Common changes of biomarkers in acute and chronic coronary syndromes: an anchored glance on pathophysiology as well as coronary microcirculation disorder prediction

Background Growing evidence supports the presence and clinical relevance of coronary microvascular dysfunction in both acute and chronic myocardial ischemic syndromes, highlighting the need for a diagnostic biomarker algorithm, with a subset of markers plausibly shared across conditions. Material and methods The circulating levels of 67 markers referred to inflammation, endothelial dysfunction, atherogenity, oxidative stress, hemostasis, NETosis, dysbiosis, neuroendocrine activation, and cardiovascular remodeling were determined after 7 days since angioplasty in consecutive 83 pts with STEMI, 83 pts with NSTEMI and at admission in 83 pts with primary diagnosed INOCA. Control series comprised 76 healthy persons. Results In regard to inflammation in all 3 series a similar significant increment (up to 86.9%) of IL-1β and soluble receptor of IL-6 level vs control (5.28±0.84 and 1.29±0.53 pg/ml respectively) was established. Commonly for endothelial dysfunction was the rise of endocan by up to 69.4%. Two markers of atherogenic statement had a common change: decrease of paraoxanase-1 by up to 56.3% and elevation of oxiHDL. The ratio Willebrand/ADAMTS13 was alone marker of hemostasis having a significant increase in all series up to 131.5% (especially in STEAMI and NSTEMI). NETosis, oxidative stress and dysbiosis assessment didn’t underline common markers. However, neuroendocrine activity exhibited by more biomarkers with matched changes in all 3 series: increase of ACE1, Ang II, ET-1, neprylisin and decrease of catestatin, ACE2 and Ang I-7. From 10 biomarkes of cardiovascular remodeling only GDF-15 elevated in all 3 series: by 108.6-112.3 in STEMI and NSTEMI and by 96.2% in INOCA vs control (1.35±0.68 ng/ml). Conclusion Application of a comprehensive multi-biomarker panel in patients with STEMI and NSTEMI (7 days post-angioplasty) and in newly diagnosed INOCA identified 13 biomarkers with similar changes vs control. The most pronounced change was observed for GDF-15, while the majority of shared markers reflected neuroendocrine activation (ACE1, ACE2, angiotensin-(1–7)/angiotensin II balance, catestatin, and neprilysin). These findings suggest a common pathophysiological basis underlying INOCA and support the diagnostic relevance of coronary microvascular dysfunction.