Background: Coronavirus disease 2019 (COVID-19) has spread worldwide, having a dramatic impact on healthcare systems. The aim of this study is to evaluate mid-term clinical impact of COVID-19 on respiratory function.Methods: 379 patients were evaluated 4 months after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) diagnosis. Patients were divided in two groups based on the presence of pneumonia during COVID-19. Clinical conditions, quality of life, symptomatology, 6-min walk test, pulmonary function test with spirometry and diffusing capacity of the lung for carbon monoxide were analysed. Data were compared to clinical evolution during COVID-19 (development of acute respiratory distress syndrome, need of invasive mechanical ventilation, partial oxygen saturation (SpO₂)/inspiratory oxygen fraction (FIO₂) ratio and pneumonia severity index (PSI)).Results: After a median 135 days, 260 (68.6%) out of 379 patients referred at least one symptom. Patients who developed pneumonia during COVID-19 showed lowerSpO₂at rest (p<0.001),SpO₂during 6-min walk test (p<0.001), total lung capacity (p<0.001), airway occlusion pressure after 0.1 s (P_0.1) (p=0.02),P_0.1/maximal inspiratory pressure ratio (p=0.005) and higher Borg category-ratio scale (p=0.006) and modified Medical Research Council breathlessness scale (p=0.003), compared to patients without pneumonia.SpO₂/FIO₂ratio and PSI during SARS-CoV-2 pneumonia were directly associated with mid-term alteration ofSpO₂at rest (p<0.001) and during 6-min walk test (p<0.001), residual volume (p<0.001), total lung capacity (p<0.001 and p=0.003, respectively) and forced vital capacity (p=0.004 and p=0.03, respectively).Conclusion: Lung damage during COVID-19 correlates to the reduction of pulmonary function 4 months after acute infection.

Background and Aims: Increasing evidence suggests that COVID-19 survivors experience long-term cardiovascular complications possibly through development of vascular damage. The study aimed to investigate whether accelerated vascular ageing occurs after COVID-19 infection, and if so, identify its determinants. Methods: This prospective, multicentric, cohort study, included 34 centres in 16 countries worldwide, in 4 groups of participants—COVID-19-negative controls (ⅰ) and three groups of individuals with recent (6 ± 3 months) exposure to SARS-CoV-2: not hospitalized (ⅱ), hospitalized in general wards (ⅲ), and hospitalized in intensive care units (ⅳ). The main outcome was carotid-femoral pulse wave velocity (PWV), an established biomarker of large artery stiffness. Results: 2390 individuals (age 50 ± 15 years, 49.2% women) were recruited. After adjustment for confounders, all COVID-19-positive groups showed higher PWV (+0.41, +0.37, and +0.40 m/s for groups 2–4, P < .001, P = .001 and P = .003) vs. controls [PWV 7.53 (7.09; 7.97) m/s adjusted mean (95% CI)]. In sex-stratified analyses, PWV differences were significant in women [PWV (+0.55, +0.60, and +1.09 m/s for groups 2–4, P < .001 for all)], but not in men. Among COVID-19 positive women, persistent symptoms were associated with higher PWV, regardless of disease severity and cardiovascular confounders [adjusted PWV 7.52 (95% CI 7.09; 7.96) vs. 7.13 (95% CI 6.67; 7.59) m/s, P < .001]. A stable or improved PWV after 12 months was found in the COVID+ groups, whereas a progression was observed in the COVID− group. Conclusions: COVID-19 is associated with early vascular ageing in the long term, especially in women.

An excess morning blood pressure surge (MBPS) may portend an increased cardiovascular risk, but the mechanisms thereof have been little investigated. The link between MBPS, short-term blood pressure (BP) variability, and arterial stiffness has not been entirely defined. In 602 consecutive untreated hypertensive patients (48 ± 12 years, 61% men, office BP 149/93 ± 17/10 mmHg), we measured carotid–femoral pulse wave velocity (cf-PWV, SphygmoCor) and 24-h ambulatory BP. Using self-reported sleep and wake times, MBPS was defined as sleep-trough (ST-MBPS), prewaking, rising. Short-term BP variability was calculated as weighted 24-h SBP SD and average real variability of 24-h SBP (ARV), that is, average of absolute differences between consecutive SBP readings. ST-MBPS (r = 0.16, P < 0.001) and rising MBPS (r = 0.12, P = 0.003) showed a direct correlation with cf-PWV, whereas prewaking MBPS had no such relation (r = 0.06, P = 0.14). Only ST-MBPS was independently associated with cf-PWV (t = 1.96, P = 0.04) after adjustment for age, sex, height, office mean arterial pressure, heart rate, and renal function. This association was lost after further adjustment for weighted 24-h SBP SD (P = 0.13) or ARV (P = 0.24). ARV was a significant mediator of the relationship between ST-MBPS and cf-PWV (P = 0.003). In untreated hypertension, ST-MBPS has a direct relation with aortic stiffness, which is mediated by an increased ARV. The adverse effects of MBPS may be partly explained by its link with arterial stiffness, mediated by short-term SBP variability.