Fabry disease is an invalidating multisystemic disorder affecting α-Galactosidase, a rate-limiting hydrolase dedicated to lipid catabolism. Non-metabolized substrates, such as Globotriaosylceramide and its derivatives trigger the direct or indirect activation of inflammatory events and endothelial dysfunction. In spite of the efficacy demonstrated by enzyme replacement therapy or pharmacological chaperones in delaying disease progression, few studies have analyzed whether these treatments can improve the pro-inflammatory state of FD patients. Therefore, the aim of this work was to assess cytokines and cardiovascular risk-related proteins detectable in plasma from FD patients, whether treated or not with ERT, to evaluate the reliability of these markers in monitoring disease stage and treatment effects. We identified inflammatory and endothelial dysfunction markers (ADAMTS-13, TNF-α, GDF-15, MIP-1β, VEGFA, MPO, and MIC-1) that cooperate in a common pathway and are increased in FD patients\' plasma samples. As shown by the assessment of these proteins over time, they can help to evaluate the risk of higher severity in FD, as well as ERT effects. Even though the analyzed proteins cannot be considered as proper biomarkers due to their non-specificity to FD, taken together they can provide a signature of reference molecules with prognostic value for early diagnosis, and evaluation of disease progression and treatment efficacy, using blood samples.

BACKGROUND: Participation in ultra-endurance races may lead to a transient decline in cardiac function and increased cardiovascular biomarkers. This study aims to assess alterations in biventricular function immediately and five days after the competition in relation to elevation of high-sensitivity cardiac Troponin I (hs-cTnI) and N-terminal-pro-brain-natriuretic-peptide (NT-proBNP).
RESULTS: Fifteen participants of an ultramarathon (UM) with a running distance of 130 km were included. Transthoracic echocardiography and quantification of biomarkers was performed before, immediately after and five days after the race. A significant reduction in right ventricular fractional area change (FAC) was observed after the race (48.0 ± 4.6% vs. 46.7 ± 3.8%, p = 0.011) that persisted five days later (48.0 ± 4.6% vs. 46.3 ± 3.9%, p = 0.027). No difference in left ventricular ejection fraction (LVEF) was found (p = 0.510). Upon stratification according to biomarkers, participants with NT-proBNP above the median had a significantly reduced LVEF directly (60.8 ± 3.6% vs. 56.9 ± 4.8%, p = 0.030) and five days after the race (60.8 ± 3.6% vs. 55.3 ± 4.5%, p = 0.007) compared to baseline values. FAC was significantly reduced five days after the race (48.4 ± 5.1 vs. 44.3 ± 3.9, p = 0.044). Athletes with hs-cTnI above the median had a significantly reduced FAC directly after the race (48.1 ± 4.6 vs. 46.5 ± 4.4, p = 0.038), while no difference in LVEF was observed. No alteration in cardiac function was observed if hs-cTnI or NT-proBNP was below the median.
CONCLUSIONS: A slight decline in cardiac function after prolonged strenuous exercise was observed in athletes with an elevation of hs-cTnI and NT-proBNP above the median but not below.

Background: Biomarkers development for prognostication or prediction of perioperative myocardial disease is critical for the evolution of treatment options in patients undergoing cardiac surgery. The aim of our prospective monocentric study was to investigate the role of selenoprotein 1 (SEEP 1) as a potential biomarker for assessing the risk of myocardial injury after cardiac surgery. Methods: Circulating SEPP1 was measured in the blood of 45 patients before surgery and at 4 h, 8 h and 12 h after CPB by enzyme-linked immunosorbent assay (ELISA); (3) Results: circulating SEPP-1 levels measured 4 h after surgery were strongly correlated with CK-MB levels measured at 48 h (R = 0.598, p < 0.0001) and at 72 h (R = 0.308, p = 0.05). Close correlations were also found between 4 h SEPP-1 and Hs-c troponin values measured at 24 h (R = 0.532, p < 0.0001), 48 h (R = 0.348, p = 0.01) and 72 h (R = 0.377, p = 0.02), as well as with cardiopulmonary bypass (CPB) (R = 0.389, p = 0.008) and cross-clamp time (R = 0.374, p = 0.001); (4) Conclusions: Early SEPP1 measurement after CPB may hold great potential for identifying cardiac surgery patients at risk of developing perioperative myocardial injury.

To examine whether household income is causally related to cardiovascular diseases and investigate the potential reasons.
Using 2-sample Mendelian randomization analyses, we obtained summary statistics from genome-wide association studies of household income and a range of cardiovascular diseases, biomarkers, and socioeconomic factors.
Higher household income was causally associated with lower risks of coronary heart disease (odd ratio [OR] = 0.63; 95% CI: 0.49-0.79; P = 0.0001), myocardial infarction (OR = 0.64; 95% CI: 0.50-0.82; P = 0.0003), and hypertension (OR = 0.71; 95% CI: 0.58-0.88; P = 0.0015). With increasing household income, the cardiovascular biomarkers including triglycerides, C-reactive protein, body mass index, fasting glucose were decreased whereas telomere length and high-density lipoprotein cholesterol were increased. Besides, individuals with higher household income were less likely to smoke (β = -0.34; 95% CI: -0.47 to -0.21; P = 1.91×10-07), intake salt (β = -0.14; 95% CI: -0.21 to -0.07; P = 0.0001), or be exposed to air pollution (β = -0.10; 95% CI: -0.15 to -0.06; P = 8.81×10-06) or depression state (β = -0.03; 95% CI: -0.04 to -0.02; P = 5.16×10-07). They were more likely to take physical activity (β = 0.06; 95% CI: 0.02 to 010; P = 0.0016) and have long years of schooling (β = 0.70; 95% CI: 0.62 to 0.78; P = 5.32×10-67).
Higher household income is causally associated with better socioeconomic factors and improved cardiovascular biomarkers, which translates into a reduced prevalence of cardiovascular diseases. Policies to improve income equality may result in a reduced burden of cardiovascular diseases.

BACKGROUND: The diagnosis and prognosis of cardiovascular disorders are greatly aided by cardiovascular biomarkers. The uses of troponin and B-type natriuretic peptide in situations involving carbon monoxide exposure are examined in this narrative review. These biomarkers are important because they help predict outcomes in cardiovascular disorders, track the effectiveness of therapy, and influence therapeutic choices.
METHODS: Clinical practice makes considerable use of B-type natriuretic peptide (BNP), which has diuretic and vasodilatory effects, and troponin, a particular marker for myocardial injury. Carbon monoxide (CO) poisoning is a major worldwide health problem because CO, a \"silent killer,\" has significant clinical consequences. Higher risk of cardiac problems, poorer clinical outcomes, and greater severity of carbon monoxide poisoning are all linked to elevated troponin and B-type natriuretic peptide levels. BNP\'s adaptability in diagnosing cardiac dysfunction and directing decisions for hyperbaric oxygen therapy is complemented by troponin\'s specificity in identifying CO-induced myocardial damage. When combined, they improve the accuracy of carbon monoxide poisoning diagnoses and offer a thorough understanding of cardiac pathophysiology.
CONCLUSIONS: To sum up, this review emphasizes the importance of troponin and B-type natriuretic peptide (BNP) as cardiac indicators during carbon monoxide exposure. While BNP predicts long-term cardiac problems, troponin is better at short-term morbidity and death prediction. When highly sensitive troponin I (hsTnI) and B-type natriuretic peptide are combined, the diagnostic accuracy of carbon monoxide poisoning patients is improved. One of the difficulties is evaluating biomarker levels since carbon monoxide poisoning symptoms are not always clear-cut. Accurate diagnosis and treatment depend on the investigation of new biomarkers and the use of standardized diagnostic criteria. The results advance the use of cardiovascular biomarkers in the intricate field of carbon monoxide exposure.

Heart failure (HF) is a widespread cardiovascular condition that poses significant risks to a wide spectrum of age groups and leads to terminal illness. Although our understanding of the underlying mechanisms of HF has improved, the available treatments still remain inadequate. Recently, long non-coding RNAs (lncRNAs) have emerged as crucial players in cardiac function, showing possibilities as potential targets for HF therapy. These versatile molecules interact with chromatin, proteins, RNA, and DNA, influencing gene regulation. Notable lncRNAs like Fendrr, Trpm3, and Scarb2 have demonstrated therapeutic potential in HF cases. Additionally, utilizing lncRNAs to forecast survival rates in HF patients and distinguish various cardiac remodeling conditions holds great promise, offering significant benefits in managing cardiovascular disease and addressing its far-reaching societal and economic impacts. This underscores the pivotal role of lncRNAs in the context of HF research and treatment.

BACKGROUND: We aimed to identify patients with subphenotypes of postacute coronary syndrome (ACS) using repeated measurements of high-sensitivity cardiac troponin T, N-terminal pro-B-type natriuretic peptide, high-sensitivity C-reactive protein, and growth differentiation factor 15 in the year after the index admission, and to investigate their association with long-term mortality risk.
RESULTS: BIOMArCS (BIOMarker Study to Identify the Acute Risk of a Coronary Syndrome) was an observational study of patients with ACS, who underwent high-frequency blood sampling for 1 year. Biomarkers were measured in a median of 16 repeated samples per individual. Cluster analysis was performed to identify biomarker-based subphenotypes in 723 patients without a repeat ACS in the first year. Patients with a repeat ACS (N=36) were considered a separate cluster. Differences in all-cause death were evaluated using accelerated failure time models (median follow-up, 9.1 years; 141 deaths). Three biomarker-based clusters were identified: cluster 1 showed low and stable biomarker concentrations, cluster 2 had elevated concentrations that subsequently decreased, and cluster 3 showed persistently elevated concentrations. The temporal biomarker patterns of patients in cluster 3 were similar to those with a repeat ACS during the first year. Clusters 1 and 2 had a similar and favorable long-term mortality risk. Cluster 3 had the highest mortality risk. The adjusted survival time ratio was 0.64 (95% CI, 0.44-0.93; P=0.018) compared with cluster 1, and 0.71 (95% CI, 0.39-1.32; P=0.281) compared with patients with a repeat ACS.
CONCLUSIONS: Patients with subphenotypes of post-ACS with different all-cause mortality risks during long-term follow-up can be identified on the basis of repeatedly measured cardiovascular biomarkers. Patients with persistently elevated biomarkers have the worst outcomes, regardless of whether they experienced a repeat ACS in the first year.

Type 2 diabetes mellitus is a major health problem worldwide with a steadily increasing prevalence reaching epidemic proportions. The major concern is the increased morbidity and mortality due to diabetic complications. Traditional but also nontraditional risk factors have been proposed to explain the pathogenesis of type 2 diabetes mellitus and its complications. Hyperglycemia has been considered an important risk factor, and the strict glycemic control can have a positive impact on microangiopathy but not macroangiopathy and its related morbidity and mortality. Thus, the therapeutic algorithm has shifted focus from a glucose-centered approach to a strategy that now emphasizes target-organ protection. Sodium-glucose transporter 2 inhibitors is an extremely important class of antidiabetic medications that, in addition to their glucose lowering effect, also exhibit cardio- and renoprotective effects. Various established and novel biomarkers have been described, reflecting kidney and cardiovascular function. In this review, we investigated the changes in established but also novel biomarkers of kidney, heart and vascular function associated with sodium-glucose transporter 2 inhibitors treatment in patients with type 2 diabetes mellitus.

Patients presenting with symptoms suggestive of acute coronary syndrome (ACS) contribute to a high workload and overcrowding in the Emergency Department (ED). Accelerated diagnostic protocols for non-ST-elevation myocardial infarction have proved challenging to implement. One obstacle is the turnaround time for analyzing high-sensitivity cardiac troponin (hs-cTn). In the WESTCOR-POC study (Clinical Trials number NCT05354804) we aim to evaluate safety and efficiency of a 0/1 h hs-cTn algorithm utilizing a hs-cTnI point of care (POC) instrument in comparison to central laboratory hs-cTnT measurements.
This is a prospective single-center randomized clinical trial aiming to include 1500 patients admitted to the ED with symptoms suggestive of ACS. Patients will receive standard investigations following the European Society of Cardiology 0/1h protocols for centralized hs-cTnT measurements or the intervention using a 0/1h POC hs-cTnI algorithm. Primary end-points are 1) Safety; death, myocardial infarction or acute revascularization within 30 days 2) Efficiency; length of stay in the ED, 3) Cost- effectiveness; total episode cost, 4) Patient satisfaction, 5) Patient symptom burden and 6) Patients quality of life. Secondary outcomes are 12-months death, myocardial infarction or acute revascularization, percentage discharged after 3 and 6 h, total length of hospital stay and all costs related to hospital contact within 12 months.
Results from this study may facilitate implementation of POC hs-cTn testing assays and accelerated diagnostic protocols in EDs, and may serve as a valuable resource for guiding future investigations for the use of POC high sensitivity troponin assays in outpatient clinics and prehospital settings.

Previous observational studies have shown that the prevalence of cardiovascular diseases (CVDs) is related to particulate matter (PM). However, given the methodological limitations of conventional observational research, it is difficult to identify causality conclusively. To explore the causality of PM on CVDs and cardiovascular biomarkers, we conducted a Mendelian randomization (MR) analysis.
In this study, we obtained summary-level data for CVDs and cardiovascular biomarkers including atrial fibrillation (AF), heart failure (HF), myocardial infarction (MI), ischemic stroke (IS), stroke subtypes, body mass index (BMI), lipid traits, fasting glucose, fasting insulin, and blood pressure from several large genome-wide association studies (GWASs). Then we used two-sample MR to assess the causality of PM on CVDs and cardiovascular biomarkers, 16 single nucleotide polymorphisms (SNPs) for PM2.5 and 6 SNPs for PM10 were obtained from UK Biobank participants. Inverse variance weighting (IVW) analyses under the fixed effects model were used as the main analytical method to calculate MR Estimates, followed by multiple sensitivity analyses to confirm the robustness of the results.
Our study revealed increases in PM2.5 concentration were significantly related to a higher risk of MI (odds ratio (OR), 2.578; 95% confidence interval (CI), 1.611-4.127; p = 7.920 × 10-5). Suggestive evidence was found between PM10 concentration and HF (OR, 2.015; 95% CI, 1.082-3.753; p = 0.027) and IS (OR, 2.279; 95% CI,1.099-4.723; p = 0.027). There was no evidence for an effect of PM concentration on other CVDs. Furthermore, PM2.5 concentration increases were significantly associated with increases in triglyceride (TG) (OR, 1.426; 95% CI, 1.133-1.795; p = 2.469 × 10-3) and decreases in high-density lipoprotein cholesterol (HDL-C) (OR, 0.779; 95% CI, 0.615-0.986; p = 0.038). The PM10 concentration increases were also closely related to the decreases in HDL-C (OR, 0.563; 95% CI, 0.366-0.865; p = 8.756 × 10-3). We observed no causal effect of PM on other cardiovascular biomarkers.
At the genetic level, our study suggested the causality of PM2.5 on MI, TG, as well HDL-C, and revealed the causality of PM10 on HF, IS, and HDL-C. Our findings indicated the need for continued improvements in air pollution abatement for CVDs prevention.