Women and non-academic institutions less likely to get work published

Fascinating study in the European Heart Journal this week. Winnik et al analyzed all 10,020 abstracts submitted to the World Congress of Cardiology 2006 in Barcelona (which combined the ESC and World Heart Federation congresses) according to whether they were accepted or rejected for presentation and whether accepted studies were oral or poster presentations. Of these, 3104 (31%) were accepted as posters and 701 (7%) for oral presentation.


Introduction and Methods: Through a 4-year follow-up of the abstracts submitted to the European Society of Cardiology Congress in 2006, we aimed at identifying factors predicting high-quality research, appraising the quality of the peer review and editorial processes, and thereby revealing potential ways to improve future research, peer review, and editorial work.Methods and resultsAll abstracts submitted in 2006 were assessed for acceptance, presentation format, and average reviewer rating. Accepted and rejected studies were followed for 4 years. Multivariate regression analyses of a representative selection of 10% of all abstracts (n= 1002) were performed to identify factors predicting acceptance, subsequent publication, and citation. A total of 10 020 abstracts were submitted, 3104 (31%) were accepted for poster, and 701 (7%) for oral presentation.

Results: At Congress level, basic research, a patient number ≥ 100, and prospective study design were identified as independent predictors of acceptance. These factors differed from those predicting full-text publication, which included academic affiliation. The single parameter predicting frequent citation was study design with randomized controlled trials reaching the highest citation rates. The publication rate of accepted studies was 38%, whereas only 24% of rejected studies were published. Among published studies, those accepted at the Congress received higher citation rates than rejected ones.

Conclusions: Research of high quality was determined by study design and largely identified at Congress level through blinded peer review. The scientometric follow-up revealed a marked disparity between predictors of full-text publication and those predicting citation or acceptance at the Congress.

Commenting on their findings for the heart.org, the authors stated that:


Female senior authors are 50% less likely than males to have their work published in a peer-reviewed journal and that nonacademic institutions are less likely than academic ones to have research published.

Any thoughts on this? I think this reinforces the need for double blinded reviewing.

Carotid plaque inflammation predicts early stroke recurrence

This study, just published in the highly respected journal 'Annals of Neurology' lends support to the concept of persisting inflammation, as detected by 18FDG PET, portends early stroke recurrence. In fact, 18FDG uptake was the only factor on multivariate analysis to predict recurrence, out-performing stenosis degree and age. If the SUV was above 2.1, 80% of subjects had recurrent events within 90 days.

What we need now is a prospective study of an FDG PET-guided approach to risk stratification and management compared with standard medical/surgical care.

The SUV value is in the same ballpark as that seen in other PET studies of atherosclerosis, and less than frequently noted in untreated active vasculitis.

This study provides a counterpart to the MRI one I published here yesterday.

Any thoughts?

Low healing rate amongst complex carotid artery plaques - a longitudinal MRI study

What surprised me the most about this elegant study was the very low rate of healing of complex plaques that had caused cerebrovascular events. We know that the risk of recurrent events is very high immediately after TIA but drops off rapidly. Presumably, even high-resolution structural imaging takes some time to reflect this change in risk.

I believe this is the first longitudinal study to address this issue in humans.

200611 04 1

Atherosclerotic plaque imaging - past, present, and future

Dr. Alistair Lindsay hosts a round table from the British Cardiovascular Society Conference in Manchester, on the topic of atherosclerotic plaque imaging; past, present, and future.

He is joined by:

  • Matthias Nahrendorf, Center for Systems Biology, Harvard University
  • Farouc Jaffer, Center for Molecular Imaging Research, Harvard University
  • James Rudd, Division of Cardiovascular Medicine, University of Cambridge
  • Robin Choudhury, Department of Cardiovascular Medicine, University of Oxford

Click here to listen.

See also:
Webcasts from all the sessions at the British Cardiovascular Society Conference 2012

Click here to watch.

HDL research must continue say experts at the EAS meeting

HDL research must continue (via the heart.org)

> After a series of negative trial results, the concept of raising high-density lipoprotein (HDL) as a therapeutic approach to reducing cardiovascular risk looks to be in a sorry state. But lipid experts at the recent European Atherosclerosis Society (EAS) 2012 Congress were adamant that the HDL hypothesis was not yet dead and that it is imperative that research in this direction continue.

What do you think? Do you hold out any hope for this method of lowering CV risk? Should we wait for the results of the phase 3 anacetrapib study? What about the HPS2-thrive study with Niacin? Do we have to wait until 2013 or should we withdraw Niacin today?

Subclinical atherosclerosis represents the vessel memory of risk factor exposure.

A very interesting review paper on coronary artery calcium screening in the European Heart Journal.

Their conclusions:

Computed coronary tomography allows for quantification and localization of CAC as a sign of subclinical atherosclerosis. The SHAPE (Screening for Heart Attack Prevention and Education) Task Force presented a practice guideline for cardiovascular screening in the asymptomatic risk population based on signs of subclinical atherosclerosis.

This practice guideline could, however, not be based on prospective observational cohort studies, which are now available and thus these aspects were further emphasized including other tasks for subclinical atherosclerosis such as ultrasound of the carotid artery and screening with biomarkers.

Coronary artery calcification can be used for risk stratification and has already received a class IIa recommendation by the ACC/AHA. Coronary artery calcification should be in the focus of cardiologists particularly for those who are interested in preventive cardiology because important and unique insights in CAD can be provided. Coronary atherosclerosis represents the memory of lifetime risk factor exposure, and has a significant short- term and intermediate term prognostic implication. Our colleagues who experienced a sudden fatal event just like thousands of other people, unaware of their risk, should stimulate us to improve primary prevention by using signs of subclinical atherosclerosis as a marker of risk.

Scientists develop new technique that could improve heart attack prediction

James Ruddweb 560x315

 

From left to right, CT, PET and combined PET/CT images of the heart arteries. The areas in white on the left and right panels demonstrate calcification of the arteries, whilst the orange spots on the middle and right panels demonstrate actively calcifying areas of atherosclerosis. These have accumulated significant amounts of NaF, and we believe that these areas represent high-risk areas for future heart attacks. Further work is, of course, needed to prove this hypothesis.

Building on work pioneered in Cambridge 10 years ago, scientists have developed a new imaging approach that could help improve how doctors predict a patient’s risk of having a heart attack.

The British Heart Foundation (BHF) funded project, a collaboration between scientists from the Universities of Cambridge and Edinburgh, is the first to demonstrate the potential of combined PET and CT imaging to highlight the disease processes causing heart attacks directly within the coronary arteries.

The research, published last week in the Journal of the American College of Cardiology (JACC), involved imaging over 100 people with a CT calcium scan to measure the amount of calcified or hardened plaques in their coronary arteries. This is a standard test, which is commonly used to predict heart attack risk but cannot distinguish calcium that has been there for some time from calcium that is actively building up.

The patients were also injected with two contrast agents that show up on PET imaging scans, and which can be used to track various metabolic pathways in the body. One of these tracers, 18F-sodium fluoride (18F-NaF), is a molecule taken up by cells in which active calcification is occurring. The 18F-NaF can then be visualised and quantified during a PET scan.

The researchers wanted to see if they could identify patients with active, ongoing calcification because these patients may be at higher risk of heart attack than patients in whom the calcium developed a long time ago. The results showed that increased 18F-NaF activity could be observed in specific coronary artery plaques in patients who had many other high-risk markers of cardiovascular disease.

Dr James Rudd, HEFCE Senior Lecturer at the Department of Medicine and joint senior author of the paper, said:

Our results show, for the first time, that certain areas of atherosclerosis within the coronary arteries, previously thought to be inert, are actually highly active and have the potential to cause heart attack. Once identified, they might be targeted with drug therapy more effectively.

Additionally, we might be able to improve our ability to predict an individual person’s future risk of heart attack using this fairly straightforward imaging test in selected people.

This research exploits longstanding scientific links between my research team in Cambridge and Professor Newby’s in Edinburgh, with core support from the Cambridge NIHR Biomedical Research Centre, HEFCE and the British Heart Foundation.

Dr Marc Dweck, lead author on the research paper and a BHF Clinical Research Fellow at the University of Edinburgh, said:

Predicting heart attacks is very difficult and the methods we’ve got now are good but not perfect. Our new technique holds a lot of promise as a means of improving heart attack prediction although further ongoing work is needed before it becomes routine clinical practice.

If we can identify patients at high risk of a heart attack earlier, we can then use intensive drug treatments, and perhaps procedures such as stents, to reduce the chances of them having a heart attack.

Dr Shannon Amoils, Research Advisor at the (BHF), which funded the study, said:

For decades cardiologists have been looking for ways to detect the high-risk plaques found in coronary arteries that could rupture to cause a heart attack, but it’s been difficult to develop a suitable imaging test that can focus in on these small vessels.

This research is a technical tour de force as it allows us to assess active calcification happening right in the problem area – inside the wall of the coronary arteries and this active calcification may correlate with a higher risk of a heart attack.

There are nearly 2.7 million people living with coronary heart disease (CHD) in the UK and it kills 88,000 people each year. Most of these deaths are caused by a heart attack. Each year there are around 124,000 heart attacks in the UK.

Koch's postulates - inflammation vs atherosclerosis

Progress and challenges in translating the biology of atherosclerosis-Libby et al Nature, 2011


Statins effectively lower LDL and CRP levels in humans. Analyses of several large studies of statins in primary- and secondary-prevention populations suggest that some of their clinical benefit accrues from an anti-inflammatory action distinct from LDL lowering. The hypothesis that an anti-inflammatory intervention can reduce cardiovascular events independent of lipoprotein effects still requires rigorous testing. Thus, despite hundreds of studies affirming a role for inflammation in atherosclerosis in mice, and many intriguing observations in humans...Koch’s postulates remain unfulfilled.

Any thoughts on this?

Non-invasive imaging of atherosclerosis review in EHJ

A very comprehensive review from an eminent group of authors appeared in EHJ recently.

Non-invasive anatomic and functional imaging of vascular inflammation and unstable plaque

It covers:

  1. Pathobiology of plaque, including lipid accumulation, oxidation, inflammation, matrix breakdown, apoptosis and calcification (both macro- and micro-).

  2. Imaging techniques PET, SPECT, CT, MRI and ultrasound

There were some interesting comments on the increasing use of FDG PET imaging for detection of inflammation in atherosclerosis : -

Despite these attractions, some issues require resolution before embracing FDG uptake in this regard. Firstly, only limited prospective data correlate FDG uptake, or changes in FDG uptake, with cardiovascular events or altered rates of such complications,42 and we eagerly await the results of larger prospective cohort studies, such as the High Risk Plaque Initiative and BioImage studies."

"In this regard, nuclear agents that image hypoxia, already in use in oncology, may be
useful in imaging atherosclerosis, as hypoxic conditions may prevail in the core of lesions."


I quite agree on point 1 and keep watching this space for point 2!