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Journal of Hypertension ; 40:e172, 2022.
Article in English | EMBASE | ID: covidwho-1937717


Objective: Endothelial dysfunction is thought to underlie many of the complications of COVID-19 but to what degree this persists after recovery is unknown. Here we examine endothelial function in subjects previously hospitalized with COVID- 19, those with mild symptoms who were not hospitalized and negative controls (absence of SARS-CoV-2-antibodies). Endothelial function was measured as pulse wave response to the β2 adrenergic agonist salbutamol (PWRS) which is mediated through the nitric oxide - cyclic guanosine monophosphate pathway (NO-cGMP). Design and method: Echocardiography was used to exclude subjects with cardiac abnormalities. Tonometry of the radial artery (SphygmoCor, AtCor Medical, Sydney, Australia) was performed in duplicate by a single operator before and after inhalation of 200 mcg of salbutamol using a spacer device. The PWRS was taken as the change from baseline in augmentation index (Aix) as calculated by the SphygmoCor system. In a sub-sample, PWRS was assessed in the presence and absence of the phosphodiesterase type 5 inhibitor sildenafil which inhibits the breakdown of cGMP. Results: We recruited 88 subjects (49 men) aged 47.9 ± 14.3 (mean ± SD) years of whom 32 were previously hospitalized with COVID-19 (~6 months). Subjects previously hospitalized with COVID-19 were all previously assessed in a dedicated pulmonary clinic. Age, gender, BMI, smoking status, diabetes and estimated 10-year cardiovascular risk (Q-RISKâ3) were similar between the groups. Administration of salbutamol reduced AIx in controls and those with mild COVID-19 but produced an increase in AIx in previously hospitalized COVID-19 cases (mean [95% CI]): -2.85 [-5.52, -0.188] %, -2.32 [-5.17,0.54] %, and 3.03 [0.06, 6.00] % respectively, P = 0.017 between the groups. In a sub-sample (11 hospitalized and 11 non-hospitalized) the PWRS was measured again 30 minutes after oral administration of sildenafil 25 mg. This produced a greater reduction in AIx: -5.28 [-9.00, -1.54] % in non-hospitalized and a reduction: -3.90 [-7.60, -0.21] % in hospitalized patients, and an overall improvement in the PWRS (P = 0.006). Conclusions: In subjects previously hospitalized with severe COVID-19, endothelial function is impaired for many months after hospital discharge and the impaired NO-cGMP mediated vasodilation may be reversed by sildenafil.

Italian Journal of Medicine ; 15(3):71, 2021.
Article in English | EMBASE | ID: covidwho-1567763


Background and Aim: Pulmonary involvement from CoViD-19 is frequent, after acute phase dyspnoea, cough, desaturation, respiratory insufficiency, can persist, pneumonia leads to interstitial disease (ground- glass) and to pulmonary fibrosis (honeycomb lung). A diagnostic algorithm can be a simple way for differential diagnoses (pulmonary embolism, PE) and to set up therapies in a systematic way. Our objective was to propose a simple and easy diagnostic algorithm, to identify with chest CT scan, excluding PE in high dimer- D patients, suggestive gait test and compatible objectivity. Methods: Prescription of: blood tests, radiological (CT chest CMC or High Resolution), respiratory physiopathology (Walking test, Global spirometry, Plethysmography, DLCO). Set drug therapies in case of PE, oral steroid (OCS) in case of extensive interstitial disease, long-acting beta 2 agonist bronchodilators (LABA), antimuscarinics (LAMA), inhaled steroids (ICS). For fibrosis and a honeycomb pattern, treatment with dipalmitoylethanolamide (PEA). Results: 258 outpatients, average 60.68 years, 115 women, 143 men, with an urgent request for pneumological visit and treated on an outpatient basis. 1 pt died during treatment, 4 pts were diagnosed with pulmonary embolism. 4 pts required a prescription for oxygen therapy. 228 pts presented ground-glass, 30 pts showed normal chest CT. Conclusions: DLCO shows progressive improvement in values after ICS treatment. Small pathway deficiency evidenced by spirometry can be treated with LABA-LAMA especially in patients with a previous history of cigarette smoking or COPD.