Neutrophil count as the centerpiece in the joined association networks of inflammatory and cell damage markers, and neuroendocrine stress markers in patients with stable angina pectoris following stenting.
Horváth. Tamás T; Serfőző. Gyöngyi G; Györkei. Ádám Á; Földesi. Imre I; Forster. Tamás T; Keresztes. Margit M
Key Findings
- Neutrophil counts, along with monocyte‑to‑lymphocyte and neutrophil‑to‑lymphocyte ratios, stayed elevated after the stent procedure.
- Plasma levels of LL‑37, lactoferrin, IL‑6, cortisol, and chromogranin A all changed significantly around the time of the procedure.
- On day 1 after the procedure, neutrophil count strongly correlated with stress markers (cortisol, chromogranin A) and liver enzyme ASAT, indicating a link between inflammation, stress, and tissue damage.
Practical Outcomes
- For most biohackers, the study offers limited direct action because it focuses on patients undergoing a specific cardiac intervention, not on healthy individuals or supplementation strategies. The main takeaway is that neutrophil count can serve as an easy, quick snapshot of combined stress and inflammation after a major physiological event, but it doesn’t provide guidance on how to manipulate LL‑37 or related pathways for performance or longevity.
Summary
In patients with stable heart disease who had a stent placed, the researchers tracked blood markers before, right after, and one day later. They found that neutrophil (a type of white blood cell) counts rose and were tightly linked to stress hormones and inflammation markers, suggesting neutrophils could be a simple way to gauge the body’s stress‑inflammation response after heart procedures.
Abstract
The primary aim of this study was to examine whether markers of cell damage and of the psycho-neuroendocrino-inflammatory/immune (PNI) system could be associated in patients with stable coronary artery disease (CAD) on the next day following percutaneous coronary intervention (PCI). Blood samples of 23 patients (18 men and five women, mean age 62.9 ± 10.6 years), were collected immediately before (pre-PCI), immediately after (post-PCI), and on the day following PCI (1d-PCI). Lactoferrin, LL-37 and interleukin-6 (IL-6) were assayed in plasma, in addition to cortisol and chromogranin A (CgA), as well as CK, ASAT and ALAT. Total and differential leukocyte counts were also analysed. At all the three time points, the monocyte fractions, the monocyte-to-lymphocyte and the neutrophil-to-lymphocyte ratios and CgA levels were elevated. We detected significant peri-procedural changes in the plasma levels of our PNI markers: IL-6 (p<0.05), lactoferrin, LL-37 (both: p <0.0001), CgA, (p<0.05), and cortisol (p<0.01). On the first day after PCI, highly significant associations were found of ASAT with IL-6 and neutrophil count (both: r>0.75, p<0.0001), and of CgA with neutrophil count and monocyte count (both: r>0.79, p<0.0001); furthermore, cortisol was also associated with neutrophil count (r>0.7, p<0.0001). The findings suggest that myocardial damage could correlate not only with an inflammatory reaction but, via neutrophil count, also with increased level of stress in stable CAD after PCI. Furthermore, 1d-PCI neutrophil count may serve as an easy-to-obtain integrative PNI measure in stable CAD.
Study Information
pubmed
2019
2019-04-11T00:00:00.000Z
10.1371/journal.pone.0215209
8
56