Cardiovascular Complications of COVID-19: Pharmacotherapy Perspective

Abstract

Coronavirus disease of 2019 (COVID-19), which is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is spreading rapidly the world over. The disease was declared "pandemic" by the World Health Organization. An approved therapy for patients with COVID-19 has yet to emerge; however, there are some medications used in the treatment of SARS-CoV-2 infection globally including hydroxychloroquine, remdesivir, dexamethasone, protease inhibitors, and anti-inflammatory agents. Patients with underlying cardiovascular disease are at increased risk of mortality and morbidity from COVID-19. Moreover, patients with chronic stable states and even otherwise healthy individuals might sustain acute cardiovascular problems due to COVID-19 infection. This article seeks to review the latest evidence with a view to explaining possible pharmacotherapies for the cardiovascular complications of COVID-19 including acute coronary syndrome, heart failure, myocarditis, arrhythmias, and venous thromboembolism, as well as possible interactions between these medications and those currently administered (or under evaluation) in the treatment of COVID-19.

COVID-19, hydroxychloroquine and sudden cardiac death: implications for clinical practice in patients with rheumatic diseases

“…Moreover, interstitial infiltrates have also been seen in non-survivors of COVID-19, further indicative of a virus attack on the myocardium [ 9 ]. In line with this, raised levels of cardiac troponin and creatine kinase in COVID patients also indicate the direct destruction of myocytes by the virus, leading on to myocarditis [ 34 ]. Further evidence is highlighted by in vitro studies whereby the SARS-Cov2 led to the destruction of contractile function and apoptosis of cardiac myocytes originated from induced pluripotent stem cells (iPSCs) leading to cardiac death within 72 h [ 36 ].…”

“…SARS-COV-2 can infect the cardiovascular system both directly and indirectly, considering the pronounced tropism of the virus for heart [ 34 – 36 ]. Several mechanisms underlie the worsening of symptoms in case of cardiac involvement:…”

“…The ensuing hypoxia results in acidosis and production of reactive oxygen species (ROS), which may damage the cell membrane of myocytes [ 28 , 52 ]. This, in addition to an increased oxygen demand from the myocytes in the face of infection-induced fever and tachycardia, results in an oxygen demand–supply mismatch, which may be contributive towards a Type 2 myocardial infarction [ 12 , 22 , 25 , 34 , 41 , 58 , 59 ] Additionally, hypotension in a severe cytokine storm may further accentuate the ischemia due to poor coronary perfusion. Moreover, hypoxemia leads to the increased entry of calcium ions into cells that further aids the apoptotic cascade [ 28 , 52 ].…”

“…It has also been noticed that patients with severe infection had raised serum levels of vWF (Von Willebrand Factor), which mediates adhesion and aggregation of platelets in vessel walls resulting in blockage [ 62 ]. Additionally, the cytokine storm in critically ill patients aids the development of a pro-coagulant and pro-thrombotic state, leading to the development of Disseminated Intravascular Coagulation (DIC) [ 34 , 49 ]. Hence, thrombi in coronary vessels, together with an exaggerated inflammatory response, may contribute to rupture of unstable atherogenic plaques, manifesting as myocardial infarction [ 40 , 44 , 58 , 59 ].…”

Research Progress of Genetic Structure, Pathogenic Mechanism, Clinical Characteristics, and Potential Treatments of Coronavirus Disease 2019

“…Recently, the WHO and the International Society on Thrombosis and Haemostasis have recommended prophylactic dose low molecular weight heparin (LMWH), which should be considered in all hospitalized patients with SARS-CoV-2 ( Bikdeli et al, 2020 ; Thachil et al, 2020 ). In fact, it is important to note the multiple roles of LMWH, on the one hand, as preventer of the thromboembolic process and thrombotic complications, on the other hand, as a powerful inhibitor of anti-viral and anti-inflammatory ( Kipshidze et al, 2020 ; Talasaz et al, 2020 ). Additionally, accumulating evidence indicated that prophylactic anticoagulation could reduce the risk of VTE and mortality in severely ill patients.…”