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1.
Annals of Hematology ; 101(10):2307-2315, 2022.
Article in English | MEDLINE | ID: covidwho-2014115

ABSTRACT

Severe acute respiratory syndrome coronavirus (SARS-CoV2) and associated COVID-19 infection continue to impact patients globally. Patients with underlying health conditions are at heightened risk of adverse outcomes from COVID-19;however, research involving patients with rare health conditions remains scarce. The amyloidoses are a rare grouping of protein deposition diseases. Light-chain and transthyretin amyloidosis are the most common disease forms, often present with systemic involvement of vital organs including the heart, nerves, kidneys, and GI tracts of affected individuals. The Amyloidosis Program of Calgary examined 152 ATTR patients and 103 AL patients analyzing rates of vaccination, COVID-19 testing, infection outcomes, influence referrals, and excess deaths. Results showed 15 total PCR-confirmed COVID-19 infections in the tested population of amyloid patients, with a higher frequency of infections among patient with AL compared to the ATTR cohort (26.2% vs 5.1%). Four patients (26.6%) required hospital admission for COVID-19 infection, 2 ATTR, and 2 AL patients. Of the confirmed cases, 1 (0.07%) unvaccinated ATTR patient died of a COVID-19 infection. An excess of deaths was found in both the ATTR and AL cohorts when comparing pre-pandemic years 2018 and 2019 to the pandemic years of 2020 and 2021. The finding suggests that amyloidosis patients are likely at a high risk for severe COVID-19 infection and mortality, especially those of advanced age, those on an active treatment with chemotherapy, and those with concomitant B-cell or plasma cell disorder. The impact of virtual healthcare visits and pandemic measures on the excess of deaths observed requires further research.

2.
Topics in Antiviral Medicine ; 30(1 SUPPL):38-39, 2022.
Article in English | EMBASE | ID: covidwho-1880187

ABSTRACT

Background: Cardiopulmonary symptoms and reduced exercise capacity can persist after SARS-CoV-2 infection. Mechanisms of post-acute sequelae of COVID-19 ("PASC" or "Long COVID") remain poorly understood. We hypothesized that systemic inflammation would be associated with reduced exercise capacity and pericardial/myocardial inflammation. Methods: As part of a COVID recovery cohort (NCT04362150) we assessed symptoms, biomarkers, and echocardiograms in adults >2 months after PCR-confirmed SARS-CoV-2 infection. In a subset, we performed cardiac magnetic resonance imaging (CMR), ambulatory rhythm monitoring (RM), and cardiopulmonary exercise testing (CPET) >12 months after acute infection. Associations between symptoms and oxygen consumption (VO2), cardiopulmonary parameters and biomarkers were evaluated using linear and logistic regression with adjustment for age, sex, BMI, and time since infection. Results: We studied 120 participants (median age 51, 42% female, and 47% had cardiopulmonary symptoms at median 7 months after acute infection). Elevated hsCRP was associated with symptoms (OR 1.32 per doubling, 95%CI 1.01-1.73, p=0.04). No differences in echocardiographic indices were found except for presence of pericardial effusions among those with symptoms (p=0.04). Of the subset (n=33) who underwent CMR at a median 17 months, all had normal cardiac function (LVEF 53-76%), 9 (27%) had pericardial effusions and none had findings suggestive of prior myocarditis. There were no differences on RM by symptoms. On CPET, 33% had reduced exercise capacity (peak VO2 <85% predicted). Individuals with symptoms had lower peak VO2 compared to those reporting recovery (28.4 vs 21.4 ml/kg/min, p=0.04, Figure). Elevated hsCRP was independently associated with lower peak VO2 after adjustment (-9.8 ml/kg/min per doubling, 95%CI-17.0 to-2.5;p=0.01, Figure). The predominant mechanism of reduced peak VO2 was chronotropic incompetence (HR 19% lower than predicted, 95%CI 11-26%;p<0.0001, Figure). Chronotropic incompetence on CPET correlated with lower peak HR during ambulatory RM (p<0.001). Conclusion: Persistent systemic inflammation (hsCRP) is associated with pericardial effusions and reduced exercise capacity > 1 year after acute SARS-CoV-2 infection. This finding appears to be driven mainly by chronotropic incompetence rather than respiratory compromise, cardiac pump dysfunction, or deconditioning. Evaluation of therapeutic strategies to target inflammation and/or chronotropy to alleviate PASC is urgently needed.

3.
PubMed; 2022.
Preprint in English | PubMed | ID: ppcovidwho-338328

ABSTRACT

BACKGROUND: Mechanisms underlying persistent cardiopulmonary symptoms following SARS-CoV-2 infection (post-acute sequelae of COVID-19 "PASC" or "Long COVID") remain unclear. The purpose of this study was to elucidate the pathophysiology of cardiopulmonary PASC using multimodality cardiovascular imaging including cardiopulmonary exercise testing (CPET), cardiac magnetic resonance imaging (CMR) and ambulatory rhythm monitoring. METHODS: We performed CMR, CPET, and ambulatory rhythm monitoring among adults > 1 year after PCR-confirmed SARS-CoV-2 infection in the UCSF Long-Term Impact of Infection with Novel Coronavirus cohort (LIINC;NCT04362150 ) and correlated findings with previously measured biomarkers. We used logistic regression to estimate associations with PASC symptoms (dyspnea, chest pain, palpitations, and fatigue) adjusted for confounders and linear regression to estimate differences between those with and without symptoms adjusted for confounders. RESULTS: Out of 120 participants in the cohort, 46 participants (unselected for symptom status) had at least one advanced cardiac test performed at median 17 months following initial SARS-CoV-2 infection. Median age was 52 (IQR 42-61), 18 (39%) were female, and 6 (13%) were hospitalized for severe acute infection. On CMR (n=39), higher extracellular volume was associated with symptoms, but no evidence of late-gadolinium enhancement or differences in T1 or T2 mapping were demonstrated. We did not find arrhythmias on ambulatory monitoring. In contrast, on CPET (n=39), 13/23 (57%) with cardiopulmonary symptoms or fatigue had reduced exercise capacity (peak VO 2 <85% predicted) compared to 2/16 (13%) without symptoms (p=0.008). The adjusted difference in peak VO 2 was 5.9 ml/kg/min lower (-9.6 to -2.3;p=0.002) or -21% predicted (-35 to -7;p=0.006) among those with symptoms. Chronotropic incompetence was the primary abnormality among 9/15 (60%) with reduced peak VO 2 . Adjusted heart rate reserve <80% was associated with reduced exercise capacity (OR 15.6, 95%CI 1.30-187;p=0.03). Inflammatory markers (hsCRP, IL-6, TNF-alpha) and SARS-CoV-2 antibody levels measured early in PASC were negatively correlated with peak VO 2 more than 1 year later. CONCLUSIONS: Cardiopulmonary symptoms and elevated inflammatory markers present early in PASC are associated with objectively reduced exercise capacity measured on cardiopulmonary exercise testing more than 1 year following COVID-19. Chronotropic incompetence may explain reduced exercise capacity among some individuals with PASC. Clinical Perspective: What is New?Elevated inflammatory markers in early post-acute COVID-19 are associated with reduced exercise capacity more than 1 year later.Impaired chronotropic response to exercise is associated with reduced exercise capacity and cardiopulmonary symptoms more than 1 year after SARS-CoV-2 infection.Findings on ambulatory rhythm monitoring point to perturbed autonomic function, while cardiac MRI findings argue against myocardial dysfunction and myocarditis. Clinical Implications: Cardiopulmonary testing to identify etiologies of persistent symptoms in post-acute sequalae of COVID-19 or "Long COVID" should be performed in a manner that allows for assessment of heart rate response to exercise. Therapeutic trials of anti-inflammatory and exercise strategies in PASC are urgently needed and should include assessment of symptoms and objective testing with cardiopulmonary exercise testing.

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