LAUSR

The world has finally emerged from the great medical, economic, and social calamity of 2020 to 2022, the COVID-19 pandemic. This Compendium of 10 articles describes various aspects of the effects of SARS-CoV-2 on the cardiovascular system, focusing on the heart. The Minotaur from Greek mythology is an apt metaphor, because this half bull/half man spike-adorned gain of function mutant slaughtered the innocent was nearly impossible to eradicate in his labyrinthian environs, inspired mass fear of the unknown, and ultimately was eliminated by resourceful, determined collaborators.1 Although SARS-CoV-2 infection has not been eliminated, it has been contained to the point of acquiring the status of a manageable infectious disease.2 As we review some of the findings of the enormous, world-wide efforts to investigate the cardiovascular effects of SARS-CoV-2, it is important to reflect on the national mood of mid-March, 2020, when through reports from China, Northern Italy, and elsewhere it became apparent that a catastrophic infectious disease was on the move, and the nascent local appearance of isolated cases indicated the United States would not be spared. Shortly thereafter, it became apparent that the cardiovascular system was not going to dodge the pandemic. At this point, something remarkable in the annals of research support occurred: The American Heart Association went into emergency mode and quickly developed and disseminated a Request for Applications as part of a COVID-19 Rapid Response initiative. The Request for Applications was announced on March 26, 2020, the proposals had to be submitted by April 6, the review of 750 grants was accomplished within 10 days (by 150 reviewers), and the notices of awards of 15 grants were distributed on April 23. In other words, an emergency funding mechanism for investigating unknown mechanisms responsible for serious cardiovascular disorders tied to a burgeoning pandemic was developed and executed in under 30 days. This Compendium includes information from multiple investigations generated by the AHA’s Rapid Response funding, in addition to other contributions. The impact of COVID-19 on cardiovascular disease outcomes and treatment was profound, as detailed by Boulos et al3 in this Compendium. Reluctance of patients to seek care for serious conditions, deferral or modification of necessary procedures, an increase in thrombotic disorders related to procoagulant effects of SARS-CoV-2 and its invoked inflammatory response, led to the exacerbation of underlying conditions, such as heart failure, as well as interaction with pharmacological treatments, such as immunosuppression regimens in transplant patients.3 Others4 have described the profound impact of COVID-19 on basic and clinical cardiovascular research. Clinical trials are one example of this, as recruitment fell precipitously in many of them in 2020. In any case, during the pandemic, the adaptation and performance of cardiovascular clinical care teams as well as the professional societies charged with issuing and updating COVID-19-related guidelines was nothing short of heroic.3 When it comes to the pathophysiology of COVID-19, a striking observation at the forefront of SARS-CoV-2 infection was the increased risk of thrombotic outcomes in patients. These included intravascular coagulation, macrothrombosis, organ microthrombosis, bleeding, and profound coagulopathy, and in certain cases an