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Reviews in Cardiovascular Medicine  2020, Vol. 21 Issue (3): 399-409     DOI: 10.31083/j.rcm.2020.03.124
Special Issue: Utilizing Technology in the COVID 19 era
Systematic Review Previous articles | Next articles
Cardiovascular system and COVID-19: manifestations and therapeutics
Ajay K. Mahenthiran1, Ashorne K. Mahenthiran2, Jo Mahenthiran1, *()
1Community Heart and Vascular Hospital, Indianapolis, IN 46250, USA
2Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA
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Abstract:

The world is currently in the midst of a daunting global pandemic due to SARS-CoV-2 viral infection and associated COVID-19 disease. Healthcare professionals are tasked with the challenge of managing diverse multisystem clinical manifestations of this infection. Although acute hypoxic respiratory failure is the hallmark of severe COVID-19 disease, there have been diverse manifestations within the cardiovascular (CV) system that each pose unique therapeutic challenges. Of these manifestations, myocardial injury and right ventricular dysfunction are the most common, however, heart failure, circulatory shock, cardiomyopathy, arrhythmia, and vascular thrombosis have been noted as well. Furthermore, these CV related manifestations portend greater morbidity and mortality, which requires clinicians to be familiar with the most recent information to provide informed patient care. Although there are limited treatment options available for COVID-19, it is imperative that the potential cardiovascular implications of these therapies are considered in these patients. This review highlights the pathophysiological mechanisms of and therapeutics for CV manifestations of COVID-19 as well as the CV implications of proposed COVID-19 therapies. Since our hospital-based providers are the frontline caregivers battling this pandemic, the aim of this review is to assist with clinical decision-making for optimal patient outcomes while maintaining a safe environment for healthcare personnel.

Key words:  Coronavirus      COVID-19      cardiovascular system      cardiac injury      heart failure      myocarditis      myocardial infarction      cardiac therapy      arrhythmia      thrombosis     
Submitted:  02 July 2020      Revised:  06 August 2020      Accepted:  07 August 2020      Published:  30 September 2020     
*Corresponding Author(s):  Jo Mahenthiran     E-mail:  jmahenthiran@ecommunity.com

Cite this article: 

Ajay K. Mahenthiran, Ashorne K. Mahenthiran, Jo Mahenthiran. Cardiovascular system and COVID-19: manifestations and therapeutics. Reviews in Cardiovascular Medicine, 2020, 21(3): 399-409.

URL: 

https://rcm.imrpress.com/EN/10.31083/j.rcm.2020.03.124     OR     https://rcm.imrpress.com/EN/Y2020/V21/I3/399

Fig. 1.  “Basic pathobiology of SARS-CoV-2 infection and possible treatment strategies”. Upon the viral spike protein priming by the transmembrane protease serine 2 (TMPRSS2), SARS-CoV-2 uses the host angiotensin-converting enzyme 2 (ACE2) to enter and infect the cell. Inhibiting TMPRSS2 activity could be used to prevent proteolytic cleavage of the SARS-CoV-2 spike protein and protect the cell against virus–cell fusion (1). Another approach could be neutralizing the virus from entering cells and keeping it in solution by activation of a disintegrin and metalloprotease 17 (ADAM17) which leads to shedding of the membrane-bound ACE2 and release of the soluble extracellular domain of ACE2 (2); additionally, administration of soluble recombinant human ACE2 protein acting as a competitive interceptor for SARS-CoV-2 (3). Title, legend (modified), image (modified) reproduced with permission from Guzik et al. (2020).

Fig. 2.  “Key symptoms, biochemical and radiological features of the clinical course of COVID-19”Title, image reproduced with permission from Guzik et al. (2020).

Fig. 3.  “Cardiovascular involvement in COVID-19—key manifestations and hypothetical mechanisms”. SARS-CoV-2 anchors on transmembrane ACE2 to enter the host cells including cardiac myocytes, leading to inflammation. In particular, the infection of endothelial cells or pericytes could lead to severe micro vascular and macro vascular dysfunction. Furthermore, in conjunction with the immune over-reactivity, it can potentially destabilize atherosclerotic plaques and explain the development of the acute coronary syndromes. Progression of systemic inflammation and immune cell over activation, leading to a ’cytokine storm’, which results in an elevated level of cytokines such as IL-6, IL-7, IL-22, and CXCL10. Subsequently, it is possible that activated T cells and macrophages may infiltrate infected myocardium, resulting in the development of fulminant myocarditis and severe cardiac damage. Similarly, the viral invasion could cause cardiac myocyte damage directly leading to myocardial dysfunction and contribute to the development of arrhythmia.Title, legend (modified), image reproduced with permission from Guzik et al. (2020).

Table 1.  Outline of common therapeutic approaches to CV manifestations of COVID-19
CV Manifestations Therapeutic Options
Cardiac Injury (Elevated Troponin)
- STEMI Primary or rescue PCI or IV Fibrinolytic (ex: tPA)
- NSTEMI Early invasive strategy-PCI in high risk patients
Anti-ischemic therapy: BB, CCB and nitrates
IV anticoagulation: LMWH/UFH (therapeutic dose)
Antiplatelet therapy (dual therapy if no contraindications)
- Myocarditis Oxygen, Cautious IV hydration, Supportive care
IV steroids, antiviral and anti-inflammatory agents (trials)
Acute Circulatory Shock (Target MAP – 60-65 mm Hg)
- Cardiogenic Coronary angiography, Inotrope: Norepinephrine, MCS
- Systemic / Sepsis Antiviral / anti-inflammatory agents
Biological immunomodulators
Inotrope: Norepinephrine or Vasopressin, MCS-ECMO
Acute Heart Failure
- HFpEF Oxygen, IV diuretic, Supportive care
- HFrEF Oxygen, IV diuretic, Inotrope: Dobutamine
Guideline directed medications: BB, ACE-I (as tolerated)
Renal replacement therapy(as indicated)
Cardiac Arrhythmia
- Atrial Fibrillation/Flutter Hemodynamic Instability: Electrical Cardioversion
IV Amiodarone for rhythm/rate control
Rate control agents: BB and CCB / Digoxin
Therapeutic LWMH/UFH and DOAC per CHA2DS2-VASc (Avoid AAD and check drug interactions)
- Ventricular Tachycardia (VT) Hemodynamic Instability: Electrical Cardioversion
IV Amiodarone for rhythm control
Correct electrolytes, volume and acidosis
IV BB-Esmolol/IV Lidocaine if refractory or recurrent
- Polymorphic VT/VF/Tdp Electrical Cardioversion
Withdrawal of all QT prolonging agents
IV Magnesium and correct electrolytes
IV Isoprenaline or Temporary Pacemaker
- Brady arrhythmia Remove offending agents
IV Isoprenaline, IV Atropine, Temporary Pacemaker
Cardiomyopathy Oxygen, Anti Inflammatory, Inotrope: Norepinephrine
- Stress Cardiomyopathy Higher preload (CVP 12-15), Ventilation, IV fluids,
- RV dysfunction Inotrope: Dopamine / Milrinone, MCS: Impella RP®
Vascular Thrombosis
- VTE/ Pulmonary embolism Anticoagulation: Therapeutic LMWH/UFH and DOAC
IV or catheter directed (EKOS) thrombolytic (ex: tPA)
- Cerebrovascular accident Thrombectomy with stent placement
IV thrombolysis, DOAC and antiplatelet therapies
STEMI: ST-elevation myocardial infarction, NSTEMI: Non-ST elevation myocardial infarction, PCI: Percutaneous coronary intervention, IV: intravenous, tPA: Tissue plasminogen activator, BB: Beta blocker, CCB: Calcium channel blockers, LMWH: Low-molecular-weight heparin, UFH: Unfractionated heparin, MAP: Mean arterial pressure, MCS: Mechanical circulatory support, ECMO: Extracorporeal membrane oxygenation, HFpEF: Heart failure with preserved ejection fraction, HFrEF: Heart failure with reduced ejection fraction, AAD: Anti-arrhythmic drug, Tdp: Torsade de pointes, ACE-I: Angiotensin converting enzyme inhibitor, CVP: Central venous pressure, EKOS: Ekosonic Endovascular System, DOAC: Direct oral anticoagulant, VTE: Venous thromboembolism, VF: ventricular fibrillation, CHA2DS2-VASC: score for atrial fibrillation stroke risk
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