A prospective study of pulmonary outcomes and chest computed tomography in the first year after COVID-19

Abstract

COVID-19 primarily affects the respiratory system. We aimed to evaluate how pulmonary outcomes develop after COVID-19 by assessing participants from the first pandemic wave prospectively 3- and 12-months following hospital discharge.Pulmonary outcomes included self-reported dyspnoea assessed with the modified Medical Research Council dyspnoea scale (mMRC), 6-minute walking distance (6MWD), spirometry, diffusion capacity of the lungs for carbon monoxide (DLCO), body plethysmography, and chest computed tomography (CT). Chest CT was repeated at 12 months in participants with pathological findings at 3 months. The WHO ordinal scale for clinical improvement defined disease severity in the acute phase.Of 262 included COVID-19 patients, 245 (94%) and 222 (90%) participants attended the 3- and 12-month follow-up, respectively. Self-reported dyspnoea and 6MWD remained unchanged between the two time points, while DLCOand total lung capacity improved (0.28 mmol min−1kPa−1, 95% CI (0.12–0.44), and 0.13 L, 95% CI (0.02–0.24), respectively). The prevalence of fibrotic-like findings on chest CT at 3 and 12 months in those with follow-up chest CT was unaltered. Those with more severe disease had worse dyspnoea, DLCO,åand TLC values than those with mild disease.There was an overall positive development of pulmonary outcomes from 3 to 12 months after hospital discharge. The discrepancy between the unaltered prevalence of self-reported dyspnoea and the improvement in pulmonary function underscores the complexity of dyspnoea as a prominent factor of long-COVID. The lack of increase in fibrotic-like findings from 3 to 12 months suggests that SARS-CoV-2 does not induce a progressive fibrotic process in the lungs.

Pulmonary function trajectories in COVID-19 survivors with- and without pre-existing respiratory disease at three and twelve months after hospital discharge

“…Although DLCO impairments mostly restore over time in Non-PRD patients [14,20,21], our cohort of PRD patients did not show improvements in DLCO abnormalities over time. These patients might already have an impaired DLCO caused by the pathological characteristics of their underlying disease including emphysema and pulmonary hypertension, which are known to negatively in uence the diffusion capacity of the lungs [22,23].…”

Estimated Global Proportions of Individuals With Persistent Fatigue, Cognitive, and Respiratory Symptom Clusters Following Symptomatic COVID-19 in 2020 and 2021

“…Faroe Islands, 24 Germany, 25,26 Sweden, 27,28 US 29 China, 30 Denmark, 31 Norway, 32 UK, 10,33,34 US 35 Australia, 36 Belgium, 37 China, 38 France, [39][40][41][42] India, 43,44 Iran, 45 Israel, 46,47 Italy, [48][49][50][51][52][53] the Netherlands, 54 Norway, 55 Saudi Arabia, 56 South Africa, 57 Spain, [58][59][60][61][62] Switzerland, 63 Turkey, 64 UK, 11,65-69 US greater in those who were admitted to ICUs (43.1% [95% UI, 22.6%-65.2%]) and in those who were admitted to general hospital wards (27.5% [95% UI, 12.1%-47.8%]) than in those who were not hospitalized (5.7% [95% UI, 1.9%-13.1%]), with higher proportions among females than males (Table 3 and eTable 14 in Supplement 1).…”

Circulating markers of extracellular matrix remodelling in severe COVID‐19 patients

“…Moreover, high levels of OPN, S100A12 and YKL‐40 during hospitalisation were associated with pathological findings on chest CT 3‐months after hospital admission, suggesting induction of persistent pulmonary pathology. However, follow‐up studies have shown a reduction in the prevalence of such findings on chest CT from 3 to 12‐months after COVID‐19 [43]. Interestingly, YKL‐40 (CHI3L1) have been shown to stimulate the expression of angiotensin‐converting enzyme 2 and host proteases implicated in SARS‐CoV‐2 infectivity [44], and YKL‐40 inhibition augmented SARS‐CoV‐2 infection in epithelial cells, including infection with omicron variants [45].…”