Author + information
- Received April 8, 2020
- Accepted April 8, 2020
- Published online May 25, 2020.
- Peter Libby, MD∗ ()
- Division of Cardiovascular Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts
- ↵∗Address for correspondence:
Dr. Peter Libby, Department of Medicine, Cardiovascular Division, Brigham and Women's Hospital, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, Massachusetts 02115.
In the throes of the current coronavirus disease-2019 (COVID-19) pandemic, interest has burgeoned in the cardiovascular complications of this virulent viral infection. As troponin, a biomarker of cardiac injury, often rises in hospitalized patients, its interpretation and actionability require careful consideration. Fulminant myocarditis due to direct viral infection can certainly occur, but in patients with increased oxygen demands due to tachycardia and fever and reduced oxygen delivery due to hypotension and hypoxemia, COVID-19 disease can cause myocardial injury indirectly. Cytokines released during the acute infection can elicit activation of cells within pre-existing atherosclerotic lesions, augmenting thrombotic risk and risk of ischemic syndromes. Moreover, microvascular activation by cytokines can cause not only myocardial injury but can also harm other organ systems commonly involved in COVID-19 infections including the kidneys. Dealing with the immense challenge of COVID-19, confronted with severely ill patients in dire straits with virtually no rigorous evidence base to guide our therapy, we must call on our clinical skills and judgment. These touchstones can help guide us in selecting patients who might benefit from the advanced imaging and invasive procedures that present enormous logistical challenges in the current context. Lacking a robust evidence base, pathophysiologic reasoning can help guide our choices of therapy for individual clinical scenarios. We must exercise caution and extreme humility, as often plausible interventions fail when tested rigorously. But act today we must, and understanding the multiplicity of mechanisms of myocardial injury in COVID-19 infection will help us meet our mission unsupported by the comfort of strong data.
Dr. Libby has received funding support from the National Heart, Lung, and Blood Institute (grants R01HL080472 and 1R01HL134892), the American Heart Association (grant 18CSA34080399), and the RRM Charitable Fund; Dr. Libby is an unpaid consultant to, or involved in clinical trials for Amgen, AstraZeneca, Baim Institute, Beren Therapeutics, Esperion, Therapeutics, Genentech, Kancera, Kowa Pharmaceuticals, Medimmune, Merck, Norvo Nordisk, Merck, Novartis, Pfizer, Sanofi-Regeneron. Dr. Libby is a member of scientific advisory board for Amgen, Corvidia Therapeutics, DalCor Pharmaceuticals, Kowa Pharmaceuticals, Olatec Therapeutics, Medimmune, Novartis, XBiotech, Inc. Dr. Libby’s laboratory has received research funding in the last 2 years from Novartis. Dr. Libby is on the Board of Directors of XBiotech, Inc. and participates in the Leducq Transatlantic Network on Clonal Hematopoiesis. Dr. Libby has a financial interest in Xbiotech, a company developing therapeutic human antibodies. Dr. Libby's interests were reviewed and are managed by Brigham and Women's Hospital and Partners HealthCare in accordance with their conflict of interest policies.
The author attests he is in compliance with human studies committees and animal welfare regulations of the author's institutions and Food and Drug Administration guidelines, including patient consent where appropriate. For more information, visit the JACC: Basic to Translational Science author instructions page.
- Received April 8, 2020.
- Accepted April 8, 2020.
- 2020 The Author
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