Long COVID is the persistence of one or more COVID-19 symptoms after the initial viral infection, and there is evidence supporting its association with lung damage. In this systematic review, we provide an overview of lung imaging and its findings in long COVID patients. A PubMed search was performed on 29 September 2021, for English language studies in which lung imaging was performed in adults suffering from long COVID. Two independent researchers extracted the data. Our search identified 3130 articles, of which 31, representing the imaging findings of 342 long COVID patients, were retained. The most common imaging modality used was computed tomography (CT) (N = 249). A total of 29 different imaging findings were reported, which were broadly categorized into interstitial (fibrotic), pleural, airway, and other parenchymal abnormalities. A direct comparison between cases, in terms of residual lesions, was available for 148 patients, of whom 66 (44.6%) had normal CT findings. Although respiratory symptoms belong to the most common symptoms in long COVID patients, this is not necessarily linked to radiologically detectable lung damage. Therefore, more research is needed on the role of the various types of lung (and other organ) damage which may or may not occur in long COVID.
Asthma is a common disorder affecting around 315 million individuals worldwide. The heterogeneity of asthma is becoming increasingly important in the era of personalized treatment and response assessment. Several radiological imaging modalities are available in asthma including chest x-ray, computed tomography (CT) and magnetic resonance imaging (MRI) scanning. In addition to qualitative imaging, quantitative imaging could play an important role in asthma imaging to identify phenotypes with distinct disease course and response to therapy, including biologics. MRI in asthma is mainly performed in research settings given cost, technical challenges, and there is a need for standardization. Imaging analysis applications of artificial intelligence (AI) to subclassify asthma using image analysis have demonstrated initial feasibility, though additional work is necessary to inform the role of AI in clinical practice.
In chronic obstructive pulmonary disease (COPD), vascular alterations have been shown to contribute to hypoxia and pulmonary hypertension, but the independent contribution of small vessel abnormalities to mortality remains unclear. We quantified artery and vein dimensions on computed tomography (CT) down to 0.2 mm. Small vessel volumes (<1 mmᴓ) were normalized by body surface area. In 7903 current and former smokers of the COPDGene study (53.2% male) the independent contribution of small artery and small vein volume to all-cause mortality was tested in multivariable Cox models. Additionally, we calculated the 95th percentile of small arteries and veins in 374 never smokers to create two groups: normal and high small artery or vein volume. We describe clinical, physiological and imaging characteristics of subjects with a high small artery and high small vein volume. Both high small artery and high small vein volumes were independently associated with mortality with an adjusted hazard ratio of 1.07 [1.01, 1.14] and 1.34 [1.21, 1.49] per mL/m2 increase, respectively. In COPDGene, 447 (5.7%) had high small artery volume and 519 (9.1%) subjects had high small vein volume and both had more emphysema, more air trapping and more severe coronary calcium. In smokers, abnormally high volumes in small arteries and veins are both relevant for mortality, which urges investigations into the aetiology of small pulmonary vessels and cardiac function in smokers. Award Number U01-HL089897 and U01-HL089856 from the NHLBI. COPD Foundation with contributions from AstraZeneca, Boehringer Ingelheim, Genentech, GlaxoSmithKline, Novartis, Pfizer, Siemens, and Sunovion.
Cigarette smoke affects the small pulmonary vasculature through mechanisms involving endothelial dysfunction, oxidative stress, inflammation, smooth muscle proliferation, and fibrosis, some of which are more acute and others more chronic [1]. These changes contribute to various lung diseases, including COPD, emphysema and pulmonary hypertension, and also increase the risk of cardiovascular complications such as right-sided heart failure [2].
Aim: In chronic obstructive pulmonary disease (COPD), emphysema can lead to microscopic artery loss and pulmonary hypertension. Left heart dysfunction can lead to enlargement of distal pulmonary veins. Aims: To evaluate pulmonary artery/vein volume on CT and associate this with clinical parameters and mortality. Methods: The artery-vein phenotyping analysis (AVX) was performed using the AI-based lung quantification platform LungQ (Thirona, The Netherlands). For this analysis we quantified large artery volume (diameter ≥2mm, AVXLA) and small vein volume (diameter <2mm, AVXSV) in participants in the COPDGene study, normalized for body height. Normal AVXLA and AVXSV volumes were determined using never smokers (95th percentile). Baseline characteristics were compared between normal and abnormal groups using independent T-tests. Results: 7980 subjects included 77 never smokers. AVXSV>97.5 mm3/cm and AVXLA>263.9 mm3/cm were defined as abnormal. Subjects with increased AVXSV or AVXLA had higher 10y mortality compared to subjects with normal AVXSV and AVXLA (41.4% and 39.4% vs. 28.0%). Results on clinical parameters are shown in the table. *p<.001 as compared to normal group **Overlap in 536 subjects Conclusions: High AVXSV and AVXLA in subjects with COPD are associated with male gender, more emphysema, higher CAC scores and higher mortality. This may reflect left heart dysfunction and pulmonary artery hypertension.