Nord AS, Jarvik GP, et al. Neurodevelopmental outcomes after staged palliation for hypoplastic left heart syndrome. Pediatrics. 2008 Mar. 121(3):476-83. [Medline].\nPuosi R, Korkman M, Sarajuuri A, et al. Neurocognitive development and behavioral outcome of 2-year-old children with univentricular heart. J Int Neuropsychol Soc. 2011 Nov. 17(6):1094-103. [Medline].\nSarajuuri A, Jokinen E, Puosi R, Mildh L, Mattila I, Lano A, et al. Neurodevelopment in children with hypoplastic left heart syndrome. J Pediatr. 2010 Sep. 157(3):414-20, 420.e1-4. [Medline].\nBlitzer D, Nguyen S, Farooqi KM, Takeda K. Orthotopic heart transplantation and concomitant aortic arch replacement in an adult Fontan patient with hypoplastic left heart syndrome. Interact Cardiovasc Thorac Surg. 2020 Nov 24. [Medline].\nPasquali SK, He X, Jacobs JP, Jacobs ML, O'Brien SM, Gaynor JW. Evaluation of failure to rescue as a quality metric in pediatric heart surgery: an analysis of the STS Congenital Heart Surgery Database. Ann Thorac Surg. 2012 Aug. 94(2):573-9; discussion 579-80. [Medline]. [Full Text].\nNorwood WI Jr. Hypoplastic left heart syndrome. Baue AF, Geha AS, Hammond GL, et al, eds. Glenn's Thoracic and Cardiovascular Surgery. Appleton & Lange; 1991.\nTakabayashi S, Kado H, Shiokawa Y, Fukae K, Nakano T. Comparison of hemodynamics between Norwood procedure and systemic-to-pulmonary artery shunt for single right ventricle patients. Eur J Cardiothorac Surg. 2005 Jun. 27(6):968-74. [Medline].\nWatson DG, Rowe RD. Aortic-valve atresia report of 43 cases. JAMA. 1962. 179:14.\nCunningham TW, Tan Y, Krawczeski CD, et al. Incidence and impact of acute kidney injury in patients with hypoplastic left heart syndrome following the hybrid stage 1 palliation. Cardiol Young. 2020 Dec 2. 1-7. [Medline].\nSurgical Treatment of Pediatric Hypoplastic Left Heart Syndrome. The main pulmonary artery and ductus arteriosus have been divided. Dashes indicate the line of incision on the hypoplastic ascending aorta. Image courtesy of Edward L. Bove, MD.\nSurgical Treatment of Pediatric Hypoplastic Left Heart Syndrome. The ascending aorta is opened and sutured to the adjacent proximal main pulmonary artery. A patch of pulmonary homograft is fashioned to create the neoaorta (inset). Image courtesy of Edward L. Bove, MD.\nSurgical Treatment of Pediatric Hypoplastic Left Heart Syndrome. Completed Norwood procedure showing reconstructed neoaorta and modified Blalock-Taussig shunt from the innominate artery to the confluence of the branch pulmonary arteries. Image courtesy of Edward L. Bove, MD.\nSurgical Treatment of Pediatric Hypoplastic Left Heart Syndrome. Hemi-Fontan procedure. The modified Blalock-Taussig shunt is ligated, and incisions are made in the right atrial appendage and pulmonary arteries (upper left). The posterior aspect of the right atriotomy is anastomosed to the inferior aspect of the pulmonary arteriotomy (upper right). A patch of polytetrafluoroethylene is placed to prevent the superior vena cava return from entering the right atrium. The cavopulmonary connection is roofed with a patch of pulmonary homograft (lower). Image courtesy of Koji Kagasaki, MD.\nSurgical Treatment of Pediatric Hypoplastic Left Heart Syndrome. Fontan procedure. Through a right atriotomy, the polytetrafluoroethylene (PTFE) patch has been removed. A new PTFE patch is placed to baffle the inferior vena cava return to the cavopulmonary connection constructed during the hemi-Fontan procedure (left). The arrows indicate the systemic venous return bypassing the right heart to directly enter the pulmonary arteries (right). Image courtesy of Edward L. Bove, MD.\nMing-Sing Si, MD Assistant Professor of Cardiac Surgery, University of Michigan Medical School\nMing-Sing Si, MD is a member of the following medical societies: American Heart Association, Biomedical Engineering Society, Society of Thoracic Surgeons, Tissue Engineering and Regenerative Medicine International Society, International Society for Stem Cell Research\nCoauthor(s)\nJennifer C Hirsch-Romano, MD, MS, FACS, FACC Assistant Professor of Cardiac Surgery, Pediatric Cardiac Surgery, Department of Cardiac Surgery, Assistant Professor, Pediatric Cardiac Intensive Cre, Department of Pediatrics, Surgical Director, Pediatric Cardiothoracic Intensive Care Unit, Co-Director, Pediatric Cardiac Extracorporeal Life Support, Pediatric Cardiac Surgeon, Fetal Diagnosis and Treatment Center, University of Michigan Medical Center\nJennifer C Hirsch-Romano, MD, MS, FACS, FACC is a member of the following medical societies: American College of Cardiology, American College of Surgeons, Association for Academic Surgery, Congenital Heart Surgeons Society, Society of Thoracic Surgeons, Association of Women Surgeons, European Association for Cardio-Thoracic Surgery, John Alexander Society, Frederick A Coller Surgical Society, Midwest Pediatric Cardiology Society\nEdward L Bove, MD Associate Director, PICU, CS Mott Children's Hospital; Director, Division of Pediatric Cardiovascular Surgery, Professor, Department of Surgery, Section of Thoracic Surgery, University of Michigan Medical Center\nEdward L Bove, MD is a member of the following medical societies: American Association for Thoracic Surgery, American College of Cardiology, American College of Chest Physicians, American College of Surgeons, American Heart Association, American Medical Association, American Surgical Association, Central Surgical Association, Congenital Heart Surgeons Society, Medical Society of the State of New York, Society of Thoracic Surgeons, Society of University Surgeons\nRichard G Ohye, MD Head, Section of Pediatric Cardiovascular Surgery, Associate Professor of Cardiac Surgery, Program Director, Pediatric Cardiac Surgery Fellowship, University of Michigan Medical Center\nRichard G Ohye, MD is a member of the following medical societies: Alpha Omega Alpha, American Association for Thoracic Surgery, Congenital Heart Surgeons Society, Society of University Surgeons, American College of Cardiology, American College of Chest Physicians, American College of Surgeons, Association for Academic Surgery, International Society for Heart and Lung Transplantation, Society of Thoracic Surgeons\nMary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference\nMary C Mancini, MD, PhD, MMM Surgeon-in-Chief and Director of Cardiothoracic Surgery, Christus Highland\nMary C Mancini, MD, PhD, MMM is a member of the following medical societies: American Association for Thoracic Surgery, American College of Surgeons, American Surgical Association, Phi Beta Kappa, Society of Thoracic Surgeons\nStuart Berger, MD Executive Director of The Heart Center, Interim Division Chief of Pediatric Cardiology, Lurie Childrens Hospital; Professor, Department of Pediatrics, Northwestern University, The Feinberg School of Medicine\nStuart Berger, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American College of Chest Physicians, American Heart Association, Society for Cardiovascular Angiography and Interventions\nJonah Odim, MD, PhD, MBA Section Chief of Clinical Transplantation, Transplantation Branch, Division of Allergy, Immunology, and Transplantation, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH)\nJonah Odim, MD, PhD, MBA is a member of the following medical societies: American College of Cardiology, American College of Chest Physicians, American Association for Physician Leadership, American College of Surgeons, American Heart Association, American Society for Artificial Internal Organs, American Society of Transplant Surgeons, Association for Academic Surgery, Association for Surgical Education, International Society for Heart and Lung Transplantation, National Medical Association, New York Academy of Sciences, Royal College of Physicians and Surgeons of Canada, Society of Critical Care Medicine, Society of Thoracic Surgeons, Canadian Cardiovascular Society\nRalph S Mosca, MD Director, Pediatric Cardiac Surgery, Associate Professor, Department of Surgery, New York Presbyterian Medical Center\nRalph S Mosca, MD is a member of the following medical societies: American College of Surgeons, Central Surgical Association, Congenital Heart Surgeons Society, International Society for Heart and Lung Transplantation, Michigan State Medical Society, and Society of Thoracic Surgeons\nencoded search term (Surgical Treatment of Pediatric Hypoplastic Left Heart Syndrome) and Surgical Treatment of Pediatric Hypoplastic Left Heart Syndrome\nFetal Surgery for Congenital Heart Disease\nCardiovascular Disease and Pregnancy\nDermatologic Manifestations of Cardiac Disease\nHigh Altitude Pulmonary Hypertension\nHigh-Altitude Cardiopulmonary Diseases\nPediatric Congenital Atrioventricular Block\nPostnatal Down Syndrome Imaging\nNeurodevelopmental Deficits in Children With Single-Ventricle Physiology Change With Age\nCardiology Clinical Practice Guidelines - 2020 Year in Review\nGetting Closer to a Lifesaving RSV Vaccine\nGrowth Disorders: 10 Cases of a Developing Problem\nAccording to Cardiologists\nChili Pepper Consumption Linked to Better Midlife Survival\nFish Oils and CV Prevention -- Now What?\nSAMSON Pins Most Muscle Pain Experienced With Statins on the Nocebo Effect\nProinflammatory Dietary Pattern Linked to Higher CV Risk\nA Pesco-Mediterranean Diet With Intermittent Fasting\n2002 2109511-overview Diseases & Conditions\nDiseases & Conditions Fetal Surgery for Congenital Heart Disease\nAddressing the Problem in HCM: The Role of Cardiac Myosin Inhibition 0.25 CME / ABIM MOC Credits\n0.25 CME / ABIM MOC\nAddressing the Problem in HCM: The Role of Cardiac Myosin Inhibition\n2002 162004-overview Diseases & Conditions\nDiseases & Conditions Cardiovascular Disease and Pregnancy\n2010 /viewarticle/940870 Practice Guideline\nPractice Guideline Adult Congenital Heart Disease Clinical Practice Guidelines (ESC, 2020)"