ABSTRACT
Background: The COVID-19 vaccines were developed unprecedentedly and have proven safe and efficacious in reducing transmissibility and severe infection. The impact of mRNA-based COVID-19 vaccines on atrial arrhythmias (AA) incidence is unknown. Objective(s): To analyze the incidence of AA after COVID-19 vaccination in patients with a cardiac implantable electronic device (CIED). Method(s): BIOTRONIK Home Monitoring data and Medicare claims data from CERTITUDE patients implanted with a CIED between 2010-20 were utilized to identify recipients of one or more doses of the COVID-19 vaccine in 2021. Those who had influenza vaccination in 2020 were also identified in the same cohort as a control. From remote monitoring data, the number of atrial high rate events (AHR) and % burden of AA in the three months post-vaccination was compared to the preceding three months using Wilcoxon signed rank test. Kruskal-Wallis test was used for group difference comparisons. New AF diagnosis was determined from ICD-10 diagnosis codes in Medicare claims. Result(s): First and 2nd doses of COVID vaccine (50% Pfizer, 47% Moderna, and 3% J&J) were administered to 7757 and 6579 individuals with a CIED (age 76.2 (+/-9.0) y, 49% males), respectively. In the same cohort, 4723 (61%) individuals received the influenza vaccine. A statistically significant increase in the number of AHR episodes and % burden of AA was noted in the three months post-vaccination compared to the preceding three months after the 1st and 2nd doses of the COVID-19 vaccine (Figure). No such association was noted following influenza vaccination. In subgroup analysis, AHR episodes increased significantly in age groups >70 and men. Post-vaccination increase in AHR episodes was more significant in those without a pre-vaccination history of AHR episodes (mean increase of AHR 6.9+/-88.4, p<0.001) and was non-significant in those with a preceding history of AHR (p=0.8). Among the 764 patients with no AF diagnosis in claims preceding the first COVID-19 vaccine, 87 (11.4%) developed a new AF diagnosis or AHR event in the first three months post-vaccination. Conclusion(s): We report a small but significant increase in the number of CIED-detected atrial arrhythmias following vaccination for COVID-19 but not influenza, specifically in men and age >70 years. Acknowledging the immense public health benefit of COVID-19 vaccines, our results should prompt increased awareness of evaluating for AF in this high-risk group following vaccination. [Formula presented]Copyright © 2023
ABSTRACT
Introduction: Transverse myelitis has previously been reported following administration of the Johnson and Johnson (J&J) vaccine against SARS-CoV-2. Brain and peripheral nervous system involvement is less well described. Aims/Methods: We report on a case series of 3 patients who developed neuro-inflammation following administration of the J&J vaccine (Ad26.COV2.S). Spinal cord was involved in all 3 patients, brain - in 2, and peripheral nervous system involvement (facial nerve enhancement, radiculitis) in 2. Result(s): Case 1: A 43F developed progressive gait difficulty and ascending paresthesias in bilateral lower extremities ~4 weeks after J&J COVID-19 vaccination. MRI revealed multiple enhancing cervical and thoracic cord lesions and 1 small enhancing subcortical brain lesion. Workup included extensive serum and CSF testing that was unremarkable, except for matching bands in CSF and serum. 3 months later she developed symptom recurrence with persistent enhancement and enlargement of one cord lesion. Case 2: A 39M developed bilateral ascending numbness, tingling, gait instability, urinary hesitancy/urgency and bilateral peripheral facial weakness 10 days after J&J COVID-19 vaccination. MRI revealed bilateral facial nerve enhancement, patchy cervical and thoracic cord and cauda equina enhancement. CSF revealed lymphocytic pleocytosis and elevated protein, with no oligoclonal bands. Extensive serum/CSF testing was otherwise unremarkable. Patient developed recurrent symptoms during steroid taper 3 months later;MRIs showed persistent enhancement and enlarging lesions. Case 3: A 34F developed blurred vision, body aches, paresthesias and urinary retention 2 weeks after J&J COVID-19 vaccination. MRI revealed large, mostly enhancing fluffy occipital/parietal lesions, cervical lesion, longitudinally extensive thoracic lesion and lumbar nerve root enhancement. CSF revealed neutrophilic pleocytosis and elevated protein. 3 months later she developed new enhancing brain lesions with persistent enhancement in the spine. Conclusion(s): Our case series highlights that central and peripheral nervous system inflammatory involvement without clear alternative explanation can rarely be seen in close temporal relationship to administration of the J&J COVID-19 vaccine. Unusual feature of our cases was clinical/radiographic worsening and persistent enhancement several months after initial presentation.Two patients required second-line immunotherapy for disease control.
ABSTRACT
Objective: We report the case of a man who presented with anterograde memory deficit due to bilateral hippocampal lesions in the setting of cocaine and amyl nitrate use. Background: A 52-year-old man with a history of alcohol, cocaine, and amyl nitrate use presented with acute encephalopathy, acute kidney injury, and rhabdomyolysis. Although encephalopathy improved with treatment of these systemic disorders, he revealed persistent anterograde greater than retrograde amnesia. Design/Methods: N/A Results: MRI brain revealed strikingly well-delineated diffusion restricting and enhancing bilateral hippocampal lesions and a diffusion restricting non-enhancing right corona radiata lesion. Stroke evaluation with MRA head and neck, MRV head, echocardiogram, lipid panel, and hemoglobin A1c were unremarkable. SARS-CoV-2 RT-PCR, lupus anticoagulant, cardiolipin, and beta-2 glycoprotein 1 antibodies were unremarkable. Video-EEG, LP with cerebrospinal autoimmune encephalitis panel, and malignancy work-up were also unremarkable. Anticoagulation was started for an incidental pulmonary embolus. A 5-day course of intravenous solumedrol was given empirically for suspected limbic encephalitis. Urine drug screen revealed cocaine metabolites, and he admitted recent amyl nitrate use. At 2-month follow-up, memory function was improved, and MRI revealed resolution of hippocampal lesions with persistent corona radiata lesion. Conclusions: The distinct imaging finding of diffusion restricting bilateral hippocampal lesions carries a broad differential including ischemic, ictal, and various toxic-metabolic causes. This patient was favored to have had a seizure due to toxic-metabolic insult from cocaine and amyl nitrate use. Cocaine induced vasculopathy resulting in bilateral hippocampal infarcts has been reported rarely in literature, but rapid resolution of hippocampal lesions in this patient suggests this was unlikely, although may explain the corona radiata stroke. Limbic encephalitis may cause bilateral hippocampal edema, but less likely to cause diffusion restriction. A detailed history and work-up for potential toxic exposures is critical for those who do not have an alternative explanation and present with such imaging findings.