Background: Chronic obstructive pulmonary disease (COPD) is increasingly recognized as a disorder linked to increased cardiovascular risk, often coexisting with coronary artery disease (CAD), yet angiographic data on coronary involvement in COPD remain limited. This study aimed to evaluate whether COPD is associated with a distinct angiographic pattern of CAD, focusing on vessel distribution. Methods: We retrospectively enrolled 94 patients who underwent coronary angiography between 2023 and 2024 for suspected or known CAD. Clinical data, comorbidities, laboratory testing, pulmonary function, electrocardiography, echocardiography, and angiography were collected. Participants were stratified into two groups: COPD (n = 47) and non-COPD (n = 47). Coronary vessels were classified by number, location, and diameter. The normality of continuous variables was assessed using the Shapiro–Wilk test. Non-normally distributed variables were compared using the Mann–Whitney U test, while Fisher’s exact test was used for categorical comparisons. A multivariable logistic regression model was performed to identify independent predictors of left main coronary artery (LMCA) disease at the patient level. The primary endpoint was the association between COPD and CAD severity. Results: Baseline characteristics, including age, sex, BMI, and smoking history, were comparable between groups. The overall extent of CAD, expressed as the number of diseased vessels, did not differ significantly (p = 0.1436). However, vessel-based analysis revealed a distinct pattern: COPD patients showed a significantly higher prevalence of left main coronary artery (LMCA) disease compared to non-COPD patients (14% vs. 4.7%, p < 0.001). At the patient level, LMCA disease was present in 15/47 (31.9%) COPD patients compared with 6/47 (12.8%) non-COPD patients (p = 0.046). Multivariable logistic regression confirmed that COPD was an independent predictor of LMCA disease (OR = 3.56, 95% CI: 1.12–11.29, p = 0.031) after adjustment for age, sex, smoking, diabetes, and chronic kidney disease. Intermediate-caliber vessels were most frequently affected in both groups, while small-caliber branches were less commonly involved in COPD patients. Conclusions: COPD is an independent predictor of LMCA disease despite a similar overall angiographic extent of CAD. These findings suggest a distinct, high-risk coronary phenotype in COPD and highlight the need for enhanced cardiovascular vigilance and integrated cardiopulmonary management in this population.

Small airway dysfunction and air trapping are increasingly recognized as important contributors to disease severity in severe asthma. Although type 2 (T2)-targeted biologics improve clinical outcomes, their effects on distal airway physiology remain incom-pletely characterized. We evaluated the longitudinal effects of biologic therapy on air trapping, lung function, and type 2 inflammatory activity in patients with severe asth-ma. In this prospective real-world study, 43 adults with severe asthma received benral-izumab (n = 16), mepolizumab (n = 21), or tezepelumab (n = 6). Clinical outcomes, pul-monary function parameters, static lung volumes, and fractional exhaled nitric oxide (FeNO) were assessed at baseline (T0), 3 months (T3), and 9 months (T9). The primary endpoint was the change in RV/TLC ratio, a physiological marker of air trapping and distal airway dysfunction. Biologic therapy was associated with significant improve-ments in asthma control and exacerbation burden. Mean asthma control test (ACT) score increased from 12.7 ± 0.6 to 23.5 ± 0.3 (p < 0.0001), while annual exacerbations decreased from 4.74 ± 0.27 to 0.63 ± 0.19 events per patient (p < 0.0001). Improvements were also observed in conventional spirometric parameters, with FEV₁ increasing from 80.3 ± 3.1% predicted at baseline to 96.3 ± 3.4% at T9 (p < 0.0001). The most pronounced functional changes involved air-trapping indices: RV decreased from 108.4 ± 6.0% predicted to 82.2 ± 4.1% (p < 0.0001), while RV/TLC decreased from 111.2 ± 5.0% to 83.7 ± 3.9% (p < 0.0001). FeNO progressively declined from 68.8 ± 6.7 ppb at baseline to 28.3 ± 2.9 ppb at T9 (p < 0.0001). T2-targeted biologics were associated with significant reductions in air trapping alongside improvements in clinical, functional, and inflammatory outcomes. The marked responsiveness of RV and RV/TLC suggests that assessment of air trapping may provide complementary information on treatment response beyond conventional spi-rometric measures and may represent a promising functional pharmacodynamic bi-omarker in severe asthma.

Background/Objectives: Alpha-1 antitrypsin deficiency (AATD) is an underdiagnosed hereditary disorder that predisposes individuals to lung and liver disease. While its prevalence is higher in Northern Europe, data from specific, isolated populations in other regions are scarce. This study assessed the prevalence of pathogenic SERPINA1 variants in the adult population of Ponte di Legno, a secluded town in the Italian Alps, to investigate potential founder effects involving rare genotypes. Methods: A cross-sectional community-based screening was conducted. Adult residents without previously diagnosed chronic respiratory diseases were invited to undergo spirometry and provide venous blood samples for serum AAT and CRP measurement. Buccal swabs were collected for genotyping, which was performed using a validated multiplex Luminex xMAP assay detecting 14 common and rare SERPINA1 variants, with isoelectric focusing and Sanger sequencing for further characterization when required. Results: Ninety-one subjects were enrolled (median age 61 years; 37.4% male). Five individuals (5.5%) carried pathogenic SERPINA1 variants: one Pi*MS heterozygote (1.1%), two Pi*MZ heterozygotes (2.2%), and two individuals heterozygous for the rare Pi*Mheerlen variant (Pi*M/Mheerlen) (2.2%). Median serum AAT levels were significantly lower in carriers of deficient alleles compared with Pi*MM individuals (100 mg/dL vs. 125 mg/dL, p = 0.0218). Conclusions: This community-based screening revealed a notable prevalence of AATD carriers in a geographically isolated Italian community, including two cases of the rare Pi*Mheerlen variant, suggesting a possible local founder effect. These findings underscore the value of targeted screening programs using rare variant panels to uncover hidden genetic architectures in isolated populations.

Background: Obstructive sleep apnea (OSA) is recognized as a systemic disorder associated with several comorbidities, including renal dysfunction, which may improve with continuous positive airway pressure (C-PAP) therapy. Sleep fragmentation and nocturnal hypoxia characteristic of OSA have been implicated in carcinogenesis, particularly affecting hypoxia-sensitive urinary tract tissues. This study aimed to assess the prevalence of different cancer types among patients with concurrent OSA and malignancy and to characterize the clinical profiles of those with urinary tract cancer. Methods: We retrospectively analyzed 50 patients with both OSA and cancer from the Vercelli Hospital Registry. Cancer diagnoses were collected at the time of OSA diagnosis, prior to C-PAP initiation. Results: Among the cohort (70% males) of OSA-cancer patients, urinary tract cancers were the most frequent (34%), followed by breast (14%), colorectal (12%), lung (10%), laryngeal and skin (8%), intracranial (6%), hematologic and parotid (4%), and other cancers (2%); 10% had multiple cancer sites. Patients with urinary tract cancer were mainly male (88%, p = 0.0043) and displayed better respiratory indices, frequent hypertension, and higher C-PAP adherence. Conclusions: These findings suggest a possible link between OSA-related hypoxia and carcinogenesis in urinary tract tissues and support increased clinical surveillance and further research to determine potential protective effects of C-PAP therapy.

Background. Alpha-1 antitrypsin deficiency (AATD) is an under-diagnosed hereditary disorder that predisposes individuals to lung and liver disease. While its prevalence is higher in Northern Europe, data from specific, isolated populations in other regions are scarce. Methods. This study assessed the prevalence of pathogenic SERPINA1 variants in the adult population of Ponte di Legno, a secluded town in the Italian Alps. A cross sectional screening was conducted on March 5–6, 2022. Asymptomatic adult residents were invited to undergo spirometry and provided venous blood samples for serum AAT and CRP measurement, while buccal swabs were collected from all participants for genotyping. Genotyping was performed using a validated multiplex Luminex xMAP assay detecting 14 common and rare SERPINA1 variants, with isoelectric focusing and Sanger sequencing for further characterization when required. Results: Ninety‑one subjects were enrolled (median age 61 years; 37.4% male). Five individuals (5.5%) carried pathogenic SERPINA1 variants: one PiMS heterozygote (1.1%), two PiMZ heterozygotes (2.2%), and two individuals homozygous for the rare PiMheerlen variant (2.2%). Median serum AAT levels were significantly lower in carriers of deficient alleles compared with PiMM individuals (100 mg/dL vs. 125 mg/dL, p = 0.0218). Conclusions: This population‑based screening revealed a notable prevalence of AATD carriers in a geographically isolated Italian community, including two cases of the rare Pi*Mheerlen variant. These findings underscore the value of targeted screening programs to identify at‑risk individuals who may benefit from counseling and clinical monitoring, and suggest that AATD may be more common than previously recognized in specific populations.

Background: Chronic obstructive pulmonary disease (COPD) is increasingly recognized as a disorder linked to increased cardiovascular risk, often coexisting with coronary artery disease (CAD), yet angiographic data on coronary involvement in COPD remain limited. This study aimed to evaluate whether COPD is associated with a distinct angiographic pattern of CAD, focusing on vessel distribution. Methods: We retrospectively enrolled 94 patients who underwent coronary angiography between 2023 and 2024 for suspected or known CAD. Clinical data, comorbidities, laboratory testing, pulmonary function, electrocardiography, echocardiography, and angiography were collected. Participants were stratified into two groups: COPD (n = 47) and non-COPD (n = 47). Coronary vessels were classified by number, location, and diameter. The primary endpoint was the association between COPD and CAD severity. Results: Baseline characteristics, including age, sex, BMI, and smoking history, were comparable between groups. The overall extent of CAD, expressed as the number of diseased vessels, did not differ significantly (p = 0.1436). However, vessel-based analysis revealed a distinct pattern: COPD patients showed a significantly higher prevalence of left main coronary artery (LMCA) disease compared to non-COPD patients (14% vs. 4.7%, p < 0.001). Intermediate-caliber vessels were most frequently affected in both groups, while small-caliber branches were less commonly involved in COPD patients. Conclusions: COPD is associated with a disproportionate burden of LMCA disease despite a similar overall angiographic extent of CAD. These findings suggest a distinct, high-risk coronary phenotype in COPD and highlight the need for enhanced cardiovascular vigilance and integrated cardiopulmonary management in this population.