Selim M Arcasoy

Columbia University, New York City, New York, United States

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Publications (140)835.29 Total impact

  • The Journal of Heart and Lung Transplantation 04/2015; 34(4):S255-S256. DOI:10.1016/j.healun.2015.01.709 · 5.61 Impact Factor
  • The Journal of Heart and Lung Transplantation 04/2015; 34(4):S15. DOI:10.1016/j.healun.2015.01.028 · 5.61 Impact Factor
  • The Journal of Heart and Lung Transplantation 04/2015; 34(4):S254-S255. DOI:10.1016/j.healun.2015.01.706 · 5.61 Impact Factor
  • The Journal of Heart and Lung Transplantation 04/2015; 34(4):S170-S171. DOI:10.1016/j.healun.2015.01.464 · 5.61 Impact Factor
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    ABSTRACT: Objective Many transplant programs are hesitant to offer lung transplantation to patients with systemic sclerosis (SSc) due to concerns about extrapulmonary involvement that might affect survival. The aim of this study was to determine whether adults with SSc have higher 1-year mortality rates after lung transplantation compared to those with interstitial lung disease (ILD) or pulmonary arterial hypertension (PAH) not due to SSc.Methods Using data provided by the United Network for Organ Sharing, we performed a retrospective cohort study of 229 adults with SSc, 201 with PAH, and 3,333 with ILD who underwent lung transplantation in the US between May 4, 2005 and September 14, 2012. We examined associations between diagnosis and 1-year survival after lung transplantation using stratified Cox models adjusted for recipient, donor, and procedure factors.ResultsAdults with SSc undergoing lung transplantation in the US had a multivariable-adjusted 48% relative increase in the 1-year mortality rate compared to those with non-SSc-related ILD (hazard ratio 1.48 [95% confidence interval 1.01-2.17]). However, we did not detect a difference in the risk of death at 1 year between those with SSc and those with non-SSc-related PAH (hazard ratio 0.85 [95% confidence interval 0.50-1.44]).ConclusionA diagnosis of SSc may confer an increased risk of death 1 year following lung transplantation compared to a diagnosis of ILD, but this risk is similar to that of PAH, a widely accepted indication for lung transplantation. Future work should identify modifiable risk factors that can improve transplant outcomes in this population.
    01/2015; 67(5). DOI:10.1002/art.39021
  • 15th Annual State of the Art Winter Symposium of the; 01/2015
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    ABSTRACT: Background Long term outcomes after lung transplantation are limited due to chronic lung allograft dysfunction (CLAD). Bronchiolitis obliterans syndrome (BOS) is the most common form of obstructive CLAD and its definition derives from spirometric measurements. Given the importance of this diagnosis, the accuracy and reliability of this definition are crucial in understanding the pathophysiology of this disease in order to develop therapeutic options and influence outcome after lung transplantation. Methods A web based survey was designed and distributed to members of the Pulmonary Council of the International Society of Heart and Lung Transplantation (ISHLT) to better understand the accuracy and reliability of pulmonary function criteria in diagnosing BOS. Spirometric data from five patient scenarios that were discordant among reviewers regarding BOS determination from the AIRSAC trial were randomly selected and summarized in this survey. Survey questions included the respondent’s general understanding of the BOS definition, the determination of BOS and difficulties with the current BOS definition. Results Eighty-seven respondents from the ISHLT pulmonary council responded to this survey. There was an overall 70% interobserver agreement regarding the presence of absence of BOS. Among those who agreed upon the presence of BOS, there was a 41% inter-observer agreement regarding the time of onset of BOS. Despite this variability, the majority of respondents not only was familiar and agreed with the BOS criteria, they also felt confident in applying these criteria. Conclusions Our survey has identified potential limitations with the current criteria for diagnosing BOS. With the recognition of the various CLAD phenotypes, further refinements of these diagnostic criteria will allow for a better ability to identify and characterize patients who develop or are at risk for BOS, prognosticate outcomes, and most importantly marshal in future strategies directed at treating and preventing chronic lung dysfunction after lung transplantation.
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    ABSTRACT: Rationale:Obesity and underweight are contraindications to lung transplantation based on their associations with mortality in studies performed prior to implementation of the Lung Allocation Score (LAS)-based organ allocation system in the United States. Objectives:To determine the associations of the body mass index(BMI) and plasma leptin levels with survival after lung transplantation. Methods:We used multivariable-adjusted regression models to examine associations between (1) BMI and 1-year mortality in 9,073 adults who underwent lung transplantation in the United States between May 2005 and June 2011, and (2) plasma leptin and mortality in 599 Lung Transplant Outcomes Group study participants. We measured body fat and skeletal muscle mass using whole-body dual x-ray absorptiometry in 142 adult lung transplant candidates. Measurements and Main Results: Adjusted mortality rates were similar among normal weight (BMI 18.5-24.9 kg/m2), overweight (BMI 25.0-29.9) and Class I obese (BMI 30-34.9) transplant recipients. Underweight (BMI<18.5) was associated with a 35% increased rate of death (95%CI 10-66%). Class II-III obesity (BMI≥35kg/m2) was associated with a nearly 2-fold increase in mortality (HR 1.9, 95%CI 1.3-2.8). Higher leptin levels were associated with increased mortality after transplant surgery performed without cardiopulmonary bypass (p for interaction=0.03). A BMI≥30 kg/m2 was 26% sensitive and 97% specific for total body fat-defined obesity. Conclusions: A BMI of 30.0-34.9kg/m2 is not associated with 1-year mortality after lung transplantation in the LAS era, perhaps due to its low sensitivity for obesity. The association between leptin and mortality suggests the need to validate alternative methods to measure obesity in candidates for lung transplantation. A BMI ≥30kg/m2 may no longer contraindicate lung transplantation.
    American Journal of Respiratory and Critical Care Medicine 09/2014; 190(9). DOI:10.1164/rccm.201405-0973OC · 11.99 Impact Factor
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    ABSTRACT: We aimed to determine the effects of treatment with intravenous immunoglobulin on bacterial infections in patients with hypogammaglobulinemia (HGG) after lung transplantation.
    PLoS ONE 08/2014; 9(8):e103908. DOI:10.1371/journal.pone.0103908 · 3.53 Impact Factor
  • The Journal of Heart and Lung Transplantation 04/2014; 33(4):S107-S108. DOI:10.1016/j.healun.2014.01.321 · 5.61 Impact Factor
  • The Journal of Heart and Lung Transplantation 04/2014; 33(4):S139. DOI:10.1016/j.healun.2014.01.375 · 5.61 Impact Factor
  • The Journal of Heart and Lung Transplantation 04/2014; 33(4):S188. DOI:10.1016/j.healun.2014.01.880 · 5.61 Impact Factor
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    ABSTRACT: Inherent recipient factors, including pretransplant diagnosis, obesity and elevated pulmonary pressures, are established primary graft dysfunction (PGD) risks. We evaluated the relationship between preoperative lung injury biomarkers and PGD to gain further mechanistic insight in recipients. We performed a prospective cohort study of recipients in the Lung Transplant Outcomes Group enrolled between 2002 and 2010. Our primary outcome was Grade 3 PGD on Day 2 or 3. We measured preoperative plasma levels of five biomarkers (CC-16, sRAGE, ICAM-1, IL-8 and Protein C) that were previously associated with PGD when measured at the postoperative time point. We used multivariable logistic regression to adjust for potential confounders. Of 714 subjects, 130 (18%) developed PGD. Median CC-16 levels were elevated in subjects with PGD (10.1 vs. 6.0, p < 0.001). CC-16 was associated with PGD in nonidiopathic pulmonary fibrosis (non-IPF) subjects (OR for highest quartile of CC-16: 2.87, 95% CI: 1.37, 6.00, p = 0.005) but not in subjects with IPF (OR 1.38, 95% CI: 0.43, 4.45, p = 0.59). After adjustment, preoperative CC-16 levels remained associated with PGD (OR: 3.03, 95% CI: 1.26, 7.30, p = 0.013) in non-IPF subjects. Our study suggests the importance of preexisting airway epithelial injury in PGD. Markers of airway epithelial injury may be helpful in pretransplant risk stratification in specific recipients.
    American Journal of Transplantation 02/2014; 14(2). DOI:10.1111/ajt.12541 · 6.19 Impact Factor
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    ABSTRACT: Rationale: Biological pathways with significant genetic conservation across human populations have been implicated in the pathogenesis of primary graft dysfunction (PGD). The evaluation of the role of recipient genetic variation in PGD has thus far been limited to single, candidate gene analyses. Objective: We sought to identify genetic variants in lung transplant recipients that are responsible for increased risk of PGD using a two-phase large-scale genotyping approach. Methods: Phase 1 was a large-scale candidate gene association study of the multicenter, prospective Lung Transplant Outcomes Group cohort. Phase 2 included functional evaluation of selected variants and a bioinformatics screening of variants identified in phase 1. Main Result: After genetic data quality control, 680 lung transplant recipients were included in the analysis. In phase 1, seventeen variants were significantly associated with PGD, four of which were in the prostaglandin E2 family of genes. Among these were a coding variant in the gene encoding prostaglandin E2 synthase (PTGES2, p=9.3x10-5) resulting in an arginine to histidine substitution at amino acid position 298, and three variants in a block containing the 5' promoter and first intron of the PTGER4 gene (encoding prostaglandin E2 receptor subtype 4, all p<5x10-5). Functional evaluation in regulatory T-cells identified that rs4434423A in the PTGER4 gene was associated with differential suppressive function of regulatory T cells. Conclusions: Further research aimed at replication and additional functional insight into the role played by genetic variation in prostaglandin E2 synthetic and signaling pathways in PGD is warranted.
    American Journal of Respiratory and Critical Care Medicine 01/2014; DOI:10.1164/rccm.201307-1283OC · 11.99 Impact Factor
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    ABSTRACT: Lungs from older adult organ donors are often unused because of concerns for increased mortality. We examined associations between donor age and transplant outcomes among 8860 adult lung transplant recipients using Organ Procurement and Transplantation Network and Lung Transplant Outcomes Group data. We used stratified Cox proportional hazard models and generalized linear mixed models to examine associations between donor age and both 1-year graft failure and primary graft dysfunction (PGD). The rate of 1-year graft failure was similar among recipients of lungs from donors age 18-64 years, but severely ill recipients (Lung Allocation Score [LAS] >47.7 or use of mechanical ventilation) of lungs from donors age 56-64 years had increased rates of 1-year graft failure (p-values for interaction = 0.04 and 0.02, respectively). Recipients of lungs from donors <18 and ≥65 years had increased rates of 1-year graft failure (adjusted hazard ratio [HR] 1.23, 95% CI 1.01-1.50 and adjusted HR 2.15, 95% CI 1.47-3.15, respectively). Donor age was not associated with the risk of PGD. In summary, the use of lungs from donors age 56 to 64 years may be safe for adult candidates without a high LAS and the use of lungs from pediatric donors is associated with a small increase in early graft failure.
    American Journal of Transplantation 08/2013; 13(10). DOI:10.1111/ajt.12428 · 6.19 Impact Factor
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    ABSTRACT: Chronic lung allograft dysfunction (CLAD) is the major factor limiting long-term success of lung transplantation. Polymorphisms of surfactant protein D (SP-D), an important molecule within lung innate immunity, have been associated with various lung diseases. We investigated the association between donor lung SP-D polymorphisms and posttransplant CLAD and survival in 191 lung transplant recipients consecutively transplanted. Recipients were prospectively followed with routine pulmonary function tests. Donor DNA was assayed by pyrosequencing for SP-D polymorphisms of two single-nucleotide variations altering amino acids in the mature protein N-terminal domain codon 11 (Met(11) Thr), and in codon 160 (Ala(160) Thr) of the C-terminal domain. CLAD was diagnosed in 88/191 patients, and 60/191 patients have died. Recipients of allografts that expressed the homozygous Met(11) Met variant of aa11 had significantly greater freedom from CLAD development and better survival compared to those with the homozygous Thr(11) Th variant of aa11. No significant association was noted for SP-D variants of aa160. Lung allografts with the SP-D polymorphic variant Thr(11) Th of aa11 are associated with development of CLAD and reduced survival. The observed genetic differences of the donor lung, potentially with their effects on innate immunity, may influence the clinical outcomes after lung transplantation.
    American Journal of Transplantation 07/2013; 13(8). DOI:10.1111/ajt.12326 · 6.19 Impact Factor
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    ABSTRACT: A third of patients with idiopathic pulmonary fibrosis (IPF) develop pulmonary hypertension (PH-IPF), which is associated with increased mortality. Whether an altered gene expression profile in the pulmonary vasculature precedes the clinical onset of PH-IPF is unknown. We compared gene expression in the pulmonary vasculature of IPF patients with and without PH with controls. Pulmonary arterioles were isolated using laser capture microdissection from 16 IPF patients: eight with PH (PH-IPF) and eight with no PH (NPH-IPF), and seven controls. Probe was prepared from extracted RNA, and hybridised to Affymetrix Hu133 2.0 Plus genechips. Biometric Research Branch array tools and Ingenuity Pathway Analysis software were used for analysis of the microarray data. Univariate analysis revealed 255 genes that distinguished IPF arterioles from controls (p<0.001). Mediators of vascular smooth muscle and endothelial cell proliferation, Wnt signalling and apoptosis were differentially expressed in IPF arterioles. Unsupervised and supervised clustering analyses revealed similar gene expression in PH-IPF and NPH-IPF arterioles. The pulmonary arteriolar gene expression profile is similar in IPF patients with and without coexistent PH. Pathways involved in vascular proliferation and aberrant apoptosis, which may contribute to pulmonary vascular remodelling, are activated in IPF patients.
    European Respiratory Journal 06/2013; 41(6):1324-1330. DOI:10.1183/09031936.00084112 · 7.13 Impact Factor
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    ABSTRACT: BACKGROUND: Cytomegalovirus (CMV) is the most common opportunistic infection in lung transplantation. A recent multicenter, randomized trial (the AIRSAC study) comparing sirolimus to azathioprine in lung transplant recipients showed a decreased incidence of CMV events in the sirolimus cohort. To better characterize this relationship of decreased incidence of CMV events with sirolimus, we examined known risk factors and characteristics of CMV events from the AIRSAC database. METHODS: The AIRSAC database included 181 lung transplant patients from 8 U.S.-based lung transplant centers that were randomized to sirolimus or azathioprine at 3 months post-transplantation. CMV incidence, prophylaxis, diagnosis and treatment data were all prospectively collected. Prophylaxis and treatment of CMV were at the discretion of each institution. RESULTS: The overall incidence of any CMV event was decreased in the sirolimus arm when compared with the azathioprine arm at 1 year after lung transplantation (relative risk [RR] = 0.67, confidence interval [CI] 0.55 to 0.82, p < 0.01). This decreased incidence of CMV events with sirolimus remained significant after adjusting for confounding factors of CMV serostatus and CMV prophylaxis. CONCLUSIONS: These data support results from other solid-organ transplantation studies and suggest further investigation of this agent in the treatment of lung transplant recipients at high risk for CMV events.
    The Journal of heart and lung transplantation: the official publication of the International Society for Heart Transplantation 05/2013; DOI:10.1016/j.healun.2013.04.010 · 5.61 Impact Factor
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    ABSTRACT: Our group has hypothesized that the frailty phenotype might help identify those at high risk of early complications after lung transplantation. The prevalence of pre-transplant frailty among transplant recipients and the impact of frailty on outcomes after transplantation is not known.Methods and MaterialsWe performed an interim analysis of the first 46 consecutive lung transplant recipients ≥50 years old enrolled in the Lung Transplant Body Composition (LTBC) study at our center. All LTBC participants undergo a structured frailty assessment during transplant evaluation. Frailty was defined as the presence of ≥3 of the following: unintentional weight loss ≥ 4.5kg, low walking speed, self-reported exhaustion, low activity level, and low grip strength. Wilcoxon rank sum tests, Chi-square tests, Fisher’s exact tests, and log-rank tests were used to compare frail and non-frail participants.ResultsThe mean (SD) age was 62 (5) yrs, 34% were ≥ 65 yrs, 44% were female, 13% were African-American, 54% had ILD, 14% had COPD, 2% had CF, 4% were underweight, 13% were obese, the median LAS was 42 (IQR 33 to 51), 48% were bilateral, and 11 (24%) were frail. Frail recipients were more frequently African-American (37% vs. 6%, p = 0.02) but were similar with regard to age, gender, BMI, diagnosis, LAS score, PA pressure, and use of cardiopulmonary bypass. There were non-significant trends toward more intraoperative complications (28% vs 6%, p = 0.08), postoperative complications (64% vs 37%, p = 0.17), unplanned returns to the OR (18% vs 6%, p = 0.24), and deaths on the ventilator (18% vs 2%, p = 0.14) among frail vs non-frail recipients, respectively. The 30-day mortality rate was 18% among frail and 0% among non-frail (p = 0.01).Conclusions The frail phenotype is prevalent among lung transplant recipients over 50 years old at our center and is not associated with diagnosis or LAS score. Our finding of an unadjusted association of frailty with poor outcomes should be interpreted cautiously. These findings merit additional study.
    The Journal of Heart and Lung Transplantation 04/2013; 32(4):S119-S120. DOI:10.1016/j.healun.2013.01.256 · 5.61 Impact Factor
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    ABSTRACT: ABSTRACT BACKGROUND: Acute rejection remains a major source of morbidity after lung transplantation. Given the importance of this diagnosis, an international grading system was developed to standardize the diagnosis of acute lung allograft rejection. The reliability of this grading system has not been adequately assessed by previous studies. METHODS: We examined the level of agreement in grading transbronchial biopsies obtained from a large multicenter study (AIRSAC trial). Biopsies were initially graded for acute rejection and lymphocytic bronchiolitis by the site pathologist and subsequently graded by a central pathologist. Reliability of interobserver grading was evaluated using Cohen's kappa coefficients. RESULTS: A total of 481 transbronchial biopsies were graded by both the site and central pathologist. The overall concordance rate was 74% for Grade A biopsies and concordance rate for Grade B biopsies was 89%. When biopsies performed at different time points after transplantation were assessed, there was a higher level of agreement early (≤6 weeks) after transplant compared to later time points for acute rejection. However, there was still only moderate agreement for both Grade A (kappa score 0.479 (95% CI 0.29-0.67)) and Grade B (kappa score 0.465 (95% CI 0.08-0.85)) rejection. CONCLUSION: These results expand upon previous reports of interobserver variability in grading transbronchial biopsies after lung transplantation. Given the variability in the grading transbronchial biopsies, we advocate further education of the histopathologic findings in lung transplant biopsies as well as revisiting the current criteria for grading transbronchial biopsies in order to improve concordance among lung transplant pathologists.
    Chest 01/2013; 143(6). DOI:10.1378/chest.12-2107 · 7.13 Impact Factor

Publication Stats

3k Citations
835.29 Total Impact Points

Institutions

  • 2004–2014
    • Columbia University
      • • College of Physicians and Surgeons
      • • Department of Medicine
      New York City, New York, United States
  • 2003–2014
    • CUNY Graduate Center
      New York, New York, United States
  • 2000–2014
    • William Penn University
      Filadelfia, Pennsylvania, United States
  • 2009–2012
    • New York Presbyterian Hospital
      New York City, New York, United States
    • Cornell University
      Итак, New York, United States
  • 2008
    • University of Toronto
      Toronto, Ontario, Canada
  • 2007
    • Yale University
      • Department of Pediatrics
      New Haven, Connecticut, United States
  • 2005
    • Vanderbilt University
      Нашвилл, Michigan, United States
  • 2002
    • West Chester University
      웨스트체스터, Pennsylvania, United States
  • 2000–2002
    • Hospital of the University of Pennsylvania
      • Division of Pulmonary Allergy and Critical Care
      Philadelphia, Pennsylvania, United States
  • 1999
    • University of Pittsburgh
      Pittsburgh, Pennsylvania, United States