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1.
J Nucl Cardiol ; 2022 May 02.
Article in English | MEDLINE | ID: covidwho-1850449

ABSTRACT

AIM: Arterial involvement has been implicated in the coronavirus disease of 2019 (COVID-19). Fluorine 18-fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG PET/CT) imaging is a valuable tool for the assessment of aortic inflammation and is a predictor of outcome. We sought to prospectively assess the presence of aortic inflammation and its time-dependent trend in patients with COVID-19. METHODS: Between November 2020 and May 2021, in this pilot, case-control study, we recruited 20 patients with severe or critical COVID-19 (mean age of 59 ± 12 years), while 10 age and sex-matched individuals served as the control group. Aortic inflammation was assessed by measuring 18F-FDG uptake in PET/CT performed 20-120 days post-admission. Global aortic target to background ratio (GLA-TBR) was calculated as the sum of TBRs of ascending and descending aorta, aortic arch, and abdominal aorta divided by 4. Index aortic segment TBR (IAS-TBR) was designated as the aortic segment with the highest TBR. RESULTS: There was no significant difference in aortic 18F-FDG PET/CT uptake between patients and controls (GLA-TBR: 1.46 [1.40-1.57] vs. 1.43 [1.32-1.70], respectively, P = 0.422 and IAS-TBR: 1.60 [1.50-1.67] vs. 1.50 [1.42-1.61], respectively, P = 0.155). There was a moderate correlation between aortic TBR values (both GLA and IAS) and time distance from admission to 18F-FDG PET-CT scan (Spearman's rho = - 0.528, P = 0.017 and Spearman's rho = - 0.480, p = 0.032, respectively). Patients who were scanned less than or equal to 60 days from admission (n = 11) had significantly higher GLA-TBR values compared to patients that were examined more than 60 days post-admission (GLA-TBR: 1.53 [1.42-1.60] vs. 1.40 [1.33-1.45], respectively, P = 0.016 and IAS-TBR: 1.64 [1.51-1.74] vs. 1.52 [1.46-1.60], respectively, P = 0.038). There was a significant difference in IAS- TBR between patients scanned ≤ 60 days and controls (1.64 [1.51-1.74] vs. 1.50 [1.41-1.61], P = 0.036). CONCLUSION: This is the first study suggesting that aortic inflammation, as assessed by 18F-FDG PET/CT imaging, is increased in the early post COVID phase in patients with severe or critical COVID-19 and largely resolves over time. Our findings may have important implications for the understanding of the course of the disease and for improving our preventive and therapeutic strategies.

2.
Int J Cardiol ; 358: 136-139, 2022 Jul 01.
Article in English | MEDLINE | ID: covidwho-1796722

ABSTRACT

BACKGROUND: Complications following COVID-19 vaccination, particularly with mRNA vaccines, rarely include myocarditis and pericarditis. This work principally aimed at defining a realistic temporal relationship between vaccination and myocarditis/pericarditis development. METHODS: All relevant cases reported from week 52/2020 through week 41/2021 in the VAERS database were retrieved and analyzed for licensed vaccines. These included BNT162b2, mRNA-1273, and AD26.COV2·S. Incidence rates were calculated using the corresponding administered vaccine doses as denominators. Additionally, analyzed parameters included demographics, dose series, hospitalization length and outcome. RESULTS: Overall, 2016 myocarditis and 1380 pericarditis cases, (4.96/106 and 3.40/106 administered vaccine doses, respectively), were recorded. Most myocarditis cases occurred following BNT162b2 (5.60/106 doses) in males <30 years. Pericarditis affected predominantly males <40, both sexes >40 years, and was most common post AD26.COV2·S (4.78/106 doses). Hospitalization was required for 40.3% and 27.2% of myocarditis and pericarditis cases, respectively. A bimodal pattern was found for both myocarditis and pericarditis, with two peaks that coincided temporally, but were reversed in intensity. The first peak was recorded 1-3 days post-vaccination and was more pronounced in myocarditis, while the second was recorded 15-30 days post-vaccination and was more intense in pericarditis. CONCLUSIONS: Myocarditis/pericarditis after COVID-19 vaccination is rare and depicts a bimodal pattern.


Subject(s)
COVID-19 , Myocarditis , Pericarditis , COVID-19/epidemiology , COVID-19/prevention & control , COVID-19 Vaccines/adverse effects , Female , Humans , Male , Myocarditis/complications , Myocarditis/etiology , Pericarditis/diagnosis , Pericarditis/epidemiology , Pericarditis/etiology , SARS-CoV-2 , Vaccination/adverse effects
4.
Hypertens Res ; 45(5): 846-855, 2022 05.
Article in English | MEDLINE | ID: covidwho-1735235

ABSTRACT

To fight the COVID-19 pandemic, messenger RNA (mRNA) vaccines were the first to be adopted by vaccination programs worldwide. We sought to investigate the short-term effect of mRNA vaccine administration on endothelial function and arterial stiffness. Thirty-two participants (mean age 37 ± 8 years, 20 men) who received the BNT162b2 mRNA COVID-19 vaccine were studied in three sessions in a sequence-randomized, sham-controlled, assessor-blinded, crossover design. The primary outcome was endothelial function (assessed by brachial artery flow-mediated dilatation (FMD)), and the secondary outcomes were aortic stiffness (evaluated with carotid-femoral pulse wave velocity (PWV)) and inflammation (measured by high-sensitivity C-reactive protein (hsCRP) in blood samples). The outcomes were assessed prior to and at 8 h and 24 h after the 1st dose of vaccine and at 8 h, 24 h, and 48 h after the 2nd dose. There was an increase in hsCRP that was apparent at 24 h after both the 1st dose (-0.60 [95% confidence intervals [CI]: -1.60 to -0.20], p = 0.013) and the 2nd dose (maximum median difference at 48 h -6.60 [95% CI: -9.80 to -3.40], p < 0.001) compared to placebo. The vaccine did not change PWV. FMD remained unchanged during the 1st dose but decreased significantly by 1.5% (95% CI: 0.1% to 2.9%, p = 0.037) at 24 h after the 2nd dose. FMD values returned to baseline at 48 h. Our study shows that the mRNA vaccine causes a prominent increase in inflammatory markers, especially after the 2nd dose, and a transient deterioration of endothelial function at 24 h that returns to baseline at 48 h. These results confirm the short-term cardiovascular safety of the vaccine.


Subject(s)
COVID-19 , Vascular Stiffness , Adult , Brachial Artery , C-Reactive Protein/metabolism , COVID-19/prevention & control , COVID-19 Vaccines , Cross-Over Studies , Female , Humans , Male , Middle Aged , Pandemics , Pulse Wave Analysis , RNA, Messenger , Vaccines, Synthetic
5.
EuropePMC; 2021.
Preprint in English | EuropePMC | ID: ppcovidwho-292295

ABSTRACT

Aim: Arterial involvement has been implicated in the coronavirus disease of 2019 (COVID-19). 18F-fluoro-2-deoxy-d-glucose positron emission tomography/computed tomography (18F-FDG PET/CT) imaging is a valuable tool for the assessment of disease severity in different types of vasculitis and is a predictor of outcome. We sought to prospectively assess the presence of aortic inflammation and its time-dependent trend by measuring the 18-FDG uptake in PET/CT in patients with severe or critical COVID-19. Methods: In this pilot case control study, we recruited 20 patients, who were admitted with severe or critical COVID-19 illness. Patients underwent imaging between 20 to 120 days after hospital admission. Ten age- and sex-matched individuals with prior history of malignancy but free of active disease served as the control group. Arterial inflammation was assessed by measuring 18-FDG uptake in PET/CT and calculating aortic target to blood ratio (TBR). Results: There was a significant correlation between aortic TBR values and time distance from diagnosis to 18F-FDG PET/CT scan (-rho- =0.547, p=0.015) even after adjustment for confounders (p=0.002). Patients who were scanned less than 60 days (median) from diagnosis had significantly higher TBR values compared to patients examined more than 60 days post-diagnosis (1.55 [1.47-1.61] vs 1.40 [1.33-1.45], respectively, p=0.013). Conclusion: This is the first study suggesting that 18 FDG PET/CT imaging could be used for assessment of arterial inflammation in patients with severe/critical COVID-19. These findings may have important implications for the understanding of the pathophysiology and the course of the disease and for improving our preventive and therapeutic strategies.

6.
Sci Rep ; 11(1): 20239, 2021 10 12.
Article in English | MEDLINE | ID: covidwho-1467128

ABSTRACT

Accurate risk stratification in COVID-19 patients consists a major clinical need to guide therapeutic strategies. We sought to evaluate the prognostic role of estimated pulse wave velocity (ePWV), a marker of arterial stiffness which reflects overall arterial integrity and aging, in risk stratification of hospitalized patients with COVID-19. This retrospective, longitudinal cohort study, analyzed a total population of 1671 subjects consisting of 737 hospitalized COVID-19 patients consecutively recruited from two tertiary centers (Newcastle cohort: n = 471 and Pisa cohort: n = 266) and a non-COVID control cohort (n = 934). Arterial stiffness was calculated using validated formulae for ePWV. ePWV progressively increased across the control group, COVID-19 survivors and deceased patients (adjusted mean increase per group 1.89 m/s, P < 0.001). Using a machine learning approach, ePWV provided incremental prognostic value and improved reclassification for mortality over the core model including age, sex and comorbidities [AUC (core model + ePWV vs. core model) = 0.864 vs. 0.755]. ePWV provided similar prognostic value when pulse pressure or hs-Troponin were added to the core model or over its components including age and mean blood pressure (p < 0.05 for all). The optimal prognostic ePWV value was 13.0 m/s. ePWV conferred additive discrimination (AUC: 0.817 versus 0.779, P < 0.001) and reclassification value (NRI = 0.381, P < 0.001) over the 4C Mortality score, a validated score for predicting mortality in COVID-19 and the Charlson comorbidity index. We suggest that calculation of ePWV, a readily applicable estimation of arterial stiffness, may serve as an additional clinical tool to refine risk stratification of hospitalized patients with COVID-19 beyond established risk factors and scores.


Subject(s)
COVID-19/mortality , Cardiovascular Diseases/epidemiology , Vascular Stiffness , Aged , Aged, 80 and over , Comorbidity , Female , Humans , Italy/epidemiology , Longitudinal Studies , Male , Middle Aged , Retrospective Studies , Risk Factors , United Kingdom/epidemiology
7.
Vaccine ; 2021.
Article in English | EuropePMC | ID: covidwho-1451636

ABSTRACT

<h4>Background</h4> COVID-19 vaccines were efficacious and safe in clinical trials. We report nine events of acute pericarditis (AP) in eight patients following COVID-19 vaccination with BNT162b2 (6/9), AZD1222 (2/9) and mRNA-1273 (1/9). <h4>Methods</h4> All patients were referred for AP temporally linked with COVID-19 vaccination. Chest pain was the most common clinical manifestation. Alternative etiologies were excluded upon thorough diagnostic work up. AP diagnosis was established according to ESC guidelines. <h4>Findings</h4> Five events occurred after the first vaccine dose and four after the second. The mean age in this cohort was 65.8±10.2 years and the men/women ratio 3/5. All events resolved without sequelae;two events were complicated by cardiac tamponade requiring emergent pericardial decompression. Hospitalization was required in four cases. <h4>Interpretation</h4> Although causality cannot be firmly established, AP has emerged as a possible complication following COVID-19 vaccination. Further investigation is indispensable to fully characterize this new entity.

8.
Ther Adv Neurol Disord ; 13: 1756286420978004, 2020.
Article in English | MEDLINE | ID: covidwho-972457

ABSTRACT

Neurological manifestations are not uncommon during infection with the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). A clear association has been reported between cerebrovascular disease and coronavirus disease 2019 (COVID-19). However, whether this association is causal or incidental is still unknown. In this narrative review, we sought to present the possible pathophysiological mechanisms linking COVID-19 and cerebrovascular disease, describe the stroke syndromes and their prognosis and discuss several clinical, radiological, and laboratory characteristics that may aid in the prompt recognition of cerebrovascular disease during COVID-19. A systematic literature search was conducted, and relevant information was abstracted. Angiotensin-converting enzyme-2 receptor dysregulation, uncontrollable immune reaction and inflammation, coagulopathy, COVID-19-associated cardiac injury with subsequent cardio-embolism, complications due to critical illness and prolonged hospitalization can all contribute as potential etiopathogenic mechanisms leading to diverse cerebrovascular clinical manifestations. Acute ischemic stroke, intracerebral hemorrhage, and cerebral venous sinus thrombosis have been described in case reports and cohorts of COVID-19 patients with a prevalence ranging between 0.5% and 5%. SARS-CoV-2-positive stroke patients have higher mortality rates, worse functional outcomes at discharge and longer duration of hospitalization as compared with SARS-CoV-2-negative stroke patients in different cohort studies. Specific demographic, clinical, laboratory and radiological characteristics may be used as 'red flags' to alarm clinicians in recognizing COVID-19-related stroke.

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