Chronic obstructive pulmonary disease (COPD) is considered one of the leading causes of mortality. Cardiovascular comorbidities are diagnosed often in COPD patients, not only because of the common risk factors these two diseases share, but also because of the systemic inflammation which characterizes COPD and has deleterious effects in the cardiovascular system. The comorbid cardiovascular diseases in COPD result in several difficulties in the holistic treatment of these patients and affect outcomes such as morbidity and mortality. Several studies have reported that mortality from cardiovascular causes is common among COPD patients, while the risk for acute cardiovascular events increases during COPD exacerbations and remains high for a long time even after recovery. In this review, we focus on the prevalence of cardiovascular comorbidities in COPD patients, presenting the evidence regarding the interaction of the pathophysiological pathways which characterize each disease. Furthermore, we summarize information regarding the effects of cardiovascular treatment on COPD outcomes and vice versa. Finally, we present the current evidence regarding the impact of cardiovascular comorbidities on exacerbations, quality of life and survival of COPD patients.

Exacerbations of Chronic Obstructive Pulmonary Disease (COPD) have a substantial effect on overall disease management, health system costs, and patient outcomes. However, exacerbations are often underdiagnosed or recognized with great delay due to several factors such as patients’ inability to differentiate between acute episodes and symptom fluctuations, delays in seeking medical assistance, and disparities in dyspnea perception. Self-management intervention plans, telehealth and smartphone-based programs provide educational material, counseling, virtual hospitals and telerehabilitation, and help COPD patients to identify exacerbations early. Moreover, biomarkers such as blood eosinophil count, fibrinogen, CRP, Serum amyloid A(SAA),together with imaging parameters such as the pulmonary artery-to-aorta diameter ratio, have emerged as potential predictors of exacerbations, yet their clinical utility is limited by variability and lack of specificity. In this review, we provide information regarding the importance of the early identification of exacerbation events in COPD patients and the available methods which can be used for this purpose.

Background: Reticulation, ground glass opacities and post-infection bronchiectasis are present three months following hospitalisation in patients recovering from SARS-CoV-2 infection and are associated with the severity of acute infection. However, scarce data exist on small airways impairment and lung hyperinflation in patients with long COVID-19. Aim: To evaluate small airways function and lung hyperinflation in previously hospitalised patients with long COVID-19 and their association with post-COVID-19 breathlessness. Methods: In total, 33 patients (mean ± SD, 53 ± 11 years) with long COVID-19 were recruited 149 ± 90 days following hospital discharge. Pulmonary function tests were performed and lung hyperinflation was defined as RV/TLC ≥ 40%. Small airways function was evaluated by measuring the closing volume (CV) and closing capacity (CC) using the single-breath nitrogen washout technique (SBN₂W). Results: CC was 115 ± 28% pred. and open capacity (OC) was 90 ± 19. CC was abnormal in 13 patients (39%), CV in 2 patients (6.1%) and OC in 9 patients (27%). Lung hyperinflation was present in 15 patients, whilst the mean mMRC score was 2.2 ± 1.0. Lung hyperinflation was associated with CC (r = 0.772, p = 0.001), OC (r = 0.895, p = 0.001) and mMRC (r = 0.444, p = 0.010). Conclusions: Long COVID-19 patients present with small airways dysfunction and lung hyperinflation, which is associated with persistent dyspnoea, following hospitalisation.

Background/Objectives: Cardiorespiratory complications are commonly reported among patients with long COVID-19 syndrome. However, their effects on exercise capacity remain inconclusive. We investigated the impact of long COVID-19 on exercise tolerance combining cardiopulmonary exercise testing (CPET) with resting echocardiographic data. Methods: Forty-two patients (55 ± 13 years), 149 ± 92 days post-hospital discharge, and ten healthy age-matched participants underwent resting echocardiography and an incremental CPET to the limit of tolerance. Left ventricular global longitudinal strain (LV-GLS) and the left ventricular ejection fraction (LVEF) were calculated to assess left ventricular systolic function. The E/e’ ratio was estimated as a surrogate of left ventricular end-diastolic filling pressures. Tricuspid annular systolic velocity (SRV) was used to assess right ventricular systolic performance. Through tricuspid regurgitation velocity and inferior vena cava diameter, end-respiratory variations in systolic pulmonary artery pressure (PASP) were estimated. Peak work rate (WRpeak) and peak oxygen uptake (VO₂peak) were measured via a ramp incremental symptom-limited CPET. Results: Compared to healthy participants, patients had a significantly (p < 0.05) lower LVEF (59 ± 4% versus 49 ± 5%) and greater left ventricular end-diastolic diameter (48 ± 2 versus 54 ± 5 cm). In patients, there was a significant association of E/e’ with WRpeak (r = −0.325) and VO₂peak (r = −0.341). SRV was significantly associated with WRpeak (r = 0.432) and VO₂peak (r = 0.556). LV-GLS and PASP were significantly correlated with VO₂peak (r = −0.358 and r = −0.345, respectively). Conclusions: In patients with long COVID-19 syndrome, exercise intolerance is associated with left ventricular diastolic performance, left ventricular end-diastolic pressure, PASP and SRV. These findings highlight the interrelationship of exercise intolerance with left and right ventricular performance in long COVID-19 syndrome.

Background: Stewart’s approach is known to have better diagnostic accuracy for the identification of metabolic acid–base disturbances compared to traditional methods based either on plasma bicarbonate concentration ([HCO₃⁻]) and anion gap (AG) or on base excess/deficit (BE). This study aimed to identify metabolic acid–base disorders using either Stewart’s or traditional approaches in critically ill COVID-19 patients admitted to the ICU, to recognize potential hidden acid–base metabolic abnormalities and to assess the prognostic value of these abnormalities for patient outcome. Methods: This was a single-center retrospective study, in which we collected data from patients with severe COVID-19 admitted to the ICU. Electronical files were used to retrieve data for arterial blood gases, serum electrolytes, and proteins and to derive [HCO₃⁻], BE, anion gap (AG), AG adjusted for albumin (AG_adj), strong ion difference, strong ion gap (SIG), and SIG corrected for water excess/deficit (SIG_corr). The acid–base status was evaluated in each patient using the BE, [HCO₃⁻], and physicochemical approaches. Results: We included 185 patients. The physicochemical approach detected more individuals with metabolic acid–base abnormalities than the BE and [HCO₃⁻] approaches (p < 0.001), and at least one acid–base disorder was recognized in most patients. According to the physicochemical method, 170/185 patients (91.4%) had at least one disorder, as opposed to the number of patients identified using the BE 90/186 (48%) and HCO₃ 62/186 (33%) methods. Regarding the derived acid–base status variables, non-survivors had greater AG_adj, (p = 0.013) and SIG_corr (p = 0.035) compared to survivors. Conclusions: The identification of hidden acid–base disturbances may provide a detailed understanding of the underlying conditions in patients and of the possible pathophysiological mechanisms implicated. The association of these acid–base abnormalities with mortality provides the opportunity to recognize patients at increased risk of death and support them accordingly.

Endobronchial ultrasound (EBUS) has evolved beyond conventional applications in mediastinal staging and central pulmonary tumor diagnosis. It encompasses the assessment of pulmonary vasculature in patients with thoracic malignancies. EBUS can visualize major vessels and allow assessment of pulmonary embolism, differential diagnosis of endovascular lesions, and T staging. Additionally, EBUS-guided transvascular needle aspiration (TVNA) has proven valuable for sampling lesions behind vessels and diagnosing conditions such as pulmonary artery sarcoma and tumor embolism, with low complication rates reported. The PubMed and SCOPUS databases were searched up to November 2024 for articles in the English language reporting the use of EBUS for pulmonary vasculature assessment. References were also searched for relevant articles. The integration of EBUS with other modalities enhances staging and diagnostic capabilities in thoracic malignancies. Despite promising findings, limitations include suboptimal image quality and challenges in extensively assessing all the vasculature. Safety concerns, particularly with transvascular biopsy, remain minimal with expert handling, although further studies are needed to assess specific risks like hematogenous tumor seeding. EBUS continues to evolve, suggesting its potential to become the cornerstone in advanced thoracic diagnostics and treatment planning. This review systematically explores the feasibility, safety, and diagnostic utility of EBUS in pulmonary vasculature assessment, highlighting its potential as an indispensable tool in thoracic diagnostics and treatment planning.