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BACKGROUND: Olfactory dysfunction is a cardinal symptom of COVID-19 infection, however, studies assessing long-term olfactory dysfunction are limited and no randomised-controlled trials (RCTs) of early olfactory training have been conducted. METHODOLOGY: We conducted a prospective, multi-centre study consisting of baseline psychophysical measurements of smell and taste function. Eligible participants were further recruited into a 12-week RCT of olfactory training versus control (safety information). Patient-reported outcomes were measured using an electronic survey and BSIT at baseline and 12 weeks. An additional 1-year follow-up was open to all participants. RESULTS: 218 individuals with a sudden loss of sense of smell of at least 4-weeks were recruited. Psychophysical smell loss was observed in only 32.1%; 63 participants were recruited into the RCT. The absolute difference in BSIT improvement after 12 weeks was 0.45 higher in the intervention arm. 76 participants completed 1-year follow-up; 10/19 (52.6%) of participants with an abnormal baseline BSIT test scored below the normal threshold at 1-year, and 24/29 (82.8%) had persistent parosmia. CONCLUSIONS: Early olfactory training may be helpful, although our findings are inconclusive. Notably, a number of individuals who completed the 1-year assessment had persistent smell loss and parosmia at 1-year. As such, both should be considered important entities of long-Covid and further studies to improve management are highly warranted.
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[Figure: see text].
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Background: Recent CMR studies have reported cardiac abnormalities after COVID-19 are common, even after mild, non-hospitalised illness with evidence of ongoing myocardial inflammation. Such a prevalence of chronic myocarditis after mild disease has prompted societal concerns in diverse domains, and suggests that screening should be considered post COVID-19, even in asymptomatic individuals. Cardiovascular magnetic resonance (CMR) has proven utility for diagnosis in patients with COVID-19 infection and elevated troponin from unclear causes by measuring cardiac structure, function, myocardial scar (late gadolinium enhancement) and oedema (T1 and T2 mapping). Objectives: We aimed to determine the prevalence and extent of late cardiac and cardiovascular sequelae after mild non-hospitalised SARS-CoV-2 infection. Methods: Participants were recruited from COVIDsortium, a three-hospital prospective study of 731 healthcare workers who underwent first wave weekly symptom, PCR and serology assessment over 4 months, with seroconversion in 21.5% (n = 157). At 6 months post infection, 74 seropositive and 75 age-, sex-, ethnicity-matched seronegative controls were recruited for cardiovascular phenotyping (comprehensive phantom-calibrated Cardiovascular Magnetic Resonance and blood biomarkers). Analysis was blinded, using objective AI analytics where available. Results: 149 subjects (mean age 37 years, range 18-63, 58% female) were recruited. Seropositive infections had been mild with case definition/ non-case definition/asymptomatic disease in 45(61%), 18(24%) and 11(15%) with one person hospitalised (for 2 days). Between seropositive and seronegative groups, there were no differences in cardiac structure (left ventricular volumes, mass;atrial area), function (ejection fraction, global longitudinal shortening, aortic distensibility), tissue characterisation (T1, T2, ECV mapping, late gadolinium enhancement) or biomarkers (troponin, NT-proBNP). With abnormal defined by the 75 seronegatives (2 standard deviations from mean, e.g. EF < 54%, septal T1 > 1072ms, septal T2 > 52.4ms), individuals had abnormalities including reduced EF (n = 2, minimum 50%), T1 elevation (n = 6), T2 elevation (n = 9), LGE (n = 13, median 1%, max 5% of myocardium), biomarker elevation (borderline troponin elevation in 4;all NTproBNP normal). These were distributed equally between seropositive and seronegative individuals. Conclusions: Cardiovascular abnormalities are no more common in seropositive vs seronegative otherwise healthy, workforce representative individuals 6 months post mild SARS-CoV-2 infection. Our study provides societal reassurance for the cardiovascular health of workingaged individuals with convalescence from mild SARS-CoV-2. Screening asymptomatic individuals following mild diseases is not indicated.
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Background: Acute myocardial damage is common in hospitalized patients with severe COVID-19, with evidence of myocardial infarction and myocarditis demonstrated on cardiovascular magnetic resonance (CMR). Post-mortem studies have also implicated microvascular thrombosis, which may cause persistent microvascular disease. Purpose: To determine the long-term coronary sequelae in recovered COVID-19 using multiparametric CMR including state-of-the-art inline quantitative stress myocardial blood flow (sMBF) mapping to assess global and regional sMBF. Methods: Prospective, multicentre observational study of recovered COVID-19 patients scanned at three London CMR units. Results were compared to a propensity-matched, pre-COVID chest pain cohort (104 patients referred for perfusion CMR, with subsequently demonstrated unobstructed coronary arteries) and 27 healthy volunteers (HV). Perfusion image analysis was performed using a novel artificial intelligence approach deriving global and regional stress and rest MBF with a cut-off of >2.25mL/g/min signifying normal sMBF and <1.82mL/g/min abnormal sMBF (Kotecha JCVI 2019). Results: 104 recovered, post-COVID patients (median age 62 years, 76% male;89[87%] hospitalised, 41/89[46%] requiring ICU) underwent adenosine-stress perfusion CMR at a median 131(IQR 43-179) days from COVID-19 diagnosis. Median LVEF was 67% (IQR 60-71%;12 (11.5%) with impaired LVEF), 51 patients (49%) had late gadolinium enhancement (LGE);18% infarct-pattern and 33% non-ischaemic LGE. Global stress MBF in post-COVID patients was no different to age-, sex-and co-morbidities-matched controls (2.57 ± 0.77 vs. 2.40 ± 0.75 ml/g/min, p = 0.11, Figure 1), though lower than HV (3.00 ± 0.76 ml/g/min, p = 0.001). Post-COVID, multivariate predictors of low sMBF were male sex (OR 0.57, 95%CI 0.41-0.80, p = 0.001) and hypertension (OR 0.67, 95%CI 0.51-0.88, p = 0.004), but not COVID-19 disease severity (ICU admission) or presence of scar (ischemic/non-ischemic). 21/42 with reduced sMBF (<2.25mL/g/min) had regional perfusion defects consistent with epicardial coronary disease. Conclusions: COVID-19 survivors do not demonstrate evidence of reduced global MBF by CMR compared to risk factor matched controls. Stress perfusion CMR identifies etiology of acute myocardial damage (infarction/myocarditis) and presence of occult coronary ischemia.