Cardiac inflammation in COVID-19: Lessons from heart failure

Abstract

Cardiovascular disease (CVD) is the most common co-morbidity associated with COVID-19 and the fatality rate in COVID-19 patients with CVD is higher compared to other comorbidities, such as hypertension and diabetes. Preliminary data suggest that COVID-19 may also cause or worsen cardiac injury in infected patients through multiple mechanisms such as ‘cytokine storm’, endotheliosis, thrombosis, lymphocytopenia etc. Autopsies of COVID-19 patients reveal an infiltration of inflammatory mononuclear cells in the myocardium, confirming the role of the immune system in mediating cardiovascular damage in response to COVID-19 infection and also suggesting potential causal mechanisms for the development of new cardiac pathologies and/or exacerbation of underlying CVDs in infected patients. In this review, we discuss the potential underlying molecular mechanisms that drive COVID-19-mediated cardiac damage, as well as the short term and expected long-term cardiovascular ramifications of COVID-19 infection in patients.

Weight loss, malnutrition, and cachexia in COVID‐19: facts and numbers

“…Such therapies SGLT2 inhibitors—one trial with dapagliflozin is running in at least 900 COVID‐19 patients (DARE‐19, started during hospitalization, duration of treatment 30 days, see clinicaltrials.gov: NCT 04350593 33 ), but studies focusing on the post COVID‐19 disease process are lacking. COVID‐19 has a high potential to induce fibrosis in the lung, 34 in the heart, 35 and elsewhere in the body, which can also contribute to a chronic wasting processes. Because of this, we believe that therapy with mineralo‐corticoid receptor antagonists may also be useful in acute COVID‐19 and in the post COVID‐19 situation.…”

Outcomes and Risk Factors for Cardiovascular Events in Hospitalized COVID-19 Patients

“…Our study demonstrated 18% incidence of cardiovascular events and carried 45.2% mortality rate in this metropolitan sample population cohort. COVID-19 can cause cardiovascular complications or deterioration of coexisting cardiovascular diseases through direct or indirect mechanisms, including viral toxicity, dysregulation of the renin–angiotensin–aldosterone system, endothelial cell damage and thromboinflammation, cytokine storm, and oxygen supply–demand mismatch 24 , 25 . Published clinical studies suggested COVID-19 itself might induce myocardial injury, arrhythmia, acute coronary syndrome, and venous thromboembolism 5 , 26 , 27 .…”

Cardiovascular Health and Disease in the Context of COVID-19

“…Circulation of these pro-inflammatory cytokines activates the endothelium, creating an environment within blood vessels that is pro-coagulant/pro-aggregatory, anti-fibrinolytic, pro-inflammatory, pro-oxidant, and characterized by impaired barrier function and vasoconstriction [ 28 ]. Acute release of pro-inflammatory cytokines, including IL-1, IL-6 and plasminogen activator inhibitor (PAI-1), have also been associated with increased risk of heart failure with preserved ejection fraction [ 21 ], and chronic inflammation is known to be an important pathogenic driver of heart failure in general [ 29 ].…”

“…For example, the possibility exists that myocardial injury as a result of COVID-19 will result in atrial or ventricular fibrosis and a subsequent increased long-term risk for cardiac arrhythmias [ 33 ]. A number of investigators similarly suggest the potential for COVID-19 survival to ultimately be identified as an independent risk factor for later development of heart failure and other long-term cardiovascular sequelae including cardiac hypertrophy, cardiac fibrosis, chronic right heart failure, decreased cardiac output, diastolic dysfunction and pulmonary hypertension, particularly among those recovering from severe illness characterized by profound hypoxemia, respiratory failure and thromboembolic complications [ 22 , 29 ]. To mitigate these risks, Kochi et al recommend the use of c-MRI to stratify patents for follow-up [ 33 ].…”