Abstract

Angiotensin Converting Enzyme 2 (ACE2) is an endothelial cell receptor used by SARS-CoV- 2 virus to enter cells. Pulmonary function tests (PFTs), mainly spirometry, are the main diagnostic tools for most respiratory diseases. PFTs are mandatory for assessing the response to therapy. We evaluated patients after the SARS-CoV-2 infection through flow-volume spirometry that evaluates the role of drugs inhibiting the ACE2 pathway. We evaluated 112 Caucasian patients 3-6months after COVID-19 disease, i.e. after the date of negative molecular or antigenic nasopharyngeal swab. The series of patients showed a great variability due to a wide spectrum of age, the severity of disease manifestations, hospitalization, invasive/non-invasive ventilation, comorbidities, the presence/absence of a previous pneumological diagnosis and the variants of the virus. Patients were divided into those who were being treated with angiotensin receptor blocker (ARB) or ACE2 inhibitors (ACEi) (ARB/ACEi, group 1, 23 females and 12 males, aged 63.63±10.40), and those who were not treated with these drugs (group 2, 38 females and 37 males, aged 55.12±16.51). Distal airflow obstruction (DAO) was evaluate as forced expiratory flow (FEF) at 25%, 50% and 75% of total flow. Group 1 presented lower peripheral oxygen saturation percentage vs group 2 (96.54±3.06 vs 97.30±1.19%, p<0.05). Spirometry data were worst in group1: Forced expiratory volume at first minute (FEV1) (91.20±17.09 vs 97.56±16.40%, p<0.05), Forced vital capacity (94.06±17.48 vs 99.13±17.71%, p<0.05), and Tiffenau Index (0.78±0.12 vs 0.84±0.10, p<0.05). There was a DAO in group1. In group 1, we found also a reduction in FEF 25 (73.97±27.28 vs 86.89±22.44%, p<0.05), FEF 50 (74.69±33.01 vs 85.67±23.74%, p<0.05), and FEF 25-75 (74.14±35.03 vs 83.92±25.38%, p<0.05) but not in FEF 75 (73.06±39.37 vs 82.27±43.33%, p<0.05). In patients treated with ARB/ACEi the indexes of respiratory function were shifted towards the lower limits (albeit within normal limits). These parameters were significantly reduced compared to patients not treated with these drugs. This indicates that the COVID-19 disease is not only a pulmonary disease, but also a vascular one.

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