Bio

Clinical Focus


  • Cardiac Critical Care
  • Pediatric Cardiology

Academic Appointments


Honors & Awards


  • Pediatric Fellows Poster Award, Columbia University, NY (5/22/2006)
  • Council on Clinical Cardiology, Women in Cardiology Travel Grant, American Heart Association Scientific Sessions (11/13/2005)
  • Finalist, Young Investigator Award in Basic Research, Section on Cardiology and Cardiac Surgery, American Academy of Pediatrics (10/7/2005)
  • Section on Cardiology and Cardiac Surgery’s Educational Travel Grant, American Academy of Pediatrics (10/7/2005)
  • Poster of Distinction, North American Society for Pediatric Gastroenterology, Hepatology & Nutrition (2002)

Professional Education


  • Fellowship:Morgan Stanley Children's Hospital (2008) NY
  • Board Certification: Pediatrics, American Board of Pediatrics (2005)
  • Medical Education:Rajah Muthiah Medical College and Hospital Annamalai University (1998) India
  • Fellowship:Children's Hospital Boston (2009) MA
  • Board Certification: Pediatric Cardiology, American Board of Pediatrics (2008)
  • Residency:Children's Hospital of Michigan (2004) MI

Publications

Journal Articles


  • Variability of Characteristics and Outcomes Following Cardiopulmonary Resuscitation Events in Diverse ICU Settings in a Single, Tertiary Care Children's Hospital PEDIATRIC CRITICAL CARE MEDICINE Gupta, P., Yan, K., Chow, V., Dao, D. T., Gossett, J. M., Leong, K., Franzon, D., Halamek, L. P., Reddy, S., Berg, R. A., Roth, S. J., Nadkarni, V. M. 2014; 15 (3): E128-E141
  • Atherosclerosis Causing Recurrent Catastrophic Aortopulmonary Shunt Dehiscence in a Patient with Alagille Syndrome PEDIATRIC CARDIOLOGY May, L., Hanley, F. L., Connolly, A. J., Reddy, S. 2013; 34 (8): 1945-1948

    Abstract

    Alagille syndrome (ALGS) is an autosomal dominant disorder associated with cholestatic liver disease, pulmonary valvar stenosis or atresia, vasculopathy, and renal disease. Although the liver and cardiac manifestations contribute to overall morbidity and mortality during their life span, these patients also carry a burden of important but often underappreciated vascular abnormalities. This report describes a 3 year-old girl with Alagille syndrome, hepatic cholestasis, systemic hypertension, hypercholesterolemia, hypertriglyceridemia, and tetralogy of Fallot, pulmonary atresia, and major aortopulmonary collaterals (TOF/PA/MAPCAs). She presented for bilateral pulmonary artery plasty and central shunt upsizing. She then experienced three shunt dehiscence episodes, necessitating emergent intervention. Autopsy showed diffuse atherosclerosis and significant atherosclerotic plaque at the site of shunt dehiscence. This is the first reported case of ALGS with TOF/PA/MAPCAs and catastrophic shunt dehiscence due to significant generalized vasculopathy caused by dyslipidemia and atherosclerosis. Dyslipidemia, a known comorbidity in ALGS, is one of few modifiable risk factors that should be screened for and treated, particularly before cardiac surgery.

    View details for DOI 10.1007/s00246-012-0484-4

    View details for Web of Science ID 000327065100039

  • Deletion of the beta 2-adrenergic receptor prevents the development of cardiomyopathy in mice JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY Fajardo, G., Zhao, M., Urashima, T., Farahani, S., Hu, D., Reddy, S., Bernstein, D. 2013; 63: 155-164

    Abstract

    Beta adrenergic receptor (β-AR) subtypes act through diverse signaling cascades to modulate cardiac function and remodeling. Previous in vitro studies suggest that β1-AR signaling is cardiotoxic whereas β2-AR signaling is cardioprotective, and may be the case during ischemia/reperfusion in vivo. The objective of this study was to assess whether β2-ARs also play a cardioprotective role in the pathogenesis of non-ischemic forms of cardiomyopathy. To dissect the role of β1 vs β2-ARs in modulating MLP (Muscle LIM Protein) cardiomyopathy, we crossbred MLP-/- with β1-/- or β2-/- mice. Deletion of the β2-AR improved survival, cardiac function, exercise capacity and myocyte shortening; by contrast haploinsufficency of the β1-AR reduced survival. Pathologic changes in Ca(2+) handling were reversed in the absence of β2-ARs: peak Ca(2+) and SR Ca(2+) were decreased in MLP-/- and β1+/-/MLP-/- but restored in β2-/-MLP-/-. These changes were associated with reversal of alterations in troponin I and phospholamban phosphorylation. Gi inhibition increased peak and baseline Ca(2+), recapitulating changes observed in the β2-/-/MLP-/-. The L-type Ca(2+) blocker verapamil significantly decreased cardiac function in β2-/-MLP-/- vs WT. We next tested if the protective effects of β2-AR ablation were unique to the MLP model using TAC-induced heart failure. Similar to MLP, β2-/- mice demonstrated delayed progression of heart failure with restoration of myocyte shortening and peak Ca(2+) and Ca(2+) release. Deletion of β2-ARs prevents the development of MLP-/- cardiomyopathy via positive modulation of Ca(2+) due to removal of inhibitory Gi signaling and increased phosphorylation of troponin I and phospholamban. Similar effects were seen after TAC. Unlike previous models where β2-ARs were found to be cardioprotective, in these two models, β2-AR signaling appears to be deleterious, potentially through negative regulation of Ca(2+) dynamics.

    View details for DOI 10.1016/j.yjmcc.2013.07.016

    View details for Web of Science ID 000325387300017

    View details for PubMedID 23920331

  • Altered ubiquitin-proteasome signaling in right ventricular hypertrophy and failure AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY Rajagopalan, V., Zhao, M., Reddy, S., Fajardo, G., Wang, X., Dewey, S., Gomes, A. V., Bernstein, D. 2013; 305 (4): H551-H562

    Abstract

    Alterations in the ubiquitin-proteasome system (UPS) have been described in left ventricular hypertrophy and failure, although results have been inconsistent. The role of the UPS in right ventricular (RV) hypertrophy (RVH) and RV failure (RVF) is unknown. Given the greater percent increase in RV mass associated with RV afterload stress, as present in many congenital heart lesions, we hypothesized that alterations in the UPS could play an important role in RVH/RVF. UPS expression and activity were measured in the RV from mice with RVH/RVF secondary to pulmonary artery constriction (PAC). Epoxomicin and MG132 were used to inhibit the proteasome, and overexpression of the 11S PA28α subunit was used to activate the proteasome. PAC mice developed RVH (109.3% increase in RV weight to body weight), RV dilation with septal shift, RV dysfunction, and clinical RVF. Proteasomal function (26S β5 chymotrypsin-like activity) was decreased 26% (P < 0.05). Protein expression of 19S subunit Rpt5 (P < 0.05), UCHL1 deubiquitinase (P < 0.0001), and Smurf1 E3 ubiquitin ligase (P < 0.01) were increased, as were polyubiquitinated proteins (P < 0.05) and free-ubiquitins (P = 0.05). Pro-apoptotic Bax was increased (P < 0.0001), whereas anti-apoptotic Bcl-2 decreased (P < 0.05), resulting in a sixfold increase in the Bax/Bcl-2 ratio. Proteasomal inhibition did not accelerate RVF. However, proteasome enhancement by cardiac-specific proteasome overexpression partially improved survival. Proteasome activity is decreased in RVH/RVF, associated with upregulation of key UPS regulators and pro-apoptotic signaling. Enhancement of proteasome function partially attenuates RVF, suggesting that UPS dysfunction contributes to RVF.

    View details for DOI 10.1152/ajpheart.00771.2012

    View details for Web of Science ID 000323549500011

    View details for PubMedID 23729213

  • FK506 activates BMPR2, rescues endothelial dysfunction, and reverses pulmonary hypertension. journal of clinical investigation Spiekerkoetter, E., Tian, X., Cai, J., Hopper, R. K., Sudheendra, D., Li, C. G., El-Bizri, N., Sawada, H., Haghighat, R., Chan, R., Haghighat, L., de Jesus Perez, V., Wang, L., Reddy, S., Zhao, M., Bernstein, D., Solow-Cordero, D. E., Beachy, P. A., Wandless, T. J., ten Dijke, P., Rabinovitch, M. 2013; 123 (8): 3600-3613

    Abstract

    Dysfunctional bone morphogenetic protein receptor-2 (BMPR2) signaling is implicated in the pathogenesis of pulmonary arterial hypertension (PAH). We used a transcriptional high-throughput luciferase reporter assay to screen 3,756 FDA-approved drugs and bioactive compounds for induction of BMPR2 signaling. The best response was achieved with FK506 (tacrolimus), via a dual mechanism of action as a calcineurin inhibitor that also binds FK-binding protein-12 (FKBP12), a repressor of BMP signaling. FK506 released FKBP12 from type I receptors activin receptor-like kinase 1 (ALK1), ALK2, and ALK3 and activated downstream SMAD1/5 and MAPK signaling and ID1 gene regulation in a manner superior to the calcineurin inhibitor cyclosporine and the FKBP12 ligand rapamycin. In pulmonary artery endothelial cells (ECs) from patients with idiopathic PAH, low-dose FK506 reversed dysfunctional BMPR2 signaling. In mice with conditional Bmpr2 deletion in ECs, low-dose FK506 prevented exaggerated chronic hypoxic PAH associated with induction of EC targets of BMP signaling, such as apelin. Low-dose FK506 also reversed severe PAH in rats with medial hypertrophy following monocrotaline and in rats with neointima formation following VEGF receptor blockade and chronic hypoxia. Our studies indicate that low-dose FK506 could be useful in the treatment of PAH.

    View details for DOI 10.1172/JCI65592

    View details for PubMedID 23867624

  • Physiologic and molecular characterization of a murine model of right ventricular volume overload. American journal of physiology. Heart and circulatory physiology Reddy, S., Zhao, M., Hu, D., Fajardo, G., Katznelson, E., Punn, R., Spin, J. M., Chan, F. P., Bernstein, D. 2013; 304 (10): H1314-27

    Abstract

    Pulmonary insufficiency (PI) is a common long-term sequel after repair of tetralogy of Fallot, causing progressive right ventricular (RV) dilation and failure. We describe the physiologic and molecular characteristics of the first murine model of RV volume overload. PI was created by entrapping the pulmonary valve leaflets with sutures. Imaging, catheterization, and exercise testing were performed at 1, 3, and 6 mo and compared with sham controls. RNA from the RV free wall was hybridized to Agilent whole genome oligonucleotide microarrays. Volume overload resulted in RV enlargement, decreased RV outflow tract shortening fraction at 1 mo followed by normalization at 3 and 6 mo (39 ± 2, 44 ± 2, and 41 ± 2 vs. 46 ± 3% in sham), early reversal of early and late diastolic filling velocities (E/A ratio) followed by pseudonormalization (0.87 ± 0.08, 0.82 ± 0.08, and 0.96 ± 0.08 vs. 1.04 ± 0.03; P < 0.05), elevated end-diastolic pressure (7.6 ± 0.7, 6.9 ± 0.8, and 7 ± 0.5 vs. 2.7 ± 0.2 mmHg; P < 0.05), and decreased exercise duration (26 ± 0.4, 26 ± 1, and 22 ± 1.3 vs. 30 ± 1.1 min; P < 0.05). Subendocardial RV fibrosis was evident by 1 mo. At 1 mo, 372 genes were significantly downregulated. Mitochondrial pathways and G protein-coupled receptor signaling were the most represented categories. At 3 mo, 434 genes were upregulated and 307 downregulated. While many of the same pathways continued to be downregulated, TNF-α, transforming growth factor-β1 (TGF-β1), p53-signaling, and extracellular matrix (ECM) remodeling transitioned from down- to upregulated. We describe a novel murine model of chronic RV volume overload recapitulating aspects of the clinical disease with gene expression changes suggesting early mitochondrial bioenergetic dysfunction, enhanced TGF-β signaling, ECM remodeling, and apoptosis.

    View details for DOI 10.1152/ajpheart.00776.2012

    View details for PubMedID 23504182

  • Hypoxia-Inducible Factor-1 alpha in Pulmonary Artery Smooth Muscle Cells Lowers Vascular Tone by Decreasing Myosin Light Chain Phosphorylation CIRCULATION RESEARCH Kim, Y., Barnes, E. A., Alvira, C. M., Ying, L., Reddy, S., Cornfield, D. N. 2013; 112 (9): 1230-U73
  • Dynamic microRNA expression during the transition from right ventricular hypertrophy to failure PHYSIOLOGICAL GENOMICS Reddy, S., Zhao, M., Hu, D., Fajardo, G., Hu, S., Ghosh, Z., Rajagopalan, V., Wu, J. C., Bernstein, D. 2012; 44 (10): 562-575

    Abstract

    MicroRNAs (miRs) are small, noncoding RNAs that are emerging as crucial regulators of cardiac remodeling in left ventricular hypertrophy (LVH) and failure (LVF). However, there are no data on their role in right ventricular hypertrophy (RVH) and failure (RVF). This is a critical question given that the RV is uniquely at risk in patients with congenital right-sided obstructive lesions and in those with systemic RVs. We have developed a murine model of RVH and RVF using pulmonary artery constriction (PAC). miR microarray analysis of RV from PAC vs. control demonstrates altered miR expression with gene targets associated with cardiomyocyte survival and growth during hypertrophy (miR 199a-3p) and reactivation of the fetal gene program during heart failure (miR-208b). The transition from hypertrophy to heart failure is characterized by apoptosis and fibrosis (miRs-34, 21, 1). Most are similar to LVH/LVF. However, there are several key differences between RV and LV: four miRs (34a, 28, 148a, and 93) were upregulated in RVH/RVF that are downregulated or unchanged in LVH/LVF. Furthermore, there is a corresponding downregulation of their putative target genes involving cell survival, proliferation, metabolism, extracellular matrix turnover, and impaired proteosomal function. The current study demonstrates, for the first time, alterations in miRs during the process of RV remodeling and the gene regulatory pathways leading to RVH and RVF. Many of these alterations are similar to those in the afterload-stressed LV. miRs differentially regulated between the RV and LV may contribute to the RVs increased susceptibility to heart failure.

    View details for DOI 10.1152/physiolgenomics.00163.2011

    View details for Web of Science ID 000304367600003

    View details for PubMedID 22454450

  • Recipient Genotype Is a Predictor of Allograft Cytokine Expression and Outcomes After Pediatric Cardiac Transplantation JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY Auerbach, S. R., Manlhiot, C., Reddy, S., Kinnear, C., Richmond, M. E., Gruber, D., McCrindle, B. W., Deng, L., Chen, J. M., Addonizio, L. J., Chung, W. K., Mital, S. 2009; 53 (20): 1909-1917

    Abstract

    This study sought to investigate the influence of recipient renin-angiotensin-aldosterone system (RAAS) genotype on cardiac function, rejection, and outcomes after heart transplantation.The RAAS influences cardiac function and up-regulates inflammatory/immune pathways. Little is known about the effect of recipient RAAS polymorphisms in pediatric cardiac transplantation.Patients <25 years of age, after cardiac transplantation, were enrolled (2003 to 2008) and genotyped for polymorphisms in genes associated with RAAS upregulation: AGT-G, ACE-D, AGTR1-C, CYP11B2-G, and CMA-A. Presence of at least 1 high-risk allele was defined as a high-risk genotype. Univariable and multivariable associations between genotypes and outcomes were assessed in time-dependent models using survival, logistic, or linear regression models. Biopsy samples were immunostained for interleukin (IL)-6, transforming growth factor (TGF)-beta, and tumor necrosis factor (TNF)-alpha during rejection and quiescence.A total of 145 patients were studied, 103 primary cohort and 42 replication cohort; 81% had rejection, 51% had graft dysfunction, and 13% had vasculopathy, 7% died and 8% underwent re-transplantation. A higher number of homozygous high-risk RAAS genotypes was associated with a higher risk of graft dysfunction (hazard ratio [HR]: 1.5, p = 0.02) and a higher probability of death (HR: 2.5, p = 0.04). The number of heterozygous high-risk RAAS genotypes was associated with frequency of rejection (+0.096 events/year, p < 0.001) and rejection-associated graft dysfunction (+0.37 events/year, p = 0.002). IL-6 and TGF-beta were markedly upregulated during rejection in patients with >/=2 high-risk RAAS genotypes.Recipient RAAS polymorphisms are associated with a higher risk of rejection, graft cytokine expression, graft dysfunction, and a higher mortality after cardiac transplantation. This may have implications for use of RAAS inhibitors in high-risk patients after transplantation.

    View details for DOI 10.1016/j.jacc.2009.02.027

    View details for Web of Science ID 000266236600012

    View details for PubMedID 19442892

  • Genomic Profiling of Left and Right Ventricular Hypertrophy in Congenital Heart Disease JOURNAL OF CARDIAC FAILURE Kaufman, B. D., Desai, M., Reddy, S., Osorio, J. C., Chen, J. M., Mosca, R. S., Ferrante, A. W., Mital, S. 2008; 14 (9): 760-767

    Abstract

    The right ventricle (RV) has a lower ability than the left ventricle (LV) to adapt to systemic load. The molecular basis of these differences is not known. We compared hypertrophy-signaling pathways between the RV and the LV in patients with congenital heart disease (CHD).Gene expression was measured using DNA microarrays in myocardium from children with CHD with LV or RV obstructive lesions undergoing surgery. The expression of 175 hypertrophy-signaling genes was compared between the LV (n=7) and the RV (n=11). Hierarchic clustering was performed.Seventeen genes (10%) were differentially expressed between the LV and the RV. Expression of genes for angiotensin, adrenergic, G-proteins, cytoskeletal, and contractile components was lower (P < .05) and expression of maladaptive factors (fibroblast growth factors, transforming growth factor-beta, caspases, ubiquitin) was higher in the RV compared with the LV (P < .05). Five of 7 LV samples clustered together. Only 4 of 11 RV samples clustered with the LV. Genes critical to adaptive remodeling correlated with the degree of LV hypertrophy but not RV hypertrophy.The transcription of pathways of adaptive remodeling was lower in the RV compared with the LV. This may explain the lower ability of the RV to adapt to hemodynamic load in CHD.

    View details for DOI 10.1016/j.cardfail.2008.06.002

    View details for Web of Science ID 000261269800008

    View details for PubMedID 18995181

  • Pyloric Stenosis AAP Textbook on Pediatric Care Sushma Reddy, Deepak M Kamat 2008; Chapter315
  • RAAS gene polymorphisms influence progression of pediatric hypertrophic cardiomyopathy HUMAN GENETICS Kaufman, B. D., Auerbach, S., Reddy, S., Manlhiot, C., Deng, L., Prakash, A., Printz, B. F., Gruber, D., Papavassiliou, D. P., Hsu, D. T., Sehnert, A. J., Chung, W. K., Mital, S. 2007; 122 (5): 515-523

    Abstract

    Hypertrophic Cardiomyopathy (HCM) is a disease with variable rate of progression. Young age is an independent risk factor for poor outcome in HCM. The influence of renin-angiotensin-aldosterone (RAAS) genotype on the progression of HCM in children is unknown. Children with HCM (n = 65) were enrolled prospectively across two centers (2001-2005). All subjects were genotyped for five RAAS gene polymorphisms previously associated with LV hypertrophy (pro-LVH): AGT M235T, ACE DD, CMA-1903 A/G, AGTR1 1666 A/C and CYP11B2-344 C/T. Linear regression models, based on maximum likelihood estimates, were created to assess the independent effect of RAAS genotype on LV hypertrophy (LVH). Forty-six subjects were homozygous for <2 and 19 were homozygous for > or =2 pro-LVH RAAS polymorphisms. Mean age at presentation was 9.6 +/- 6 years. Forty children had follow-up echocardiograms after a median of 1.5 years. Indexed LV mass (LVMI) and LV mass z-scores were higher at presentation and follow-up in subjects with > or =2 pro-LVH genotypes compared to those with <2 (P < 0.05). Subjects with > or =2 pro-LVH genotypes also demonstrated a greater increase in septal thickness (IVST) and in LV outflow tract (LVOT) obstruction on follow-up (P < 0.05). On multivariate analysis, a higher number of pro-LVH genotypes was associated with a larger effect size (P < 0.05). Pro-LVH RAAS gene polymorphisms are associated with progressive septal hypertrophy and LVOT obstruction in children with HCM. Identification of RAAS modifier genes may help to risk-stratify patients with HCM.

    View details for DOI 10.1007/s00439-007-0429-9

    View details for Web of Science ID 000251143900011

    View details for PubMedID 17851694

  • Failure of right ventricular adaptation in children with tetralogy of Fallot CIRCULATION Reddy, S., Osorio, J. C., Duque, A. M., Kaufman, B. D., Phillips, A. B., Chen, J. M., Quaegebeur, J., Mosca, R. S., Mital, S. 2006; 114: I37-I42

    Abstract

    The left ventricle (LV) adapts to chronic hypoxia by expressing protective angiogenic, metabolic, and antioxidant genes to improve O2 delivery and energy production, and to minimize reoxygenation injury. The ability of the right ventricle (RV) to adapt to hypoxia in children with tetralogy of Fallot (TOF) is unknown.Gene expression using real-time polymerase chain reaction was measured in RV myocardium obtained during surgical repair of TOF from 23 patients: 13 cyanotic and 10 acyanotic. Results were compared between the 2 groups and correlated with age at surgery, severity of cyanosis, and early postoperative course. The cyanotic patients were younger at surgery compared with acyanotic (5+/-3 versus 9+/-4 months; P=0.01), had higher hematocrit (43+/-4 versus 38+/-3 grams/dL; P=0.004), and lower O2 saturations (84+/-4% versus 98+/-2%; (P<0.001). Cyanotic patients had a significantly lower expression of vascular endothelial growth factor (VEGF), glycolytic enzymes, and glutathione peroxidase (GPX) (P<0.05), and a higher expression of collagen (P<0.01) compared with acyanotic patients. Gene expression correlated inversely with severity of cyanosis ie, preoperative hematocrit (P<0.01) and positively with preoperative saturation (P<0.05). The relationship between gene expression and cyanosis was independent of age at surgery. Ca2+ handling genes did not correlate with the severity of hypoxia. Lower angiogenic, glycolytic, and antioxidant gene expression correlated with increasing postoperative lactate (P<0.05).The RV fails to up regulate adaptive pathways in response to increasing hypoxia in children with TOF. The implications of an early maladaptive response of the RV on long-term RV function require further investigation.

    View details for DOI 10.1161/CIRCULATIONAHA.105.001248

    View details for Web of Science ID 000238688200008

    View details for PubMedID 16820602

  • Inlet patch: Heterotopic gastric mucosa - Another contributor to supraesophageal symptoms? JOURNAL OF PEDIATRICS Macha, S., Reddy, S., Rabah, R., Thomas, R., Tolia, V. 2005; 147 (3): 379-382

    Abstract

    To determine prospectively the incidence of an inlet patch (IP) in children requiring esophagogastroduodenoscopy (EGD) and assess the prevalence of presenting symptoms between children with and without an IP.All patients undergoing EGD in a 2-year period were assessed for the presence of an IP with biopsy confirmation. IP, distal esophagus, and stomach biopsy specimens were blindly reviewed by a pathologist for the presence and degree of inflammation and intestinal metaplasia. Symptoms from children with and without an IP were compared.From 407 EGDs done by a single endoscopist, 24 patients had confirmed IP (incidence of 5.9%). The presence and degree of inflammation were always relatively greater in the columnar mucosa of the IP than in the antral/body gastric mucosa in the same patient (P = .0027) Inflammation was similar in the squamous epithelium around the IP and in the distal esophagus (P=.46). Two patients had intestinal metaplasia of the IP. The patients with IPs had a higher prevalence of respiratory symptoms than the control group (P = .03).Children with IPs may have a higher frequency of respiratory symptoms. Periodic surveillance should be performed in children with intestinal metaplasia of an IP.

    View details for DOI 10.1016/j.jpeds.2005.03.002

    View details for Web of Science ID 000232412100023

    View details for PubMedID 16182679

  • Restrictive interatrial communication in hypoplastic left heart syndrome after modified Fontan repair ANNALS OF THORACIC SURGERY Nemeh, H. W., Reddy, S., Walters, H. L., Hakimi, M., Ross, R. D. 2003; 76 (6): 2089-2091

    Abstract

    The occurrence of pulmonary venous obstruction after total cavopulmonary connection with intraatrial lateral tunnel is a rare occurrence. We present two cases of hypoplastic left heart syndrome with restrictive interatrial communication presenting late after this type of modified Fontan repair. This occurred even after complete excision of the atrial septum at the time of Stage 1 Norwood in both cases. A novel approach to this problem of resecting the roof of the coronary sinus was utilized to enlarge the interatrial communication.

    View details for DOI 10.1016/S0003-4975(03)01173-1

    View details for Web of Science ID 000186986500072

    View details for PubMedID 14667654

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