Heart failure (HF) remains a major cause of morbidity and mortality worldwide. Therefore, there is a need to identify robust biomarkers to improve early diagnosis, stratify disease severity and predict outcomes. Biomarkers such as galectin-3 (Gal-3), TIMP-1, BNP, NT-proBNP, CysC, CA125, ST2 and MMP9 have shown the potential to reflect the pathophysiology of HF. Despite their clinical potential, their integration into routine practice is still limited. The use of bioinformatics may help uncover critical associations between these biomarkers and the progression of HF, providing opportunities for personalized disease management.

Following PRISMA guidelines, a systematic review of clinical studies was performed using databases with time constraints. The major proteins associated with HF were identified and their diagnostic and prognostic roles were analysed.

The study emphasizes that galectin-3 (Gal-3) and TIMP-1 serve as key indicators of fibrosis and inflammation, while BNP and NT-proBNP are reliable markers of cardiac stress. Cystatin C (CysC) reflects renal dysfunction, and CA125 correlates strongly with venous congestion. In addition, ST2 and MMP9 provide valuable insights into inflammation and tissue remodelling processes. These biomarkers are consistently elevated in patients with HF, emphasizing their critical role in detecting the systemic and cardiac manifestations of the disease.

Our results emphasize the importance of including biomarkers such as Gal-3, TIMP-1, BNP, NT-proBNP, CysC, CA125, ST2 and MMP9 in the diagnosis and treatment of HF. Their upregulation reflects the complex pathophysiological processes of HF and supports their use in the clinical setting to improve diagnostic accuracy, prognostic precision and personalized therapeutic strategies.

Heart failure is the leading cause of hospital admissions in Germany. The prevention of hospitalizations due to heart failure has recently improved, encompassing guideline-based basic therapy, targeted medication escalation options, and structured outpatient care incorporating telemedicine. An early identification of parameters that precede or indicate acute heart failure is crucial. The term "worsening heart failure" is broader than the term "acute heart failure". Worsening heart failure includes patients identified through clinical examination, biochemical methods (especially natriuretic peptides), and imaging (echocardiography, chest X-ray, lung ultrasound, computed tomography, magnetic resonance imaging), and innovative cardiac telemonitoring. Early detection of worsening heart failure is only beneficial if followed by appropriate management that stabilizes heart failure, reduces mortality, and decreases hospital admissions and emergency contacts. Dedicated guidelines for the treatment of worsening heart failure are not yet available. It is recommended to start or up-titrate guideline-recommended medical therapy and additionally initiate treatment with the soluble guanylate cyclase stimulator Vericiguat in patients with heart failure with a reduced ejection fraction. Initiation and up-titration should begin during hospitalization and should be completed during careful follow-up within the first 6 weeks after discharge. This guide provides recommendations for the comprehensive and coordinated treatment of worsening heart failure, considering all these aspects which are crucial for improving patient outcomes.

Short-chain fatty acids (SCFAs), produced through fermentation of dietary fibers by gut bacteria, play a central role in modulating cardiovascular function and heart failure (HF) development. The progression of HF is influenced by intestinal barrier dysfunction and microbial translocation, where SCFAs serve as key mediators in the gut-heart axis. This review examines the complex metabolic interactions between SCFAs and other gut microbiota metabolites in HF, including their relationships with trimethylamine N-oxide (TMAO), aromatic amino acids (AAAs), B vitamins, and bile acids (BAs). We analyze the associations between SCFA production and clinical parameters of HF, such as left ventricular ejection fraction (LVEF), N-terminal pro-B-type natriuretic peptide (NT-proBNP), and glomerular filtration rate (GFR). Gaining insights into metabolic networks offers new potential therapeutic targets and prognostic markers for managing heart failure, although their clinical significance needs further exploration.

N-terminal pro B-type natriuretic peptide (NT-proBNP) is a natriuretic peptide that is strongly associated with congestive heart failure (CHF). The utility of NT-proBNP for prediction of cardiovascular events and renal endpoints, compared with clinical risk factors, has not been evaluated in detail. We hypothesise that NT-proBNP can improve risk stratification and prediction of cardiorenal events in type 2 diabetes, beyond that provided by clinical risk factors.

NT-proBNP was measured in 1993 samples from the Hong Kong Diabetes Biobank, a multicentre prospective diabetes cohort and biobank. A cut-off of ≥125 pg/ml was used to define elevated NT-proBNP. Associations between elevated NT-proBNP and incident cardiovascular and renal endpoints were examined using Cox regression, adjusted for sex, age and duration of diabetes, as well as other covariates. Prognostic and incremental predictive values of NT-proBNP in diabetes cardiorenal complications, compared with those of the Joint Asia Diabetes Evaluation risk equations for CHD, CHF and kidney failure, were evaluated using the concordance index (C index), net reclassification improvement index, integrated discrimination improvement index and relative integrated discrimination improvement index.

A total of 24.7% of participants had elevated NT-proBNP. Participants with elevated NT-proBNP at baseline had a more adverse cardiometabolic profile, with 2-4-fold higher frequency of complications at baseline. Adjusting for age at baseline, sex and duration of diabetes, elevated NT-proBNP was associated with incident atrial fibrillation (HR 4.64 [95% CI 2.44, 8.85]), CHD (HR 4.21 [2.46, 7.21]), CVD (HR 3.32 [2.20, 5.01]) and CHF (HR 4.18 [2.18, 8.03]; all p<0.001). All these associations remained significant after further adjustment for additional covariates. Elevated NT-proBNP had good discriminative ability for various cardiorenal endpoints, with C index of 0.83 (95% CI 0.76, 0.90) for CHD, 0.88 (0.81, 0.94) for atrial fibrillation, 0.89 (0.83, 0.95) for CHF, 0.81 (0.77, 0.84) for 40% drop in eGFR and 0.88 (0.84, 0.92) for kidney failure. Models incorporating NT-proBNP had improved prediction compared with established clinical risk models. Sensitivity analyses including alternative cut-off of NT-proBNP, as well as use of other risk engines of CHD, yielded similar results.

NT-proBNP demonstrated a promising ability to serve as a prognostic marker for a variety of cardiorenal complications in type 2 diabetes. Considering NT-proBNP in clinical assessments could potentially help identify high-risk individuals who may benefit from more intensive therapies.

This study aimed to develop a reliable and effective nomogram model to identify high-risk populations with non-response to prone position ventilation (PPV) in acute respiratory distress syndrome (ARDS) patients.

This retrospective cohort study included 175 patients with ARDS undergoing PPV. An improvement of ≥ 20 mmHg in the PaO2/FiO2 after the first PPV was defined as a 'response'. For the construction of the model, all patients were randomly assigned to the train and validation cohort according to 2:1. Multivariate logistic regression was useed to develop the nomogram. The area under the receiver operating characteristic curve (AUC), decision curve and calibration curve were assessed to evaluate the efficiency, clinical utility and calibration of the model.

The overall rate of non-response to PPV in ARDS patients was approximately 32.6 %. In the training cohort and validation cohort, the rate are 29.9 % and 34.5 % respectively. Murray score ≥ 2.5 (OR: 4.29), procalcitonin (PCT) ≥ 2 ng/mL (OR: 2.52), N-terminal pro-B-type natriuretic peptide (Nt-proBNP) ≥ 2000 pg/ml (OR: 2.44), and hemoglobin ≤ 90 g/L (OR: 2.39) were independently associated with the rate of non-response to PPV and combined in prediction model. The model demonstrated good predictive value with AUC of 0.817 and 0.828 in the train and validation cohort. Calibration curve showed good calibration and decision curve analysis indicated favorable clinical utility.

This study constructed a risk prediction model for non-response to PPV, which demonstrated good predictive value and clinical utility.

Early identification of prone position response in ARDS is essential for timely alternative treatments, improving patient prognosis and healthcare efficiency. The predictive model included representative indicators of patients with ARDS, encompassing parameters such as the acute lung injury (Murray score), cardiac function (Nt-proBNP), infectious status (PCT), and hemoglobin levels.

The therapeutic efficacy of Ershen Zhenwu Decoction (ESZWD)-a famous formulation from Xin'an for patients with chronic heart failure heart-kidney Yang deficiency (CHF-HKYD)-is well established. Still, the underlying molecular mechanism is not clear.

This study investigated mechanisms by which ESZWD suppresses cardiac pathology, including myocardial fibrosis, in CHF-HKYD model rats and Ang II-stimulated cardiac fibroblasts (CFs).

The components in ESZWD were analyzed by ultra-high-performance liquid chromatography coupled with Quadrupole Time-Of-Flight mass spectrometry (UHPLC-Q-TOF-MS). CHF-HKYD model was established in the male Sprague-Dawley rats through bilateral thyroidectomy and intraperitoneal administration of 0.02% doxorubicin (DOX), twice weekly for 3 weeks. Subsequently, the CHF-HKYD model rats were randomly categorized into the Model, ESZWD-L (3.96 g/kg/d ESZWD), ESZWD-M (7.92 g/kg/d ESZWD), ESZWD-H (15.84 g/kg/d ESZWD), and Sac/Val (68 mg/kg/d sacubitril/valsartan) groups and treated daily for 4 weeks. As a control, the sham surgery group (Sham) was used. Primary cardiac fibroblasts (CFs) were categorized into Control, Model, ESZWD, and Sac/Val groups. Then, the CFs were stimulated with Ang-II. The ESZWD and Sac/Val groups were incubated with different concentrations of drug-containing sera and their effects on CF viability were assessed via the CCK-8 assay. The ESZWD and Sac/Val groups received drug-containing serum concentrations determined by CCK-8 assay results. The cardioprotective effects of ESZWD were determined using echocardiography, Hematoxylin & Eosin (H&E) staining, Masson staining, and Sirius red staining, and the Enzyme Linked Immunosorbent Assay (ELISA). ESZWD's effects on the Ras Homolog Gene Family Member A (RhoA)/Rho-Associated Coiled-Coil Kinases (ROCKs) signaling pathway and myocardial fibrosis were assessed by Western blotting and Quantitative Real-Time PCR (qRT-PCR) analyses. Immunofluorescence was used to observe fibrotic markers in CFs.

ESZWD treatment improved cardiac function in the CHF-HKYD rats by significantly reducing myocardial fibrosis and ventricular remodeling. ESZWD treatment increased the rats' body temperature (Tb) and 24-h urine volume, left ventricular ejection fraction (LVEF) and LV fractional shortening (LVFS), and decreased LV internal systolic diameter (LVIDs), LV internal diastolic diameter (LVIDd), and heart weight/body weight (HW/BW) compared to the Model group. In comparison to the model rats, ESZWD treatment decreased serum levels of B-type natriuretic peptide precursor (NT-proBNP), tumor necrosis factor-alpha (TNF-α), interleukin-11 (IL-11), and IL-17A. ESZWD treatment significantly down-regulated the protein and mRNA expression levels of collagen I A1, α-SMA, RhoA, ROCK1, and ROCK2 in the heart tissues of the CHF-HKYD rats and the Ang II-stimulated CFs.

ESZWD significantly improved cardiac function and attenuated myocardial fibrosis and inflammation in the CHF-HKYD rats by inhibiting the RhoA/ROCKs signaling pathway.

The recurrence of atrial fibrillation (AF) in patients after successful radiofrequency catheter ablation (RFCA) appears to be an unresolved clinical issue and needs to be clearly elucidated. There are many factors associated with AF recurrence, such as duration of AF, male sex, concomitant heart failure, hemodynamic parameters, chronic obstructive pulmonary disease, hypertension, obstructive sleep apnea, hyperthyroidism, smoking and obesity. However, the inflammatory changes are strongly associated with electrical and structural cardiac remodeling, cardiac damage, myocardial fibrotic changes, microvascular dysfunction and altered reparative response. In this context, biomarkers reflecting the different stages of AF pathogenesis deserve thorough investigation. The authors of the retrospective study revealed that one-year recurrence rate of non-valvular AF in the high systemic immune inflammation (SII) index group was significantly increased compared to that of the low SII index group and provided additional predictive value to the APPLE. Furthermore, the authors suggest that this biomarker may help physicians to optimize the selection of AF patients and to develop a personalized treatment approach. In conclusion, the SII index may serve as a valuable indicator of recurrent AF in patients after RFCA and may be a biomarker with plausible predictive value for poor clinical outcomes.

Atrial fibrillation (AF) is a common treatable risk factor for stroke. Screening for paroxysmal AF in general practice is difficult, but biomarkers might help improve screening strategies.

We investigated six blood biomarkers for predicting paroxysmal AF in general practice.

This was a pre-specified sub-study of the SCREEN-AF RCT done in Germany. Between 12/2017-03/2019, we enrolled ambulatory individuals aged 75 years or older with a history of hypertension but without known AF. Participants in the intervention group received active AF screening with a wearable patch, continuous ECG monitoring for 2x2 weeks and usual care in the control group. The primary endpoint was ECG-confirmed AF within six months after randomisation. High-sensitive Troponin I (hsTnI), brain natriuretic peptide (BNP), N-terminal pro-B-type natriuretic peptide (NT-pro BNP), N-terminal pro atrial natriuretic peptide (NT-ANP), mid-regional pro atrial natriuretic peptide (MR-pro ANP) and C-reactive protein (CRP) plasma levels were investigated at randomisation for predicting AF within six months after randomisation.

Blood samples were available for 291 of 301 (96.7%) participants, including 8 with AF (3%). Five biomarkers showed higher median results in AF-patients: BNP 78 vs. 41 ng/L (p = 0.012), NT-pro BNP 273 vs. 186 ng/L (p = 0.029), NT-proANP 4.4 vs. 3.5 nmol/L (p = 0.027), MR-pro ANP 164 vs. 125 pmol/L (p = 0.016) and hsTnI 7.4 vs. 3.9 ng/L (p = 0.012). CRP levels were not different between groups (2.8 vs 1.9 mg/L, p = 0.1706).

Natriuretic peptide levels and hsTnI are higher in patients with AF than without and may help select patients for AF screening, but larger trials are needed.

AI-CAC provides more actionable information than the Agatston coronary artery calcium (CAC) score. We have recently shown in the MESA (Multi-Ethnic Study of Atherosclerosis) that AI-CAC automated left atrial (LA) volumetry enabled prediction of atrial fibrillation (AF) as early as 1 year.

In this study, the authors evaluated the performance of AI-CAC LA volumetry versus LA measured by human experts using cardiac magnetic resonance imaging (CMRI) for predicting incident AF and stroke and compared them with Cohorts for Heart and Aging Research in Genomic Epidemiology model for atrial fibrillation (CHARGE-AF) risk score, Agatston score, and N-terminal pro b-type natriuretic peptide (NT-proBNP).

We used 15-year outcomes data from 3,552 asymptomatic individuals (52.2% women, age 61.7 ± 10.2 years) who underwent both CAC scans and CMRI in the MESA baseline examination. CMRI LA volume was previously measured by human experts. Data on NT-proBNP, CHARGE-AF risk score, and the Agatston score were obtained from MESA. Discrimination was assessed using the time-dependent area under the curve.

Over 15 years follow-up, 562 cases of AF and 140 cases of stroke accrued. The area under the curve for AI-CAC versus CMRI volumetry for AF (0.802 vs 0.798) and stroke (0.762 vs 0.751) were not significantly different. AI-CAC LA significantly improved the continuous net reclassification index for prediction of 5-year AF when added to CHARGE-AF risk score (0.23), NT-proBNP (0.37, 0.37), and Agatston score (0.44) (P for all <0.0001).

AI-CAC automated LA volumetry and CMRI LA volume measured by human experts similarly predicted incident AF and stroke over 15 years. Further studies to investigate the clinical utility of AI-CAC for AF and stroke prediction are warranted.

Elevated liver stiffness has been associated with atrial fibrillation (AFib) in the general population. The mechanism underlying this association is unclear.

Participants were recruited from the general population and prospectively enrolled with follow-up for 5 years. The fibrosis-4 (FIB-4) index was used as a surrogate marker for liver fibrosis. Proteomics analysis was performed using the 92-target Olink inflammation panel. Validation was performed using the NAFLD fibrosis score (NFS), aspartate aminotransferase to platelet index (APRI), and repeat confirmation proteomics.

A sample of 11,509 participants with a mean age of 54.0 ± 11.1 years, 51.3% women, and a median FIB-4 index of 0.85 (0.65/1.12), was used. The FIB-4 index was predictive for prevalent (FIB-4 index adjusted odds ratio (aOR) per SD: 1.100 with 95% CI 1.011-1.196; p = 0.026), but not incident AFib (log[FIB-4 index]) adjusted hazard ratio: 1.125 with 95% CI 0.943-1.342, p = 0.19). Elastic net regularized regression identified CCL20, DNER, and CXCL10 for prevalent AFib, and AXIN1, CXCL10, and Flt3L for the log(FIB-4 index) (per SD) as most important in common regulated proteins. The relationship between the FIB-4 index, the identified proteins, and AFib was relevant and reproduced at the 5-year follow-up for CXCL10 after adjusting for confounders (log[FIB-4 index] per SD - CXCL10 [per SD] adjusted β 0.160 with 95% CI 0.127-0.194, p <0.0001; CXCL10 [per SD] - AFib aOR 1.455 with 95% CI 1.217-1.741, p <0.0001), reproduced using the NFS and APRI, and corresponding to increased serum levels.

CXCL10 is linked to liver fibrosis, as determined by the FIB-4 index, and to prevalent AFib.

How elevated liver stiffness relates to atrial fibrillation in the general population remains to be clarified. We hypothesized that systemic inflammation against a background of liver fibrosis produced from metabolic dysfunction-associated steatotic liver disease (MASLD), is involved in the pathophysiology of atrial fibrillation. Using large-scale targeted proteomics, we found that CXCL10 is related to both liver fibrosis, as defined by the fibrosis-4 index, and to atrial fibrillation. These results can aid evidence-based drug development for patients with atrial fibrillation and MASLD-related liver fibrosis.

Post-operative atrial fibrillation (POAF) is a frequent complication after cardiac surgery. It is associated with prolonged hospital stay, increased morbidity, mortality rate and economic costs. The aim of the study was to determine the association between the values of Galectin3 and N-terminal pro-B-type natriuretic peptide (NTproBNP) with POAF after cardiac surgery.

A prospective study enrolled patients aged 18-85 years old admitted due to elective coronary artery bypass graft surgery (CABG) or CABG + aortic valve replacement. The plasma Galectin-3 and NT-proBNP levels were measured one day before surgery postoperative days 1 and 7.

The study included a total of 103 patients. POAF was registered in 45 patients. The mean age of patients in whom POAF occurred was 68.8 years, while other patients' mean age was 65.5 years (p=0.028). Patients with POAF did not differ from the group without POAF in the values of Galectin-3 and NT-proBNP preoperatively as well as on the first and seventh postoperative days. Changes in Galectin-3 levels on the first postoperative day had statistically significant value for predicting POAF (AUC=0.627 0.509-0.745 , p<0.05). Decrease in Galectin-3 level con centration on the first postoperative day over 17% increases the risk of developing AF.

Preoperative values of Galectin-3 and NTproBNP are not associated with POAF development after cardiac surgery.

(1) Background: Given its high cardiac specificity and its capacity to directly assess the cardiac function, cardiac myosin-binding protein (MyBP-C) is a promising biomarker in patients with acute heart failure (AHF). The aim of our study was to investigate the clinical utility of this novel marker for diagnosis and short-term prognosis in subjects with AHF. (2) Methods: We measured plasma levels of MyBP-C at admission in 49 subjects (27 patients admitted with AHF and 22 controls). (3) Results: The plasma concentration of MyBP-C was significantly higher in patients with AHF compared to controls (54.88 vs. 0.01 ng/L, p < 0.001). For 30-day prognosis, MyBP-C showed significantly greater AUC (0.972, p < 0.001) than NT-proBNP (0.849, p = 0.001) and hs-TnI (0.714, p = 0.047). In a multivariate logistic regression analysis, an elevated level of MyBP-C was the best independent predictor of 30-day mortality (OR = 1.08, p = 0.039) or combined death/recurrent 30-days rehospitalization (OR = 1.12, p = 0.014). (4) Conclusions: Our data show that circulating MyBP-C is a sensitive and cardiac-specific biomarker with potential utility for the accurate diagnosis and prognosis of AHF.

The diagnosis of cardiac syncope remains a challenge. This study sought to develop and validate a diagnostic model for the early identification of individuals likely to have a cardiac cause.

877 syncope patients with a determined cause were retrospectively enrolled at a tertiary heart center. They were randomly divided into the training set and validation set at a 7:3 ratio. We analyzed the demographic information, medical history, laboratory tests, electrocardiogram, and echocardiogram by the least absolute shrinkage and selection operator (LASSO) regression for selection of key features. Then a multivariable logistic regression analysis was performed to identify independent predictors and construct a diagnostic model. The receiver operating characteristic curves, area under the curve (AUC), calibration curves, and decision curve analysis were used to evaluate the predictive accuracy and clinical value of this nomogram.

Five independent predictors for cardiac syncope were selected: BMI (OR 1.088; 95% CI 1.022-1.158; P =0.008), chest symptoms preceding syncope (OR 5.251; 95% CI 3.326-8.288; P <0.001), logarithmic NT-proBNP (OR 1.463; 95% CI 1.240-1.727; P <0.001), left ventricular ejection fraction (OR 0.940; 95% CI 0.908-0.973; P <0.001), and abnormal electrocardiogram (OR 6.171; 95% CI 3.966-9.600; P <0.001). Subsequently, a nomogram based on a multivariate logistic regression model was developed and validated, yielding AUC of 0.873 (95% CI 0.845-0.902) and 0.856 (95% CI 0.809-0.903), respectively. The calibration curves showcased the nomogram's reasonable calibration, and the decision curve analysis demonstrated good clinical utility.

A diagnostic tool providing individualized probability predictions for cardiac syncope was developed and validated, which may potentially serve as an effective tool to facilitate early identification of such patients.

Patients with stroke often remain bedridden despite rehabilitation. Serum N-terminal pro-B-type natriuretic peptide (NT-pro-BNP) levels increase after stroke. Our study aimed to investigate the difference in NT-pro-BNP levels between bedridden and non-bedridden patients with stroke and to explore the factors influencing NT-pro-BNP levels in bedridden patients.

A single-centre, cross-sectional study.

This study was conducted in a hospital, Shenzhen, China.

Between January 2019 and December 2022, 465 participants were included in this study.

The collected data included basic information, laboratory data and echocardiographic parameters. Binary logistic regression analysis and receiver operating characteristic curves were used to identify factors associated with high NT-pro-BNP levels.

Bedridden patients with stroke had higher levels of NT-pro-BNP, D-dimer, high-sensitivity C reactive protein (hs-CRP) and lower levels of creatinine, high-density lipoprotein cholesterol, albumin and haemoglobin, as well as lower left ventricular ejection fraction, fractional shortening and the ratio between the peak velocities of early and late diastolic filling than non-bedridden patients. In bedridden patients, age ≥75 years, high levels of hs-CRP and creatinine, and low levels of albumin were associated with high NT-pro-BNP levels. In non-bedridden patients, age ≥75 years and high creatinine levels were associated with high NT-pro-BNP levels. In bedridden patients with stroke, the area under the curve (AUC) of hs-CRP was 0.700 (p<0.001, 95% CI 0.638 to 0.762) with a cut-off value of 5.12 mg/L. The AUC of albumin was 0.671 (p<0.001, 95% CI 0.606 to 0.736) with a cut-off value of 37.15 g/L.

NT-pro-BNP levels were higher in bedridden patients with stroke than in non-bedridden patients. Decreased albumin and elevated hs-CRP levels were associated with high levels of NT-pro-BNP in bedridden patients. Further studies are needed to explore the risk stratification and potential treatments for elevated NT-pro-BNP in bedridden patients with stroke.

N terminal pro brain natriuretic peptide (NT-proBNP) plays an important role in the diagnosis and prognosis of heart failure (HF). The plasma level of NT-proBNP in atrial fibrillation (AF) patients was higher than of sinus rhythm patients. In HF, NT-proBNP levels are affected by the concomitant presence of AF, making it difficult to distinguish between HF and AF in patients with elevated NT-proBNP. Several other diseases, such as renal failure and pulmonary embolism, are known to further increase NT-proBNP levels in patients with concomitant HF. Therefore, NT-proBNP is a sensitive but non-specific marker for the detection of HF. AF is very important in this regard because among patients with HF regardless of ejection fraction, symptoms such as shortness of breath and atrial enlargement develop and can mimic HF. In the present study, we investigated whether the prognostic value of natriuretic peptides in HF holds true for patients with concomitant AF.

Atrial fibrillation (AF) is the most diagnosed arrhythmia in clinical settings. The fatty liver index (FLI) is a marker of liver steatosis with potential cardiovascular implications. This study investigated whether FLI could predict the risk of AF.

We used data from the Suita Study, a Japanese population-based prospective cohort study. A total of 2,346 men and 3,543 women, aged 30-84 years, without prevalent AF were included and followed up. The diagnosis of AF was established during follow-up using electrocardiograms, hospital records, and death certificates. FLI was assessed during a baseline health checkup. Hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated for incident AF per FLI quintile and log-transformed FLI. Within a median 14.5 years of follow-up, 142 men and 105 women developed AF. Compared with women in the third (middle) FLI quintile, women in the first (lowest), fourth, and fifth (highest) quintiles showed a higher risk of AF, with multivariable-adjusted HRs of 2.37 (95% CI 1.06-5.31), 2.60 (95% CI 1.30-5.17), and 2.04 (95% CI 1.00-4.18), respectively. No corresponding associations were observed in men. The change in log-transformed FLI was not associated with the risk of AF in either sex.

A U-shaped association between FLI and AF risk was detected in Japanese women. FLI could be a screening tool to detect women at high risk of developing AF.

Atrial fibrillation (AF) is the most common type of cardiac arrhythmia. Proteins are a component of cardiac biomarkers containing cell structures that are released into the circulation when a myocardial injury occurs. They are essential in the diagnosis, risk assessment, and treatment of patients who have chest pain, are thought to have acute coronary syndrome, or are experiencing acute heart failure exacerbations. There are numerous biochemical cardiac markers, but this article summarizes the basic role of major biochemical cardiac markers, including cardiac natriuretic peptides, cardiac troponins, C-reactive protein (CRP), creatine kinase-MB, heart-type fatty acid-binding protein, ischemia-modified albumin, lipoprotein (a), osteopontin (OPN), and soluble suppression of tumorigenicity 2 (sST2), in AF. Atrial natriuretic peptide may serve as an indicator of atrial integrity, which may help to select appropriate treatment approaches for AF. Higher levels of N-terminal pro-B-type natriuretic peptide and brain natriuretic peptide are predictive of incidental AF. Increased troponin T release may indicate better clinical results following AF ablation. Similarly, CRP increases the risk of the AF-increasing calcium (Ca) influx in atrial myocytes, but not because of atrial fibrosis. Patients with postoperative AF have lower FABP3 gene expression in the atrium. Lipoprotein (a) (Lp[a]) may play a causative role in the onset of AF and impact various cardiac tissues. Clinical trials for Lp(a)-lowering drugs should assess their impact on preventing AF. Also, OPN was highly expressed in the circulation of AF patients and further increased with the progression of AF. sST2 was a reliable predictor of new-onset AF and can improve the accuracy of the AF risk model. There is a greater chance that these cardiac biomarkers might be employed to enhance clinical risk stratification in AF.

The aim of this narrative review is to summarize contemporary evidence on the use of circulating cardiac biomarkers of heart failure (HF) and to identify a promising biomarker model for clinical use in personalized point-of-care HF management. We discuss the reported biomarkers of HF classified into clusters, including myocardial stretch and biomechanical stress; cardiac myocyte injury; systemic, adipocyte tissue, and microvascular inflammation; cardiac fibrosis and matrix remodeling; neurohumoral activation and oxidative stress; impaired endothelial function and integrity; and renal and skeletal muscle dysfunction. We focus on the benefits and drawbacks of biomarker-guided assistance in daily clinical management of patients with HF. In addition, we provide clear information on the role of alternative biomarkers and future directions with the aim of improving the predictive ability and reproducibility of multiple biomarker models and advancing genomic, transcriptomic, proteomic, and metabolomic evaluations.

Most studies, especially in primary prevention patients, have evaluated N-terminal B-type natriuretic peptide (NT-proBNP) at one time point. Evaluation of change in NT-proBNP may improve risk stratification for incident cardiovascular events.

To assess the association between change in NT-proBNP and risk for incident heart failure (HF) and death.

Participants were recruited from 4 US communities enrolled in the Atherosclerosis Risk in Community (ARIC) study. Individuals who attended ARIC visits 2 and 4 (approximately 6 years apart) with measurements of NT-proBNP and without prevalent HF were included. Assays of NT-proBNP were conducted between 2011 and 2013, and analysis took place between July 2021 and October 2022.

The primary exposure variable was NT-proBNP change between visits 2 and 4, modeled as change categories (<125 pg/mL or ≥125 pg/mL) and as percent change.

The primary outcome measures were incident HF hospitalization and all-cause death. The association between changes in cardiovascular risk factors with change in NT-proBNP was further assessed.

A total of 9776 individuals (mean [SD] age, 57.1 [5.7] years at visit 2; 5523 [56.5%] women) were included in the study. Compared with participants with NT-proBNP level less than 125 pg/mL at both visits, participants with NT-proBNP level of 125 pg/mL or higher at both visits had an increase in incident HF (adjusted hazard ratio [HR], 2.40 [95% CI, 2.00-2.88]) and mortality risk (HR, 1.68 [95% CI, 1.47-1.91). Participants with NT-proBNP levels of 125 pg/mL or higher at visit 2 and less than 125 pg/mL at visit 4 had similar risk for HF and death (HR, 1.01 [95% CI, 0.71-1.43]; HR, 0.79 [95% CI, 0.61-1.01]) compared with the group with NT-proBNP levels of less than 125 pg/mL at both visits. The percent change in NT-proBNP was positively associated with HF and death (HR, 1.06 [95% CI, 1.02-1.10]; HR, 1.05 [95% CI, 1.03-1.08] per 1-SD increase, respectively). Change in systolic blood pressure, low-density lipoprotein cholesterol, triglyceride level, body mass index, and estimated glomerular filtration rate were significantly associated with change in NT-proBNP.

In this study, 6-year change in NT-proBNP reflected dynamic change in risk for HF events and death among community-dwelling adults without prevalent clinical HF. These results support the utility of serial NT-proBNP measurements to improve risk stratification of patients with pre-HF.

The syndrome heart failure with preserved ejection fraction (HFpEF) represents patients with different comorbidities and specific etiologies, but with a key and common alteration: an elevation in left ventricular (LV) filling pressure or pulmonary capillary wedge pressure (PCWP). Expert consensuses, society guidelines, and diagnostic scores have been stated to diagnose HFpEF syndrome based mainly on the determination of elevated LV filling pressure or PCWP by transthoracic echocardiography (TTE). Echocardiographic parameters such as early (E) and late diastolic mitral inflow velocity (mitral E/A ratio), septal and lateral mitral annular early diastolic velocity (E'), ratio of the early diastolic mitral inflow and annular velocity (E/E'-ratio), maximal left atrial volume index (LAVI_max), and tricuspid regurgitation peak velocity (V_TR) constitute the pivotal parameters for determining elevated LV filling pressure or PCWP in patients with suspected HFpEF symptoms. Notwithstanding this, taking into consideration the heterogeneity of patients with HFpEF symptoms, the term "HFpEF" should be considered as a syndrome rather than an entity since HFpEF results from different pathological entities that should and can be characterized by echocardiography and multimodality imaging. Comprehensive TTE might help diagnose specific diseases and etiologies by characterization of specific cardiac phenotypes.