Atrial fibrillation is a disease with a complex pathophysiology, whose occurrence and persistence are caused not only by aberrant electrical signaling in the heart, but by the development of a susceptible heart substrate. These changes, such as the accumulation of adipose tissue and interstitial fibrosis, are characterized by the presence of inflammation. N-glycans have shown great promise as biomarkers in different diseases, specifically those involving inflammatory changes. To assess the changes in the N-glycosylation of the plasma proteins and IgG in atrial fibrillation, we analyzed the N-glycosylation of 172 patients with atrial fibrillation, before and six months after a pulmonary vein isolation procedure, with 54 cardiovascularly healthy controls. An analysis was performed using ultra-high-performance liquid chromatography. We found one oligomannose N-glycan structure from the plasma N-glycome and six IgG N-glycans, mainly revolving around the presence of bisecting N-acetylglucosamine, that were significantly different between the case and control groups. In addition, four plasma N-glycans, mostly oligomannose structures and a derived trait that was related to them, were found to be different in the patients who experienced an atrial fibrillation recurrence during the six-month follow-up. IgG N-glycosylation was extensively associated with the CHA2DS2-VASc score, confirming its previously reported associations with the conditions that make up the score. This is the first study looking at the N-glycosylation patterns in atrial fibrillation and warrants further investigation into the prospect of glycans as biomarkers for atrial fibrillation.
Background and aim: Patients with non-infarct-related artery chronic total occlusion (non-IRA CTO) found during percutaneous coronary intervention (PCI) in acute coronary syndromes (ACSs) are not rare and have worse clinical outcomes. We aimed to analyze their long-term clinical outcomes in regard to clinical characteristics, revascularization strategies, and adherence to medical therapy. Patients and methods: The dual-center ACS registry of patients treated from Jan 2017 to May 2023 was used to identify 1950 patients with timely PCI in ACS who survived to discharge with documented adequate demographic, clinical, and angiographic characteristics, treatment strategies, and medical therapy adherence during a median follow-up time of 49 months. Results: There were 171 (9%) patients with non-IRA CTO. In comparison to patients without non-IRA CTO, they were older, with more diabetes mellitus (DM), higher Syntax scores (median 27.5 vs. 11.5), and lower left ventricular ejection fraction (LVEF) at discharge (median LVEF 50% vs. 55%). There was also a lower proportion of patients with high adherence to medical therapy (32% vs. 46%). Patients with non-IRA CTO had significantly higher cardiovascular mortality during follow-up (18% vs. 8%, RR 1.87, 95% CI 1.27–2.75). After adjusting for relevant clinical and treatment characteristics in a multivariate Cox regression analysis, only lower LVEF, worse renal function, the presence of DM, and lower adherence to medical therapy were independently associated with higher cardiovascular mortality during follow-up, with low adherence to medical therapy as the strongest predictor (RR 3.18, 95% CI 1.76–5.75). Time to cardiovascular death was significantly lower in patients who did not receive non-IRA CTO revascularization, although CTO revascularization did not show independent association with survival in the multivariate analysis. Conclusions: Patients with non-IRA CTO found during ACS treatment have more unfavorable clinical characteristics, worse adherence to medical therapy, and higher cardiovascular mortality. They need a more scrutinized approach during follow-up to increase adherence to optimal medical therapy and to receive revascularization of the non-IRA CTO whenever it is clinically indicated and reasonably achievable without excess risks.
Background: Pulmonary embolism (PE) is a major cause of cardiovascular morbidity and mortality. Guidelines favor direct oral anticoagulants (DOACs) over vitamin K antagonists (VKAs), but real-world Croatian data are scarce. Methods: A prospective dual-center registry included 773 patients discharged with acute PE between 2013 and 2024. Clinical, laboratory, and socioeconomic data were collected. The primary outcome was all-cause mortality; secondary outcomes were recurrent venous thromboembolism (VTE) and major bleeding. Results: DOAC users were younger, with higher education and income, than VKA or heparin patients. Median follow-up was 1106 days. Mortality reached 60.3% with VKA, 26.0% with DOAC, and 84.1% with heparin (p < 0.001). VTE recurrence did not differ significantly. Major bleeding occurred in 9.3% of VKA versus 2.9% of DOAC patients (p = 0.003). Adjusted analysis showed a lower mortality risk with DOAC versus VKA (HR 0.62, 95% CI 0.48–0.80, p < 0.001), while heparin predicted higher mortality (HR 3.63, 95% CI 2.54–5.21, p < 0.001). Higher PESI class independently increased mortality and recurrence. Conclusion: In the first Croatian PE cohort, DOACs were linked to reduced mortality and bleeding risk compared with VKAs, with similar recurrence. Clinical, socioeconomic, and policy factors strongly influenced prescribing patterns and outcomes.