High-sensitivity C-reactive protein (hs-CRP) is a biomarker used for risk prediction for cardiovascular disease by assessing low concentration of inflammation. Measurements of regular CRP have become very sensitive with a lower detection limit of 0.3 mg/L. This study aimed to compare and explore the association between CRP and hs-CRP. Data from 607 consecutive patients referred for cardiovascular risk assessment with hs-CRP were reviewed retrospectively. In total, 570 patients were included in the analysis and classified into 3 (low-, medium-, and high-risk) groups (hs-CRP cutoff: 3 mg/L). Correlation between hs-CRP and CRP was assessed with the kappa statistic and visualized with a Bland–Altman plot. The association between hs-CRP and occurrence of the composite outcome (acute myocardial infarction, stroke, coronary intervention [percutaneous coronary intervention or bypass surgery], or death) was determined with Cox regression analysis and visualized with Kaplan–Meier curves. A total number reclassification occurred in 8.6% of the cases for CRP risk groups, which demonstrates an agreement of 91.4% (kappa 0.87; P < 0.001). The correlation between CRP and hs-CRP was significant (P < 0.001), Spearman regression R² = 0.98. A Bland–Altman plot displayed an average difference of 0.19 mg/L (95%CI, 0.17 to 0.23) between the CRP and hs-CRP. Cardiovascular events were more likely to occur in patients who were older, with hs-CRP or CRP >3 mg/L and a history of coronary artery disease. The usual laboratory tests for CRP values in the lower range highly correlate with the hs-CRP tests and can therefore replace the costlier hs-CRP measurements.

Introduction. The renin-angiotensin system (RAS) is the main target of neurohumoral therapy in heart failure with reduced ejection fraction (HFrEF) effectively reducing mortality. Reasonably, renin might serve as a biomarker for risk prediction and therapy response. Renin indeed bears some additional value to clinical risk models, albeit the effect is not pronounced. Whether assessing renin trajectories can overcome the weaknesses of single renin measurements has not been reported. Methods. A total of 505 patients with stable HFrEF were enrolled prospectively and followed through routine clinical visits. Active plasma renin concentration was documented up to 5 years. Changes in renin were analyzed throughout the disease course, and survival was compared for different renin trajectories within the first year. Results. Baseline renin levels were not related to all-cause mortality (crude HR for an increase of 100 μiE/ml: 1.01 (95% CI: 0.99–1.02), ) but associated with unplanned HF hospitalizations (crude HR: 1.01 (95% CI: 1.00-1.02), ). Renin increased during the disease course from baseline to 1-year and 2-year FUP (122.7 vs. 185.6 μIU/ml, , and 122.7 vs. 258.5 μIU/ml, ). Both survival and unplanned HF hospitalization rates were comparable for different renin trajectories at 1-year FUP ( , ). Conclusions. Intriguingly, renin is not a good biomarker to indicate prognosis in HF, while renin trajectories over a 1-year period do not have an additional value. Rapid physiologic plasma renin variations, but also opposing effects of angiotensinogen-derived metabolites under presence of RAS blockade, might obscure the predictive ability of renin.

Cardiac magnetic resonance (CMR) studies reported CMR abnormalities in patients with mild–moderate SARS-CoV-2 infection, suggesting ongoing myocardial inflammation. Patients (n = 278, 43 ± 13 years, 70.5% female) with post-acute sequelae of SARS-CoV-2 cardiovascular syndrome (PASC-CVS) were included prospectively into the Vienna POSTCOV Registry between March 2021 and March 2023 (clinicaltrials.gov NCT05398952). Clinical, laboratory, and CMR findings were recorded. Patients with abnormal CMR results were classified into isolated chronic pericardial (with/without pleural) effusion, isolated cardiac function impairment, or both (myopericarditis) groups. Medical treatment included a nonsteroidal anti-inflammatory agent (NSAID) for pericardial effusion and a condition-adapted maximal dose of heart failure (HF) treatment. Three months after medical therapy, clinical assessment and CMR were repeated in 82 patients. Laboratory analyses revealed normal hematological, inflammatory, coagulation, and cardiac biomarkers. CMR abnormalities were found in 155 patients (55.8%). Condition-adapted HF treatment led to a significant increase in the left ventricular ejection fraction (LVEF) in patients with initially reduced LVEF (from 49 ± 5% to 56 ± 4%, p = 0.009, n = 25). Low–moderate doses of NSAIDs for 3 months significantly reduced pericardial effusion (from 4/3;5.75/mm to 2/0;3/mm, median/interquartile ranges/p < 0.001, n = 51). Clinical symptoms improved markedly with a decrease in CMR abnormalities, which might be attributed to the maintenance of NSAID and HF medical treatment for PASC-CVS.

Interpersonal trust declined worldwide during the COVID-19 pandemic; strategies are needed to restore it. We surveyed 3,065 quota-sampled German-speaking adults residing in the D-A-CH region. Using multinomial logistic regression models and backward elimination for variable selection, we calculated multivariable-adjusted odds ratios (OR) and 95% confidence intervals (95% CIs) to appraise correlates of interpersonal trust using the Interpersonal Trust Short Scale (KUSIV3). Participants with high levels of interpersonal trust (top KUSIV3 tertile (T3)) tended to be older, male, residents of Switzerland, university degree holders, and workers with higher income and work satisfaction (all P_diff5 times a week (OR = 0.48; 95%CI = 0.36–0.66, versus none); and scored high on conspiracy belief (OR_T3vsT1 = 0.53; 95%CI = 0.41–0.69). Results differed minimally by gender and country. These findings may be helpful in devising targeted strategies to strengthen interpersonal trust and social engagement in European societies, especially during times of crises.

Endothelial dysfunction mediated by elevated levels of autoantibodies against vasoactive peptides occurring after COVID-19 infection is proposed as a possible pathomechanism for orthostatic intolerance in long COVID patients. This case-control study comprised 100 long COVID patients from our prospective POSTCOV registry and three control groups, each consisting of 20 individuals (Asymptomatic post-COVID group; Healthy group = pan-negative for antispike protein of SARS-CoV-2; Vaccinated healthy group = no history of COVID-19 and vaccinated). Autoantibodies towards muscarinic acetylcholine receptor M3, endothelin type A receptor (ETAR), beta-2 adrenergic receptor (Beta-2 AR), angiotensin II receptor 1 and angiotensin 1-7 (Ang1-7) concentrations were measured by enzyme-linked immunosorbent assay in long COVID patients and controls. Orthostatic intolerance was defined as inappropriate sinus tachycardia, postural tachycardia, orthostatic hypotonia and other dysautonomia symptoms, such as dizziness or blurred vision (n = 38 long COVID patients). Autoantibody concentrations were compared with routine laboratory parameters and quality of life questionnaires (EQ-5D). The concentration of ETAR autoantibodies were significantly higher in long COVID, Asymptomatic and Vaccinated groups compared to the antispike protein pan-negative Healthy group. A trend towards higher plasma levels of Beta-2 AR and Ang1-7 was measured in long COVID patients, not related to presence of orthostatic intolerance. ETAR autoantibody concentration showed significant positive correlation with the EQ-5D item “Problems in performing usual activities”.

Navigating today’s crises requires transcending one-dimensional, exclusively science-centered approaches. This article advocates a transdisciplinary strategy, integrating diverse perspectives to address complex issues like poly-crises. It emphasizes the potential of mutual learning and knowledge co-generation between science and society for fostering creative, sustainable solutions within a multilayered innovation system.