Tag: troponin

Three new papers published – part II

~ BS

In my last post, I explained why I am at the moment not writing one post per new paper. Instead, I group them. This time with a common denominator, namely the role of cardiac troponin and stroke:

High-Sensitivity Cardiac Troponin T and Cognitive Function in Patients With Ischemic Stroke. This paper finds its origins in the PROSCIS study, in which we studied other biomarkers as well. In fact, there is a whole lot more coming. The analyses of these longitudinal data showed a – let’s say ‘medium-sized’ – relationship between cardiac troponin and cognitive function. A whole lot of caveats – a presumptive learning curve, not a big drop in cognitive function to work with anyway. After all, these are only mild to moderately affected stroke patients.

Association Between High-Sensitivity Cardiac Troponin and Risk of Stroke in 96 702 Individuals: A Meta-Analysis. This paper investigates several patient populations -the general population, increased risk population, and stroke patients. The number of patients individuals in the title might, therefore, be a little bit deceiving – I think you should really only look at the results with those separate groups in mind. Not only do I think that the biology might be different, the methodological aspects (e.g. heterogeneity) and interpretation (relative risks with high absolute risks) are also different.

Response by Siegerink et al to Letter Regarding Article, “Association Between High-Sensitivity Cardiac Troponin and Risk of Stroke in 96 702 Individuals: A Meta-Analysis”. We did the meta-analysis as much as possible “but the book”. We pre-registered our plan and published accordingly. This all to discourage ourselves (and our peer reviewers) to go and “hunt for specific results”. But then there was a letter to the editor with the following central point: Because in the subgroup of patients with material fibrillation, the cut-offs used for the cardiac troponin are so different that pooling these studies together in one analysis does not make sense. At first glance, it looks like the authors have a point: it is difficult to actually get a very strict interpretation from the results that we got. This paper described our response. Hint: upon closer inspection, we do not agree and make a good counterargument (at least, that’s what we think).

Messy epidemiology: the tale of transient global amnesia and three control groups

~ BS

Clinical epidemiology is sometimes messy. The methods and data that you might want to use might not be available or just too damn expensive. Does that mean that you should throw in the towel? I do not think so.

I am currently working in a more clinical oriented setting, as the only researcher trained as a clinical epidemiologist. I could tell about being misunderstood and feeling lonely as the only who one who has seen the light, but that would just be lying. The fact is that my position is one privilege and opportunity, as I work with many different groups together on a wide variety of research questions that have the potential to influence clinical reality directly and bring small, but meaningful progress to the field.

Sometimes that work is messy: not the right methods, a difference in interpretation, a p value in table 1… you get the idea. But sometimes something pretty comes out of that mess. That is what happened with this paper, that just got published online (e-pub) in the European Journal of Neurology.  The general topic is the heart brain interaction, and more specifically to what extent damage to the heart actually has a role in transient global amnesia. Now, the idea that there might be a link is due to some previous case series, as well as the clinical experience of some of my colleagues. Next step would of course to do a formal case control-study, and if you want to estimate true measure of rate ratios, a lot effort has to go into the collection of data from a population based control group. We had neither time nor money to do so, and upon closer inspection, we also did not really need that clean control group to answer some of our questions that would progress to the field.

So instead, we chose three different control groups, perhaps better referred as reference groups, all three with some neurological disease. Yes, there are selections at play for each of these groups, but we could argue that those selections might be true for all groups. If these selection processes are similar for all groups, strong differences in patient characteristics of biomarkers suggest that other biological systems are at play. The trick is not to hide these limitations, but as a practiced judoka, leverage these weaknesses and turn them into a strengths. Be open about what you did, show the results, so that others can build on that experience.

So that is what we did. Compared patients with migraine with aura, vestibular neuritis and transient ischemic attack, patients with transient global amnesia are more likely to exhibitsigns of myocardial stress. This study was not designed – nor will if even be able to – understand the cause of this link, not do we pretend that our odds ratios are in fact estimates of rate ratios or something fancy like that. Still, even though many aspects of this study are not “by the book”, it did provide some new insights that help further thinking about and investigations of this debilitating and impactful disease.

The effort was lead by EH, and the final paper can be found here on pubmed.