Impact of COVID-19 on cardiovascular testing in the United States versus the rest of the world

Objectives: This study sought to quantify and compare the decline in volumes of cardiovascular procedures between the United States and non-US institutions during the early phase of the coronavirus disease-2019 (COVID-19) pandemic. Background: The COVID-19 pandemic has disrupted the care of many non-COVID-19 illnesses. Reductions in diagnostic cardiovascular testing around the world have led to concerns over the implications of reduced testing for cardiovascular disease (CVD) morbidity and mortality. Methods: Data were submitted to the INCAPS-COVID (International Atomic Energy Agency Non-Invasive Cardiology Protocols Study of COVID-19), a multinational registry comprising 909 institutions in 108 countries (including 155 facilities in 40 U.S. states), assessing the impact of the COVID-19 pandemic on volumes of diagnostic cardiovascular procedures. Data were obtained for April 2020 and compared with volumes of baseline procedures from March 2019. We compared laboratory characteristics, practices, and procedure volumes between U.S. and non-U.S. facilities and between U.S. geographic regions and identified factors associated with volume reduction in the United States. Results: Reductions in the volumes of procedures in the United States were similar to those in non-U.S. facilities (68% vs. 63%, respectively; p = 0.237), although U.S. facilities reported greater reductions in invasive coronary angiography (69% vs. 53%, respectively; p < 0.001). Significantly more U.S. facilities reported increased use of telehealth and patient screening measures than non-U.S. facilities, such as temperature checks, symptom screenings, and COVID-19 testing. Reductions in volumes of procedures differed between U.S. regions, with larger declines observed in the Northeast (76%) and Midwest (74%) than in the South (62%) and West (44%). Prevalence of COVID-19, staff redeployments, outpatient centers, and urban centers were associated with greater reductions in volume in U.S. facilities in a multivariable analysis. Conclusions: We observed marked reductions in U.S. cardiovascular testing in the early phase of the pandemic and significant variability between U.S. regions. The association between reductions of volumes and COVID-19 prevalence in the United States highlighted the need for proactive efforts to maintain access to cardiovascular testing in areas most affected by outbreaks of COVID-19 infection

Cellular prion protein neither binds to alpha-synuclein oligomers nor mediates their detrimental effects

\u3b1-Synuclein oligomers are crucial players in the pathogenesis of Parkinson's disease. Some mechanisms involved in \u3b1-synuclein oligomer detrimental effects include membrane damage, neuroinflammation and protein-protein interactions. Recently, the cellular prion protein (PrP C) emerged as an interactor of \u3b1-synuclein oligomers, apparently mediating their detrimental activities. Through direct in vivo and in vitro approaches we herein investigated the existence of a direct cross-talk between \u3b1-synuclein oligomers and PrP C. In vitro, we assessed \u3b1-synuclein oligomer toxicity by comparing the effect in Prnp +/+ versus PrP C knockout (Prnp 0/0) hippocampal neurons. Through an in vivo acute mouse model, where \u3b1-synuclein oligomers injected intracerebroventricularly induce memory impairment and neuroinflammation, we verified whether these detrimental effects were preserved in Prnp 0/0 mice. In addition, PrP C -\u3b1-synuclein oligomer direct binding was investigated through surface plasmon resonance. We found that PrP C was not mandatory to mediate \u3b1-synuclein oligomer detrimental effects in vitro or in vivo. Indeed, \u3b1-synuclein oligomer toxicity was comparable in Prnp +/+ and Prnp 0/0 neurons and both Prnp +/+ and Prnp 0/0 mice injected with \u3b1-synuclein oligomers displayed memory deficit and hippocampal gliosis. Moreover, surface plasmon resonance analyses ruled out PrP C -\u3b1-synuclein oligomer binding. Our findings indicate that PrP C neither binds \u3b1-synuclein oligomers nor mediates their detrimental actions. Therefore, it is likely that PrP C -dependent and PrP C -independent pathways co-exist in Parkinson's disease