Structural analysis of retinal blood vessels in patients with COPD during a pulmonary rehabilitation program

Abstract

cardiovascular diseases are frequently present in chronic obstructive pulmonary disease (copD). population-based studies found associations between retinal vessel diameters and cardiovascular health, but it is unknown whether this also applies to COPD patients. Therefore, we measured retinal vessel diameters in copD patients and aimed to determine the association with cardiovascular risk factors, lung function, and functional outcomes. In addition, we investigated whether an exercisebased pulmonary rehabilitation (PR) program would change retinal vessel diameters, as a proxy for improved microvascular health. Demographics and clinical characteristics, including pulmonary function, exercise capacity, blood pressure, blood measurements and level of systemic inflammation were obtained from 246 patients during routine assessment before and after PR. Retinal vessel diameters were measured from digital retinal images. older age and higher systolic blood pressure were associated with narrower retinal arterioles (β: −0.224; p = 0.042 and β: −0.136; p < 0.001, respectively). Older age, higher systolic blood pressure and lower level of systemic inflammation were associated with narrower retinal venules (β: −0.654; −0.229; and −13.767, respectively; p < 0.05). No associations were found between retinal vessel diameters and lung function parameters or functional outcomes. After PR, no significant changes in retinal venular or arteriolar diameter were found. To conclude, retinal vessel diameters of COPD patients were significantly associated with systolic blood pressure and systemic inflammation, whilst there was no evidence for an association with lung function parameters, functional outcomes or other cardiovascular risk factors. Furthermore, an exercise-based PR program did not affect retinal vessel diameter. Chronic obstructive pulmonary disease (COPD) is characterized by persistent respiratory symptoms and airflow limitation due to airway and/or alveolar abnormalities usually caused by significant exposure to noxious particles or gases 1. Although the diagnosis of COPD is based on spirometry, it is well recognized that COPD is associated with a range of systemic extrapulmonary effects 1. Indeed, comorbidities are frequently present and contribute to the severity of disease 2-4. Cardiovascular disease (including hypertension, coronary artery disease, congestive heart failure, stroke and peripheral arterial disease) is a common comorbidity in COPD 2,5. Smoking is the most important risk factor for the development of COPD, but it is also a major risk factor for the development of cardiovascular disease 6,7. Indeed, cigarette smoke not only affects the airway epithelium, but also causes vascular endothelial damage and loss of microvascular integrity in several organs, including the heart, brain, and kidney 8,9. In addition, systemic inflammatory processes, oxidative stress, and hypoxia may contribute

Optical coherence tomography angiography as a surrogate marker for end-organ resuscitation in sepsis: A review

“…COPD patients also had a larger FAZ diameter than healthy participants ( p = 0.002) ( 35 ), and there was a moderate correlation between partial pressure of oxygen (pO 2 ) and superficial/deep vascular density ( r = 0.559/0.800 respectively), and a highly negative correlation between pO 2 and FAZ size ( r = −0.876) ( 35 ), suggesting that retinal vascular density by OCTA may be useful to monitor disease progression in COPD patients ( 35 ). Retinal imaging in COPD has also shown that older age, higher systolic BP and lower levels of systemic inflammation are associated with narrower retinal venules ( p < 0.05) ( 36 ).…”

Vascular Endothelial Damage in COPD: Where Are We Now, Where Will We Go?

“…COPD often occurs with some relevant cardiovascular comorbidities, such as arterial hypertension, heart failure, acute myocardial infarction, stroke, or peripheral arterial disease. These comorbidities largely contribute to Diagnostics 2024, 14, 950 2 of 13 increasing COPD's severity and accelerate the disease's progression, leading to progressive deterioration in quality of life, resulting in poorer clinical outcomes [3][4][5][6][7][8][9][10]. In-depth studies of this pathology and progress in our knowledge of the underlying pathogenetic mechanisms have led to evidence in the literature that support a strict correlation between chronic systemic inflammation, which characterizes COPD patients, and comorbidities that are commonly associated with COPD, especially cardiovascular comorbidities [11][12][13][14][15][16][17][18][19][20].…”

“…COPD is a virtually untreatable disease; it is defined as chronic airflow obstruction, not fully manageable, and with an inevitable progression over time [5][6][7][8][9]. In this chronic lung disease, there is increased inflammation in the airways and pulmonary remodelling, often related to parenchymal destruction and primarily responsible for emphysema; in addition, mucous hyper-secretion and loss of elastic recoil are major events that are related to the development of airflow obstruction [6][7][8][9][10]. These mechanisms underlie the typical symptomatology of COPD, in particular dyspnoea, wheezing, fatigue, cough, and possibly sputum production [6][7][8][9][10].…”

“…It is stated that cigarette smoking is the main risk factor of COPD; in fact, the literature has proven that non-smokers develop this disease less frequently [7][8][9][10]. Nevertheless, smoking is not the only cause of this disease, and as a matter of fact, only 30% to 50% of smokers develop COPD, so there are other major risk factors that play an almost equally key role related to the disease [5,8].…”

Possibilities of drug correction of the state of the main arteries and microcirculation in patients with chronic heart failure and chronic obstructive pulmonary disease

“…По мнению ряда авторов, тяжелое клиническое состояние таких коморбидных пациентов и высокая смертность связаны с нарушениями функционирования сосудистого русла [3][4][5][6][7][8]. Как при ХСН, так и при ХОБЛ происходят изменения как в крупных сосудах, так и на уровне микроциркуляторного звена.…”