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A fluorescence antibody microarray has been developed for the determination of relevant cardiovascular disease biomarkers for the analysis of human plasma samples. Recording characteristic protein molecular fingerprints to assess individual's states of health could allow diagnosis to go beyond the simple identification of the disease, providing information on its stage or prognosis. Precisely, cardiovascular diseases (CVDs) are complex disorders which involve different degenerative processes encompassing a collection of biomarkers related to disease progression or stage. The novel approach that we propose is a fluorescent microarray chip has been developed accomplishing simultaneous determination of the most significant cardiac biomarkers in plasma aiming to determine the CVD status stage of the patient. As proof of concept, we have chosen five relevant biomarkers, C-reactive protein (CRP) as biomarker of inflammation, cystatin C (CysC) as biomarker of renal failure that is directly related with heart failure, cardiac troponin I (cTnI) as already established biomarker for cardiac damage, heart fatty acid binding protein as biomarker of ischemia (H-FABP), and finally, NT-proBNP (N-terminal pro-brain natriuretic peptide), a well-established heart failure biomarker. After the optimization of the multiplexed microarray, the assay allowed the simultaneous determination of 5 biomarkers in a buffer solution reaching LODs of 15 ± 5, 3 ± 1, 24 ± 3, 25 ± 3, and 3 ± 1 ng mL-1, for CRP, CysC, H-FABP, cTnI, and NT-proBNP, respectively. After solving the matrix effect, and demonstrating the accuracy for each biomarker, the chip was able to determine 24 samples per microarray chip. Then, the microarray has been used on a small pilot clinical study with 29 plasma samples from clinical patients which suffered different CVD and other related disorders. Results show the superior capability of the chip to provide clinical information related to the disease in terms of turnaround time (

Innate immune activation during Covid-19 infection is associated with pernicious clinical outcome. Coronavirus disease 2019 (Covid-19) is a worldwide threat that has already caused more than 3 000 000 deaths. It is characterized by different patterns of disease evolution depending on host factors among which old-age and pre-existing comorbidities play a detrimental role. Previous coronavirus epidemics, notably SARS-CoV, were associated with increased serum neopterin levels, which can be interpreted as a sign of acute innate immunity in response to viral infection. Here we hypothesize that neopterin may serve as a biomarker of SARS-CoV-2 viral infection and Covid-19 disease severity. We measured neopterin blood levels by ELISA. Seric concentration was quantified from 256 healthy donors and 374 Covid-19 patients at hospital admission. Enrolled Covid-19 patients were all symptomatic and displayed a large spectrum of comorbidities. Patients were followed until disease resolution or death. Severe and critically ill SARS-CoV-2 infected patients were characterized by a profound exacerbation of immune activation characterized by elevated neopterin blood levels. Systemic neopterin levels above 19nM stratified healthy individuals from Covid-19 patients with 87% specificity and 100% sensitivity. Moreover, systemic neopterin levels above 53nM differentiated non-survivors from survivors with 64% specificity and 100% sensitivity. We propose that neopterin concentration measured at arrival to hospital is a hallmark of severe Covid-19 and identifies a high-risk population of pernicious clinical outcome with a need for special medical care.

Our aim was to evaluate the association between the soluble form of neprilysin () levels and long-term all-cause, cardiovascular, and acute heart failure () recurrent admissions in an ambulatory cohort of patients with heart failure. has emerged as a new biomarker with promising implications for prognosis and therapy in patients with heart failure. Reducing the recurrent admission rate of heart failure patients has become an important target of public health planning strategies. We measured levels in 1021 consecutive ambulatory heart failure patients. End points were the number of all-cause, cardiovascular, and hospitalizations during follow-up. We used covariate-adjusted incidence rate ratios to identify associations. At a median follow-up of 3.4 years (interquartile range: 1.8-5.7), 391 (38.3%) patients died, 477 (46.7%) patients had 1901 all-cause admissions, 324 (31.7%) patients had 770 cardiovascular admissions, and 218 (21.4%) patients had 488 admissions. The medians for and amino-terminal pro-brain natriuretic peptide were 0.64 ng/mL (interquartile range: 0.39-1.22) and 1248 pg/mL (interquartile range: 538-2825), respectively. In a multivariate setting, the adjusted incidence rate ratios for the top (>1.22 ng/mL) versus the bottom (≤0.39 ng/mL) quartiles of were 1.37 (95% confidence interval: 1.03-1.82), P =0.032; 1.51 (95% confidence interval: 1.10-2.06), P =0.010; and 1.51 (95% confidence interval: 1.05-2.16), P =0.026 for all-cause, cardiovascular, and admissions, respectively. Elevated levels predicted an increased risk of recurrent all-cause, cardiovascular, and admissions in ambulatory patients with heart failure.

The number of recreational/non-elite athletes participating in marathons is increasing, but data regarding impact of endurance exercise on cardiovascular health are conflicting. This study evaluated 79 recreational athletes of the 2016 Barcelona Marathon (72% men; mean age 39 ± 6 years; 71% ≥35 years). Blood samples were collected at baseline (24–48 h before the race), immediately after the race (1–2 h after the race), and 48-h post-race. Amino-terminal pro-B type natriuretic peptide (NT-proBNP, a marker of myocardial strain), ST2 (a marker of extracellular matrix remodeling and fibrosis, inflammation, and myocardial strain), and high-sensitivity troponin T (hs-TnT, a marker of myocyte stress/injury) were assayed. The median (interquartile range, IQR) years of training was 7 (5–11) years and median (IQR) weekly training hours was 6 (5–8) h/week, respectively. The median (IQR) race time (h:min:s) was 3:32:44 (3:18:50–3:51:46). Echocardiographic indices were within normal ranges. Immediately after the race, blood concentration of the three cardiac biomarkers increased significantly, with 1.3-, 1.6-, and 16-fold increases in NT-proBNP, ST2, and hs-TnT, respectively. We found an inverse relationship between weekly training hours and increased ST2 (p = 0.007), and a direct relationship between race time and increased hs-TnT (p < 0.001) and ST2 (p = 0.05). Our findings indicate that preparation for and participation in marathon running may affect multiple pathways affecting the cardiovascular system. More data and long-term follow-up studies in non-elite and elite athletes are needed., Postprint (author's final draft)