Pulmonary Circulation receives Impact Factor of 3.017

We are delighted to announce that Pulmonary Circulation has received a new Impact Factor of 3.017. This is an excellent result and we would like to congratulate Chief Editors, Jason Yuan, Nick Morrell, and Anna Hemnes for this achievement. Congratulations also, to all editors, deputy editors, associate editors, scientific advisers, and editorial board members who have contributed to this achievement.

Impact Factors are awarded to quality journals and are a measure of the frequency that an average article in a journal has been cited in a given year.  

This score is Pulmonary Circulation's highest impact factor so far, up from 2.075 in 2020. Pulmonary Circulation is now ranked higher, at 73/142 in the “Cardiac & Cardiovascular Systems” category, and 37/64 in “Respiratory System”, compared with 78/138 and 42/64 respectively last year.

This achievement confirms Pulmonary Circulation as a leading journal featuring the high-quality material on the pulmonary circulation and pulmonary vascular disease.  

Anna Hemnes appointed new Editor in Chief of Pulmonary Circulation journal

Posted 06 July 2021

The PVRI is delighted to welcome Anna Hemnes to the Pulmonary Circulation journal editorial board, and joins Jason Yuan as one of our two Editors in Chief.

“I have been an active member of the PVRI and an Associate Editor of Pulmonary Circulation for several years. I am excited to work with Dr Yuan in my new role as Co-Editor in Chief to advance the journal's mission and impact.” - Dr Hemnes

 Read more…Link to full text

Pulmonary Circulation receives Impact Factor of 2.205

Posted 30 June 2020

We are delighted to announce that Pulmonary Circulation has received a new Impact Factor of 2.205. This is a tremendous result and a tribute to our Chief Editors, Jason Yuan and Nick Morrell, and editorial team. Congratulations to all editors, deputy editors, associate editors, scientific advisers, and editorial board members for this achievement. 

Impact Factors are awarded to quality journals and are a measure of the frequency that an average article in a journal has been cited in a given year.  

The Impact Factor’s increase over the 2018 score places Pulmonary Circulation 78 out of 138 journals in the category Cardiac & Cardiovascular Systems and 42 out of 64 in the Respiratory System category. 

This achievement confirms Pulmonary Circulation as a leading journal featuring the high-quality material on the pulmonary circulation and pulmonary vascular disease.  

Congratulations to the entire Pulmonary Circulation team and a big thank you to all its contributors. 

Pulmonary Circulation Editors-in-Chief Jason Yuan and Nick Morrell commented:

'We are very glad about the upward trajectory of the journal's Impact Factor and its scientific and academic impact. Our editorial team will continue to work hard to make Pulmonary Circulation the venue for our colleagues and readers to publish their scientific discoveries and clinical advances in the field of pulmonary circulation, lung vascular disease and right heart dysfunction.'

PC journal supports statement from the Wellcome Trust

In partnership with our publisher SAGE, the PVRI and Pulmonary Circulation journal support the statement from the Wellcome Trust which calls on researchers, journals and funders to ensure that research findings and data relevant to the COVID-19 outbreak are shared rapidly and openly to inform the public health response and help save lives.

In support of the principles set out in the statement we would like to remind authors considering submitting their article to Pulmonary Circulation that:

  • All articles accepted in Pulmonary Circulation are open access and free to read as soon as they are published.
  • Production of articles focused on COVID-19 are fast-tracked and deposited in Pubmed Central (PMC) for indexing.
  • All papers published on COVID-19 are promoted via the PVRI website and also collated on the SAGE Journals microsite for COVID-19 research.
  • We encourage authors of COVID-19 research and findings to share their findings with the WHO as early as possible.
  • Authors may post versions of their papers on institutional sites or on preprint servers before they are accepted, such as medRxiv or bioRxiv.

Pulmonary Circulation 2020 update

In partnership with our publisher SAGE, the PVRI and Pulmonary Circulation journal support the statement from the Wellcome Trust which calls on researchers, journals and funders to ensure that research findings and data relevant to the COVID-19 outbreak are shared rapidly and openly to inform the public health response and help save lives.

In support of the principles set out in the statement we would like to remind authors considering submitting their article to Pulmonary Circulation that:

  • All articles accepted in Pulmonary Circulation are open access and free to read as soon as they are published.
  • Production of articles focused on COVID-19 are fast-tracked and deposited in Pubmed Central (PMC) for indexing.
  • All papers published on COVID-19 are promoted via the PVRI website and also collated on the SAGE Journals microsite for COVID-19 research.
  • We encourage authors of COVID-19 research and findings to share their findings with the WHO as early as possible.
  • Authors may post versions of their papers on institutional sites or on preprint servers before they are accepted, such as medRxiv or bioRxiv.

 

We would like to reassure all our Pulmonary Circulation authors that, in light of the COVID-19 pandemic, SAGE publishing has: 

  • Removed the subscription gateway to articles that we believe will be of value to researchers and practitioners at this time. 
  • Signed and committed to the Wellcome coordinated statement on Sharing research data and findings relevant to the novel coronavirus (COVID-19) outbreak 
  • Created and will maintain a microsite that highlights both social and behavioural sciences and medical sciences research on COVID-19 and more broadly on managing pandemics. 
  • Collated a collection of blog posts on impacts for researchers, instructors, and the public in general on Social Science Space. 
  • Decided to prioritise publishing open access research relevant to the current pandemic and move it through production as fast as they can. 
  • Planned to further promote our free online SAGE Campus ‘How to Get Published’ course to support the global author community, many of whom are preparing articles for publication in remote and challenging circumstances.  

 If you have any queries, please email: admin@pvrinstitute.org.

Pulmonary Circulation 2019 update

2019 has been another great year for Pulmonary Circulation. We continue to see increasing numbers of articles submitted and we now receive many good quality papers that we have been able to raise the bar for acceptance and we are pleased to say that it is becoming more difficult to get published in Pulmonary Circulation!

As can be seen from the list of most downloaded articles below, our most popular articles tend to be clinical rather than basic science, and comprehensive review articles are also frequently downloaded. A highlight, amongst the review articles we have published recently, was the report of the PVRI Task Force on lung vascular imaging. While we are pleased to have many high-quality clinical manuscripts submitted to the journal, we would encourage our audience, especially the Editorial Board members and the Pulmonary Vascular Research Institute members, to submit and publish more basic and translational research manuscripts in Pulmonary Circulation.

As at the time of writing this report (end October 2019) we have published 100 articles, including high-quality reviews, original research articles, and case reports.

Since the first volume in 2011, we have now published 845 articles in Pulmonary Circulation

  •           Editorials – (53) 6%
  •           Reviews – (148) 18%
  •           Original Research Articles – (443) 52%
  •           Guidelines & Other – (103) 12%
  •           Case Reports – (98) 12%

 We receive most submissions from the USA, followed by China, the UK, Japan, and Germany, though we receive articles from all around the world. Please consider us when deciding where to publish your article – we would be delighted to receive it.

Strong Impact Factor

Our impact factor remains strong for a journal at our stage at 2.075. The Impact Factor is a measure of the frequency that an average article in a journal has been cited in a given year. To have an impact factor consistently over 2.0 is an excellent indicator for a young journal when we have been increasing the number of articles published.

Editorial Team

Our Editors in Chief Jason Yuan (University of California, San Diego) and Nick Morrell (University of Cambridge) work alongside Deputy Editors Kurt Stenmark (University of Colorado) and Irene Lang (Medical University of Vienna).  In addition, our Associate Editors who also handle manuscripts are Anna Hemnes (Vanderbilt University), Patricia Thistlethwaite (University of California, San Diego).

Publishing Team

Pulmonary Circulation is published in collaboration with SAGE Publishing, who handle the production and online hosting of published articles and carry out promotional activities, and Editorial Office Ltd, who support the Editors in managing peer review and liaising with authors and reviewers. Michael Brown, Business Manager, oversees the business elements of the journal, liaises with the publisher and, together with the Editors, develops the future commercial strategy for the journal.

Promotional Activities

Pulmonary Circulation’s Editors and SAGE Publishing promoted the journal at various international conferences, including the PVRI Annual World Congress in Barcelona, the PVRI Drug Discovery and Development Symposium, the American Thoracic Society (ATS) International Conference, and the American Heart Association Scientific Sessions. In addition, we have increased promotional email campaigns and continue to grow our mailing lists.

Pulmonary Circulation Summer 2018 Update

PC Featured Articles

Review Article

Non-invasive imaging of global and regional cardiac function in pulmonary hypertension

Tim Crowe, Geeshath Jayasekera, Andrew J. Peacock

First published December 28, 2017, Volume: 8, Issue: 1

Stable URL: http://journals.sagepub.com/doi/full/10.1177/2045893217742000

Abstract:

Non-invasive tests of RV function to determine prognosis and response to treatment in patients with PH is essential. Although the right ventricle is the focus of attention, it is clear that cardiac interaction can cause left ventricular dysfunction, thus biventricular assessment is paramount. There is also focus on the atrial chambers in their contribution to cardiac function in PH. Furthermore, there is evidence of regional dysfunction of the two ventricles in PH, so it would be useful to understand both global and regional components of dysfunction. In order to understand global and regional cardiac function in PH, the most obvious non-invasive imaging techniques are echocardiography and cardiac magnetic resonance imaging (CMRI). Both techniques have their advantages and disadvantages. Echocardiography is widely available, relatively inexpensive, provides information regarding RV function, and can be used to estimate RV pressures. CMRI, although expensive and less accessible, is the gold standard of biventricular functional measurements. The advent of 3D echocardiography and techniques including strain analysis and stress echocardiography have improved the usefulness of echocardiography while new CMRI technology allows the measurement of strain and measuring cardiac function during stress including exercise. In this review, we have analyzed the advantages and disadvantages of the two techniques and discuss pre-existing and novel forms of analysis where echocardiography and CMRI can be used to examine atrial, ventricular, and interventricular function in patients with PH at rest and under stress.

Keywords: pulmonary arterial hypertension, pulmonary hypertension, magnetic resonance imaging, echocardiography, right ventricle function and dysfunction

 Read more…Link to full text

Original Research Article

Myosin light chain kinase (MYLK) coding polymorphisms modulate human lung endothelial cell barrier responses via altered tyrosine phosphorylation, spatial localization, and lamellipodial protrusions

Ting Wang, Mary E. Brown, Gabriel T. Kelly, Sara M. Camp, Joseph B. Mascarenhas, Xiaoguang Sun, Steven M. Dudek, Joe G.N. Garcia

First published March 9, 2018, Volume: 8, Issue: 1

Stable URL: http://journals.sagepub.com/doi/full/10.1177/2045894018764171

Abstract:

Sphingosine 1-phosphate (S1P) is a potent bioactive endogenous lipid that signals a rearrangement of the actin cytoskeleton via the regulation of non-muscle myosin light chain kinase isoform (nmMLCK). S1P induces critical nmMLCK Y464 and Y471 phosphorylation resulting in translocation of nmMLCK to the periphery where spatially-directed increases in myosin light chain (MLC) phosphorylation and tension result in lamellipodia protrusion, increased cell-cell adhesion, and enhanced vascular barrier integrity. MYLK, the gene encoding nmMLCK, is a known candidate gene in lung inflammatory diseases, with coding genetic variants (Pro21His, Ser147Pro, Val261Ala) that confer risk for inflammatory lung injury and influence disease severity. The functional mechanisms by which these MYLK coding single nucleotide polymorphisms (SNPs) affect biologic processes to increase disease risk and severity remain elusive. In the current study, we utilized quantifiable cell immunofluorescence assays to determine the influence of MYLK coding SNPs on S1P-mediated nmMLCK phosphorylation and translocation to the human lung endothelial cell (EC) periphery . These disease-associated MYLK variants result in reduced levels of S1P-induced Y464 phosphorylation, a key site for nmMLCK enzymatic regulation and activation. Reduced Y464 phosphorylation resulted in attenuated nmMLCK protein translocation to the cell periphery. We further conducted EC kymographic assays which confirmed that lamellipodial protrusion in response to S1P challenge was retarded by expression of a MYLK transgene harboring the three MYLK coding SNPs. These data suggest that ARDS/severe asthma-associated MYLK SNPs functionally influence vascular barrier-regulatory cytoskeletal responses via direct alterations in the levels of nmMLCK tyrosine phosphorylation, spatial localization, and lamellipodial protrusions.

Keywords: sphingosine 1-phosphate, S1P, nmMLCK, SNP

Read more…Link to full text

Original Research Article

Pulmonary arterial hypertension and atrial arrhythmias: incidence, risk factors, and clinical impact

Valentina Mercurio, Grace Peloquin, Khalil I. Bourji, Nermin Diab, Takahiro Sato, Blessing Enobun, Traci Housten-Harris, Rachel Damico, Todd M. Kolb, Stephen C. Mathai, Ryan J. Tedford, Carlo G. Tocchetti, Paul M. Hassoun
First published April 17, 2018, Volume: 8, Issue: 1

Stable URL: http://journals.sagepub.com/doi/full/10.1177/2045894018769874

Abstract:

Atrial arrhythmia (AA) occurrence in pulmonary arterial hypertension (PAH) may determine clinical deterioration and affect prognosis. In this study we assessed AA incidence in idiopathic (IPAH) and systemic sclerosis related PAH (SSc-PAH) and evaluated risk factors, management, and impact on mortality. We collected baseline data from consecutive IPAH or SSc-PAH patients prospectively enrolled in the Johns Hopkins Pulmonary Hypertension Registry between January 2000 and July 2016. During follow-up AA onset, treatment, and outcome were recorded. Among 317 patients (201 SSc-PAH, 116 IPAH), 42 developed AA (19 atrial fibrillation, 10 flutter-fibrillation, 9 atrial flutter, and 4 atrial ectopic tachycardia) with a 13.2% cumulative incidence. Most events were associated with hospitalization (90.5%). Electrical or pharmacological cardioversion was attempted in most cases. Patients with AA had higher right atrial pressure, pulmonary wedge pressure (P < 0.005), NT-proBNP (P < 0.05), and thyroid disease prevalence (P < 0.005). Higher mortality was observed in patients with AA, though not statistically significant (LogRank P = 0.323). Similar long-term mortality between IPAH with AA and SSc-PAH without AA was observed (LogRank P = 0.098). SSc-PAH with AA had the worst prognosis. In PAH patients AA occurrence is a matter of significant concern. Therapeutic strategies aimed at restoring sinus rhythm may represent an important goal.

Keywords: atrial arrhythmias, pulmonary arterial hypertension, systemic sclerosis

Read more…Link to full text

Original Research Article

Clinical trial protocol for TRANSFORM-UK: A therapeutic open-label study of tocilizumab in the treatment of pulmonary arterial hypertension

Jules Hernández-Sánchez, Louise Harlow, Colin Church, Sean Gaine, Emily Knightbridge, Kate Bunclark, Dee Gor, Alun Bedding, Nicholas Morrell, Paul Corris, Mark Toshner

First published December 3, 2017, Volume: 8, Issue: 1

Stable URL: http://journals.sagepub.com/doi/full/10.1177/2045893217735820

Abstract:

Our aim is to assess the safety and potential efficacy of a novel treatment paradigm in pulmonary arterial hypertension (PAH), immunomodulation by blocking interleukin-6 (IL6) signaling with the IL6 receptor antagonist, tocilizumab. Inflammation and autoimmunity are established as important in PAH pathophysiology. One of the most robust observations across multiple cohorts in PAH has been an increase in IL6, both in the lung and systemically. Tocilizumab is an IL-6 receptor antagonist established as safe and effective, primarily in rheumatoid arthritis, and has shown promise in scleroderma. In case reports where the underlying cause of PAH is an inflammatory process such as systemic lupus erythematosus, mixed connective tissue disease (MCTD), and Castleman’s disease, there have been case reports of regression of PAH with tocilizumab. TRANSFORM-UK is an open-label study of intravenous (IV) tocilizumab in patients with group 1 PAH. The co-primary outcome measures will be safety and the change in resting pulmonary vascular resistance (PVR). Clinically relevant secondary outcome measurements include 6-minute walk distance, WHO functional class, quality of life score, and N-terminal pro-brain natriuretic peptide (NT-proBNP). If the data support a potentially useful therapeutic effect with an acceptable risk profile, the study will be used to power a Phase III study to properly address efficacy.

Keywords: clinical studies, immunotherapy, pulmonary hypertension

 Read more…Link to full text

Back to top



Researcher Spotlight

Dustin-Fraidenburg_hs.jpg

A conversation with Dustin R. Fraidenburg, M.D., Chief Fellow in Pulmonary, Critical Care Medicine at the University of Illinois at Chicago.

Dr. Dustin Fraidenburg earned his M.D. at Wayne State University in Detroit, Michigan and did his residency in Internal Medicine at the University of Illinois at Chicago. He is in his final year of fellowship training in Pulmonary, Critical Care medicine at the University of Illinois at Chicago, where he has served as Chief Fellow since 2015. Dr. Fraidenburg serves on the Pulmonary Circulation Writing and Consulting Committee.

PC: What is your area of research interest and what projects are you currently involved in?

DF: My research focuses primarily on studying the cellular and molecular mechanisms of hypoxic pulmonary vasoconstriction and my current project is concentrated on how acute lung inflammation and injury affects hypoxic pulmonary vasoconstriction. In particular, how upregulation of the NFAT transcription factor during acute lung inflammation can affect pulmonary artery vasoreactivity through its effects on functional and transcriptional regulation of calcium channels in pulmonary artery smooth muscle cells. My project takes a unique approach to tackling the ventilation-perfusion mismatch which leads to profound hypoxemia in patients with acute respiratory distress syndrome. I believe a better understanding of mechanisms that impair hypoxic pulmonary vasoconstriction, a product of evolution meant to protect the diseased lung, could very well lead to distinctive therapeutic targets in ARDS among many other lung diseases.

PC: Why did you specialize in PVD?

DF: Pulmonary vascular disease was and still is a rapidly expanding area of research in respiratory diseases and there have been such great strides recently in both basic science, translational, and clinical research that I knew there was abundant opportunity to do research to discover the disease mechanisms involved, help patients, and develop a solid academic career. The people that have been on my side throughout my training are definitely the reason that I have both enjoyed and prospered in research on pulmonary vascular disease. I have had the pleasure of working with some amazing mentors as well as colleagues that shared my desire to produce really great research.

PC: What is the most exciting new topic in PVD research right now?

DF: There are so many researchers doing great work in the field. One of the really interesting things out there to read about right now is the lung-on-a-chip coming out of Harvard. New technologies and innovative techniques are really going to revolutionize both drug development as well as our understanding of many disease processes.

PC: What’s “lung-on-a-chip”?

DF: The lung-on-a-chip is a really unique three dimensional model of the human lung. It is a small chip containing airway epithelial cells on one side of a membrane that are exposed to oxygenated gas and pulmonary vascular cells on the opposite side of the membrane with culture media or solutions mimicking blood that flow across it. Additionally, there is a vacuum to create stretching forces on each side to mimic the changes of respiration. This allows experimental modeling of various injuries or therapies which will have wide ranging implications in basic science and translational research. (For more information, see the Wyss Institute at Harvard's website.)

PC: Where do you hope to see the field of PVD research in five years?

DF: In 5 to 10 years from now I very much expect the divisions between basic science and clinical research to become further blurred. I fully expect that the continued challenges researchers are faced with (for example, securing research funding and the distribution of public dollars to science) will lead to a revolution in how research is now divided as a necessary step to improve our effectiveness. Additionally, with mobile technology and social media making the world ever smaller, collaboration will be essential to our efficiency as researchers. Removing the redundancy from the system and illuminating the strengths of each group will help everyone to focus on our ultimate goal, the eradication of human disease. For research on pulmonary vascular disease in particular, I feel that a new generation of therapeutic agents for pulmonary hypertension will become available. It will be interesting to see therapies that shift from the pulmonary vasodilators, which will remain mainstays in treatment, to focus on mechanisms of maladaptive right ventricular remodeling or reversal of vascular remodeling with unique cellular and genetic targets.

Back to top


2016, No. 1, First Quarter Edition

PH in the News

Study Reports an Association Between Pulmonary Hypertension and Non-Dialysis Dependent Chronic Kidney Disease

Mariella Vélez Martínez
PVRI Committee for Young Clinicians & Scientists

Chronic kidney disease (CKD) carries an increased risk for incurring cardiovascular disease morbidity and mortality. Traditional factors influencing an elevated risk in CKD patients include hypertension, diabetes, and hypercholesterolemia. Pulmonary hypertension (PH) is also an important contributor to cardiovascular disease morbidity, and has not yet been fully studied in the non-dialysis dependent CKD population. However, authors from a recently published article in theJournal of the American Society of Nephrology concluded that PH is an independent predictor of cardiovascular and all-cause mortality in non-dialysis dependent CKD. (Navaneethan S, et al. Journal of the American Society of Nephrology, published online before print September 18, 2015, doi: 10.1681/ASN.2014111111).

This study used the data from the Chronic Renal Insufficiency Cohort (CRIC) Study to evaluate the prevalence, risk factors and clinical outcomes of pulmonary hypertension, as measured by echocardiography (pulmonary artery systolic pressure [PASP] > 35 mmHg and/or tricuspid regurgitant velocity [TRV] >2.5 m/s), in this patient population. The CRIC Study was established in 2003 and enrolled approximately 3000 patients, with a broad spectrum of renal disease severity, at seven sites and followed participants for up to 5 years.

The investigators found a prevalence of PH of 21% in this population. They also identified the following risk factors associated with PH in this patient population: older age, non-Hispanic blacks, a lower estimated glomerular filtration rate (eGFR), and comorbid conditions, such as obesity and diabetes. In a cross-sectional multivariable model, those patients who were older, with anemia, lower left ventricular ejection fraction, and left ventricular hypertrophy had a higher chance of having PH as measured at the year 1 CRIC study visit.

After a median follow up of approximately 4 years and adjusting for confounders, the investigators found that the presence of PH was associated with an elevated risk for all-cause mortality and cardiovascular outcomes. In addition, higher ranges of TRV and PASP were shown to predict a higher risk of cardiovascular events and all-cause mortality, including a higher risk for congestive heart failure, even in those without preexisting heart failure.

The authors concluded having used an echo-based definition of PH in their study is a well-known limitation, given that “the sensitivity and specificity of echocardiography to diagnose PH are modest (83% and 72% respectively).” They did perform sensitivity analyses in light of this known limitation. The analyses indeed confirmed that a TRV > 2.9 m/sec imparts a higher risk of cardiovascular events and mortality. The investigators also noted that their study did not determine the etiology of the association between PH and poor outcomes in this population, due to the epidemiologic nature of the investigation. Finally, the authors concluded that more mechanistic studies are needed in order to further investigate the etiology of this association.

Back to top


Our research platform is the world.

Through worldwide collaboration, we can begin to answer the question of a global disease.

Join the PVRI
standard-example-image.jpg