COVID-19 and the cardiovascular system. Thrombotic events in COVID-19. Interprofessional collaboration.


Cardiovascular medicine and surgery

COVID-19 and the cardiovascular system

With the global outbreak of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) ongoing, there is increased awareness of the cardiovascular manifestations and implications of COVID-19. Approximately 20% of inpatients with COVID-19 have acute cardiac injury (defined as cardiac troponin elevation) (Shi S, et al. JAMA Cardiol. 2020 Mar 25. doi: 10.1001/jamacardio.2020.0950). Moreover, in one cohort, both acute cardiac injury and preexisting cardiovascular disease (CVD) were associated with COVID-19 hospital mortality: 69% with elevated troponin levels and underlying CVD vs 7.6% with neither (Guo T, et al. JAMA Cardiol. 2020 Mar 27. doi: 10.1001/jamacardio.2020.1017). Moreover, case reports suggest COVID-19 may present as myopericarditis, cardiomyopathy, acute on chronic decompensated heart failure, and acute coronary syndrome (Fried JA, et al. Circulation. 2020 Apr 3. doi: 10.1161/circulationaha.120.047164). Adding to this clinical variability, one case series suggests that electrocardiographic ST-segment elevation may not reliably identify obstructive coronary disease (Bangalore S, et al. N Engl J Med. 2020 Apr 17. doi: 10.1056/NEJMc2009020). Intriguingly, the angiotensin-converting enzyme 2 (ACE2) protein is the functional receptor for SARS-CoV-2 cell entry, and ACE2 is highly expressed in pulmonary and cardiac cells (Driggin E, et al. J Am Coll Cardiol. 2020;75[18]:2352). Given the central role of ACE2 and the renin-angiotensin-aldosterone (RAAS) system in cardiovascular pathophysiology and pharmacotherapy, RAAS modulation could have beneficial and/or detrimental effects with COVID-19 (Vaduganathan M, et al. N Engl J Med. 2020;382:1653). Available evidence and societal guidelines support continuing RAAS antagonists in patients per established clinical practice (Mancia G, et al. N Engl J Med. 2020 May 1. doi: 10.1056/NEJMoa2006923); (Mehra MR, et al. N Engl J Med. 2020 May 1. doi: 10.1056/NEJMoa2007621). A better understanding of the direct and indirect effect of SARS-CoV-2 on the cardiovascular system will require additional evidence.

Dr. Benjamin Kenigsberg

Dr. Benjamin Kenigsberg

Benjamin B. Kenigsberg, MD

Fellow-in-Training Steering Committee Member

Thrombotic events in COVID-19: Implications and evolving practice recommendations

A startling potential complication of infection with SARS-CoV2 has been the reported predisposition to thrombotic events. Mortality in COVID-19 patients is associated with notable increases in hemostatic parameters such as levels of d-dimer (Bikdeli, et al. J Am Coll Cardiol. 2020 Apr 15. pii: S0735-1097(20)35008-7. doi: 10.1016/j.jacc.2020.04.031. Available autopsy findings suggest that microvascular thrombosis may contribute to development of hypoxemic respiratory failure in COVID-19 (Wichmann, et al. Ann Intern Med. 2020 May 6. doi: 10.7326/M20-2003. Hence, the role of anticoagulation in COVID-19 merits serious discussion.

Dr. Saiprakash B. Venkateshiah

Dr. Saiprakash B. Venkateshiah

Vascular societies led by International Society on Thrombosis and Haemostasis (ISTH) have published consensus recommendations for guidance. If no contraindications exist, pharmacologic venous thromboembolism (VTE) prophylaxis with unfractionated heparin (UFH) or low-molecular-weight heparin (LMWH) is recommended for hospitalized patients with moderate or severe COVID-19 without disseminated intravascular coagulation (DIC). VTE prophylaxis should also be considered for patients with moderate or severe COVID-19 and in DIC but without overt bleeding. There is insufficient evidence to consider routine therapeutic or intermediate-dose parenteral anticoagulation with UFH or LMWH. Many institutions have developed protocols advising therapeutic-intensity anticoagulation when certain thresholds of d-dimer levels are observed, even in the absence of documented VTE. It is unclear how long the prothrombotic milieu in COVID-19 persists after recovery, and consensus recommendations (and some centers) are considering extended prophylaxis (30-45 days) post-discharge after individual VTE risk stratification (Kreuziger LB, et al. American Society of Hematology, April 17, 2020.. Further well-designed research is needed to inform clinicians of anticoagulation strategies in COVID-19 population.

Saiprakash B. Venkateshiah, MD, FCCP,


Gabriela Magda, MD

Fellow-in-Training Steering Committee Member


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