Background: The World Health Organization (WHO) declared a pandemic in March 2020 caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Given the neurotropism feature of the coronavirus and growing number of COVID-19 associated neurological disorders, including Guillain Barre syndrome (GBS), we conducted a systematic review to thoroughly describe the clinical features, diagnostic workup, and clinical outcome of COVID-19 associated GBS in 78 cases. Methods: We identified case reports and case series of COVID-19 associated GBS by conducting a search in the PubMed/MEDLINE and EMBASE databases. We assessed the quality of studies using an appraisal checklist presented by Cochrane Murad et al. Extracted data included demographic characteristics, clinical presentation, diagnostic workup, and outcome. Results: The systematic search yielded a total of 60 articles reporting 78 patients with a diagnosis of COVID-19 associated GBS. The patients were mainly male (65.3%) with an average age of 57 years. The ascending symmetrical paresis was the most common presentation (79.4%), with demyelinating pattern in 54 patients (79.4%). The CSF analysis showed albuminocytologic dissociation in 48 patients (75%). The mortality of COVID-19 associated GBS was estimated as 6.4% attributable to progressive respiratory failure. Conclusion: Given the associated morbidities such as respiratory failure in patients with COVID-19 associated GBS, its timely detection is crucial to prevent poor clinical outcomes. On the other hand, clinicians must be vigilant to identify the clinical findings of SARS-CoV-2 infection in newly diagnosed GBS patients, as this might be a neurological complication of the subclinical viral infection.

Introduction: Cardiac complications are the leading cause of death in thalassemia patients. It is assumed that progressive iron accumulation results in myocyte damage. Myocardial T2* measurement by cardiac MRI quantifies iron overload. We aimed to study the association between left and right ventricular (LV and RV) function and iron deposition estimation by cardiac MRI T2* in a sample of Iranian patients. Methods: Cardiac MRI exams of 118 transfusion-dependent thalassemia major patients were evaluated retrospectively. Biventricular function and volume and myocardial and liver T2* values were measured. The demographic and lab data were registered. Poisson and chi-square regression analyses investigated the correlation between the T2* value and ventricular dysfunction. Results: The study participants’ mean (SD) age was 32.7y (9.02), and 47.46% were female. Forty-nine cases (41.52%) revealed at least uni-ventricular dysfunction. LV dysfunction was noted in 20 cases, whereas 47 patients revealed RV dysfunction. The risk of LV dysfunction was 5.3-fold higher in patients with cardiac T2* value less than 10msec (RR=5.3, 95% CI=1.6, 17.1, P<0.05). No association was found between age, liver T2* value, serum ferritin level, and chelation therapy with the risk of LV and RV dysfunction. Conclusion: Cardiac MRI T2* measure is a good indicator of LV dysfunction. Moreover, MRI parameters, especially RV functional measures, may have a substantial role in patient management. Therefore, cardiac MRI should be included in beta-thalassemia patients’ management strategies.

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Purpose: Left ventricular (LV) replacement fibrosis is a marker of adverse cardiac events in hypertrophic cardiomyopathy (HCM). We aimed to assess the efficacy of the feature-tracking cardiac magnetic resonance (FT-CMR) in the detection of LV replacement fibrosis. Material and methods:Fifty-one patients with HCM (51% female, mean age = 21 ± 5.2 years) and significant myocardial hypertrophy, who underwent CMR between February 2018 and December 2019 were enrolled. Functional and 3D FT-CMR parameters were measured. LV global longitudinal strain, global radial strain (GRS), and global circumferential strain (GCS) were recorded. The percentage of enhanced myocardial mass was calculated. Univariate and multivariate regression analyses were performed to determine the predictors of fibrosis. A p-value of less than 0.05 was considered significant. Results:The mean enhanced mass percentage was 15.2 ± 10.53%. Among LV volumetric parameters, end-systolic and end-diastolic volume indices predicted fibrosis (fitness [F] = 8.11 and p = 0.006 vs. F = 6.6 and p = 0.012, correspondingly). The univariate linear regression demonstrated that GCS and GRS predicted total enhanced mass (%) (F = 12.29 and p = 0.001 vs. F = 7.92 and p = 0.007, respectively). After the inclusion of all volumetric and deformation parameters, the multivariate analysis identified the model of a combination of LV end-diastolic volume index (LV EDVI) and LV GCS as a robust predictor of the fibrosis percentage (F = 8.86 and p = 0.005). Conclusions:Non-contrast CMR parameters including LV GCS and LV EDVI are valuable markers of replacement fibrosis in HCM patients with notable myocardial hypertrophy.