Background In heart failure (HF), various biomarkers have been established for prognosis. However, little is known about the relevance of copeptin measurements to HF. This study aimed to explore the prognostic value of copeptin for predicting cardiovascular (CV) death or HF-related re-hospitalisation in patients with acute decompensated HF. Materials and Methods We prospectively enrolled 155 consecutive patients with acute signs and symptoms of HF. Plasma copeptin and N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels were measured at admission. Patients were monitored for 90 days regarding the composite endpoint of CV death or acute HF-related re-hospitalisation. Results Of the 155 patients enrolled, 40 reached the endpoint, and 115 were in a stable condition during follow-up. Patients who reached an adverse endpoint showed higher NT-proBNP and copeptin levels compared to patients in stable condition. Receiver operating characteristic curve analysis revealed that the area under curve of copeptin 0.844 (95% CI, 0.753-0.935) was superior to that of NT-proBNP 0.809 (95% CI, 0.729-0.890) for the prediction of adverse events within 90 days. Meanwhile, compared to the group with lower copeptin levels (= 34 pmol/L) were at a 10.672-times higher risk of CV death or acute HF-related re-hospitalisation. Multivariate Cox proportional hazards regression analysis revealed that increased copeptin level was a significantly independent predictor of adverse events (risk ratio, 1.051; 95% CI, 1.020-1.083;p < 0.001). Conclusion Copeptin was found to be a strong, novel marker for predicting CV death or HF-related re-hospitalisation in patients with acute decompensated HF.

Pulmonary embolism (PE) is a potentially life-threatening condition and the fact that 90% of PE originate from lower limb veins highlights the significance of early detection and treatment of deep vein thrombosis. Massive/high risk PE involving circulatory collapse or systemic arterial hypotension is associated with an early mortality rate of approximately 50%, in part from right ventricular (RV) failure. Intermediate risk/submassive PE, on the other hand, is defined as PE-related RV dysfunction, troponin and/or B-type natriuretic peptide elevation despite normal arterial pressure. Without prompt treatment, patients with intermediate risk PE may progress to the massive category with a potentially fatal outcome. In patients with PE and right ventricular dysfunction (RVD), in hospital mortality ranges from 5% to 17%, significantly higher than in patients without RVD.

Cryoballoon-based pulmonary vein isolation (PVI) is a treatment option for atrial fibrillation (AF). Left atrial volume (LAV) and left atrial volume index (LAVi) are important parameters for long term success of PVI. Galectin-3 (Gal-3) and neutrophil to lymphocyte ratio (N/L ratio) are biomarkers to demonstrate the cardiac fibrosis and remodelling. 50 patients with symptomatic PAF despite ≥1 antiarrhythmic drug(s), who underwent PVI were enrolled. LAV, LAVi, Gal-3 and N/L ratio were calculated before ablation and after ablation at 6 and 12 months. According to AF recurrence patients were divided into two groups, recurrent AF (n = 14) and non-recurrent AF (n = 36). In both groups (recurrent and non-recurrent), initial and 12 months follow-up LAV values were 41.39 ± 18.13 ml and 53.24 ± 22.11 ml vs 48.85 ± 12.89 ml and 42.08 ± 13.85 (p = 0.037). LAVi were 20.9 ± 8.91 ml/m2 and 26.85 ± 11.28 ml/m2 vs 25.36 ± 6.21 and 21.87 ± 6.66 (p = 0.05) for recurrent and non-recurrent AF groups, respectively. In both groups PVI had no significant effect on serum Gal-3 levels and N/L ratio during 12 months follow-up. The comparison between two groups at the end of 12th month showed Gal-3 values of 6.66 ± 4.09 ng/ml and 6.02 ± 2.95 ng/ml (p = 0.516), N/L ratio values of 2.28 ± 1.07 103/μl and 1.98 ± 0.66 103/μl (p = 0.674). LAV and LAVi are useful to predict the remodelling of the left atrium and AF recurrence after cryoballoon-based PVI. However, biomarkers such as Gal-3 and N/L ratio are not associated with AF recurrence.

Objectives: Vascular inflammation is a key feature of Behçet’s disease (BD), with studies showing increased vein wall thickness. The pulmonary artery, sharing structural features with veins, is of particular importance in BD. This study aimed to assess pulmonary artery wall thickness (PAWT) using transthoracic echocardiography and examine its association with disease manifestations, including major organ involvement (MOI) and mucocutaneous-limited disease (MLD), in comparison to healthy controls (HCs). Methods: This cross-sectional study included 67 patients with BD (43 with MOI, 24 with MLD) and 46 HCs. PAWT was measured from the middle of the pulmonary valve and pulmonary artery bifurcation in the parasternal short axis by an experienced cardiologist blinded to clinical data. Results: PAWT was significantly higher in patients with BD (3.5 ± 0.9 mm) than in HCs (2.7 ± 0.5 mm) (P < .001). Patients with MOI had significantly greater thickness than those with MLD and HCs (3.9 ± 0.7, 2.7 ± 0.6, 2.7 ± 0.5 mm, respectively; P < .001). The increase in thickness was most pronounced in patients with vascular involvement (P = .03). Conclusions: PAWT is greater in BD with MOI. Routine measurement may help detect vascular complications.