>Also, and this is something I'm not clear on, but is this just an abstract? It doesn't seem like there's an associated paper or any data beyond what's mentioned there.

It's from a report presented at the American Heart Association (AHA) Scientific Sessions 2021;
https://www.thecardiologyadvisor.com/home/topics/acs/acute-c... . Presumably the actual paper is upcoming.

>"...there is no data in the abstract regarding myocardial T-cell infiltration, there are no statistical analyses for significance provided, and the author is not clear that only anecdotal data was used."

Presumably deeper analysis will be presented in the actual paper. The author claims the data is from 566 people at a preventative cardiology practice, so unless the PULS measurements have an incredibly high degree of variance, it'd be quite unlikely to see such a large increase in the underlying factors measured purely by chance when there are 500+ samples.

>they don't compare mRNA vaccine recipients to people who have recovered from COVID-19

This would be useful for comparing the relative safety of the mRNA vaccines vs getting covid. Such comparison is however not necessary to assess the safety of mRNA vaccines; an mRNA vaccine does not become safe just because covid is more dangerous. The absolute, not relative, risk is important to know as even if the risk of covid is greater, the chance of getting covid is not 100%. And with regular boosters, one might be exposed to the risk of the mRNA vaccine more often than one is exposed to the risk of covid.

> the PULS test the publishing doctor developed doesn't seem to explain how it turns a set of arbitrary biological markers into a score that correlates to risk of heart issues

https://pulstest.com/articles/analytical-performance the PULS test "measures the most clinically-significant protein biomarkers that measure the body's immune system response to arterial injury". There's peer-reviewed research demonstrating its effectiveness: https://pubmed.ncbi.nlm.nih.gov/23530883/.

"The original studies for the PULS Cardiac Test were initiated at Stanford University and Kaiser Permanente. Researchers analyzed gene expression profiles in the lesions of mouse models of ACS (mice do not form hard plaque) . Over 250 candidate proteins were identified in mice lesions and many of them were shown to be conserved in humans by analysis of soft lesions during CABG. The number of biomarker candidates was narrowed from 50 to 9 pathways during additional studies. Various permutations of these biomarkers with existing biomarkers like LP-PLA2 and hsCRP, and global risk factors were tested by 3 software systems (Akaike, Bayesian, and Drop-inDeviance) to predict a 5 year risk of ACS. This process resulted in all three systems identifying the same 9 biomarkers and 4 global risk factors (age, sex, diabetic status, and family history). These biomarkers and global risk factors were then incorporated into a benchmark algorithm format with performance superior to gold standard measures of risk such as Framingham, Reynolds, etc. The resulting algorithm yielded a clinical net reclassification index of 43% (this index penalizes an algorithm for falsely up-classifying and down-classifying patients; values above 10% when compared to Framingham are considered good). The algorithm (PULS) was then independently validated by the NIH NHLBI group in MESA which confirmed the findings. These clinical trials were all longitudinal outcome-based studies."