Group 1 of PAH patients encompasses patients with a diverse underlying etiological condition, having histological modifications that can affect gas exchange across the alveolar-capillary membrane, as reflected by decreased DLCO. Values of DLCO did not identify the exact reason for their decrease, but they can provide insights into the underlying pathobiology and prognosis of PAH patients. Our aim was to explore whether PAH patients with low DLCO constitute a different subpopulation and describe their characteristics and response to treatment. A total of 69 PAH patients were studied retrospectively and divided into two groups: group 1: DLCO ≥ 45% and group 2: DLCO < 45%. IPAH and PAH-CTD mainly constituted our population. The proportion of IPAH to PAH-CTD was almost the same between the two groups. Patients in group 2 were older (66.83 ± 11.61 vs. 59.27 ± 111.90, p = 0.035), mostly male (47.5% vs. 11.5% p = 0.008), and ever smokers (59% vs. 22%, p = 0.049). They mainly had WHO-FC III (68% vs. 32%) and had received more advanced therapy (40% on triple combination therapy vs. 16%). The two groups had similar mean PAP (group 1 = 32 (22.00–38.00) vs. group 2 = 35 (28.50–48.50) mmHg), while PVR was higher in group 2 (6.49 (4.10–9.52) vs. 3.61 (2.95–5.22) WU). In group 2, neither IPAH nor PAH-CTD patients improved WHO-FC, 6MWD, or NT-proBNP after treatment. In our center, PAH patients with low DLCO had some distinct clinical characteristics, such as poor prognosis and poor treatment response to vasodilatory therapy. Understanding the role of DLCO in both phenotyping PAH patients and in treatment response would be useful in guiding therapeutic approaches, especially now that new therapeutic targets are involved in PAH treatment.

Cardiac sarcoidosis (CS) is a complex inflammatory cardiomyopathy resulting from myocardial granulomatous inflammation. Its variable clinical presentation and lack of a single definitive test make diagnosis challenging. CS causes significant morbidity and mortality through conduction abnormalities, ventricular arrhythmias, heart failure (HF), and sudden cardiac death (SCD). This review synthesizes current knowledge on CS epidemiology, pathophysiology, diagnosis, and management. A comprehensive, non-systematic literature search was performed using PubMed/MEDLINE, Embase, and Google Scholar for English-language articles focusing on publications from January 2010-May 2025. Original research, systematic reviews, meta-analyses, consensus statements, and guidelines were included. Recent evidence indicates a paradigm shift in CS diagnosis, with advanced cardiac imaging gaining central place in international algorithms. Cardiac magnetic resonance (CMR), 18F-fluorodeoxyglucose positron emission tomography (FDG-PET), and hybrid CMR/FDG-PET have revolutionized CS diagnosis and management. Histological confirmation of sarcoidosis, when pursued, is obtained via extracardiac biopsy; cardiac involvement is then established using clinical and imaging criteria. Endomyocardial biopsy is reserved for select cases. Immunomodulation, primarily corticosteroids, remains the therapeutic cornerstone, with adjunctive steroid-sparing agents and biologics. Implantable cardioverter-defibrillators are indicated in high-risk patients to prevent ventricular arrhythmias and SCD. HF management follows guideline-directed therapy, reserving advanced therapies for CS-related advanced HF. CS is "the cardiomyopathy of a thousand faces". International consensus emphasizes advanced imaging and multidisciplinary approaches for timely diagnosis and management. While immunomodulation and device therapy have improved outcomes, knowledge gaps persist regarding optimal treatment strategies. Future research should refine diagnostic algorithms, identify CS-specific biomarkers, and develop optimal and novel therapeutics to improve CS management.

Group of PAH patients encompasses patients with a diverse underlying aetiological condition, having histological modifications that can affect gas exchange across the alveolar-capillary membrane as it is reflected by decreased DLCO. DLCO values did not identify the exact reason of its decrease, but can provide insights into the underlying pathobiology and prognosis of PAH patients. Our aim was to explore if PAH patients with low DLCO constitute a different subpopulation and describe their characteristics and response to treatment. 69 PAH patients were studied retrospectively and divided into group1: DLCO≥45% and group2: DLCO< 45%. IPAH and PAH-CTD constituted mainly our population. The proportion of IPAH and PAH-CTD was almost the same. Patients in group 2 were older (66.83± 11.61 vs 59.27±111.90, p=0.035), more often male (47.5% vs 11.5% p=0.008) and ever smokers (59% vs 22%, p=0.049). They had mainly WHO-FC III ((68%) vs 32%) and have received more advanced therapy (40% on triple combination therapy vs 16%). The two groups had the same mean PAP (group1=32 (22.00-38.00) vs group2=35 (28.50-48.50) mmHg) and PVR was higher in group 2 (6.49(4.10-9.52) vs 3.61 (2.95-5.22) WU). In group 2 neither IPAH nor PAH-CTD patients did improve WHO-FC, 6MWD, or NT-proBNP after treatment. In our centre PAH patients with low DLCO have some distinct clinical characteristics. poor prognosis and treatment response in vasodilatory therapy. Understanding the role of DLCO in phenotyping PAH patient and in treatment response would be useful in guide therapeutic approaches, especially now that new therapeutic targets are involved in the PAH treatment.

The use of bioprosthetic valves in the surgical aortic valve replacement (SAVR) or transcatheter aortic valve implantation (TAVI) of severe aortic stenosis has been associated with post-implantation thrombocytopenia, usually reversible and rarely combined with severe bleeding events. The purpose of this study was to compare the grade of thrombocytopenia and the presence of bleeding events following the implantation of bioprosthetic valves, where either surgery (Solo, Perceval, Trifecta) or transcatheter method (self-expandable TAVI) was followed. 89 patients with severe aortic stenosis were included in the study. All patients underwent either SAVR or TAVI. In each group 3 different types of bioprosthetic valves were used [59 patients in SAVR group: Solo (14), Perceval (27), Trifecta (18), 30 patients in TAVI group: Evolut R (10), Portico (15), Acurate (5)]. All patients had normal or slightly reduced platelet count at baseline. Patients previously receiving anticoagulants, patients with a primary blood disorder affecting the number of platelets, as well as patients with a post-surgery complication that could affect the number of platelets (e.g., HIT syndrome, etc.) were excluded from the study. Blood samples were taken in the morning before intervention and every morning during the first week of follow-up. Platelet count values before and after implantation were compared with paired t-test (SPSS V21.0, Inc., Chicago, IL, USA), while the reduction of platelets was compared between the 4 different valves with independent t-test. P-values of <0.05 were considered significant. Mean age was 76.8±5.1 years. There was no statistically significant difference between the 2 groups of patients concerning the baseline characteristics and the administered anticoagulants. Statistically significant reduction of the blood count was observed in all groups [Solo: 136±80x10³/μl (p=0.009), Perceval: 129±75x10³/μl (p<0.001), Trifecta: 74±32x10³/μl (p<0.001, TAVI: 60±103μl)]. There was no observed statistically significant difference between Solo and Perceval group (p=0.85) or Solo and Trifecta group (p=0.053), but in the case of Perceval and Trifecta group, a statistically significant difference was noted (p=0.047). A statistically significant difference in both SAVR and TAVI groups was demonstrated (p=0.040) regarding blood count reduction. There was no occurrence of any major bleeding events. 3 patients (3.3%) presented mild bleeding disorders (1 patient epistaxis and 2 patients mild hematuria). Both methods, surgical and transcatheter severe aortic stenosis replacement and all the different bioprosthetic valves that were implanted, were associated with statistically significant reduction of platelet count post-implantation. This reduction was linked to the procedure due to endothelial damage, shear stress injury, inflammation-related platelet consumption, and was not associated with clinically significant bleeding events. Type of funding sources: None.