Date Published: April 11, 2019
Publisher: Public Library of Science
Author(s): Tamás Horváth, Gyöngyi Serfőző, Ádám Györkei, Imre Földesi, Tamás Forster, Margit Keresztes, Byoung-Kwon Lee.
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.
Mainly due to advanced interventional cardiology and improved prevention, the mortality rate of coronary artery disease (CAD) decreased considerably in the last decade. Still, myocardial infarction probably remains a major obstacle to human longevity also in the coming decade . According to a recent model, development and progression of CAD are determined mostly by the atherosclerotic inflammatory events and by the subsequent arterial repair . Following percutaneous coronary intervention (PCI) with stent implantation, a secondary inflammatory response is initiated, which is triggered by endothelial denudation and disruption, in addition to plaque rupture and myocardial ischemia-reperfusion injury [3, 4]. Peri-procedural myocardial injury still represents a frequent complication of PCI (even in uneventful cases) . It is mostly related to myocardial ischemia, that is elicited primarily by plaque disruption (leading to side branch occlusion or distal embolization) or by coronary vasoconstriction; ischemia and reperfusion are associated with inflammatory reactions [5–6].
The main finding of our study is that myocardial cell damage is tightly associated with inflammation and, via neutrophils, also with enhanced level of stress in patients with stable CAD, on the day following stenting. During the correlational analysis of 12 parameters, two major association networks emerged: one that is composed of a cell damage marker (ASAT), a major inflammatory marker (IL-6) and neutrophil count, and an another one, which involves a marker of neuroendocrine-sympathetic activity (CgA), monocyte count and neutrophil count; these two networks are apparently linked by neutrophil count.