ABSTRACT
Coronavirus disease 2019 (COVID-19) has caused a global pandemic that continues to cause numerous deaths to date. Four vaccines have been approved by the Food and Drug Administration as of July 2021 to prevent the transmission of COVID-19: Pfizer, Moderna, AstraZeneca, and Janssen. These vaccines have shown great efficacy and safety profile. One side effect that has been widely reported is post-COVID-19 vaccination lymphadenopathy. Due to the mimicry of the lymphadenopathy for metastases in some oncologic patients, there have been reports of patients who underwent biopsies that showed pathologic confirmation of benign reactive lymphadenopathy secondary to the COVID-19 vaccine. Therefore, understanding the incidence of lymphadenopathy post-COVID-19 vaccinations will help guide radiologists and oncologists in their management of patients, both present oncologic patients, and patients with concerns over their newly presenting lymphadenopathy. A systematic literature search was performed using several databases to identify relevant studies that reported lymphadenopathy post-COVID-19 vaccination. Our results revealed that several cases have been detected in patients undergoing follow-up fluorodeoxyglucose (FDG)-positron emission tomography-computerized tomography scans where lymph nodes ipsilateral to the vaccine injection site show increased uptake of FDG. Thus, knowledge of the incidence of lymphadenopathy may help avoid unnecessary biopsies, interventions, and changes in management for patients, especially oncologic patients who are at risk for malignancies.
Subject(s)
COVID-19 , Lymphadenopathy , COVID-19/prevention & control , COVID-19 Vaccines/adverse effects , Fluorodeoxyglucose F18 , Humans , Lymphadenopathy/diagnostic imaging , Lymphadenopathy/etiology , Positron Emission Tomography Computed Tomography/adverse effects , Positron Emission Tomography Computed Tomography/methods , SARS-CoV-2 , United States , Vaccination/adverse effectsABSTRACT
The coronavirus disease 2019 (COVID-19), induced by the severe acute respiratory syndrome coronavirus 2, is responsible for a global pandemic following widespread transmission and death. Several vaccines have been developed to counter this public health crisis using both novel and conventional methods. Following approval based on promising efficacy and safety data, the AstraZeneca, Janssen, Moderna, Pfizer/BioNTech, and Sinovac vaccines have been administered globally among different populations with various reported side effects. Reports of life-threatening anaphylaxis following administration were of particular concern for both health care providers and the public. A systematic literature search using PubMed, Embase, Scopus, Web of Science, Science Direct, MedRxiv, and Lens.org databases identified relevant studies reporting anaphylaxis following vaccine administration. This systematic review includes 41 studies reporting anaphylaxis. A total of 7942 cases, including 43 deaths, were reported across 14 countries. Most cases occurred following the administration of the first dose. Importantly, the benefits of vaccination outweigh the risks of anaphylaxis. Subsequently, as populations continue to get vaccinated, it is important for health care providers to be able to recognize individuals at risk of developing anaphylaxis. Furthermore, they must be familiar with both the clinical hallmarks and treatment of anaphylactic reactions to minimize long-term sequalae and prevent death in vaccinated individuals.
Subject(s)
Anaphylaxis , COVID-19 , Vaccines , Anaphylaxis/chemically induced , COVID-19/prevention & control , COVID-19 Vaccines/adverse effects , Humans , Vaccination/adverse effects , Vaccination/methods , Vaccines/therapeutic useABSTRACT
BACKGROUND: Left ventricular (LV) ischemia has been variably associated with functional mitral regurgitation (FMR). Determinants of FMR in patients with ischemia are poorly understood. OBJECTIVES: This study sought to test whether contractile mechanics in ischemic myocardium underlying the mitral valve have an impact on likelihood of FMR. METHODS: Vasodilator stress perfusion cardiac magnetic resonance was performed in patients with coronary artery disease (CAD) at multiple centers. FMR severity was confirmed quantitatively via core lab analysis. To test relationship of contractile mechanics with ischemic FMR, regional wall motion and strain were assessed in patients with inducible ischemia and minimal (≤5% LV myocardium, nontransmural) infarction. RESULTS: A total of 2,647 patients with CAD were studied; 34% had FMR (7% moderate or greater). FMR severity increased with presence (P < 0.001) and extent (P = 0.01) of subpapillary ischemia: patients with moderate or greater FMR had more subpapillary ischemia (odds ratio [OR]: 1.13 per 10% LV; 95% CI: 1.05-1.21; P = 0.001) independent of ischemia in remote regions (P = NS); moderate or greater FMR prevalence increased stepwise with extent of ischemia and infarction in subpapillary myocardium (P < 0.001); stronger associations between FMR and infarction paralleled greater wall motion scores in infarct-affected territories. Among patients with inducible ischemia and minimal infarction (n = 532), wall motion and radial strain analysis showed impaired subpapillary contractile mechanics to associate with moderate or greater FMR (P < 0.05) independent of remote regions (P = NS). Conversely, subpapillary ischemia without contractile dysfunction did not augment FMR likelihood. Mitral and interpapillary dimensions increased with subpapillary radial strain impairment; each remodeling parameter associated with impaired subpapillary strain (P < 0.05) independent of remote strain (P = NS). Subpapillary radial strain (OR: 1.13 per 5% [95% CI: 1.02-1.25]; P = 0.02) and mitral tenting area (OR: 1.05 per 10 mm2 [95% CI: 1.00-1.10]; P = 0.04) were associated with moderate or greater FMR controlling for global remodeling represented by LV end-systolic volume (P = NS): when substituting sphericity for LV volume, moderate or greater FMR remained independently associated with subpapillary radial strain impairment (OR: 1.22 per 5% [95% CI: 1.02-1.47]; P = 0.03). CONCLUSIONS: Among patients with CAD and ischemia, FMR severity and adverse mitral apparatus remodeling increase in proportion to contractile dysfunction underlying the mitral valve.
Subject(s)
Mitral Valve Insufficiency , Humans , Infarction , Ischemia , Magnetic Resonance Spectroscopy , Mitral Valve Insufficiency/diagnostic imaging , Myocardium , Perfusion , Predictive Value of TestsABSTRACT
Since the discovery of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), numerous research has been undertaken to delineate the various effects of the virus which manifests in many ways all over the body. The association between the SARS-CoV-2 invasion mechanism and the renin-angiotensin-aldosterone system (RAAS) receptors, created many debates about the possible consequences of using RAAS-modulating drugs including angiotensin-converting enzyme inhibitors (ACEi) and angiotensin II receptor blockers (ARBs) during the pandemic. Many clinical studies were conducted to assess the outcomes of coronavirus disease 2019 (COVID-19) in patients who use ACEi/ARBs following the arguments claiming to discontinue these drugs as a precautionary measure. Although several studies mainly analyzed the outcomes of the disease, this review aimed to compare specific blood markers in both groups of COVID-19 patients to gain better insight into the interaction of ACEi/ARBs with different body functions during the infection. Several databases were searched using a combination of keywords followed by screening and data extraction. Only 28 studies met our inclusion criteria, the majority of which showed no significant difference between the inflammation markers of COVID-19 patients who used or did not use ACEi/ARBs. Interestingly, 6 studies reported lower inflammatory markers in COVID-19 patients who used ACEi/ARBs, and 6 studies reported better outcomes among the same group. We therefore concluded that the use of ACEi/ARBs may not lead to worse prognosis of COVID-19 and may even play a protective role against the hyperinflammatory response associated with COVID-19.