This article aims to analyze the relationship between non-obstructive coronary artery disease (NOCAD) and atrial fibrillation (AF), exploring the underlying pathophysiological mechanisms and implications for clinical management. NOCAD and AF are prevalent cardiovascular conditions that often coexist, yet their interrelation is not well understood. NOCAD can lead to ischemic necrosis of cardiomyocytes and their replacement with fibrous tissue, sustaining focal ectopic activity in atrial myocardium. Atrial fibrillation, on the other hand, the most common sustained cardiac arrhythmia, is able to accelerate atherosclerosis and increase oxygen consumption in the myocardium, creating a mismatch between supply and demand, and thus promoting the development or worsening of coronary ischemia. Therefore, NOCAD and AF seem to be a complex interplay with one begets another.

Background: Acute pulmonary embolism (PE) is a condition with increased morbidity and mortality. It is important to identify patients with high mortality risk. Inflammation and thrombosis are interconnected in the pathophysiology of PE. The aim of the study was to investigate the prognostic value of multiple blood cellular indices such as neutrophil-to-lymphocyte ratio (NLR), lymphocyte-to-monocyte ratio (LMR), platelet-to-lymphocyte ratio (PLR), neutrophil-to-lymphocyte platelet ratio (NLPR), systemic immune–inflammation index (SII), systemic inflammation response index (SIRI) and aggregate index of systemic inflammation (AISI) in acute PE. Methods: A total of 157 patients with acute PE confirmed by chest computed tomographic angiography (CTPA) were enrolled. These patients were divided into two categories according to the simplified pulmonary embolism severity index (sPESI): high risk and low risk. Results: Univariate logistic regression analysis showed that right ventricle dysfunction, NLR, SII and SIRI were significantly associated with high risk of acute PE. NLR of 4.32 was associated with high-risk PE with a sensitivity of 57.4% and specificity of 65.7% (AUC = 0.635). SII of 1086.55 was associated with high-risk PE with a sensitivity of 55.7% and specificity of 71.4% (AUC = 0.614). SIRI of 2.87 was associated with high-risk PE with a sensitivity of 59% and specificity of 62.9% (AUC = 0.624). Multivariate logistic regression analysis demonstrated that right ventricle dysfunction, NLR, PLR and NLPR are independent predictors of high-risk acute PE. Secondly, NLR, NLPR, SII and SIRI were significantly correlated with in-hospital mortality of acute PE. Based on receiver-operating characteristic (ROC) curve values of 7.66 for NLR (AUC 0.911, sensitivity of 85.7% and sensibility of 83%), 0.02 for NLPR (AUC 0.871, sensitivity of 85.7% and sensibility of 70%), 1542.71 for SII (AUC 0.782, sensitivity of 71.4% and sensibility of 72%) and 5.72 for SIRI (AUC 0.788, sensitivity of 71.4% and sensibility of 73%) could predict in-hospital mortality. Conclusions: The blood cellular indices (NLR, NLPR, SII and SIRI) are associated with high-risk acute PE and in-hospital mortality. Right ventricular dysfunction, NLR and NLPR are independent predictors for high-risk acute PE.

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/Objectives: Coronary artery disease (CAD) remains the leading cause of death primarily in patients over 65 years old, with an increasing incidence, especially in Eastern European countries. Primary and secondary prevention protocols are based on a large number of cardiovascular (CV) risk factors, but low-density lipoprotein cholesterol (LDL-C) remains the main treatment target and one of the central determinants of CV risk. Apolipoprotein B (apoB) is the main structural protein in all atherogenic lipoproteins, and, unlike LDL-C, which only reflects the cholesterol content of LDL, apoB directly quantifies the total number of all circulating atherogenic particles. Over the past decade, a growing amount of data has supported the utility of apoB for CV risk assessment; however, its superiority over LDL-C remains unclear. Our study aimed to investigate the predictive value of apoB for both the presence and the severity of CAD in a statin-treated cohort from an Eastern European hospital and to compare it with standard lipid biomarkers. Methods: A total of 121 statin-treated patients, who were evaluated using coronary angiography, were consecutively enrolled and subdivided into three groups: 52 patients with significant coronary artery disease (S-CAD), 36 patients with non-significant coronary artery disease (NS-CAD), and 33 patients without coronary atherosclerosis (N-CAD). Apolipoprotein B was measured at the moment of enrollment using the immunoturbidimetric assay. Results: The mean values of LDL-C, TC, non-HDL-C, and apoB increased progressively across the three studied groups. Unlike traditional lipid biomarkers, apoB levels differed significantly not only between N-CAD and S-CAD, but also between N-CAD and NS-CAD. The diagnostic superiority of apoB extended beyond group mean differences, as it also demonstrated the strongest correlation with CAD severity. ApoB showed a moderate correlation with the Gensini score (r = 0.43, p < 0.001), which was markedly higher compared to LDL-C, TC, or non-HDL-C, all of which presented only a weak correlation (r = 0.26, r = 0.23, and r = 0.28, respectively). Additionally, in a logistic regression analysis, apoB demonstrated the highest predictive power for the presence of significant CAD (per SD increase: OR 2.386, 95% CI 1.52–3.75, p = 0.000), and it was the only biomarker able to predict left main disease (per SD increase: OR 2.433, 95% CI 1.38–4.30, p = 0.002) and three vessel disease (per SD increase: OR 1.639, 95% CI 1.012–2.654, p = 0.044). Residual apoB was also calculated and remained significantly associated with the presence of coronary atherosclerosis. Conclusions: ApoB proved to be a reliable predictor for CAD, independent of LDL-C. Compared to standard lipid biomarkers, apoB was superior in detecting NS-CAD and showed a better correlation with the severity of CAD. Additionally, in our study, only apoB was significantly correlated with left main disease and three vessel disease.

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.