- Angiotensin-converting enzyme 2 (ACE2), which is a membrane bound aminopeptidase that is highly expressed in the heart and lungs, acts as a receptor for SARS-CoV-2, allowing the virus to enter the cell upon binding
- Binding of the virus to ACE2 can cause alterations of ACE2 signaling pathways, which leads to acute myocardial and lung injury

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- Myocardial injury (injury to the muscular tissue of the heart)
- Myocarditis (inflamed heart muscle tissue)
- Myocardial infarction (heart attack)
- Heart failure
- Dysrhythmias (Irregular heart rhythm)
- Venous thrombosis (blood clotting)
- Aortic thrombosis
- Heart palpitations 
- Chest tightening 
- Endothelial dysfunction
- Systemic inflammation 

Cardiovascular Complications & Symptoms Associated with COVID-19

Bansal M. (2020). Cardiovascular disease and COVID-19. Diabetes & metabolic syndrome, 14(3), 247–250. https://doi.org/10.1016/j.dsx.2020.03.013

Cardiovascular disease and COVID-19

Severe infection with COVID-19 attributes to rapid systematic inflammation, sepsis, and pro-inflammatory cytokine storm, which eventually can cause mulitorgan failure and death. 

Cardiovascular Manifestations of COVID-19 (graphic) 

Viral infections are related to metabolic dysfunction, myocardial inflammation, and sympathetic nervous system activation, which all predispose patients to cardiac arrhythmia. 
In a report of 138 hospitalized COVID-19 patients, 16.7% developed arrhythmias. Arrhythmia was observed in only 7% of those who did not need ICU treatment while 44% of those admitted to the ICU developed arrhythmia. 
Instances of developed arrhythmia include: atrial fibrillation, conduction block, ventricular tachycardia, and ventricular fibrillation. Though more research is needed on the associated manifestations. 

COVID-19 and Cardiac Arrhythmia (irregular heart  rhythm) 

Cardiac injury and acute myocarditis are well-established results of viral infections. In regards to COVID-19, reports of myocyte necrosis and mononuclear cell infiltrates suggests that myocarditis could be important in the occurrence of cardiac injury in patients. Mycarditis has the potential to turn into a conduciton block, tachyarrhythmia, and impairment of left ventricular function. Though the details of these findings are still unclear. 
Clinically, COVID-19 related myocarditis may only manifest as mild chest pain and could be rather indistinguishable from other causes in most patients. Sympotoms of myocarditis in COVID-19 patients usually do not present themselves until 10-14 days after the initial onset of symptoms. Data suggests that the delay in myocardial inflammation has to two with two pathogenic mechanisms. First, 'cytokine storm' promotes subclinical autoimmune myocarditis. Secondly, myocardial damage and/or molecular mimicry "initiate a de Novo autoimmune reaction". 


COVID-19 and Myocarditis 

Endothelial dysfunction is a cardiac condition that is the precursor of atherosclerosis.  It is controlled by the so called "cardiovascular risk factors", and when these risk factors are treated, this condition can be reversed.  Endothelial dysfunction leads to:

- plaque buildup in vascular tissue
- thrombosis
- vasoconstriction
- inflammation
- oxidative stress 
- vascular tissue remodeling

Endothelial dysfunction is a comorbidity of conditions that have been shown to aggravate a SARS-CoV-2, including obesity.  It also causes phenomena that might mechanistically enhance COVID-19.

Endothelial Dysfunction and COVID-19

Mechanism for direct myocardial injury in COVID-19 patients 

"Aortic thrombosis is a rare event that can occur in hypercoagulable state as found in patients with COVID-19. A 58-year-old man presented with COVID-19
respiratory failure and elevated D-dimers (4063 lg/l). Computed tomography scanning showed a floating thrombus in the aortic arch." 


Aortic Thrombosis and COVID-19

COVID-19 may predispose patients to thrombotic disease in both the venous and arterial circulations. This predisposition is caused by:

1. Direct and indirect effects of COVID-19 infection (e.g., severe illness and hypoxia).
2. Adverse interactions between therapies for COVID-19 and antithrombotic drugs (e.g., antiplatelet agents and anticoagulants).
3. Negative impacts on the timely treatment of patients with thrombotic events due to pandemic-related resource allocations and social distancing recommendations.

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