Karol Adam Kamiński

Background. Atherosclerotic plaques in carotid arteries (APCA) are a prevalent condition with severe potential complications. Studies continuously search for innovative biomarkers for APCA, including those participating in cellular metabolic processes, cell adhesion, immune response, and complement activation. This study aimed to assess the relationship between APCA presence and a broad range of cardiometabolic biomarkers in the general population. Methods. The study group consisted of consecutive participants of the population study Bialystok PLUS. The proximity extension assay (PEA) technique from the Olink Laboratory (Uppsala, Sweden) was used to measure the levels of 92 cardiometabolic biomarkers. Results. The study comprised 693 participants (mean age 48.78 ± 15.27 years, 43.4% males, N = 301). APCA was identified in 46.2% of the participants (N = 320). Of the 92 biomarkers that were investigated, 54 were found to be significantly linked to the diagnosis of APCA. After adjusting for the traditional risk factors for atherosclerosis in multivariate analysis, the only biomarker that remained significantly associated with APCA was FCGR2A. Conclusion. In the general population, the prevalence of APCA is very high. A range of biomarkers are linked with APCA. Nonetheless, the majority of these associations are explained by traditional risk factors for atherosclerosis. The only biomarker that was independently associated with APCA was the FCGR2A.

Background. There is a raising awareness that heart failure (HF) is a highly heterogeneous, multiorgan syndrome with an increasing global prevalence and still poor prognosis. The comorbidities of HF are one of the key reasons for presence of various phenotypes with different clinical profile and outcome. Heterogeneity of skeletal muscles (SMs) quantity and function may have an impact on patient’s phenotype. Aim. We intended to compare clinical characteristics of phenotypes defined by a combination of various SM mass taken as a fat-free compartment from DEXA scans and different levels of SUCR (Spot Urinary Creatinine). All-cause mortality with mortality predicted by MAGGIC in such phenotypes were compared. Methods. In 720 HF patients with reduced ejection fraction (age: 52.3 ± 10 years, female: 14%, NYHA: 2.7 ± 0.7, LVEF: 24.3 ± 7.3%), admitted to the hospital for heart transplantation candidacy assessment, morning SUCR along with body composition scanning (DEXA) was performed. All study participants were dichotomized twice, first by low or normal appendicular muscle mass index (ASMI) and second by SUCR (Spot Urinary Creatinine) < and ≥of 1.34 g/L. Four study groups (phenotypes) were created as combinations of lower or higher SUCR and low or normal ASMI. Results. Low ASMI was found in 242 (33.6%) patients, while the remaining 478 had normal muscle mass. In 446 patients (61.9%), SUCR was <1.34 g/L. During 3 years of follow-up, 223 (31.0%) patients died (all-cause). The phenotype of lower both ASMI and SUCR was associated with the highest mortality. The death rate in phenotype with both low ASMI and SUCR exceeded by 70% the risk estimated by MAGGIC. This difference was significant as judged by the 95% confidence interval for MAGGIC estimation. In Cox regression analysis adjusted for MAGGIC and parameters known to increase risk, the relative risk of patients with phenotype of low both ASMI and SUCR was elevated by 45–55% as compared to patients with all other phenotypes. The protective role of higher SUCR in patients with muscle wasting was, therefore, confirmed in Cox analysis. Conclusions. Measurement of SUCR in HF patients can identify clinical phenotypes with skeletal muscle wasting but strikingly different risk of death that is actually not captured by MAGGIC score. The higher level of SUCR was associated with similar risk independently of presence of muscle wasting. As the analysis of SUCR is cheap and easy to perform, it should be further tested as a potentially useful biomarker, which may precisely phenotype HF patients independently of their skeletal muscle status.