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Bio

Bio

Dr. Sweatt is board certified in internal medicine, pulmonary diseases, and critical care medicine. He sub-specializes in the evaluation and treatment of pulmonary hypertension. He recently completed his subspecialty fellowship training in 2016, and thereafter joined the multidisciplinary pulmonary hypertension team at Stanford University as a clinician and translational researcher. He sees patients at the main Stanford University campus and East Bay site in Emeryville.

Clinical Focus

  • Pulmonary Hypertension
  • Pulmonary Disease

Academic Appointments

Administrative Appointments

  • Stanford East Bay Pulmonary Hypertension Clinic Site Physician, Stanford Health Care (2017 - Present)

Honors & Awards

  • Research Support, NIH/NHLBI K12 Career Development Program in ?Omics? of Lung Diseases (2016- Present)
  • Research Support, Blue Lips Foundation- Early Detection of Pulmonary Arterial Hypertension (2016- Present)
  • Chief Fellow, Stanford University- Pulmonary and Critical Care Medicine Fellowship Program (2015-2016)
  • Presidential Poster and Fellow-In-Training Awards, American College of Gastroenterology (2015)
  • Resident Travel Award, American Thoracic Society (2012)
  • Resident Teaching Award, University of Colorado Internal Medicine (2012)
  • Colorado Governor's Presentation Selection, American College of Physicians (2011)
  • Student Research Award, Society of Toxicology (2004)
  • Team Captain, University of Connecticut Mens' Varsity Tennis Team (2004)
  • New England and Nutmeg Scholar, University of Connecticut (2003-2004)
  • University Scholar Program Participant, University of Connecticut (2003-2004)
  • Director of Athletics Scholar-Athlete Award, University of Connecticut (2002-2004)
  • Altshuler Family Scholarship, University of Connecticut (2002)
  • Academic Merit Annual Award, University of Connecticut School of Engineering (2002)
  • Academic-Athlete All-Star Team, Big East Conference (2001-2004)
  • Magna Cum Laude with Honors Degree Distinction, University of Connecticut (2004)
  • Salutatorian, Galena High School- Reno, NV (2000)
  • Finalist, Wendy's High School Heisman Scholar Athlete Award (2000)
  • Nationally ranked junior tennis player and Nevada High School Individual State Champion, United States Tennis Association (1998-2000)

Boards, Advisory Committees, Professional Organizations

  • Member, American College of Chest Physicians (2014 - Present)
  • Member, American Thoracic Society (2011 - Present)
  • Representative, University of Colorado Housestaff Association (2011 - 2012)
  • Member and Key Advocate, American College of Physicians (2010 - 2013)
  • Member and Advocate, Physicians for Human Rights (2006 - 2009)
  • Student Representative, Georgetown University School of Medicine Social Justice Committee (2006 - 2009)
  • Member, American Medical Association (2005 - 2009)
  • Member, Tau Beta Pi- international engineering honor society (2002 - 2005)
  • Member, Eta Kappa Nu- international engineering honor society (2002 - 2005)
  • Team Representative, University of Connecticut Student Athlete Advisory Council (2001 - 2004)

Professional Education

  • Medical Education: Georgetown University School of Medicine Registrar (2009) DC
  • Fellowship: Stanford University Pulmonary and Critical Care Fellowship CA
  • Board Certification: American Board of Internal Medicine, Critical Care Medicine (2016)
  • Board Certification: American Board of Internal Medicine, Internal Medicine (2012)
  • Residency: University of Colorado Internal Medicine Residency (2012) CO
  • Board Certification: American Board of Internal Medicine, Pulmonary Disease (2015)
  • Bachelor of Science, University of Connecticut School of Engineering, Major- Biomedical Engineering (Chemical Engineering focus) Minor- Biotechnology (2004)
  • Board Certification, Critical Care Medicine, American Board of Internal Medicine (2017)

Contact

  • Critical Care Medicine 300 Pasteur Dr Rm H2143 MC 5236 Stanford, CA 94305
    • Tel: (650) 723-6381
    Fax: (650) 725-5489

Research & Scholarship

Current Research and Scholarly Interests

Dr. Sweatt currently participates in the NIH/NHLBI K12 Career Development Program in ?Omics? of Lung Diseases. The focus of his ongoing research is to characterize novel immunophenotypes in pulmonary arterial hypertension (PAH), by employing informatics-based methods to delineate peripheral blood proteomic and transcriptomic signatures. A move beyond the traditional PAH classification scheme, this multimodal deep phenotyping approach may have the potential to provide new mechanistic insights, help explain heterogeneity in observed clinical outcomes, and someday identify patients who are more likely to benefit from targeted immunomodulatory therapy.

Dr. Sweatt has also recently been involved in multiple other pulmonary hypertension clinical research projects. In the first study of patients with serial acute vasodilator testing, he showed that changes in vasoreactivity status occur during PAH treatment. He demonstrated that the evolution of vasoreactivity status reflects alterations in static and pulsatile hemodynamic responses to inhaled nitric oxide, tracks with well-established clinical end-points, and could inform clinical decision-making. Furthermore, he has been a collaborator in pulmonary hypertension studies that have evaluated change in diffusion capacity of the lung for carbon monoxide as a prognostic biomarker, explored the relationship between insulin resistance and right ventricular function, investigated the peripheral tissue oxygenation response to vasodilator therapy, and evaluated the prognostic value of a novel right ventricular echocardiographic parameter.

Publications

All Publications

  • Genetic Admixture and Survival in Diverse Populations with Pulmonary Arterial Hypertension. American journal of respiratory and critical care medicine Karnes, J. H., Wiener, H. W., Schwantes-An, T. H., Natarajan, B., Sweatt, A. J., Chaturvedi, A., Arora, A., Batai, K., Nair, V., Steiner, H. E., Giles, J. B., Yu, J., Hosseini, M., Pauciulo, M. W., Lutz, K. A., Coleman, A. W., Feldman, J., Vanderpool, R., Tang, H., Garcia, J. G., Yuan, J. X., Kittles, R., de Jesus Perez, V., Zamanian, R. T., Rischard, F., Tiwari, H. K., Nichols, W. C., Benza, R. L., Desai, A. A. 2020

    Abstract

    Limited information is available on racial/ethnic differences in pulmonary arterial hypertension (PAH).Determine effects of race/ethnicity and ancestry on mortality and disease outcomes in diverse patients with PAH.Group 1 PAH patients were included from two national registries with genome-wide data and two local cohorts and further incorporated in a global meta-analysis. Hazard ratios (HRs) were calculated for transplant-free all-cause mortality in Hispanics with Non-Hispanic whites (NHWs) as the reference group. Odds ratios (ORs) for inpatient-specific mortality in PAH patients were also calculated for race/ethnic groups from an additional National Inpatient Sample (NIS) dataset, not included in the meta-analysis.After covariate adjustment, self-reported Hispanics (n=290) exhibited significantly reduced mortality versus NHWs (n=1970) after global meta-analysis (HR 0.60[0.41-0.87], p=0.008). Although not significant, increasing Native American genetic ancestry appeared to account for part of the observed mortality benefit (HR 0.48[0.23-1.01], p=0.053) in the two national registries. Finally, in the NIS, an inpatient mortality benefit was also observed for Hispanics (n=1524) versus NHWs (n=8829; OR 0.65[0.50-0.84], p=0.001). An inpatient mortality benefit was observed for Native Americans (n=185; OR 0.38[0.15-0.93], p=0.034).This study demonstrates a reproducible survival benefit for Hispanic Group 1 PAH patients in multiple clinical settings. Our results implicate contributions of genetic ancestry to differential survival in PAH.

    View details for DOI 10.1164/rccm.201907-1447OC

    View details for PubMedID 31916850

  • Mural Cell SDF1 Signaling is Associated with the Pathogenesis of Pulmonary Arterial Hypertension. American journal of respiratory cell and molecular biology Yuan, K., Liu, Y., Zhang, Y., Nathan, A., Tian, W., Yu, J., Sweatt, A. J., Condon, D., Chakraborty, A., Agarwal, S., Auer, N., Zhang, S., Wu, J. C., Zamanian, R. T., Nicolls, M. R., de Jesus Perez, V. A. 2020

    Abstract

    Pulmonary artery smooth muscle cells (PASMCs) and pericytes are NG2+ mural cells that provide structural support to pulmonary arteries and capillaries. In pulmonary arterial hypertension (PAH), both mural cell types contribute to PA muscularization but whether similar mechanisms are responsible for their behavior is unknown.RNA-Seq was used to compare the gene profile of pericytes and PASMCs from PAH and healthy lungs. NG2-Cre-ER mice were used to generate NG2-selective reporter mice (NG2tdT) for cell lineage identification and tamoxifen-inducible mice for NG2-selective SDF1 knockout (SDF1NG2-KO).Hierarchical clustering of RNA-seq data demonstrated that the genetic profile of PAH pericytes and PASMCs is highly similar. Cellular lineage staining studies on NG2tdT mice in chronic hypoxia showed that similar to PAH, tdT+ cells accumulate in muscularized microvessels and demonstrate significant upregulation of SDF1, a chemokine involved in chemotaxis and angiogenesis. Compared to controls, SDF1NG2-KO mice in chronic hypoxia had reduced muscularization and lower abundance of NG2+ cells around microvessels. SDF1 stimulation in healthy pericytes induced greater contractility and impaired their capacity to establish endothelial-pericyte communications. In contrast, SDF1 knockdown reduced PAH pericyte contractility and improved their capacity to associate with vascular tubes in co-culture.SDF1 is upregulated in NG2+ mural cells and is associated with PA muscularization. Targeting SDF1 could help prevent and/or reverse muscularization in PAH.

    View details for DOI 10.1165/rcmb.2019-0401OC

    View details for PubMedID 32084325

  • Discovery of Distinct Immune Phenotypes Using Machine Learning in Pulmonary Arterial Hypertension CIRCULATION RESEARCH Sweatt, A. J., Hedlin, H. K., Balasubramanian, V., Hsi, A., Blum, L. K., Robinson, W. H., Haddad, F., Hickey, P. M., Condliffe, R., Lawrie, A., Nicolls, M. R., Rabinovitch, M., Khatri, P., Zamanian, R. T. 2019; 124 (6): 904?19

    View details for DOI 10.1161/CIRCRESAHA.118.313911

    View details for Web of Science ID 000469341600015

  • Discovery of Distinct Immune Phenotypes Using Machine Learning in Pulmonary Arterial Hypertension. Circulation research Sweatt, A. J., Hedlin, H. K., Balasubramanian, V., Hsi, A., Blum, L. K., Robinson, W. H., Haddad, F., Hickey, P. M., Condliffe, R. A., Lawrie, A., Nicolls, M. R., Rabinovitch, M., Khatri, P., Zamanian, R. T. 2019

    Abstract

    Accumulating evidence implicates inflammation in pulmonary arterial hypertension (PAH) and therapies targeting immunity are under investigation, though it remains unknown if distinct immune phenotypes exist.Identify PAH immune phenotypes based on unsupervised analysis of blood proteomic profiles.In a prospective observational study of Group 1 PAH patients evaluated at Stanford University (discovery cohort, n=281) and University of Sheffield (validation cohort, n=104) between 2008-2014, we measured a circulating proteomic panel of 48 cytokines, chemokines, and factors using multiplex immunoassay. Unsupervised machine learning (consensus clustering) was applied in both cohorts independently to classify patients into proteomic immune clusters, without guidance from clinical features. To identify central proteins in each cluster, we performed partial correlation network analysis. Clinical characteristics and outcomes were subsequently compared across clusters. Four PAH clusters with distinct proteomic immune profiles were identified in the discovery cohort. Cluster 2 (n=109) had low cytokine levels similar to controls. Other clusters had unique sets of upregulated proteins central to immune networks- cluster 1 (n=58)(TRAIL, CCL5, CCL7, CCL4, MIF), cluster 3 (n=77)(IL-12, IL-17, IL-10, IL-7, VEGF), and cluster 4 (n=37)(IL-8, IL-4, PDGF-?, IL-6, CCL11). Demographics, PAH etiologies, comorbidities, and medications were similar across clusters. Non-invasive and hemodynamic surrogates of clinical risk identified cluster 1 as high-risk and cluster 3 as low-risk groups. Five-year transplant-free survival rates were unfavorable for cluster 1 (47.6%, CI 35.4-64.1%) and favorable for cluster 3 (82.4%, CI 72.0-94.3%)(across-cluster p<0.001). Findings were replicated in the validation cohort, where machine learning classified four immune clusters with comparable proteomic, clinical, and prognostic features.Blood cytokine profiles distinguish PAH immune phenotypes with differing clinical risk that are independent of World Health Organization Group 1 subtypes. These phenotypes could inform mechanistic studies of disease pathobiology and provide a framework to examine patient responses to emerging therapies targeting immunity.

    View details for PubMedID 30661465

  • Circulating plasmablasts are elevated and produce pathogenic anti-endothelial cell autoantibodies in idiopathic pulmonary arterial hypertension. European journal of immunology Blum, L. K., Cao, R. R., Sweatt, A. J., Bill, M., Lahey, L. J., Hsi, A. C., Lee, C. S., Kongpachith, S., Ju, C. H., Mao, R., Wong, H. H., Nicolls, M. R., Zamanian, R. T., Robinson, W. H. 2018

    Abstract

    Idiopathic pulmonary arterial hypertension (IPAH) is a devastating pulmonary vascular disease in which autoimmune and inflammatory phenomena are implicated. B cells and autoantibodies have been associated with IPAH and identified as potential therapeutic targets. However, the specific populations of B cells involved and their roles in disease pathogenesis are not clearly defined. We aimed to assess the levels of activated B cells (plasmablasts) in IPAH, and to characterize recombinant antibodies derived from these plasmablasts. Blood plasmablasts are elevated in IPAH, remain elevated over time, and produce IgA autoantibodies. Single-cell sequencing of plasmablasts in IPAH revealed repertoires of affinity-matured antibodies with small clonal expansions, consistent with an ongoing autoimmune response. Recombinant antibodies representative of these clonal lineages bound known autoantigen targets and displayed an unexpectedly high degree of polyreactivity. Representative IPAH plasmablast recombinant antibodies stimulated human umbilical vein endothelial cells to produce cytokines and overexpress the adhesion molecule ICAM-1. Together, our results demonstrate an ongoing adaptive autoimmune response involving IgA plasmablasts that produce anti-endothelial cell autoantibodies in IPAH. These antibodies stimulate endothelial cell production of cytokines and adhesion molecules, which may contribute to disease pathogenesis. These findings suggest a role for mucosally-driven autoimmunity and autoimmune injury in the pathogenesis of IPAH. This article is protected by copyright. All rights reserved.

    View details for PubMedID 29369345

  • Right Heart End-Systolic Remodeling Index Strongly Predicts Outcomes in Pulmonary Arterial Hypertension: Comparison With Validated Models. Circulation. Cardiovascular imaging Amsallem, M., Sweatt, A. J., Aymami, M. C., Kuznetsova, T., Selej, M., Lu, H., Mercier, O., Fadel, E., Schnittger, I., McConnell, M. V., Rabinovitch, M., Zamanian, R. T., Haddad, F. 2017; 10 (6)

    Abstract

    Right ventricular (RV) end-systolic dimensions provide information on both size and function. We investigated whether an internally scaled index of end-systolic dimension is incremental to well-validated prognostic scores in pulmonary arterial hypertension.From 2005 to 2014, 228 patients with pulmonary arterial hypertension were prospectively enrolled. RV end-systolic remodeling index (RVESRI) was defined by lateral length divided by septal height. The incremental values of RV free wall longitudinal strain and RVESRI to risk scores were determined. Mean age was 49±14 years, 78% were female, 33% had connective tissue disease, 52% were in New York Heart Association class ?III, and mean pulmonary vascular resistance was 11.2±6.4 WU. RVESRI and right atrial area were strongly connected to the other right heart metrics. Three zones of adaptation (adapted, maladapted, and severely maladapted) were identified based on the RVESRI to RV systolic pressure relationship. During a mean follow-up of 3.9±2.4 years, the primary end point of death, transplant, or admission for heart failure was reached in 88 patients. RVESRI was incremental to risk prediction scores in pulmonary arterial hypertension, including the Registry to Evaluate Early and Long-Term PAH Disease Management score, the Pulmonary Hypertension Connection equation, and the Mayo Clinic model. Using multivariable analysis, New York Heart Association class III/IV, RVESRI, and log NT-proBNP (N-Terminal Pro-B-Type Natriuretic Peptide) were retained (?(2), 62.2; P<0.0001). Changes in RVESRI at 1 year (n=203) were predictive of outcome; patients initiated on prostanoid therapy showed the greatest improvement in RVESRI. Among right heart metrics, RVESRI demonstrated the best test-retest characteristics.RVESRI is a simple reproducible prognostic marker in patients with pulmonary arterial hypertension.

    View details for DOI 10.1161/CIRCIMAGING.116.005771

    View details for PubMedID 28592589

  • Features and Outcomes of Methamphetamine Associated Pulmonary Arterial Hypertension. American journal of respiratory and critical care medicine Zamanian, R. T., Hedlin, H., Greuenwald, P., Wilson, D. M., Segal, J. I., Jorden, M., Kudelko, K., Liu, J., Hsi, A., Rupp, A., Sweatt, A. J., Tuder, R., Berry, G. J., Rabinovitch, M., Doyle, R. L., De Jesus Perez, V., Kawut, S. M. 2017

    Abstract

    While amphetamines are recognized as "likely" agents to cause drugs and toxins associated pulmonary arterial hypertension (PAH), (meth)amphetamine associated PAH (Meth-APAH) has not been well described.To prospectively characterize the clinical presentation, histopathology, and outcomes of Meth-APAH compared to those of idiopathic PAH (iPAH).We performed a prospective cohort study of Meth-APAH and iPAH patients presenting to the Stanford University Pulmonary Hypertension Program between 2003-2015. Clinical, pulmonary angiography, histopathology, and outcomes data were compared. We used data from the Healthcare Cost and Utilization Project to estimate the epidemiology of PAH in (meth)amphetamine abusers hospitalized in California.The study sample included 90 Meth-APAH and 97 iPAH patients. Meth-APAH patients were less likely to be female, but similar in age, body mass index, and six minute walk distance to iPAH patients. Meth-PAH patients reported more advanced heart failure symptoms, had significantly higher right atrial pressure (12.7±6.8 vs. 9.8±5.1 mmHg, p=0.001), and lower stroke volume index (22.2±7.1 vs 25.5±8.7 mL/m2, p=0.01). Event-free survival in Meth-APAH was 64.2%, 47.2%, and 25% at 2.5, 5, and 10 years respectively, representing more than double the risk of clinical worsening or death compared to iPAH (HR 2.04, 95% CI 1.28-3.25, p=0.003) independent of confounders. California data demonstrated a 2.6 fold increase in risk of PAH diagnosis in hospitalized (meth)amphetamine users.Meth-APAH is a severe and progressive form of PAH with poor outcomes. Future studies should focus on mechanisms of disease and potential therapeutic considerations.

    View details for PubMedID 28934596

  • Serial Vasoreactivity Reassessment is a Prognostic Tool in Pulmonary Arterial Hypertension American Journal of Respiratory and Critical Care Medicine Sweatt, A., Spiekerkoetter, E., Hsi, A., Sung, Y., De Jesus Perez, V., Kudelko, K., Zamanian, R. 2016; 193: A6464
  • Interventional pulmonologist perspective: treatment of malignant pleural effusion. Current treatment options in oncology Sweatt, A. J., Sung, A. 2014; 15 (4): 625-643

    Abstract

    The management of known malignant pleural effusions focuses around the initial thoracentesis and subsequent objective and subjective findings. A completely reexpanded lung after fluid removal and with symptomatic improvement predicts successful pleurodesis. Pleurodesis method depends on center expertise as well as patient preference. Medical thoracoscopy does not require the operating room setting and is performed on the spontaneously breathing patient with similar success rate to surgical thoracoscopy in the appropriately selected patients. However, it is not widely available. Talc insufflation is preferred for even distribution of sprayed particles to pleural surfaces. Most often, patients can be discharged home within 24 to 48 hours after continuous chest tube suction. Indwelling pleural catheter has become popular given the ease of insertion and patient centered home drainage. Coordinated care with good patient and family education and support is paramount to maximizing the beneficial potential of the catheter. Complications are minimal, and catheters are easily removed if patients can no longer benefit from drainage, or if pleurodesis has occurred. In the setting of trapped lung as a result of visceral pleura encasement from tumor, indwelling catheter can still be useful if the patient improves with thoracentesis. However, if no subjective improvement is seen after thoracentesis for trapped lung, then no procedure is recommended and other modes of palliation should be sought.

    View details for DOI 10.1007/s11864-014-0312-6

    View details for PubMedID 25240411

  • Evolving epidemiology and definitions of the acute respiratory distress syndrome and early acute lung injury. Clinics in chest medicine Sweatt, A. J., Levitt, J. E. 2014; 35 (4): 609-624

    Abstract

    This article reviews the evolving definitions and epidemiology of the acute respiratory distress syndrome (ARDS) and highlights current efforts to improve identification of high-risk patients, thus to target prevention and early treatment before progression to ARDS. This information will be important for general practitioners and intensivists interested in improving the care of patients at risk for ARDS, and clinical researchers interested in designing clinical trials targeting the prevention and early treatment of acute lung injury.

    View details for DOI 10.1016/j.ccm.2014.08.002

    View details for PubMedID 25453413

  • Quantifying the Influence of Wedge Pressure, Age, and Heart Rate on the Systolic Thresholds for Detection of Pulmonary Hypertension. Journal of the American Heart Association Amsallem, M., Tedford, R. J., Denault, A., Sweatt, A. J., Guihaire, J., Hedman, K., Peighambari, S., Kim, J. B., Li, X., Miller, R. J., Mercier, O., Fadel, E., Zamanian, R., Haddad, F. 2020: e016265

    Abstract

    Background The strong linear relation between mean (MPAP) and systolic (SPAP) pulmonary arterial pressure (eg, SPAP=1.62*MPAP) has been mainly reported in precapillary pulmonary hypertension. This study sought to quantify the influence of pulmonary arterial wedge pressure (PAWP), heart rate, and age on the MPAP-SPAP relation. Methods and Results An allometric equation relating invasive MPAP and SPAP was developed in 1135 patients with pulmonary arterial hypertension, advanced lung disease, chronic thromboembolic pulmonary hypertension, or left heart failure. The equation was validated in 60885 patients from the United Network for Organ Sharing (UNOS) database referred for heart and/or lung transplant. The MPAP/SPAP longitudinal stability was assessed in pulmonary arterial hypertension with repeated right heart catheterization. The equation obtained was SPAP=1.39*MPAP*PAWP-0.07*(60/heart rate)0.12*age0.08 (P<0.001). It was validated in the UNOS cohort (R2=0.93, P<0.001), regardless of the type of organ(s) patients were listed for (mean bias [-1.96SD; 1.96SD] was 0.94 [-8.00; 9.88] for heart, 1.34 [-7.81; 10.49] for lung and 0.25 [-16.74; 17.24] mmHg for heart-lung recipients). Thresholds of SPAP for MPAP=25 and 20mmHg were lower in patients with higher PAWP (37.2 and 29.8mmHg) than in those with pulmonary arterial hypertension (40.1 and 32.0mmHg). In 186 patients with pulmonary arterial hypertension, the predicted MPAP/SPAP was stable over time (0.63±0.03 at baseline and follow-up catheterization, P=0.43). Conclusions This study quantifies the impact of PAWP, and to a lesser extent heart rate and age, on the MPAP-SPAP relation, supporting lower SPAP thresholds for pulmonary hypertension diagnosis in patients with higher PAWP for echocardiography-based epidemiological studies.

    View details for DOI 10.1161/JAHA.119.016265

    View details for PubMedID 32419583

  • PROGNOSTIC VALUE OF THE RELATIVE PULMONARY PRESSURE RATIO AND ITS TRAJECTORY IN PATIENTS WITH PULMONARY ARTERIAL HYPERTENSION Bagherzadeh, S. P., Amsallem, M., Denault, A., Sweatt, A., Kudelko, K., Sung, Y., Haddad, F., Zamanian, R. ELSEVIER SCIENCE INC. 2020: 2096

    View details for Web of Science ID 000522979102081

  • Survival implications of pulmonary hypertension in end-stage COPD Kapasi, A., Halloran, K., Hirji, A., Lien, D., Mooney, J., Raj, R., Sweatt, A., Weinkauf, J., Zamanian, R. EUROPEAN RESPIRATORY SOC JOURNALS LTD. 2019

    View details for DOI 10.1183/13993003.congress-2019.PA1426

    View details for Web of Science ID 000507372401438

  • Elevated pulmonary vascular resistance is associated with increased risk of death in IPF Kapasi, A., Halloran, K., Hirji, A., Lien, D., Mooney, J., Raj, R., Sweatt, A., Weinkauf, J., Zamanian, R. EUROPEAN RESPIRATORY SOC JOURNALS LTD. 2019

    View details for DOI 10.1183/13993003.congress-2019.PA1428

    View details for Web of Science ID 000507372401440

  • Identification of Biomarkers Predictive of Pulmonary Arterial Hypertension in Systemic Sclerosis Kolstad, K. D., Holmes, T., Rosenberg-Hasson, Y., Sweatt, A., Zamanian, R. T., Li, S., Steen, V. D., Utz, P. J., Chung, L. WILEY. 2017

    View details for Web of Science ID 000411824101041

  • Kaposiform Lymphangiomatosis: An Unforeseen Cause of Spontaneous Hemothorax and Episodic Hemoptysis American Journal of Respiratory and Critical Care Medicine Sweatt, A., Regalia, K. 2016; 193: A3346
  • Comprehensive Characterization of Insulin Resistance and its Association with Ventricular Function in Pulmonary Hypertension American Journal of Respiratory and Critical Care Medicine Wells, R., Sweatt, A., Cuttica, M., Dash, R., Abbasi, F., Van de Veerdonk, M., Preston, I., Hemnes, A., Gomberg-Maitland, M., Zamanian, R. 2016; 193: A6462
  • Using Near-Infrared Spectroscopy to Characterize the Effects of Inhaled Nitric Oxide on Skeletal Muscle Oxygen Saturation in Adults with Pulmonary Arterial Hypertension American Journal of Respiratory and Critical Care Medicine Brian, S., Kholdani, C., Sweatt, A., Hedlin, H., Hsi, A., Spiekerkoetter, E., Zamanian, R. 2016; 193: A3961
  • DLCO Change in Pulmonary Arterial Hypertension Reflects Vascular Function as Determined by Longitudinal Response to Inhaled Nitric Oxide American Journal of Respiratory and Critical Care Medicine Sweatt, A., Spiekerkoetter, E., Hsi, A., Sung, Y., Kudelko, K., De Jesus Perez, V., Zamanian, R. 2016; 193: A7320
  • Right Heart End-Systolic Remodeling Index Strongly Predicts Outcomes in Pulmonary Arterial Hypertension, Insights From a Network Analysis Circulation Amsallem, M., Sweatt, A., Aymami, M., Kuznetsova, T., Mercier, O., Fadel, E., McConnell, M., Rabinovitch, M., Zamanian, R., Haddad, F. 2016; 134: A18038
  • Evaluation of Changes in Static and Pulsatile Hemodynamic Indices Across Longitudinal Vasoreactivity Tests in Pulmonary Arterial Hypertension American Journal of Respiratory and Critical Care Medicine Sweatt, A., Spiekerkoetter, E., Hsi, A., Sung, Y., Kudelko, K., De Jesus Perez, V., Zamanian, R. 2016; 193: A7319
  • Spastic Esophageal Motility Disorders in Post-Lung Transplant Patients 59th Annual Aspen Lung Conference Regalia, K., Sweatt, A., Chhatwani, L., Mooney, J., Dhillon, G., Nguyen, L. 2016
  • High Prevalence of Gastroparesis in Post-Lung Transplant Patients and Pyloric Botox for the Prevention of Bronchiolitis Obliterans Syndrome American Journal of Gastroenterology Regalia, K., Sweatt, A., Wang, L., Nguyen, L. 2015; 110: S1028
  • Interventional Pulmonologist Perspective: Treatment of Malignant Pleural Effusion CURRENT TREATMENT OPTIONS IN ONCOLOGY Sweatt, A. J., Sung, A. 2014; 15 (4): 625-643

    Abstract

    The management of known malignant pleural effusions focuses around the initial thoracentesis and subsequent objective and subjective findings. A completely reexpanded lung after fluid removal and with symptomatic improvement predicts successful pleurodesis. Pleurodesis method depends on center expertise as well as patient preference. Medical thoracoscopy does not require the operating room setting and is performed on the spontaneously breathing patient with similar success rate to surgical thoracoscopy in the appropriately selected patients. However, it is not widely available. Talc insufflation is preferred for even distribution of sprayed particles to pleural surfaces. Most often, patients can be discharged home within 24 to 48 hours after continuous chest tube suction. Indwelling pleural catheter has become popular given the ease of insertion and patient centered home drainage. Coordinated care with good patient and family education and support is paramount to maximizing the beneficial potential of the catheter. Complications are minimal, and catheters are easily removed if patients can no longer benefit from drainage, or if pleurodesis has occurred. In the setting of trapped lung as a result of visceral pleura encasement from tumor, indwelling catheter can still be useful if the patient improves with thoracentesis. However, if no subjective improvement is seen after thoracentesis for trapped lung, then no procedure is recommended and other modes of palliation should be sought.

    View details for DOI 10.1007/s11864-014-0312-6

    View details for Web of Science ID 000344532800009

  • Evolving Epidemiology and Definitions of the Acute Respiratory Distress Syndrome and Early Acute Lung Injury CLINICS IN CHEST MEDICINE Sweatt, A. J., Levitt, J. E. 2014; 35 (4): 609-?

    Abstract

    This article reviews the evolving definitions and epidemiology of the acute respiratory distress syndrome (ARDS) and highlights current efforts to improve identification of high-risk patients, thus to target prevention and early treatment before progression to ARDS. This information will be important for general practitioners and intensivists interested in improving the care of patients at risk for ARDS, and clinical researchers interested in designing clinical trials targeting the prevention and early treatment of acute lung injury.

    View details for DOI 10.1016/j.ccm.2014.08.002

    View details for Web of Science ID 000346214200002

  • A Microarray Biosensor for Multiplexed Detection of Microbes Using Grating-Coupled Surface Plasmon Resonance Imaging ENVIRONMENTAL SCIENCE & TECHNOLOGY Marusov, G., Sweatt, A., Pietrosimone, K., Benson, D., Geary, S. J., Silbart, L. K., Challa, S., Lagoy, J., Lawrence, D. A., Lynes, M. A. 2012; 46 (1): 348-359

    Abstract

    Grating-coupled surface plasmon resonance imaging (GCSPRI) utilizes an optical diffraction grating embossed on a gold-coated sensor chip to couple collimated incident light into surface plasmons. The angle at which this coupling occurs is sensitive to the capture of analyte at the chip surface. This approach permits the use of disposable biosensor chips that can be mass-produced at low cost and spotted in microarray format to greatly increase multiplexing capabilities. The current GCSPRI instrument has the capacity to simultaneously measure binding at over 1000 unique, discrete regions of interest (ROIs) by utilizing a compact microarray of antibodies or other specific capture molecules immobilized on the sensor chip. In this report, we describe the use of GCSPRI to directly detect multiple analytes over a large dynamic range, including soluble protein toxins, bacterial cells, and viruses, in near real-time. GCSPRI was used to detect a variety of agents that would be useful for diagnostic and environmental sensing purposes, including macromolecular antigens, a nontoxic form of Pseudomonas aeruginosa exotoxin A (ntPE), Bacillus globigii, Mycoplasma hyopneumoniae, Listeria monocytogenes, Escherichia coli, and M13 bacteriophage. These studies indicate that GCSPRI can be used to simultaneously assess the presence of toxins and pathogens, as well as quantify specific antibodies to environmental agents, in a rapid, label-free, and highly multiplexed assay requiring nanoliter amounts of capture reagents.

    View details for DOI 10.1021/es201239f

    View details for Web of Science ID 000298762900047

    View details for PubMedID 22029256

  • The effect of plasma transfusion on oxygenation in critically ill patients with chronic liver disease American Journal of Respiratory and Critical Care Medicine Sweatt, A., Biggins, S., Rosen, H., Clark, B., Smart, A., Moss, M., Benson, A. 2012; 185: A1151
  • When a Pain in the Neck May Have Helped: Painless Subacute Granulomatous Thyroiditis Causing Fever of Unknown Origin American College of Physicians National Meeting Sweatt, A., Mascolo, M. 2012
  • A Case of Multi-Organ Langerhans Cell Histiocytosis Responsive to Tobacco Cessation American Journal of Respiratory and Critical Care Medicine Sweatt, A., Rizeq, M., Sandberg, M. 2012; 185: A5429
  • A dosing formula for INR-targeted plasma transfusion in bleeding patients with chronic liver disease American Journal of Respiratory and Critical Care Medicine Sweatt, A., Moss, M., Tripputi, M., Benson, A. 2011; 183: A5828

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