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Dive into the research topics where Geoffrey L. Rosenthal is active.

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Featured researches published by Geoffrey L. Rosenthal.


Pediatric Infectious Disease Journal | 2004

Risk factors for surgical site infections after pediatric cardiovascular surgery

Amanda L. Allpress; Geoffrey L. Rosenthal; Kathy M. Goodrich; Flavian M. Lupinetti; Danielle M. Zerr

Background. Although risk factors for surgical site infection (SSI) after cardiovascular (CV) surgery have been well-documented among adults, few studies have been conducted in children. We performed a case-control study to identify risk factors for hospitalized SSI in children undergoing CV surgery. Methods. National Nosocomial Infections Surveillance System criteria were used prospectively to identify cases of hospitalized SSI in patients who underwent CV surgery. Seventy-nine patients who underwent CV surgery without hospitalized SSI were randomly selected as controls. Cases were compared with controls to determine preoperative, intraoperative and postoperative risk factors for hospitalized SSI. Multivariable logistic regression was performed. Results. An SSI developed in 19 of the 826 patients who underwent CV surgery (2.3 cases per 100 surgeries) during the study period. Infection was limited to soft tissue in 12, whereas deeper infection occurred in 7. Causative agents included Staphylococcus aureus (11), coagulase-negative Staphylococcus (5) and Escherichia coli (2). One patient did not have a pathogen isolated. In a multivariable analysis, duration of surgery (odds ratio, 1.4; 95% confidence interval, 1.2 to 1.8) and age <1 month (odds ratio, 14; 95% confidence interval, 3.3 to 58.4) were independently associated with SSI. Conclusions. Age <1 month and longer duration of surgery were independently associated with hospitalized SSI after CV surgery in children.


The Journal of Thoracic and Cardiovascular Surgery | 2000

Vascular endothelial growth factor and basic fibroblast growth factor in children with cyanotic congenital heart disease

Sandra L. Starnes; Brian W. Duncan; James M. Kneebone; Geoffrey L. Rosenthal; Thomas K. Jones; Ronald G. Grifka; Frank Cecchin; David J. Owens; Collette T Fearneyhough; Flavian M. Lupinetti

OBJECTIVE Vascular endothelial growth factor and basic fibroblast growth factor are potent stimulators of angiogenesis. Children with cyanotic congenital heart disease often experience the development of widespread formation of collateral blood vessels, which may represent a form of abnormal angiogenesis. We undertook the present study to determine whether children with cyanotic congenital heart disease have elevated serum levels of vascular endothelial growth factor and basic fibroblast growth factor. METHODS Serum was obtained from 22 children with cyanotic congenital heart disease and 19 children with acyanotic heart disease during cardiac catheterization. Samples were taken from the superior vena cava, inferior vena cava, and a systemic artery. Vascular endothelial growth factor and basic fibroblast growth factor levels were measured in the serum from each of these sites by enzyme-linked immunosorbent assay. RESULTS Vascular endothelial growth factor was significantly elevated in the superior vena cava (P =.04) and systemic artery (P =.02) but not in the inferior vena cava (P =.2) of children with cyanotic congenital heart disease compared to children with acyanotic heart disease. The mean vascular endothelial growth factor level, determined by averaging the means of all 3 sites, was also significantly elevated (P =.03). Basic fibroblast growth factor was only significantly elevated in the systemic artery (P =.02). CONCLUSION Children with cyanotic congenital heart disease have elevated systemic levels of vascular endothelial growth factor. These findings suggest that the widespread formation of collateral vessels in these children may be mediated by vascular endothelial growth factor.


The Annals of Thoracic Surgery | 2008

Melbourne Shunt Promotes Growth of Diminutive Central Pulmonary Arteries in Patients With Pulmonary Atresia, Ventricular Septal Defect, and Systemic-to-Pulmonary Collateral Arteries

Muhammad A. Mumtaz; Geoffrey L. Rosenthal; Athar M. Qureshi; Lourdes R. Prieto; Tamar J. Preminger; Richard Lorber; Larry A. Latson; Brian W. Duncan

BACKGROUND We manage patients with pulmonary atresia, ventricular septal defect, major systemic-to-pulmonary collateral arteries, and diminutive central pulmonary arteries with a staged approach. The first procedure is a central end-to-side aortopulmonary shunt (Melbourne shunt) intended to cause growth and development of the central pulmonary arteries. We subsequently measured central pulmonary artery growth after Melbourne shunt. METHODS Forty consecutive patients were followed after Melbourne shunt. The maximum pulmonary artery diameter was measured at the time of surgery and at subsequent catheterizations or surgery. RESULTS Median pulmonary artery size at surgery was 2 mm. The median pulmonary artery diameter was 5.5 mm at first assessment (median, 6.35 months) and 7 mm at most recent assessment (19.7 months). Mean modified Nakata index increased from 27 mm(2)/m(2) at surgery to 138 mm(2)/m(2) at first assessment, and 176 mm(2)/m(2) at final assessment. There was one acute shunt failure from anastomotic stenosis. Thirteen patients (32.5%) required 21 percutaneous interventions. There were 4 deaths during a median follow-up of 68 months. At the time of complete repair (n = 25) all patients required pulmonary artery augmentation, and 8 are in various stages of palliation. The remaining patients are considered not reparable owing to irreversible pulmonary hypertension (n = 4) or have required fenestration of ventricular septal defect after complete repair (n = 2). CONCLUSIONS Melbourne shunt promotes modest growth of central pulmonary arteries leading to complete repair in the majority of patients. There is considerable need for further interventions in these patients to augment the size of the pulmonary arteries.


American Journal of Preventive Medicine | 2009

Effects of body size and body fatness on left ventricular mass in children and adolescents: Project HeartBeat!

Shifan Dai; Ronald B. Harrist; Geoffrey L. Rosenthal; Darwin R. Labarthe

BACKGROUND Left ventricular mass (LVM) is a strong predictor of cardiovascular disease in adults. Available study findings on effects of body fatness on LVM in children are inconsistent. Understanding the impact of body fat on LVM in children may help prevent excessive LVM through measures to reduce overweight and obesity. METHODS Healthy children (n=678) aged 8, 11, and 14 years at baseline were examined at 4-month intervals for up to 4 years (1991-1995); 4608 valid measurements of LVM were obtained with M-mode echocardiography. A multilevel linear model was used for analysis. The impact of body size was examined by adding separately nine body-size indicators to a basic LVM-gender-age model. The impact of body fatness was tested by introducing four body-fatness indicators into the nine models, yielding 36 models. RESULTS All body-size indicators showed strong, positive effects on LVM. In models containing weight or body surface area (measuring both fat-free and fat contributions to body size), additional effects of body fatness were negative; in models containing fat-free mass (FFM) or height (both measuring body size independent of body fat), increased body fatness was related to a significant increase in LVM. For example, in models with FFM as a body-size indicator, a 1-SD increase in percent body fat or fat mass was related to a 5.4- or 7.2-g increase in LVM, respectively. CONCLUSIONS Effects of body size on LVM attributable to fat-free body mass can be distinguished from those attributable to fat body mass; both are independent, positive predictors, but the former is the stronger determinant. When a body-size indicator not independent of body fat is used as a predictor, effects of fat-free body mass and fat body mass are forced to relate to the same indicator; because their magnitudes are estimated to be equal, the effect of fat body mass is overestimated. Thus, when an additional body-fatness indicator is included in the prediction of LVM, the additional estimated effect related to the indicator appears to be negative.


The Annals of Thoracic Surgery | 2001

First-stage palliation of complex univentricular cardiac anomalies in older infants

Brian W. Duncan; Geoffrey L. Rosenthal; Thomas K. Jones; Flavian M. Lupinetti

BACKGROUND Poor outcomes have been reported for children older than 30 days of age with cardiac anomalies treated with first-stage palliation. METHODS Our institution has offered first-stage palliation for all such patients regardless of age. The results of this policy were reviewed. RESULTS Nine patients older than 30 days (median age 67 days, range 36 to 108 days) with diagnoses of hypoplastic left heart syndrome (n = 5), double-outlet right ventricle with hypoplastic aortic arch (n = 2), unbalanced atrioventricular septal defect (n = 1), or single left ventricle with subaortic stenosis (n = 1) underwent surgical palliation. Patients underwent a Norwood (n = 7) or Damus-Kaye-Stancel (n = 2) procedure with a 4- or 5-mm modified Blalock-Taussig shunt; all patients survived the operation. Eight patients underwent a subsequent bidirectional Glenn (2 perioperative deaths, both due to pneumonia; 6 survivors). Two of the 6 surviving patients have undergone Fontan reconstruction and 4 are awaiting Fontan. CONCLUSIONS Surgical palliation for complex univentricular cardiac malformations can be performed in older infants with results comparable to those in neonates. The use of a larger shunt may contribute to these improved outcomes.


Pediatrics International | 2013

Chylopericardium and chylothorax: Unusual mechanical complications of central venous catheters

Khaldoun Alkayed; Gregory E. Plautz; Kate Gowans; Geoffrey L. Rosenthal; Oliver S. Soldes; Athar M. Qureshi

Obstruction and thrombosis of major systemic veins can occur due to indwelling central venous catheters. If obstruction of the innominate vein or superior vena cava occurs, lymphatic drainage can be impaired due to an increase in pressure in the thoracic duct and lymphatics. We describe a case where superior vena cava syndrome, chylopericardium and chylothorax occurred in a 16‐year‐old girl due to an indwelling central venous catheter. This was successfully treated with removal of the line, anticoagulation and angioplasty of the innominate vein and superior vena cava.


American Journal of Cardiology | 2003

Usefulness of echocardiography in infants with supraventricular tachycardia

Christopher S. Snyder; Arnold L. Fenrich; Richard A. Friedman; Geoffrey L. Rosenthal; Naomi J. Kertesz

1. Stampfer MJ. Estrogen replacement and coronary heart disease: a quantitative assessment of the epidemiologic evidence. Prev Med 1991;20:47–63. 2. Grodstein F, Stampfer MJ, Colditz GA, Willett WC, Manson JE, Joffe M, Rosner B, Fuchs C, Hankinson SE, Hunter DJ, Hennekens CH, Speizer FE. Postmenopausal hormone therapy and mortality. N Engl J Med 1997;336:1769– 1776. 3. Rossouw JE, Anderson GL, Prentice RL, LaCroix AZ, Kooperberg C, Stefanick ML, Jackson RD, Beresford SA, Howard BV, Johnson KC, Kotchen JM, Ockene J. Risks and benefits of estrogen plus progestin in healthy postmenopausal women: principal results from the Women’s Health Initiative randomized controlled trial. JAMA 2002;288:321–333. 4. Grady D, Herrington D, Bittner V, Blumenthal R, Davidson M, Hlatky M, Hsia J, Hulley S, Herd A, Khan S, et al. Cardiovascular disease outcomes during 6.8 years of hormone therapy. Heart and Estrogen/progestin Replacement Study follow-up (HERS II). N Engl J Med 2002;288:49–57. 5. Furberg CD, Vittinghoff E, Davidson M, Herrington DM, Simon JA, Wenger NK, Hulley S. Subgroup interactions in the Heart and Estrogen/progestin Replacement Study: lessons learned. Circulation 2002;105:917–922. 6. Kannel WB. Lipids, diabetes and coronary heart disease: insights from the Framingham study. Am Heart J 1985;110:1100–1107. 7. Kleinman J, Donahue R, Harris M, Finucane F, Madans J, Brock D. Mortality among diabetics in a national sample. Am J Epidemiol 1988;128:389–401. 8. Harris MI. Prevalence of diabetes and impaired glucose tolerance and plasma glucose levels in US population aged 20–74 years. Diabetes 1987;36:523–534. 9. Keating NL, Cleary PD, Rossi AS, Zaslavsky AM, Ayanian JZ. Use of hormone replacement therapy by postmenopausal women in the United States. Ann Intern Med 1999;130:545–553. 10. Gillum RF, Fortmann SP, Prineas RJ, Kottke TE. WHO criteria for diagnosis of acute myocardial infarction. Am Heart J 1984;108:150–158. 11. Hulley S, Grady D, Bush T, Furberg C, Herrington D, Riggs B, Vittinghoff E. Randomized trial of estrogen plus progestin for secondary prevention of coronary heart disease in postmenopausal women. Heart and Estrogen/progestin Replacement Study (HERS) Research Group. JAMA 1998;280:605–613.


Journal of The American College of Surgeons | 2000

Angiogenic proteins in the lungs of children after cavopulmonary anastomosis

Sandra L. Starnes; Brian W. Duncan; James M. Kneebone; Geoffrey L. Rosenthal; Kathy Patterson; Charles H. Fraga; Flavian M. Lupinetti

Methods: Lung specimens were obtained from 13 children after cavopulmonary anastomosis and from 6 control subjects. Specimens were stained with antibodies against vascular endothelial growth factor and its receptor (flk-1/KDR), basic fibroblast growth factor, α-smooth muscle actin, CD31, collagen IV, fibronectin, and proliferating cell nuclear antigen. Staining was graded on a scale of 0 to 3. Vessels positive for proliferating cell nuclear antigen were counted in 10 fields per specimen, and the results were averaged.


The Journal of Thoracic and Cardiovascular Surgery | 2000

Triiodothyronine repletion in infants during cardiopulmonary bypass for congenital heart disease

Michael A. Portman; Collette Fearneyhough; Xue Han Ning; Brian W. Duncan; Geoffrey L. Rosenthal; Flavian M. Lupinetti


The Journal of Thoracic and Cardiovascular Surgery | 1999

A detailed histologic analysis of pulmonary arteriovenous malformations in children with cyanotic congenital heart disease.

Brian W. Duncan; James M. Kneebone; Emil Y. Chi; Viktor Hraska; F.Frank Isik; Geoffrey L. Rosenthal; Thomas K. Jones; Sandra L. Starnes; Flavian M. Lupinetti

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James M. Kneebone

Boston Children's Hospital

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Athar M. Qureshi

Baylor College of Medicine

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Larry A. Latson

Boston Children's Hospital

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