Chronic coronary syndrome (CCS) and atrial fibrillation (AF) are prevalent cardiovascular conditions between whom there is a dual relationship, with significant morbidity and mortality. Recent studies have highlighted the roles of galectin-3 and pentraxin-3 as potential biomarkers in coronary atherosclerosis, yet their specific interactions and implications in patients with CCS and AF remain underexplored. This proof-of-concept study aimed to evaluate the levels of galectin-3 and pentraxin-3 in a cohort of patients with CCS and AF. A total of 131 patients diagnosed with CCS or/and AF were stratified based on coronary stenosis severity (significant, S-CCS and nonsignificant, N-CCS coronary lesions) and arrhythmia burden. Blood samples were collected to measure serum levels of galectin-3 and pentraxin-3 using enzyme-linked immunosorbent assay (ELISA) techniques. Clinical data, including demographic information, comorbidities, medication use, and biological markers of systemic inflammation, were recorded. The galectin-3 value was more than double in patients with S-CCS compared with those with N-CCS (17.39 ± 4.459 ng/mL versus 7.49 ± 2.732 ng/mL, p < 0.001). Atrial fibrillation was not associated with statistically significant variations in galectin-3 values, neither overall nor separately in the group of S-CCS or N-CCS. However, pentraxin-3 values were similar in S-CCS compared with those with N-CCS (2839.18 ± 1521.639 pg/mL versus 2564.07 ± 1299.055 pg/mL, p = 0.417). These values were lower in patients with sinus rhythm, with a mean of 2469.91 ± 1253.782 pg/mL, and steadily increased in those with paroxysmal, persistent, and permanent AF, for whom they reached a mean of 3162.87 ± 1893.068 pg/mL. Elevated levels of galectin-3 appear to correlate with coronary stenosis severity and may inform future strategies for risk stratification, patients’ selection for invasive coronarography or therapeutic targeting in CCS.

Chronic coronary syndrome (CCS) and atrial fibrillation (AF) are prevalent cardiovascular conditions that share numerous risk factors and pathophysiological mechanisms. While clinical scores commonly used in AF—such as CHA₂DS₂VA (which includes congestive heart failure, hypertension, age ≥ 75, diabetes, stroke/TIA, vascular disease, and age 65–74), HAS-BLED (which incorporates hypertension, abnormal renal/liver function, stroke, bleeding history, labile INR, elderly age, and drug/alcohol use), and C₂HEST (incorporating coronary artery disease, COPD, hypertension, elderly age ≥ 75, systolic heart failure, and thyroid disease)—are traditionally applied to rhythm or bleeding risk prediction, their value in estimating the angiographic severity of coronary artery disease (CAD) remains underexplored. We conducted a prospective, single-center study including 131 patients with suspected stable CAD referred for coronary angiography, stratified according to coronary angiographic findings into two groups: significant coronary stenosis (S-CCS) and non-significant coronary stenosis (N-CCS). At admission, AF-related scores (CHA₂DS₂, CHA₂DS₂VA, CHA₂DS₂VA-HSF, CHA₂DS₂VA-RAF, CHA₂DS₂VA-LAF, HAS-BLED, C₂HEST, and HATCH) were calculated. CAD severity was subsequently assessed using the SYNTAX and Gensini scores. Statistical comparisons and Pearson correlation analyses were performed to evaluate the association between clinical risk scores and angiographic findings. Patients in the S-CCS group had significantly higher scores in CHA₂DS₂VA (4.09 ± 1.656 vs. 3.20 ± 1.338, p = 0.002), HAS-BLED (1.98 ± 0.760 vs. 1.36 ± 0.835, p < 0.001), CHA₂DS₂VA-HSF (6.00 ± 1.854 vs. 5.26 ± 1.712, p = 0.021), and C₂HEST (3.49 ± 1.501 vs. 2.55 ± 1.279, p < 0.001). Multivariate logistic regression identified HAS-BLED and C₂HEST as independent predictors of significant coronary lesions. A threshold value of HAS-BLED ≥ 1.5 and C₂HEST ≥ 3.5 demonstrated moderate discriminative ability (AUC = 0.694 and 0.682, respectively), with acceptable sensitivity and specificity. These scores also demonstrated moderate to strong correlations with both Gensini and SYNTAX scores. AF-related clinical scores, especially HAS-BLED and C₂HEST, may serve as practical and accessible tools for early CAD risk stratification in patients with suspected CCS. Their application in clinical practice may serve as supplementary triage tools to help prioritize patients for further diagnostic evaluation, but they are not intended to replace standard imaging or testing.

Background: Cardiovascular implications in systemic lupus erythematosus (SLE) are common and varied, including impacts on the pericardium, myocardium, valves, coronary arteries, and conduction system; all of these could be potential substrates or triggers of cardiac arrhythmias by interfering with disease severity and specific medication. Therefore, this narrative review aimed to assess the cardiac involvement in SLE underlying, mainly, cardiac arrhythmias. Methods: We analyzed studies, published between 2015 and 2025 on PubMed, which explore cardiovascular involvement with a focus on arrhythmias in SLE from the perspectives of epidemiology, underlying mechanisms, diagnostic techniques, and the impact of standard and biologic therapies. Results: The cardiac manifestation of LES (lupus pericarditis, lupus myocarditis, Libman–Sacks endocarditis, coronary artery disease, coronary vasculitis or myocardial fibrosis) represents a substrate for arrhythmia risk. These substrates, in association with other arrhythmias mechanisms considered as triggers or conduction abnormalities, determined arrhythmogenic conditions in these patients. In addition to structural heart disease, arrhythmias in SLE are caused by ongoing inflammation, immune system irregularities, microvascular problems, autonomic imbalance, oxidative stress, and side effects from treatments. Despite this complex background, arrhythmias are often overlooked and not routinely investigated in SLE care. Data that show how disease-modifying drugs may affect arrhythmias are limited and inconsistent, highlighting significant gaps in knowledge. Cardiac arrhythmias are a significant but, as yet, insufficiently underrecognized aspect of SLE, with serious implications for prognosis. Conclusions: Systemic lupus erythematosus causes cardiovascular involvement that is associated with arrhythmias through various and complexes mechanisms, mainly related to direct cardiovascular structural damage, systemic inflammation or specific therapies. Data on arrhythmias secondary to cardiovascular damage in patients with SLE in the literature are limited. Therefore, early detection of electrical issues, regular cardiovascular evaluation in high-risk patients, and careful management of treatment effects are vital. A coordinated, multidisciplinary cardio-rheumatology approach is essential to improving arrhythmia detection, tailoring treatments, and ultimately decreasing cardiovascular complications and deaths in SLE patients.

Chronic coronary syndrome (CCS) and atrial fibrillation (AF) are prevalent cardiovascular conditions, between whom there is a dual relationship, with significant morbidity and mortality. Recent studies have highlighted the roles of galectin-3 and pentraxin-3, as potential biomarkers in coronary atherosclerosis, yet their specific interactions and implications in patients with CCS and AF remain underexplored. This study aimed to evaluate the levels of galectin-3 and pentraxin-3 in a cohort of patients with CCS and AF. A total of 131 patients diagnosed with CCS or/and AF were stratified based on coronary stenosis severity (significant, S-CCS and non-significant, N-CCS coronary lesions) and arrhythmia burden. Blood samples were collected to measure serum levels of galectin-3 and pentraxin-3 using enzyme-linked immunosorbent assay (ELISA) techniques. Clinical data, including demographic information, comorbidities, medication use and biological markers of systemic inflammation, were recorded. The galectin-3 value was more than double in patients with S-CCS compared to those with N-CCS (17.39 4.459 ng/mL versus 7.49 2.732 ng/mL, p<0.001). Atrial fibrillation was not associated with statistically significant variations in galectin-3 values, neither overall nor separately in the group of S-CCS or N-CCS. However, pentraxin-3 values, were similar in S-CCS compared to those with N-CCS (2839.18 1521.639 pg/mL versus 2564.07 1299.055 pg/mL, p=0.417). These values were lower in patients with sinus rhythm, with a mean of 2469.91 1253.782 pg/mL and steadily increase in those with paroxysmal, persistent and permanent AF, for whom they reach a mean of 3162.87 1893.068 pg/mL. This study underscores the potential of galectin-3 and pentraxin-3 as biomarkers in patients with CCS and AF. Elevated levels of galectin-3 correlate with coronary stenosis severity and could serve as indicator for risk stratification, patients’ selection for invasive coronarography or therapeutic targeting in CCS.

Background: Systemic sclerosis (SSc) is a rare autoimmune disease characterized by progressive fibrosis, systemic inflammation and vascular dysfunction, with manifestations that can affect multiple organs, including the heart. Cardiac involvement in SSc is often underdiagnosed, although it can have serious consequences on the prognosis, especially the occurrence of arrhythmias. These rhythm disturbances can result from direct damage to the myocardium, the conduction system, or the coronary microcirculation. Equally, the medication used can have iatrogenic consequences manifested by severe arrhythmias. Methodology: The aim of this study was to provide a synthesis of incidence, pathogenic mechanisms, diagnostic methods, and therapeutic strategies of arrhythmias associated with SSc. The potential effects of immunomodulatory therapies, such as conventional immunosuppressants and biological therapies, on cardiac electrical function were also analyzed. This narrative review could present the state of the art on arrhythmias associated with SSc, which could serve as a practical guide. In clinical practice, it is necessary to establish a team that includes cardiologists and rheumatologists as well as other specialists to contribute to a correct diagnosis followed by an optimal therapy in patients with SSc. Results: Current data suggest that diffuse myocardial fibrosis, silent ischemia, and inflammatory infiltration may alter the propagation of the electrical impulse in the heart, favoring the occurrence of arrhythmias. Atrioventricular blocks, ventricular tachyarrhythmias, and atrial fibrillation are the most commonly reported rhythm abnormalities in SSc. Also, some therapies used in the treatment of the disease may influence the arrhythmic risk. Conclusions: Cardiac arrhythmias in SSc can have a significant impact on the prognosis of patients, which is why a multidisciplinary approach is essential. Collaboration between rheumatologists, cardiologists, and electrophysiologists is crucial for the early identification and appropriate management of arrhythmic risk in this patient group.

Chronic coronary syndrome (CCS) and atrial fibrillation (AF) are prevalent cardiovascular conditions that share numerous risk factors and pathophysiological mechanisms. While clinical scores such as CHA₂DS₂VA, HAS-BLED, and C₂HEST are traditionally used for AF-related outcomes, their value in predicting angiographic coronary artery disease (CAD) severity remains underexplored. We conducted a prospective, single-center study including 131 patients with suspected stable CAD referred for coronary angiography, stratified according to coronary angio-graphic findings into two groups: significant coronary stenosis (S-CCS) and non-significant coronary stenosis (N-CCS). At admission, AF-related scores (CHA₂DS₂, CHA₂DS₂VA, CHA₂DS₂VA-HSF, CHA₂DS₂VA-RAF, CHA₂DS₂VA-LAF, HAS-BLED, C₂HEST, and HATCH) were calculated. CAD severity was subsequently assessed using the SYNTAX and Gensini scores. Statistical comparisons and Pearson correlation analyses were per-formed to evaluate the association between clinical risk scores and angiographic findings. Patients in the S-CCS group had significantly higher scores in CHA2DS2VA (4.09 ± 1.656 vs. 3.20 ± 1.338, p = 0.002), HAS-BLED (1.98 ± 0.760 vs. 1.36 ± 0.835, p < 0.001), CHA2DS2VA-HSF (6.00 ± 1.854 vs. 5.26 ± 1.712, p = 0.021), and C2HEST (3.49 ± 1.501 vs. 2.55 ± 1.279, p < 0.001). Multivariate logistic regression identified HAS-BLED and C2HEST as independent predictors of significant coronary lesions. A threshold value of HAS-BLED ≥1.5 and C2HEST ≥3.5 demonstrated moderate discriminative ability (AUC = 0.694 and 0.682, respectively), with acceptable sensitivity and specificity. These scores also demonstrated moderate to strong correlations with both Gensini and SYNTAX scores. AF-related clinical scores, especially HAS-BLED and C₂HEST, may serve as practical and accessible tools for early CAD risk stratification in patients with suspected CCS. Their application in clinical practice could complement existing diagnostic algorithms and help prioritize patients for invasive evaluation.