Table 1.
Mechanism of action and cardiovascular side effects of common drugs used in COVID-19 patients.
| Drugs | Mechanism of Action | Cardiovascular Side Effects |
|---|---|---|
| Aminoquinoline | ||
| Hydroxychloroquine/chloroquine | -Interfere with lysosomal activity and autophagy, altering the PH of the lysosomes reduces low affinity self-antigen presentation. -Inhibits terminal glycosylation of ACE2 in SARS-COV-2. |
-Conduction abnormalities (bundle branch block, atrioventricular block) -QTc prolongation -Hypoglycemia (mostly in diabetic patients) |
| Ivermectin | -Interfere with Spike protein attachment to RBCs -Block nuclear entry of SARS-CoV-2 -Modulate intracellular messengers of inflammation |
None |
| Antiviral drug nucleoside analogue |
||
| Remdesevir | Remdesevir is a phosphoramidate prodrug that contains an active nucleoside triphosphate and inhibits the RNA-dependent RNA polymerase of coronaviruses. | -Sinus bradycardia -QTc prolongation and torsade de point -AF trigger -T-wave abnormalities -Cardiac arrest -Significantly increased risk of acute kidney injury |
| Janus kinase inhibitor | ||
| Baricitinib | -Reduces the inflammatory response through the inhibition of the Janus-Kinase signaling transducer and activator of transcription pathway. -It acts on AP2-associated protein kinase 1 inhibition, reducing viral endocytosis. |
- Thrombosis, including deep venous thrombosis and pulmonary embolism -Higher rate of major adverse cardiovascular events (cardiovascular death, myocardial infarction, and stroke) compared to the placebo |
| Corticosteroids | ||
| Dexamethasone | -Inhibits the pro-inflammatory pathway that encodes for chemokines, cytokines, cell adhesion molecules, and the acute inflammatory activation in response to SARS-CoV-2 infection. | -Elevations of total plasma cholesterol and triglycerides -Abnormal glycemic control -Increased systolic blood pressure and weight -Fluid and sodium retention, HF occurrence |
| Interleukin antagonists | ||
| Anakinra | -Is a recombinant, non-glycosylated form of the human IL-1 receptor antagonist that binds the IL-1 receptor, reducing the inflammatory response. | Not described |
| Interleukin-6 inhibitors | ||
| Tolicizumab | Tocilizumab and sarilumab are both IL-6 receptor antagonists that prevent the downstream activation of IL-6. | -Hypertension -Increased levels of cholesterol and/or triglycerides |
| Sarilumab | -Cardiac failure -Embolic and thrombotic event |
|
| Interleukin-1 inhibitors | ||
| Canakinumab | It is a human IgG1k monoclonal antibody that neutralizes soluble IL-1β. | Not described |
| Monoclonal Antibodies | ||
| Etesevimab | Monoclonal antibodies specifically bind the virus’ surface spike protein receptor binding domain. This high affinity is related to the strong binding of the ACE2 host cell surface receptor. | -Hypertension |
| Bamlanivimab | -Hypertension -Ischemic heart disease |
|
| Casirivimab | -Hypertension -Ischemic heart disease |
Angiotensin converting enzyme 2 (ACE2), Heart Failure (HF), Atrial Fibrillation (AF), Interleukin-1 receptor (IL-1R).